Section 00.

1 - Table of CONTENTS -

00.1 Table of CONTENTS

00.2 Front Matter: TITLE Page
00.3 Acknowledgements/Copyright
00.4 About ECG-2014-ePub
00.5 About the Author/Other Material by the Author
00.6 ECG Crib Sheet
00.7 The 6 Essential Lists
01.0 Review of Basics
01.1 Systematic Approach to 12-Lead ECG Interpretation
01.2 The 2 Steps to Systematic Interpretation
01.3 WHY 2 Separate Steps for Interpretation?
02.0 Rate & Rhythm
02.1 Assessing the 5 Parameters of Rhythm
02.2 Calculating Rate: The Rule of 300
02.3 How to Define Sinus Rhythm?
02.4 FIGURE 02.4-1: Is the Rhythm Sinus?
02.5 Sinus Mechanism Rhythms/Arrhythmias
02.6 Norms for Children: Different than Adults
02.7 Sinus Arrhythmia
02.8 FIGURE 02.8-1: What Happens to the P in Lead II?
02.9 FIGURE 02.9-1: When there is NO long Lead II Rhythm Strip ...
02.10 Advanced POINT: What is a Wandering Pacemaker?
02.11 FIGURE 02.11-1: Why is this NOT Wandering Pacer?
02.12 Other Supraventricular Rhythms
02.13 FIGURE 02.13-1: Why is this Rhythm Supraventricular?
02.14 Atrial Fibrillation
02.15 Advanced POINT: Very Fast AFib Think WPW!
02.16 Multifocal Atrial Tachycardia
02.17 FIGURE 02.17-1: Why is this Not AFib?
02.18 Atrial Flutter
02.19 FIGURE 02.19-1: Easy to Overlook AFlutter ...
02.20 How NOT to Overlook AFlutter (Figure 02.19-1)
02.21 FIGURE 02.21-1: Vagal Maneuvers to Confirm AFlutter
02.22 FIGURE 02.22-1: Some KEY Aspects about AFlutter
02.23 TRACING B: AFlutter with 3:1 AV Conduction
02.24 TRACING C: AFib-Flutter

02.25 TRACING D: AFlutter vs Artifact

02.26 Use of VAGAL Maneuvers (Carotid Massage, Valsalva)
02.27 FIGURE 02.27-1: Clinical Response to Vagal Maneuvers
02.28 Using ADENOSINE = Chemical Valsava
02.29 PSVT/AVNRT
02.30 FIGURE 02.30-1: Retrograde Conduction with PSVT
02.31 The Every-other-Beat Method (for fast rates)
02.32 Junctional Rhythms
02.33 Junctional Rhythms: P Wave Appearance in Lead II
02.34 Junctional Rhythms: Escape vs Accelerated
02.35 Low Atrial vs Junctional Rhythm?
02.36 VENTRICULAR (= wide QRS) Rhythms
02.37 Slow IdioVentricular Escape Rhythm
02.38 AIVR
02.39 Ventricular Tachycardia
02.40 ESCAPE Rhythms: ECG Recognition
02.41 PRACTICE TRACINGS: What is the Rhythm?
02.42 PRACTICE: Tracing A
02.43 PRACTICE: Tracing B
02.44 PRACTICE: Tracing C
02.45 PRACTICE: Tracing D
02.46 PRACTICE: Tracing E
02.47 LIST #1: Regular WCT
02.48 List #1: KEY Points
02.49 Suggested Approach to WCT/Presumed VT
02.50 Use of the 3 Simple Rules
02.51 FIGURE 02.51-1: 12 Leads are BETTER than One
02.52 LIST #2: Regular SVT
02.53 The Regular SVT: Differential Diagnosis?
02.54 Suggested Treatment Approach for a Regular SVT
02.55 FIGURE 02.55-1: Which SVT is present?
02.56 Premature Beats
02.57 ESCAPE Beats: Timing is Everything ...
02.58 Narrow-Complex Escape Beats
02.59 PVC Definitions: Repetitive Forms and Runs of VT
02.60 Blocked PACs/Aberrant Conduction
02.61 PRACTICE Tracings-2: What is the Rhythm?
02.62 PRACTICE: Tracing F
02.63 PRACTICE: Tracing G
02.64 PRACTICE: Tracing H

02.65 PRACTICE: Tracing I

02.66 PRACTICE: Tracing J
02.67 AV Blocks / AV Dissociation
02.68 Blocked PACs: Much More Common than AV Block
02.69 The 3 Degrees of AV Block
02.70 1st Degree AV Block
02.71 The 3 Types of 2nd Degree AV Block
02.72 Mobitz I 2nd Degree AV Block (= AV Wenckebach)
02.73 Mobitz II 2nd Degree AV Block
02.74 2-to-1 AV Block: Mobitz I or Mobitz II?
02.75 3rd Degree (Complete) AV Block
02.76 PEARLS for Recognizing/Confirming Complete AV Block
02.77 AV Dissociation
02.78 FIGURE 02.78-1: Is there any AV Block?
02.79 SUMMARY: Complete AV Block vs AV Dissociation
02.80 High-Grade 2nd-Degree AV Block
02.81 Ventricular Standstill vs AV Block
02.82 Hyperkalemia vs AV Block
02.83 FIGURE 02.83-1: Is there any AV Block at all?
03.0 Doing an ECG / Technical Errors
03.1 Limb Leads: Basic Concepts/Placement
03.2 Why 10 Electrodes but 12 Leads?
03.3 Derivation of the Standard Limb Leads (Leads I,II,III)
03.4 The 3 Augmented Leads (Leads aVR,aVL,aVF)
03.5 The Hexaxial Lead System
03.6 Precordial Lead Placement
03.7 Use of Additional Leads
03.8 Technical Errors: Angle of Louis and Lead V1
03.9 Technical Mishaps: Important Caveats
03.10 Important Concepts: Lead Misplacement/Dextrocardia
03.11 Dextrocardia: ECG Recognition
03.12 PRACTICE: Identifying Technical Errors
03.13 PRACTICE: Tracing A
03.14 PRACTICE: Tracing B
03.15 PRACTICE: Tracing C
03.16 PRACTICE: Tracing D
03.16.1 ADDENDUM: Prevalence/Types of Limb Lead Errors
03.16.2 ECG Findings that Suggest Limb Lead Misconnection
03.17 PRACTICE: Tracing E
03.18 PRACTICE: Tracing F
03.19 PRACTICE: Tracing G

03.20 PRACTICE: Tracing H

03.21 PRACTICE: Tracing I
03.22 PRACTICE: Tracing J
03.23 PRACTICE: Tracing K
04.0 Intervals (PR/QRS/QT)
04.1 What are the 3 Intervals in ECG Interpretation?
04.2 The PR Interval: What is Normal?
04.3 The PR Interval: Clinical Notes
04.4 Memory Aid: How to Recall the 3 ECG Intervals
05.0 Bundle Branch Block/IVCD
05.1 The QRS Interval: What is Normal QRS Duration?
05.2 IF the QRS is Wide: What Next? (BBB Algorithm)
05.3 FIGURE 05.3-1: Why the Need for the BBB Algorithm?
05.4 Typical RBBB: Criteria for ECG Recognition
05.5 RBBB: Clinical Notes
05.6 Typical LBBB: Criteria for ECG Recognition
05.7 FIGURE 05.7-1: LBBB alters Septal Activation
05.8 FIGURE 05.8-1: Clinical Example of Complete LBBB
05.9 LBBB: Clinical Notes
05.10 Incomplete LBBB: Does it Exist?
05.11 IVCD: Criteria for ECG Recognition
05.12 IVCD: Clinical Notes
05.13 FIGURE 05.13-1: Clinical Example of IVCD
05.14 ST-T Wave Changes: What Happens with BBB?
05.15 FIGURE 05.15-1: Assessing ST-T Wave Changes with BBB
05.16 RBBB Equivalent Patterns
05.17 FIGURE 05.17-1: Is this RBBB?
05.18 Incomplete RBBB: How is it Diagnosed?
05.19 PRACTICE: Bundle Branch Block
05.20 PRACTICE: Tracing A
05.21 PRACTICE: Tracing B
05.22 PRACTICE: Tracing C
05.23 PRACTICE: Tracing D
05.24 Diagnosing BBB + Acute MI
05.25 Begin with the ST Opposition Rule
05.26 RBBB: You Can See Q Waves!
05.27 Underlying RBBB: How to Diagnose Acute MI?
05.28 Underlying LBBB: How to Diagnose Acute MI?
05.29 FIGURE 05.29-1: Acute STEMI despite LBBB/RBBB?
05.30 Diagnosing BBB + LVH

05.31 LBBB: What Criteria to Use for LVH/RVH?

05.32 RBBB: What Criteria to Use for LVH/RVH?
05.33 Brugada Syndrome
05.34 ECG Recognition: Distinction Between Type I and II
05.35 WHAT to DO? - when a Brugada Pattern is Found?
05.36 WPW (Wolff-Parkinson-White)
05.37 WPW: Pathophysiology / ECG Recognition
05.38 WPW: The Great Mimic of other Conditions
05.39 FIGURE 05.39-1: Recognizing WPW on a 12-Lead
05.40 FIGURE 05.40-1: Recognizing WPW
05.41 FIGURE 05.41-1: Atypical RBBB or WPW?
05.42 WPW Addendum #1: How to Localize the AP?
05.43 WPW: The Basics of AP Localization
05.44 FIGURE 05.44-1: Where is the AP?
05.45 FIGURE 05.45-1: Where is the AP?
05.46 FIGURE 05.46-1: Where is the AP?
05.47 Addendum #2: Arrhythmias with WPW
05.48 PSVT with WPW: When the QRS During Tachycardia is Narrow
05.49 Very Rapid AFib with WPW
05.50 Atrial Flutter with WPW
05.51 PSVT with WPW: When the QRS is Wide
05.52 FIGURE 05.52-1: VT or WPW? What to Do?
06.0 QT Interval / Torsades de Pointes
06.1 How to Measure the QT
06.2 LIST #3: Causes of QT Prolongation
06.3 A Closer Look at LIST #3: Drugs Lytes CNS
06.4 Conditions Predisposing to a Long QT/Torsades
06.5 The QTc: Corrected QT Interval
06.6 Torsades: WHY Care about QT Prolongation?
06.7 FIGURE 06.7-1: Torsades vs PMVT vs Something Else?
06.8 FIGURE 06.8-1: Is the QT Long?
06.9 FIGURE 06.9-1: Is the QT Long?
06.10 QTc Addendum: Using/Calculating the QTc
06.11 BEYOND-the-Core: Estimating the QTc Yourself
06.12 FIGURE 06.12-1: Approximate the QTc
06.13 FIGURE 06.13-1: Approximate the QTc
07.0 Determining Axis / Hemiblocks
07.0 Determining Axis / Hemiblocks

07.1 Overview: Limb Lead Location

07.2 AXIS: The Quadrant Approach
07.3 AXIS: The Concept of Net QRS Deflection
07.4 FIGURE 07.4-1: How to Rapidly Determine Axis Quadrant
07.5 AXIS: Refining the Quadrant Approach
07.6 FIGURE 07.6-1: What is the Axis?
07.7 FIGURE 07.7-1: What is the Axis?
07.8 FIGURE 07.8-1: What is the Axis?
07.9 Hemiblocks: LAHB and LPHB
07.10 Hemiblocks: Anatomic Considerations
07.11 Advanced Concept: LSFB (a 3rd type of Fascicular Block)
07.12 Hemiblocks: An Approach to Rapid ECG Diagnosis
07.13 LAHB: ECG Diagnosis = pathologic LAD
07.14 FIGURE 07.13-1: Is there LAD? IF so Is there LAHB?
07.15 SUMMARY: ECG Diagnosis of LAHB in 3 Seconds
07.16 Bifascicular Block
07.17 Definition/Types of Bifascicular Block
07.18 RBBB/LAHB: ECG Recognition
07.19 The Meaning of Axis when there is RBBB
07.20 Clinical Implications of Bifascicular Block
07.21 RBBB/LPHB: ECG Recognition
07.22 RBBB/LPHB: Finer Points on ECG Recognition
07.23 FIGURE 07.23-1: Is there Bifascicular Block?
07.24 FIGURE 07.24-1: Is there Bi- or Tri-Fascicular Block?
07.25 FIGURE 07.25-1: Isolated LPHB vs Right Axis Deviation?
08.0 LVH: Chamber Enlargement
08.1 ECG Diagnosis of LVH: Simplified Criteria
08.2 LVH: Physiologic Rationale for Voltage Criteria
08.3 LVH: ECG Diagnosis using Lead aVL
08.4 FIGURE 08.4-1: Is there Voltage for LVH?
08.5 Standardization Mark: Is Standardization Normal?
08.6 LVH: Additional Voltage Criteria
08.7 LVH: Voltage Criteria for Patients Less than 35
08.8 FIGURE 08.8-1: Which Leads for What with LVH?
08.9 LV Strain: ECG Recognition
08.10 LV Strain: Voltage for LVH vs True Chamber Enlargement
08.11 FIGURE 08.11-1: Is there True Chamber Enlargement?
08.12 Can there be both LV Strain and Ischemia?
08.13 Strain Equivalent Patterns: Clinical Implications
08.14 Atrial Enlargement
08.15 Terminology: Enlargement vs Abnormality?

08.16 FIGURE 08.16-1: ECG Criteria for RAA/LAA

08.17 Physiologic Rationale for Normal P Wave Appearance
08.18 A Closer Look: The P Wave with Normal Sinus Rhythm
08.19 ECG Diagnosis of RAA: P Pulmonale
08.20 ECG Diagnosis of LAA: P Mitrale
08.21 FIGURE 08.21-1: Is there ECG Evidence of RAA/LAA?
08.22 FIGURE 08.22-1: Is there ECG Evidence of RAA/LAA?
08.23 RVH/Pulmonary Disease
08.24 ECG Diagnosis of RVH: Simplified Criteria
08.25 ECG Diagnosis: Review of Specific RVH Criteria
08.26 RVH: Review of Additional Criteria
08.27 Schamroths Sign for RVH: A Null Vector in Lead I
08.28 RVH: Tall R Wave in V1; RV Strain
08.29 Schematic FIGURE 08.29-1: Example of RVH + RV Strain
08.30 Schematic FIGURE 08.30-1: Example of Pulmonary Disease
08.31 Pediatric RVH: A few Brief Thoughts ...
08.32 FIGURE 08.32-1: Is there RVH?
08.33 FIGURE 08.33-1: Is there RVH?
08.34 Acute Pulmonary Embolus
08.35 Acute PE: Key Clinical Points
08.36 FIGURE 08.36-1: Should You Look for an S1-Q3-T3?
08.37 FIGURE 08.37-1: The Cause of Anterior T Inversion?
08.38 FIGURE 08.38-1: Is there Acute Anterior STEMI?
09.0 Q-R-S-T Changes
09.1 FIGURE 09.1-1: Assessing Q-R-S-T Changes
09.2 Septal Depolarization: Reason for Normal Septal Q Waves
09.3 Precordial Lead Appearance: What is Normal?
09.4 Basic Lead Groups: Which Leads look Where?
09.5 R Wave Progression: Where is Transition?
09.6 Old Terminology: R Wave Progression CW, CCW Rotation
09.7 FIGURE 09.7-1: Poor R Wave Progression
09.8 FIGURE 09.8-1: Anterior MI vs Lead Placement Error?
09.9 FIGURE 09.9-1: What is the Cause of PRWP?
09.10 FIGURE 09.10-1: QS in V1,V2 vs Anterior MI?
09.11 FIGURE 09.11-1: PRWP from LVH vs Anterior MI?
09.12 FIGURE 09.12-1: Normal Q Waves; Normal T Inversion
09.13 FIGURE 09.13-1: Inferior Infarction/Ischemia?
09.14 ST Elevation: Shape/What is the Baseline?
09.15 ST Elevation or Depression: What is the Baseline?
09.16 J-Point ST Elevation: Recognizing the J-Point
09.17 SHAPE of ST Elevation: More Important than Amount!

09.18 HISTORY: Importance of Clinical Correlation

09.19 FIGURE 09.19-1: Early Repolarization or Acute MI?
09.20 What is EARLY REPOLARIZATION?
09.21 Early Repolarization: Variations in the Definition
09.22 ERP: Is Early Repolarization Benign?
09.23 FIGURE 09.23-1: Acute MI or Repolarization Variant?
09.24 FIGURE 09.24-1: Acute MI or Repolarization Variant?
09.25 ST Segment Depression
09.26 LIST #4: Causes of ST Depression
09.27 ST-T Wave Appearance: A Hint to the Cause
09.28 FIGURE 09.28-1: What is the Cause(s) of ST Depression?
09.29 Recognizing Subtle ST Changes: ST Segment Straightening
09.30 FIGURE 09.30-1: Are the ST Segments Normal?
09.31 Clinical Uses of Lead aVR
09.32 Lead aVR: Recognizing Lead Misplacement/Dextrocardia
09.33 Lead aVR: in Acute Pulmonary Embolus
09.34 Lead aVR: in Acute Pericarditis
09.35 Lead aVR: in Atrial Infarction
09.36 Lead aVR: in Supraventricular Arrhythmias
09.37 Lead aVR: for Definitive Diagnosis of VT
09.38 Lead aVR: in TCA Overdose
09.39 Lead aVR: in Takotsubo Syndrome
09.40 Lead aVR: Severe CAD/Left Main Disease
10.0 Acute MI / Ischemia
10.1 The Patient with Chest Pain: WHY Do an ECG?
10.2 What is a Silent MI?
10.3 The ECG in Acute MI: What are the Changes?
10.4 ECG Indicators: 1) ST Segment Elevation
10.5 ECG Indicators of Acute MI: 2) T Wave Inversion
10.6 ECG Indicators of Acute MI: 3) Q Waves
10.7 Q Waves: Why Do they Form?
10.8 ECG Terminology: Distinction between Q, q and QS waves?
10.9 Summary: When are Q Waves Normal?
10.10 ECG Indicators of Acute MI: 4) ST Segment Depression
10.11 Acute MI: The Sequence of ECG Changes
10.12 Variation in the Sequence of Acute MI Changes
10.13 KEY Points: ECG Changes of Acute MI
10.14 Assessing Acute ECG Changes
10.15 FIGURE 10.15-1: Use of Serial ECGs in Acute STEMI
10.16 The Coronary Circulation

10.17 Overview of Normal Coronary Anatomy & Variants

10.18 The RCA: Taking a Closer Look
10.19 The LEFT Coronary Artery: Taking a Closer Look
10.20 LEFT-Dominant Circulation: Taking a Closer Look
10.21 LAD Wrap-Around: Taking a Closer Look
10.22 Identifying the Culprit Artery
10.23 Acute RCA Occlusion
10.24 Acute LMain Occlusion
10.25 Acute LAD Occlusion
10.26 Anterior ST Elevation: Not Always an Anterior MI
10.27 Acute Occlusion of an LAD Wrap-Around
10.28 Acute LCx (Left Circumflex) Occlusion
10.29 Acute Right Ventricular Infarction
10.30 Acute RV MI: Hemodynamics
10.31 Acute RV MI: Use of Right-Sided Leads
10.32 Acute RV MI: Making the Diagnosis by ECG
10.33 Posterior MI: Use of the Mirror Test
10.34 BEYOND-the-Core: Is there Truly a Posterior Wall?
10.35 FIGURE 10.35-1: Applying the Mirror Test
10.36 FIGURE 10.36-1: Anatomic Landmarks for Posterior Leads
10.37 FIGURE 10.37-1: Isolated Posterior Infarction
10.38 Acute MI: PRACTICE Tracings
10.39 FIGURE 10.39-1: What is the Culprit Artery?
10.40 Schematic PRACTICE Tracings: Acute MI/Ischemia
10.40.1 FIGURE 10.40-1: Ischemia/Infarction?
10.40.2 FIGURE 10.40-2: Ischemia/Infarction?
10.40.3 FIGURE 10.40-3: Ischemia/Infarction?
10.40.4 FIGURE 10.40-4: Ischemia/Infarction?
10.40.5 FIGURE 10.40-5: Ischemia/Infarction?
10.40.6 FIGURE 10.40-6: Ischemia/Infarction?
10.40.7 FIGURE 10.40-7: Ischemia/Infarction?
10.40.8 FIGURE 10.40-8: How to Date an Infarct?
10.40.9 FIGURE 10.40-9: Ischemia/Infarction?
10.40.10 FIGURE 10.40-10: Ischemia/Infarction?
10.40.11 FIGURE 10.40-11: Ischemia/Infarction?
10.40.12 FIGURE 10.40-12: Ischemia/Infarction?
10.41 LIST #5: Ant. ST Depression with Acute Inf. MI
10.42 LIST #5: Causes of Anterior ST Depression
10.43 FIGURE 10.43-1: Ant. ST Depression with Acute Inf. MI

10.44 LIST #6: Tall R Wave in Lead V1

10.45 Normal Appearance of the QRS in Lead V1
10.46 The Purpose of List #6
10.47 LIST #6: Causes of a Tall R Wave in Lead V1
10.48 PRACTICE Tracings: The Cause of the Tall R in V1?
10.49 Hypertrophic Cardiomyopathy: How to Recognize on ECG?
10.50 FIGURE 10.50-1: WHY the Tall R in V1?
10.51 Giant T Wave Syndrome
10.52 When Inverted T Waves are GIANT in Size!
10.53 FIGURE 10.53-1: Cause of the Giant T Waves?
10.54 Wellens Syndrome
10.55 Wellens Syndrome: Clinical Implications & ECG Recognition
10.56 FIGURE 10.56-1: What Wellens Syndrome is Not!
10.57 DeWinter T Waves
10.58 ECG Recognition: What are DeWinter T Waves?
10.59 DeWinter T Waves: Clinical Characteristics
10.60 FIGURE 10.60-1: What is the Culprit Artery?
10.61 Takotsubo Cardiomyopathy
10.62 FIGURE 10.62-1: Acute STEMI or Something Else?
10.63 Takotsubo CMP: Clinical Features
10.64 Muscular Dystrophy
10.65 Muscular Dystrophy: Common ECG Abnormalities
10.66 FIGURE 10.66-1: Abnormal ECG in a Young Subject
10.67 Hypothermia (Osborn Wave)
10.68 FIGURE 10.68-1: ECG Features of Hypothermia
11.0 Electrolyte Disorders
11.1 CALCIUM: ECG Changes of Hyper- & HypoCalcemia
11.2 Figure 11.2-1: Acute STEMI or HyperCalcemia?
11.3 HYPERKALEMIA: ECG Manifestations/Clinical Features
11.4 Figure 11.4-1: Ventricular Rhythm vs Hyperkalemia?
11.5 Figure 11.5-1: Ischemia vs Hyperkalemia?
11.6 Figure 11.6-1: Hyperkalemia vs Normal Variant?
11.7 HYPOKALEMIA: ECG Manifestations/Clinical Features
11.8 HYPOMAGNESEMIA: Clinical Features/ ECG Signs
11.9 U Waves: Definition/Clinical Significance
11.10 Figure 11.10-1: Electrolyte Disturbance or Ischemia?
12.0 Acute Pericarditis

12.1 Acute Pericarditis: How to Make the Diagnosis?

12.2 ECG FINDINGS of Acute Pericarditis
12.3 Stage I of Acute Pericarditis
12.4 PR Depression: How Helpful a Sign is this?
12.5 What is Spodicks Sign?
12.6 Differential Diagnosis: Acute MI vs Early Repolarization?
12.7 Acute Myocarditis/Endocarditis: ECG Changes?
12.8 FIGURE 12.8-1: Acute MI or Pericarditis?
12.9 FIGURE 12.9-1: Pericarditis or Early Repolarization?
13.0 Computerized ECG Interpretations
13.1 Computerized Systems: Pros & Cons
13.2 Suggested Approach: How to Use the Computer
13.3 FIGURE 13.3-1: Do You Agree with the Computer?
14.0 Electrical Alternans
14.1 Electrical Alternans: Definition/Features/Mechanisms
14.2 Electrical Alternans: KEY Clinical Points
14.3 FIGURE 14.3-1: Alternans in an SVT Rhythm?
14.4 FIGURE 14.4-1: Alternans in a Patient with Lung Cancer?

Section 00.2 - Front Matter: TITLE PAGE

Mail KG/EKG Press; PO Box 141258; Gainesville, Florida 32614-1258

E-Mail [email protected]
Web site www.kg-ekgpress.com
Fax (352) 641-6137
ECG Blog www.ecg-interpretation.blogspot.com
ECG Competency www.ecgcompetency.com
Author Page www.amazon.com/author/kengrauer

Section 00.3 - Acknowledgements/Copyright

Sole Proprietor Ken Grauer, MD

Design of All Figures Ken Grauer, MD
Printing by Renaissance Printing (Gainesville, Florida)
Special Acknowledgement to Colleen Kay (for making the hard copy version of this book
happen) and to Jay (for all things technical).

Special Dedication:
To Cathy Duncan (who is my wife, my best friend, and the LOVE of My Life).

Additional Acknowledgements:
Rick & Stephanie of Iveys Restaurant (great food, staff and atmosphere that inspired my
ACLS creativity).
Abbas, Jane, Jenny & Gerald of the Haile Village Bistro (for great food at my other writing
space).

COPYRIGHT to ECG-2014-PB (Expanded Version):

1st Edition 1998 by KG/EKG Press.
2nd Edition (2000).
3rd Edition (2005).
4th Edition (2007).
5th Edition (2011) plus ePub-2011 edition.
6th Edition (2014) plus ePub-2014 edition.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or
transmitted in any form by any means, electronic, mechanical, recording, or otherwise without prior

written consent from the publisher.

ISBN # 978-1-930553-30-9 (# 1-930553-30-7)

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Section 00.4 About ECG-2014-ePub

Electrocardiography is not difficult. At least it is not difficult to obtain a basic understanding of the
art and apply this understanding to interpreting the majority of 12-lead ECGs and arrhythmias that
you will encounter. The most difficult part of electrocardiography is learning (and then
remembering) the various criteria used to diagnose complex ECG findings such as chamber
enlargement and bundle branch block.
Practically speaking there is much less to learn (and memorize) than most people think.
Herein lies the secret of the ECG Pocket Brain: it facilitates understanding of basic ECG
concepts and lightens the "memory load" by providing ready recall of those KEY facts and
figures needed for successful 12-lead interpretation.
We have completely revised and updated this 6th Edition (2014) of our book. We have more
than doubled our content enhanced our explanations and have greatly improved the quality
of our figures. This book now stands as an independent concise text on key aspects of ECG
interpretation.
Development of this ePub takes ECG-2014-PB (Expanded) to a higher level. Nothing beats the
instant access of a well organized electronic file.

Our goal is to provide key information fast. Near-instant access is now possible with this electronic
ePub. We suggest you begin your review of ECG-2014-ePub by an overview of our CONTENTS at
the front of this ePub.
There are immediate links to each subsection in our Contents.
Instant search and localization is facilitated by our new numbering system. For example
typing in 05.0 in the Search bar instantly brings up all places in this ePub where reference to
Section 05.0 on Bundle Branch Block is found.
NOTE-1: This ePub book begins in Section 01.0 with Review of Basics. We have intentionally
placed our ECG Crib Sheet in Section 00.6 before Section 01.0 so that it will be easy to find.
For readers who are less experienced in systematic ECG interpretation We suggest you refer
to the ECG Crib Sheet often. Doing so will facilitate ready recall of the 6 KEY parameters (of
Rate-Rhythm-Intervals-Axis-Hypertrophy-QRST Changes).
HINT: Making a bookmark Searching for, 00.6 or simply scrolling to the front of this
ePub are easy ways to rapidly access the ECG Crib Sheet.

Please CHECK OUT our ECG Crib Sheet!

NOTE-2: We have placed review of the 6 Essential Lists in Section 00.7. This also appears at the
front of this ePub (before Section 01.0) for ready access.

You will want to refer to these 6 Lists often until you know them by heart. With minimal practice
they will be easy to remember!
HINT: Making a bookmark Searching for, 00.7 or simply scrolling toward the front of
this ePub (just after the ECG Crib Sheet) are easy ways to rapidly access the 6 Essential Lists.

The choice is YOURS to either read through this ePub from beginning-to-end or to read
selectively depending on whatever topic you are looking up.

Please WRITE Me! = [email protected]. I want to know your impressions so that I can
improve on what I have written.
I sincerely hope you enjoy this ePub and find it valuable for increasing your comfort and
abilities in ECG interpretation.

Section 00.5 About the AUTHOR

About the Author www.kg-ekgpress.com/about/

Amazon Author Page amazon.com/author/kengrauer

12-Lead ECG Interpretation

ECG-2014-PB (Expanded) the hard copy version of this ePub (260 pages in the hard copy
book): www.kg-ekgpress.com/shop/item/30/
ECG-2011 Pocket Brain (5th Edition) which we still offer as a smaller Essentials version
(100 pages): www.kg-ekgpress.com/shop/item/1/
For Those Who Teach ECGs Please check out information about the following resources on my
web site (www.kg-ekgpress.com):
My ECG-PDF Course (lecture slides learner notes for any level of learner)
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Section 00.6 ECG Crib Sheet

00.6.1 The ECG Crib Sheet: How BEST to Use It

This ePub book begins in Section 01.0 with Review of Basics. We intentionally place this ECG
Crib Sheet before Section 01.0 so that it will be easy to access.
For readers who are less experienced in systematic ECG interpretation We suggest you refer
often to this ECG Crib Sheet. This will facilitate ready recall of the 6 KEY parameters in the
Systematic Approach (= Rate-Rhythm-Intervals-Axis-Hypertrophy-QRST Changes).
With regular use Youll quickly learn the information contained within this ECG Crib Sheet.
In case there is something you forget the Crib Sheet is always here for a quick refresher.
HINT: Making a bookmark Searching for, 00.6 or simply scrolling to the front of this
ePub are easy ways to rapidly access the ECG Crib Sheet.
NOTE: All parameters in our Systematic Approach to ECG interpretation are discussed in
detail throughout the pages of this ePub. We begin with Section 01.0 on Review of Basics and
continue through to Section 14.0. We simply want you to know that this ECG Crib Sheet
(Section 00.6) and Section 00.7 that follows (which reviews the 6 Essential Lists) are
located at the very front of this ePub in order to facilitate your ready access to this material.

00.6.2 The Systematic Approach: Rate & Rhythm

The first 2 parameters in the Systematic Approach are Rate and Rhythm. They are discussed in
detail in Section 02.0.
RATE If the rhythm is regular rate can easily be determined by the Rule of 300. Divide 300
by the number of boxes in R-R Interval (Section 02.2).
IF the rhythm is regular and rapid rate can be accurately estimated by the every-other-beat
method (Section 02.31) in which you figure out the rate for every-other-beat (which is half
the rate); and then double this number.
RHYTHM First ensure that the patient is hemodynamically stable. Then assess the 5 KEY
components for rhythm. These are conveniently remembered by the phrase: Watch your P's & Q's
and the 3 R's (Section 02.1).
Are there P waves? If so Are P waves upright in lead II?
P waves should always be upright in lead II IF there is sinus rhythm (unless there is lead

reversal or dextrocardia).
Is the QRS complex wide or narrow?
What is the Rate?
Is the rhythm Regular?
Are P waves Related (ie, "married" with fixed PR interval) to the QRS? If P waves are
married then they are being conducted to the ventricles.

00.6.3 Parameter #3: Intervals

INTERVALS Look at intervals at an early point in the process!
The PR Interval is prolonged IF >0.20-0.21 second (if clearly more than a LARGE box in
duration) Section 04.0.
The QRS Complex is wide IF >0.10 sec. (if more than HALF a large box in duration)
Section 05.0.
The QT Interval is prolonged IF clearly more than half the R-R interval (provided that
heart rate is not more than 100 beats/minute) Section 06.0. If the QT interval is prolonged
Think of Drugs-Lytes-CNS ( = List #3) as the possible cause(s) of QT prolongation
(Section 06.2).
KEY Clinical Point: IF the rhythm is sinus but the QRS is wide then STOP before going
further. Figure out WHY the QRS is wide be this due to RBBB, LBBB, IVCD, WPW (Section
05.2). Criteria for infarction, ischemia, and chamber enlargement will all be different IF there is a
conduction defect. This is the reason for determining early on the cause of QRS widening.
00.6.4 Parameter #4: Axis
Axis is discussed in detail in Section 07.0.
AXIS Determine the axis quadrant by looking at lead I (at 0 degrees) and lead aVF (at +90
degrees):
The axis is normal IF the net QRS deflection is positive in leads I and aVF (this defines the
axis to be between 0 degrees to +90 degrees).
There is RAD IF the net QRS deflection is negative in I but positive in aVF (Think RVH,
LPHB or normal variant as the common causes for RAD).
There is LAD IF the net QRS is positive in I but negative in aVF. There is pathologic LAD =
LAHB (Left Anterior HemiBlock) IF the net QRS deflection is more negative than positive
in lead II (Section 07.13).
The axis is indeterminate IF the net QRS deflection is negative in leads I and aVF (Think
RVH, COPD, obesity as the common causes of an indeterminate axis).

00.6.5 Parameter #5: Chamber Enlargement

Chamber Enlargement is discussed in detail in Section 08.0.
HYPERTROPHY (Chamber Enlargement):
The "magic numbers" for LVH are 35 (sum of the deepest S wave in V1,V2 plus the
tallest R wave in V5,V6 in a patient at least 35 years of age) and 12 (for R wave
amplitude in lead aVL) Section 08.1. True chamber enlargement is much more likely IF
"strain" also present!
There is RAA (P Pulmonale) IF P waves are prominent (2.5 mm tall) and peaked (ie,
"uncomfortable to sit on") in the pulmonary leads (II, III, and aVF) Section 08.19.
There is LAA (P Mitrale) IF P waves are notched ("m"-shaped) in mitral leads (I, II, or
aVL) or if the P wave in V1 has a deep terminal negative component Section 08.20.
Consider pulmonary disease IF there is RAA, RAD (or indeterminate axis), incomplete
RBBB (or rSr pattern in lead V1), low voltage, or persistent precordial S waves Section
08.24.
Consider RVH IF there is also a tall R wave in V1 and/or right ventricular "strain"
Section 08.24.
Criteria for LVH/RVH are different when there is BBB (Sections 05.31 and 05.32).
Consider acute pulmonary embolus IF the ECG shows signs of acute right heart strain
(Section 08.34).

00.6.6 Parameter #6: Infarct (= Q-R-S-T Changes)

Assessment of QRST Changes is discussed in detail in Section 09.0.
INFARCT (= Q-R-S-T changes) Look at all 12 leads on the ECG to assess for QRST Changes.
Lead aVR will usually be globally negative under normal circumstances (negative P wave,
QRS and T wave). We therefore expect to see a Q wave and T wave inversion in lead aVR as
part of a normal ECG.
The finding of an upright P, QRS and T wave in lead aVR should suggest the possibility of lead
misplacement (especially if lead I manifests global negativity) Section 03.10.
For the more experienced interpreter We suggest review of Sections 09.31-through-09.39,
which highlight situations for which attention to lead aVR may provide important additional
information.
NOTE: Localization of the Basic Lead Groups is shown in Figure 00.6.6-1. Lead localization is
discussed in detail in Section 09.4.

Figure 00.6.6-1: Basic Lead Groups.

Assessment of Q-R-S-T Changes:
Q Waves Small and normal septal q waves are commonly seen in one or more of the lateral
leads (I,aVL,V4,V5,V6).
Moderate or large-sized Q waves may be normal IF they occur as an isolated finding in one
or more of the following leads: leads III, aVF, aVL, and/or V1. Figure 00.6.6-2 suggests that
thinking of a reverse Z (as in Zorro) may help recall which leads may normally manifest a
large isolated Q wave (Section 09.12).

Figure 00.6.6-2: Reverse Z memory aid (Q waves/T inversion).

R Wave Progression Does transition occur as it normally should between leads V2-to-V4?
(Figure 00.6.6-3 Section 09.5).
Is there a Tall R in Lead V1? = List #6 (Section 10.47).
Normally the QRS is predominantly negative in right-sided lead V1. Is there an rSr pattern in
lead V1? (which could be a normal variant or incomplete RBBB) Section 05.18.

Figure 00.6.6-3: Precordial lead placement. Normal R wave progression.

ST Segments Judge ST segment deviation (elevation or depression) with respect to the PR

segment baseline (Section 09.25). Much more than the amount of ST segment deviation
Focus on shape ("smiley" or "frowny).
T Waves May normally be inverted in leads III, aVF, aVL and/or V1. Note that these are
the same leads that may normally manifest isolated Q waves (Figure 00.6.6-2).
Remember that criteria for ischemia/infarction are different when there is BBB (Sections 05.24through-05.29).

00.6.7 Suggested Approach: Systematic ECG Interpretation

As we discuss in Section 01.0 Use the elements in Sections 00.6.2 through 00.6.6 as a guide for
descriptive analysis; then formulate your clinical impression. Whenever possible WRITE OUT
(or at least think out) your findings. Above all, even when time is short BE systematic!

Section 00.7 The 6 Essential Lists

00.7.1 The 6 Lists: What They Are

We have developed 6 Essential Lists to remember for optimal ECG and arrhythmia interpretation.
The purpose of a List is that it readily recalls the most common/important causes to remember
for the particular entity. For example as soon as you recognize that the QT interval is prolonged
Think Drugs-Lytes-CNS as possible causes (= LIST #3).
We intentionally limit the number (and length) of our lists so as not to overwhelm. Use of these
6 Lists will prove invaluable to you in saving time and improving the accuracy of your
interpretation.
You will want to refer to these 6 Lists often until you know them by heart. With minimal practice
they will be easy to remember!
For clarity (and easy reference ) we reproduce the 6 Lists here. Youll find them again
intermingled with relevant content throughout this electronic file.
HINT: Making a bookmark Searching for, 00.7 or simply scrolling to the front of this
ePub are convenient ways to instantly access the 6 Essential Lists (The 6 Lists are found just
after the ECG Crib Sheet).

00.7.2 LIST #1: The Common Causes of a Regular WCT:

LIST #1 is discussed in detail in Section 02.47.
KEY Point: The 1st thing to do in assessment of any tachycardia is to ensure hemodynamic
stability. IF the patient is unstable immediately cardiovert! But IF the patient in WCT
(Wide-Complex Tachycardia) is stable you have at least a moment of time to contemplate
management.
Always assume a regular WCT rhythm is VT until proven otherwise (Figure 00.7.2-1). This
is true regardless of whether the patient is hypotensive or alert with a systolic BP>160mmHg.
Some patients may be stable and alert despite remaining in VT for hours (or even days)!
The reason we list VT as the first 8 causes in LIST #1 (Figure 00.7.2-1) is twofold: i) VT is
the worst thing the WCT could be; and ii) Statistically at least 80-90% of cases of WCT of
uncertain etiology will turn out to be VT.

Figure 00.7.2-1: LIST #1 = Causes of a Monomorphic Regular WCT. Always assume VT until
proven otherwise.
00.7.3 LIST #2: Common Causes of a Regular SVT:
LIST #2 is discussed in detail in Section 02.52.
We define the term, SVT as a rapid rhythm (rate >100/minute) in which the QRS
complex is narrow (not more than 0.10 second) in all 12 leads. The 3 entities included in
LIST #2 (Figure 00.7.3-1) make up over 90% of the causes of a regular SVT seen by primary
care or emergency providers.
Awareness of the usual rate ranges for these 3 common causes of SVT may help with distinction
between them:
Sinus Tachycardia rarel y exceeds 160/minute in adults (children may have sinus
tachycardia at much faster rates).
Untreated Atrial Flutter usually conducts with 2:1 ratio. Since the atrial rate of untreated
atrial flutter is almost always close to 300/minute (250-350/minute is the range) this means
that the ventricular response to AFlutter will usually be between 140-to-160/minute.
As a result IF a regular SVT in an adult is faster than 160-170/minute it is most likely to
be PSVT (= AVNRT = AtrioVentricular Nodal Reentry Tachycardia).
On the other hand A regular SVT rhythm at a rate under 160-170/minute could be any of the
3 entities on LIST #2 (Fig. 00.7.3-1).
NOTE: A vagal maneuver or use of Adenosine (= chemical Valsalva) may help in making a
definitive diagnosis.

Figure 00.7.3-1: LIST #2 = Causes of a Regular SVT.

00.7.4 LIST #3: Common Causes of QT Prolongation:

LIST #3 is discussed in detail in Section 06.2.
Be aware that in addition to the 3 entities in LIST #3 (Figure 00.7.4-1) ischemia/MI/BBB
may all lengthen the QT. That said IF the only ECG abnormality on the tracing is a long QT
Think Drugs-Lytes-CNS as the likely cause. Then correlate clinically.
NOTE: Many combinations of drugs may contribute to lengthening the QT interval. These
potential drug-drug interactions extend beyond the scope of this ECG-ePub and are not
reflected in List #3. Suffice it to say that risk of QT prolongation (and risk of Torsades ) is
generally minimal IF an otherwise healthy adult takes a single new drug for a limited period
of time. Risk goes up when several agents are taken especially if the drugs utilize the p450
system for metabolism and the patient has other underlying medical problems that may
predispose to Torsades. BOTTOM Line: Consider the possibility of Drugs (or drug-drug
interactions) as one of the main clinical causes of QT prolongation.

Figure 00.7.4-1: LIST #3 = Causes of a Prolonged QT.

00.7.5 LIST #4: Common Causes of ST Segment Depression:
LIST #4 is discussed in detail in Section 09.26.
There are over 50 causes of ST depression. Many of these causes are noncardiac related to
factors such as hyperventilation, temperature extremes, severe medical illness. The entities in
LIST #4 (Figure 00.7.5-1) are simply the ones we feel it most important to remember.
A similar list of entities as shown in List #4 may produce T wave inversion.

Figure 00.7.5-1: LIST #4 = Causes of ST Depression.

00.7.6 LIST #5: Causes of Anterior ST Depression with Inferior MI:
LIST #5 is discussed in detail in Section 10.42.
Use of LIST #5 (Figure 00.7.6-1) is limited to the setting of acute inferior STEMI. The
purpose of List #5 is to remind us of the 3 common causes of anterior ST depression in this
situation.
Helpful General Rule: The more ST depression that is seen on the ECG the more likely the
MI is both acute and large.
Clinically we may not be able to determine with certainty which of the 3 entities in List #5
is/are operative. This does not matter! What counts is awareness of a more extensive MI (that
is more likely to benefit from acute intervention) when significant anterior ST depression is
seen in conjunction with acute inferior infarction.

Figure 00.7.6-1: LIST #5 = Causes of Anterior ST Depression in the Setting of Acute Inferior MI.
00.7.7 LIST #6: Common Causes of a Tall R in Lead V1:
LIST #6 is discussed in detail in Section 10.47.
Normally the QRS is predominantly negative (a QS or rS complex) in right-sided lead V1. As a
result, the finding of even a relatively tall R wave in lead V1 (that equals or exceeds S wave
amplitude in this lead) should prompt consideration of the 6 entities on LIST #6 (Figure
00.7.7-1).
Determining which of the 6 entities in List #6 is present is decided by assessing associated
ECG findings. A normal variant ( Cause #6) should be considered only after the first 5 causes
have been ruled out.
Not all patients need an Echo. On occasion, however an Echo may be needed to rule out
structural heart disease (especially if hypertrophic cardiomyopathy is a consideration).

Figure 00.7.7-1: LIST #6 = Causes of a Tall R Wave in Lead V1.

Section 01.0 Review of Basics

01.1 Systematic Approach to 12-Lead ECG Interpretation

The KEY to interpretation of any ECG is to utilize a Systematic Approach. The approach we suggest
for interpreting each 12-lead ECG you encounter entails sequential systematic assessment of the
following parameters:
Rate
Rhythm
Intervals (PR/QRS/QT )
Axis
Hypertrophy
Infarct (QRST changes )
We outline KEY elements to assess for each of the above parameters on our ECG Crib Sheet (See
Section 00.6). Discussion here is limited to the following:
The purpose of having (and regularly using) a sequential systematic approach is simple: It
provides you with an easy-to-remember mental checklist that prevents you from overlooking
potentially important findings.
Additional benefits include increased accuracy, improved organization, and surprisingly
increased speed in completing your interpretation. With regular use applying the system soon
becomes automatic!

01.2 The 2 Steps to Systematic Interpretation

The process of 12-lead ECG interpretation should be thought of as consisting of two major steps.
The secret to successful interpretation depends on keeping these 2 steps separate in your mind:
Step #1 = Descriptive Analysis is accomplished first: Simply describe what is seen on the
tracing (as per the checklist review on the ECG Crib Sheet in Section 00.6). Ideally WRITE
OUT your findings (or at least THINK out your findings if you do not have time to write them
out).
Step #2 = The Clinical Impression should only come after Step #1 has been completed.
Those specific findings identified in descriptive analysis should now be interpreted in light of
the clinical context (ie, as defined by the patient's age, presenting complaint, and additional
relevant clinical history).

01.3 WHY 2 Separate Steps for Interpretation?

Review of the ECG shown in Figure 01.3-1 provides insight as to why there is need for 2 separate
steps to interpretation.

Figure 01.3-1: How would you interpret this 12-lead ECG?

Answer to Figure 01.3-1: We interpret the 12-lead ECG shown above by the 2-Step Systematic
Approach:
Step #1 (Descriptive Analysis):
Rate and Rhythm Sinus arrhythmia at a rate of between 60-70 beats/minute.
Intervals (PR/QRS/QT) are normal.
Axis There is RAD (Right Axis Deviation) with a mean QRS axis of ~ +100 degrees.
Hypertrophy None.
Q-R-S-T changes Small Q waves in inferolateral leads; R wave progression is normal
(transition occurs between leads V3-4); Assessment of ST-T wave changes reveals fairly deep
symmetric T wave inversion in anterior precordial leads (arrows in Fig. 01.3-1).
Step #2 (Clinical Impression) It depends! That is How we would interpret the ECG in Figure
01.3-1 will vary greatly depending on the age and clinical history of the patient.
Symmetric T wave inversion as seen in the anterior leads (V1,V2,V3) of Fig. 01.3-1 is common
in pediatric patients. In an otherwise healthy child (with no heart murmur) this finding
represents a benign normal variant (referred to as a Juvenile T Wave Pattern).
BUT the same ECG (with identical T wave inversion) would have to be interpreted very
differently IF the patient in question was an older adult with chest pain (in which case ischemia
would be suggested). And, if new-onset dyspnea was the primary concern from the history
acute pulmonary embolism would also have to be considered (Section 08.34).
KEY Clinical Point: Descriptive Analysis is the same in both cases (= symmetric T wave
inversion in V1-to-V3) but the Clinical Impression is very different!

Bottom Line: Keep Steps #1 and 2 separate in your mind. Always do Descriptive Analysis first!
Then decide on your Clinical Impression of the findings identified in light of the clinical situation
(age of patient; clinical history).

02.0 Rate & Rhythm

02.1 Assessing the 5 Parameters of Rhythm

The most important clinical point (and the real KEY to rhythm interpretation) is to utilize a
Systematic Approach. The system we favor is based on assessing the rhythm for the following 5
parameters:
P waves?
QRS width ?
Regular rhythm ?
Related (P waves related to QRS ? )
Rate (heart rate ? )
Memory Aid (to remember the 5 Parameters):
"Watch your P's and Q's and the 3 R's"
NOTE: It does not matter in what sequence you look at these 5 parameters for rhythm as long as
you always check each of them every time you look at an ECG or rhythm strip! We often begin with
that parameter that is easiest to assess (be this presence of P waves, QRS width or regularity).
First Ensure that the patient is hemodynamically stable (precise rhythm diagnosis is of
secondary importance if the patient is acutely decompensating and about to code) . Always
look at the patient first before beginning to study the rhythm.
IF there is normal sinus rhythm then P waves should be present and clearly upright in lead
II (See Section 02.3).
In adults, the QRS is defined as narrow IF it is 0.10 second = not more than HALF a large
box in duration (Figure 02.1-1).

Figure 02.1-1: Is the QRS wide? Normally in adults the QRS should not be more than half a large

box in duration (= not more than 0.10 second).

Regularity Look to see IF the rhythm is regular?
Determine if P waves are "Related" to QRS complexes (ie, conducting) Look in front of
each QRS to see IF there is a P wave with a fixed PR interval.
Rate is most easily calculated by the Rule of 300 (Section 02.2).

02.2 Calculating Rate: The Rule of 300

Provided that the rhythm is regular the Rule of 300 states that heart rate can be estimated IF you
divide 300 by the number of large boxes in the R-R interval. The rule is derived as follows:
With the ECG machine set at the standard recording speed of 25 mm/second the time required
to record each little box on ECG grid paper is 0.04 second (Figure 02.2-1). Vertically each
little box is 1 mm in amplitude (a measurement we will use often in assessing for chamber
enlargement).
As seen in Figure 02.2-1 the time required to record each large box on ECG grid paper is
0.20 second. That is there are 5 little boxes in each large box, and 5 X 0.04 second = 0.20
second ( = 1/5th of a second).

Figure 02.2-1: Deriving the Rule of 300 (See text).

Thus, the time required to record 5 large boxes will be one full second (0.20 X 5 = 1.0 sec) . IF a
QRS complex occurs each large box (as in Figure 02.2-1) then the R-R interval will be 0.20
second and the rate of the rhythm is 300 beats/minute (ie, 5 beats occur each second X 60
seconds/minute = a rate of 300/minute).
IF the R-R interval is 2 large boxes then the rate will be half as fast (ie, 300 2 = 150
beats/minute).

IF the R-R is 3 boxes, the rate = 100/minute (300/3).

IF the R-R is 4 boxes, the rate = 75/min (300/4)
NOTE: Use the every-other-beat method when the rhythm is regular and the rate is fast (See
Section 02.31).
02.3 How to Define Sinus Rhythm?
By definition (under normal circumstances, assuming the heart lies in the left side of the thorax)
the P wave should always be upright in standard lead II when the mechanism of the rhythm is
sinus. This is because the overall direction of the electrical depolarization wavefront as it travels
from the SA node toward the AV node and the ventricles is oriented toward standard lead II, which
lies at +60 degrees in the frontal plane (Panel A in Figure 02.3-1).
The only 2 exceptions to the above stated rule (ie, when the rhythm may still be sinus despite a
negative P wave in lead II) are: i) if there is dextrocardia; or ii) if there is lead misplacement.

Figure 02.3-1: IF the rhythm is sinus then the P wave should always be upright in lead II (Panel
A). The only exception is IF there is dextrocardia or lead misplacement. Therefore Panel B is not
a sinus rhythm (See text).
In contrast to the situation with sinus rhythm the P wave will not be positive (upright) in lead II
when the electrical impulse originates from the AV node ( Panel B in Figure 02.3-1). Instead
spread of atrial activation is now directed away from lead II.
Therefore, with junctional beats or junctional (AV nodal) rhythm a negative P wave may be
seen to precede the QRS complex in lead II (Panel B in Fig. 02.3-1).
Alternatively (with AV nodal rhythm) a negative P wave may follow the QRS or no P wave
at all is seen in lead II.

02.4 FIGURE 02.4-1: Is the Rhythm Sinus?

Interpret the 3 rhythm strips shown in Figure 02.4-1.

How can you tell at a glance IF the rhythm is sinus? (Assume no dextrocardia and no lead
misplacement).

Figure 02.4-1: How to tell IF the rhythm is sinus?

Answer to Figure 02.4-1: The very 1st thing we do when assessing any cardiac rhythm or 12-lead
ECG is to look for a lead II rhythm strip. It takes no more than 2 brief seconds to look in front of
each QRS in lead II.
Panel A (in Figure 02.4-1) Regular upright P waves precede each QRS with fixed PR
interval in this lead II. Therefore there is NSR (Normal Sinus Rhythm). The QRS is narrow
(not more than half a large box ) and the ventricular rhythm is regular with an R-R interval
just under 4 large boxes in duration. IF the R-R interval was precisely 4 large boxes in duration
then by the Rule of 300 the rate would be 300/4 = 75/minute (Section 02.2). Since the R-R
interval is slightly less than 4 large boxes in duration the rate must be slightly faster than
75/minute, or about 78/minute.
Panel B (in Figure 02.4-1) does not represent sinus rhythm. It cant (provided there is no
dextrocardia or lead misplacement) since the QRS in lead II is not preceded by an upright P
wave. Whether the rhythm in Panel B represents AV nodal or low atrial rhythm is less important.
The KEY point is that the rhythm is not sinus!
Otherwise the QRS is narrow and the rhythm is regular with an R-R interval of 4 large boxes
in duration. Therefore the rate = 300/4 = 75/minute. The negative P waves in this lead II are
conducting because the PR interval preceding each QRS is fixed!
Panel C (in Figure 02.4-1) is not a sinus rhythm (since no P wave at all is seen). The QRS
is narrow and the rhythm is regular with an R-R interval of 6 large boxes. Therefore, the rate =
300/6 = 50/minute. This is an AV nodal rhythm (See Sections 02.32-to 02.34).

02.5 Sinus Mechanism Rhythms/Arrhythmias

Once the mechanism of the rhythm is defined as sinus the rate (and regularity) of the rhythm
determine our terminology. There are 4 principal sinus mechanism rhythms (Figure 02.5-1):
NSR (Normal Sinus Rhythm) regular rhythm with a rate between 60-99/minute in an adult
(Panel A in Figure 02.5-1). Norms for rate differ in children (Section 02.6).
Sinus Bradycardia regular sinus rhythm at a rate below 60/minute (Panel B). The rate here is
50/minute.
Sinus Tachycardia sinus rhythm at a rate of 100/minute or faster in an adult (Panel C in Fig.
02.5-1).
Sinus Arrhythmia an irregular rhythm despite the presence of a sinus mechanism (Figure
02.7-1 Section 02.7).

Figure 02.5-1: Sinus mechanism rhythms (See text).

02.6 Norms for Children: Different than Adults
Normal limits for heart rate are different in children. While we primarily concern ourselves with the
adult ECG in this book it is nevertheless helpful to be aware of some differences between
pediatric and adult findings.
Rate limits are different in children with norms depending on the age of the child. Much
more important than specific cut-off points for each age category is appreciation of the
general concept that slightly faster rates (say ~110/minute ) may be normal for a crying but
otherwise healthy young child. By the same token a rate within the seemingly normal range
of 65/minute might be relatively slow for an active young child. Clinical context is everything!
Upper limits for PR and QRS interval duration are also different (shorter) in the smaller
pediatric heart (Section 04.3).
Similarly Escape rate ranges differ in children. Whereas the normal AV nodal escape
rate in an adult is between 40-to-60/minute it is between 50-80/minute in a young child.
Therefore, the AV nodal rhythm at 75/minute seen below in Figure 02.6-1 would be slightly
fast IF the patient was an adult but is clearly within the normal AV nodal escape rate range IF
the patient is a child (See also Sections 02.32-to-02.34 on AV nodal rhythms).

Figure 02.6-1: AV nodal rhythm at 75/minute (See text).

02.7 Sinus Arrhythmia
Sinus Arrhythmia is a common normal variant in infants and young children. At times, variability in
sinus rate may be marked in which case one might initially think some other arrhythmia is present.
Sinus Arrhythmia is confirmed by the finding of identical-appearing P waves that are
upright in lead II with fixed PR interval (Figure 02.7-1). In contrast other phenomena
(wandering atrial pacemaker; sinus rhythm with PACs ) will manifest changes in P wave
morphology and/or in the PR interval. The P waves will be different!

Figure 02.7-1: Sinus Arrhythmia. Despite irregularity in the rhythm sinus mechanism is present as
defined by regularly-occurring upright P waves with fixed PR interval preceding each QRS complex
in this lead II rhythm strip (See text).
Sinus arrhythmia often exhibits respiratory variation. This is especially true in healthy young
children for whom some variation in sinus regularity is the norm rather than the exception.
Sinus arrhythmia is a normal cardiac rhythm in this setting.
Some degree of sinus variability (ie, sinus arrhythmia) may persist in young and even older
adults. This is not necessarily abnormal. Clinical correlation is key.
Beyond-the-Core: The technical definition of sinus arrhythmia is that sinus-initiated R-R
intervals vary by at least 0.08-0.12 second (2-3 little boxes). This definition is clearly satisfied in
Figure 02.7-1. That said, most of the time the presence of sinus arrhythmia (vs sinus rhythm) is
of little-to-no clinical significance.
An exception to the statement that sinus arrhythmia is benign occurs in older patients with SSS
(Sick Sinus Syndrome). Among the many manifestations of SSS (which include sinus pauses,
sinus arrest, tachy- as well as bradyarrhythmias) sinus bradycardia with sinus arrhythmia
is the most common. The usual course of SSS is prolonged over years (if not decades). Many
patients who go on to develop full-fledged symptoms (with need for a permanent pacemaker)
manifest no more than sinus bradycardia/sinus arrhythmia for a period of many years. Therefore
the finding of an inappropriately slow and variable sinus rhythm in an older patient with

symptoms of fatigue, worsening heart failure and/or syncope/presyncope is cause for potential
concern. IF not due to rate-slowing drugs, ischemia or hypothyroidism Consider SSS as the
probable cause.

02.8 FIGURE 02.8-1: What Happens to the P in Lead II?

Although specifics of the rhythm diagnosis in Figure 02.8-1 are advanced the concept of routinely
seeking out a long lead II rhythm strip each time you interpret a 12-lead ECG is fundamental!
Always begin with this step.

Figure 02.8-1: What happens to the P wave in this lead II rhythm strip? (See text).
Answer to Figure 02.8-1: Use the Ps, Qs & 3R Approach to assess the rhythm. As noted Section
02.1 it does not matter in what sequence you look at the 5 parameters (as long as you check them
all each time you assess an ECG):
The overall rhythm in Figure 02.8-1 is not regular.
The QRS complex is narrow.
Each QRS is preceded by a P wave BUT the shape of these P waves is not the same. The
rhythm begins with a taller peaked P wave with fixed PR interval preceding beats #1,2,3; and
#7,8. A 2nd P wave shape ( of smaller amplitude and notched) is then seen to precede beats
#4,5,6. Thus, the underlying rhythm in Figure 02.8-1 is sinus arrhythmia with transient
change to another atrial focus for beats #4,5,6 followed by resumption of the original sinus
focus at the end of the tracing.
Key Points about Figure 02.8-1: In our experience the most common error in 12-lead ECG
interpretation is failure to recognize when normal sinus rhythm is not present. The solution is easy:
Ideally there will be a simultaneously recorded long lead II rhythm strip. IF so Begin by:
i) assessing IF the rhythm is regular; and ii) Looking to see IF P wave morphology stays the
same throughout the rhythm strip.
It suffices to recognize that the underlying rhythm in Figure 02.8-1 is sinus with a change in P
wave morphology. It is easy to see this as long as you consciously look at P wave shape before
each QRS.
It is clearly more difficult without a long lead rhythm strip. How would you assess the rhythm
in Figure 02.9-1?

02.9 FIGURE 02.9-1: When there is NO long Lead II Rhythm Strip

The reality is that you will not always have access to a long lead rhythm strip. This was the case
for the 12-lead ECG previously shown in Figure 01.3-1 (Section 01.3). We reproduce that 12-lead
tracing below in Figure 02.9-1:
How would you assess the rhythm in Figure 02.9-1?
How many total beats are there on this 12-lead ECG?

Figure 02.9-1: 12-lead ECG previously shown in Figure 01.3-1. How many total beats are there on
this tracing? What is the rhythm? Unfortunately there is no long lead II rhythm strip (See text).
Answer to Figure 02.9-1: The problem is that only 3 beats are seen in lead II of this ECG (arrows)
before the leads switch to simultaneous recording of leads aVR/aVL/aVF. In addition the R-R
interval for these 3 beats that are seen in lead II is not the same (ie, the R-R interval between beats
#1-2 is longer than the R-R between beats #2-3). That said, we can still diagnose the mechanism as
sinus because a similarly-shaped upright P wave with fixed PR interval precedes each of these 3
beats in lead II (red arrows in Figure 02.9-1).
There are 9 total beats on this tracing. With simultaneous 3-channel recordings we get 3
looks at each beat (vertical time line in leads I II III ). The QRS is narrow. Note
irregularity of the R-R interval for beats #1-thru-9. Thus the rhythm is sinus arrhythmia.

02.10 Advanced POINT: What is a Wandering Pacemaker?

Occasionally the site of the atrial pacemaker may shift (wander) away from its usual site of origin
in the SA (Sino-Atrial) Node. In most cases wandering atrial pacemaker is a benign normal
variant that occurs in patients without underlying heart disease. It may result from variations in vagal
tone (that slow SA nodal discharge and allow other atrial sites to temporarily emerge ) or there
may be no obvious cause (Figure 02.10-1).

ECG recognition of wandering pacer requires a long enough rhythm strip to appreciate
gradual change over a period of beats from one P wave morphology to another. While possible
that the rhythm in Figure 02.8-1 could reflect a wandering pacemaker this rhythm strip is
simply not long enough to tell.

Figure 02.10-1: Wandering pacemaker. Initially the P wave in lead II is an upright sinus complex (1st
red arrow preceding beat #4 ) with gradual change to an isoelectric P wave (1st blue arrow
preceding beat #5) followed by resumption of sinus rhythm with beat #17 (2nd red arrow in
bottom rhythm strip). It would be easy-to-overlook the diagnosis of wandering pacer IF one did not
pay careful attention to P wave morphology!
Bottom Line: True wandering atrial pacemaker is not a common diagnosis. As noted it is
difficult to recognize because most 12-lead ECGs (even if accompanied by a simultaneous lead II
rhythm strip) will simply not be long enough to manifest gradual transition back-and-forth between
SA node and two or more additional atrial sites. The point to emphasize for interpreters of any
experience level is the need to always look carefully at lead II when assessing for atrial activity:
Is an upright sinus P wave present in lead II?
Does P wave morphology change during the rhythm?
Is the underlying rhythm regular? Are there any early beats?

02.11 FIGURE 02.11-1: Why is this NOT Wandering Pacer?

While not yet worrying about the specific diagnosis Why is wandering pacer not present in Figure
02.11-1?

Figure 02.11-1: Why is wandering pacemaker not present in either of the rhythm strips shown here?
Answer to Figure 02.11-1: The rhythm in Panel A is MAT ( See Section 02.16). There are too many
different P waves that change from beat-to-beat for this to be wandering pacer. In Panel B the
underlying rhythm is sinus. Beats #3 and #6 are PACs; they occur early and P shape is different
(See Section 02.56).
True wandering pacemaker should manifest gradual transition from one P wave morphology to
another and then either on to yet another atrial pacemaker site or back to the original focus.
This gradual transition was seen in Figure 02.10-1. It is definitely not seen in either Panel A or
B of Figure 02.11-1.

02.12 Other Supraventricular Rhythms

A supraventricular rhythm is defined to be one in which the electrical impulse originates at or above
the AV node (at or above the double dotted line in Figure 02.12-1).
The good news is that the number of sites from where a supraventricular impulse may
arise is limited. These include: i) the SA Node; ii) from somewhere in the atria; or iii) the AV
node. Awareness of this clinical reality greatly facilitates arrhythmia diagnosis because once
you establish that the QRS complex in an adult is truly narrow in all 12 leads you are
virtually assured that the rhythm is supraventricular (>99% of the time)!
The exception (occurs 0.1% of the time) in which a narrow QRS may arise from a
ventricular site in an adult is IF the impulse originates from the His, fascicles or bundle
branches.
The above generality does not hold true in children (the QRS is normally narrower in the
smaller pediatric heart).

Figure 02.12-1: IF the QRS is truly narrow in all 12 leads then for practical purposes the rhythm
is supraventricular (and therefore originates from at or above the double dotted red line in this
Figure). NOTE: The opposite is not true. That is the etiology of a rhythm is not at all certain IF
the QRS is wide (could be either ventricular or supraventricular See Figure 02.13-1).
Other Supraventricular Rhythms: In addition to the sinus mechanism rhythms (Section 02.5) the
other principal entities in the supraventricular rhythm category include:
AFib (Atrial Fibrillation) See Section 02.14.
MAT (Multifocal Atrial Tachycardia) See Section 02.16.
AFlutter (Atrial Flutter) See Section 02.18.
PSVT/AVNRT See Section 02.29.
Junctional (AV nodal) rhythms See Sections 02.32-to-02.34.
NOTE: Although there are many types of supraventricular rhythms those listed above make up
the great majority of rhythms that primary care and emergency providers most often will see.
Unless there is preexisting bundle branch block or aberrant conduction the QRS will be
narrow IF the rhythm is supraventricular.

02.13 FIGURE 02.13-1: Why is this Rhythm Supraventricular?

Despite the slow rate and very wide QRS complex WHY is the rhythm in Figure 02.13-1
supraventricular?

Figure 02.13-1: Despite the wide QRS Why is this rhythm supraventricular?
Answer to Figure 02.13-1: By the Ps, Qs & 3R Approach We interpret the rhythm in Figure
02.13-1 as follows:

Regular wide QRS rhythm at ~40/minute.

Upright P waves precede each QRS complex with a fixed and normal PR interval in this lead II
rhythm strip. Therefore the rhythm is sinus bradycardia with QRS widening as a result of
preexisting BBB (Bundle Branch Block).

02.14 Atrial Fibrillation

AFib (Atrial Fibrillation) is characterized by the presence of an irregularly irregular rhythm in
the absence of P waves (Figure 02.14-1). Undulations in the baseline (known as fib waves) may
sometimes be seen. Such fib waves are coarse in Tracing B of Fig. 02.14-1 fine in Tracing C
and are barely detectable in Tracing A.
As might be imagined the diagnosis of AFib is clearly more difficult when fib waves are of
minimal amplitude (in which case diagnosis is based solely on recognizing an irregularly
irregular rhythm in the absence of P waves).

Figure 02.14-1: Atrial fibrillation (See text).

KEY Clinical Point: Far better than simply saying the rhythm is AFib is to clarify the
ventricular response. Thus, AFib will conduct with either a rapid, controlled, or slow ventricular
response:
AFib with a rapid ventricular response is present IF the average rate is over ~120/minute
(Tracing A in Fig. 02.14-1) . New-onset AFib is most often rapid (unless slowed by drugs,
ischemia/infarction or sick sinus syndrome).
AFib with a controlled ventricular response is present IF the average rate of AFib is
between ~70-110/minute (Tracing B in Fig. 02.14-1). An important goal of medical treatment is
to attain rate control.
AFib with a slow ventricular response is present IF the average rate is less than 5060/minute (Tracing C). New-onset slow AFib is unusual and should suggest a different set of

diagnostic consideration (rate-slowing drugs; hypothyroidism; ischemia/infarction; sick

sinus).
Clinical PEARL: When AFib is rapid the irregularity in the rhythm may be subtle. As a result
rapid AFib may sometimes simulate PSVT. We see this toward the end of Tracing A (in Fig. 02.141).
Calipers may be needed to verify that the rhythm is in fact irregular throughout the tracing.

02.15 Advanced POINT: Very Fast AFib Think WPW!

The usual rate range for rapid A Fib is between ~110-180/minute . IF ever the rate of A Fib is
significantly above this (ie, >200-220/minute) the patient probably has an AP ( Accessory
Pathway) that is bypassing the AV node (ie, WPW = Wolff-Parkinson-White Syndrome).
The intrinsic refractory period of the normal AV node generally does not allow conduction of
more than 200-220 impulses per minute.

Figure 02.15-1: The QRS complex is wide. AFib is diagnosed by the irregular irregularity in the
absence of P waves. The rate attains 250-300/minute in parts of the tracing. This is virtually
diagnostic of WPW (See Section 05.49).
02.16 Multifocal Atrial Tachycardia
AFib should be distinguished from MAT (Multifocal Atrial Tachycardia) in which the rhythm is
also irregularly irregular, but in which definite P waves are present (arrows in Figure 02.16-1).
Note that P wave morphology changes from beat-to-beat with MAT which is what distinguishes
MAT from wandering atrial pacemaker ( Se e Figure 02.10-1). The name tells all about its ECG
appearance: Multiple Atrial foci (P waves) are seen at a fast rate (ie, Tachycardia).
In our experience MAT is the 2nd most commonly overlooked arrhythmia diagnosis (next to
AFlutter). MAT is easy to overlook because the overwhelming majority of sustained
irregular SVT rhythms are AFib.
Clinically MAT is most often seen in patients who have either: i) pulmonary disease or ii)
severe multisystem problems (sepsis, shock, acidosis, electrolyte abnormalities, etc.). The best
way to avoid overlooking MAT is to think of this diagnosis whenever you see an irregularly
irregular rhythm in either of the above settings.
12 leads are better than one. You may not always see different P wave shapes in a single

monitoring lead. Get a 12-lead ECG and look for atrial activity in all 12 leads.

Figure 02.16-1: MAT is distinguished from AFib by the presence of multiple different-looking P
waves. The importance of recognizing MAT is its different treatment (Section 02.17).
02.17 FIGURE 02.17-1: Why is this Not AFib?
Why is the irregularly rhythm seen in Figure 02.17-1 not AFib? HINT: This ECG was obtained from
a patient with COPD (Chronic Obstructive Pulmonary Disease).
Can you see atrial activity in some of the 12 leads? If so in which ones?
Clinically Why is it important to make the correct rhythm diagnosis?

Figure 02.17-1: What is the rhythm on this 12-lead ECG? What else do you see on this tracing that
supports your rhythm diagnosis? 152
Answer to Figure 02.17-1: The rhythm is irregularly irregular. The QRS complex is narrow. The
rhythm in Fig. 02.17-1 is not AFib because P waves are clearly seen in lead II. P waves are also
seen in leads III and aVF but not in other leads.
P wave morphology in lead II changes from beat to beat. This observation plus knowing this
patient has COPD helps to solidify the ECG rhythm diagnosis of MAT.
Additional support of the diagnosis of MAT is forthcoming from recognition of several ECG
findings that suggest significant pulmonary disease. These include: i) Schamroths sign (very
low QRST amplitude in lead I) ; ii) tall pointed P waves in lead II among the P wave
morphologies seen; and iii) persistence of precordial S waves through to V5,V6 (See Section
08.33).

The clinical importance of recognizing MAT ( and distinguishing it from AFib) is that
treatment of these two entities is different! Treatment of MAT is best directed at correcting
the underlying cause (optimizing oxygenation in this case). In contrast Treatment of AFib
focuses on rate control; converting the rhythm; and anticoagulation considerations.
KEY Clinical Point: Rather than a discrete entity think of MAT as part of a spectrum. At one end
is sinus rhythm with occasional PACs ( Tracing B in Figure 02.11-1). At the other is MAT in
which P wave morphology (and the PR interval) change from beat-to-beat. Along the way you may
see sinus rhythm with multiple PACs ( but not quite enough beat-to-beat change to diagnose
MAT).
Clinically implications of the various arrhythmias that may be seen throughout this spectrum
are similar. These are to diagnose and treat the underlying disorder as first priority (usually
hypoxemia from pulmonary disease; electrolyte or acid-base disturbance; other metabolic
problems).

02.18 Atrial Flutter

AFlutter (Atrial Flutter) is characterized by a special pattern of regular atrial activity that in
adults almost always (and almost magically) occurs at a rate of 300/minute (250-350/minute =
usual range). Atrial flutter typically manifests a sawtooth appearance that is usually best seen in the
inferior leads although at times, flutter waves may be subtle and only seen in a few leads (Figure
02.18-1).
The most common ventricular response to atrial flutter (by far!) is with 2:1 AV conduction. As
a result, the ventricular rate with untreated atrial flutter will usually be close to 150/minute (ie,
~300 2). NOTE: The atrial rate may slower IF antiarrhythmic drugs are used.
Less commonly with AFlutter there is 4:1 AV conduction ( ventricular rate ~75/minute) or a
variable (= irregular) ventricular response.
Odd ratios (ie, 1:1, 3:1, 5:1) are possible but extremely uncommon (unless the patient has
WPW or is already on antiarrhythmic drugs).

Figure 02.18-1: Atrial Flutter with 2:1 AV conduction ( Tracing A ). Note how much easier it is to
identify AFlutter when the AV conduction ratio is slower ( as it is with 4:1 AV conduction in Tracing

B). Tracing B shows the effect that a vagal maneuver might have (See Sections 02.26, 02.27).
02.19 FIGURE 02.19-1: Easy to Overlook AFlutter
In our experience AFlutter is by far the most commonly overlooked rhythm diagnosis. It is easy
to overlook because flutter waves may not always be evident in the lead you are monitoring.
Always suspect AFlutter (until proven otherwise) whenever there is a regular SVT at
~150/minute without clear sign of normal atrial activity. This is precisely what is seen in
(Figure 02.19-1). The patient was stable.

Figure 02.19-1: There is a regular SVT (narrow QRS rhythm) at a rate of ~150/minute. Normal
atrial activity is not seen (no clear upright P wave is evident in this lead II monitoring lead). IF the
patient is stable Look for atrial activity in other leads!
IF the patient is hemodynamically stable and tolerating the tachycardia then a look at additional
leads may facilitate diagnosis:
A 12-lead ECG is obtained (Figure 02.19-2). Note how this helps to verify our suspicion of
non-sinus atrial activity (red and blue arrows).

Figure 02.19-2: 12-lead ECG obtained on the patient whose initial rhythm was shown in Figure
02.19-1.
02.20 How NOT to Overlook AFlutter (Figure 02.19-1)
We were not initially certain of the rhythm diagnosis in Figure 02.19-1. We assessed this rhythm as a
regular narrow-complex tachycardia (ie, a regular SVT) at a rate of ~150/minute without sinus P
waves.

We saw one ( if not two) negative deflections within each R-R interval in Figure 02.19-1
suggesting atrial activity.
Remembering the statement: AFlutter until proven otherwise for any regular SVT at
~150/minute without sinus P waves We suspected this diagnosis (but were not certain).
Since the patient was hemodynamically stable (as they usually will be with SVT rhythms)
We obtained a 12-lead ECG (Figure 02.19-2). The 12-lead confirmed that the QRS was truly
narrow in all leads. It also suggested regularly occurring atrial activity at rapid rate in many
leads (red and blue arrows in Figure 02.19-2).
NOTE: There is no indication of atrial activity during the regular SVT in several leads in Fig.
02.19-2 (leads I, aVL,V6). Flutter waves are not always seen in all leads. That said leads with the
arrows clearly demonstrate that the deflections we see are real.
PEARL Using Calipers: Use of calipers greatly facilitates the diagnostic process. There is
no easier way to identify if baseline deflections are regularly occurring or not. Using calipers
enables us to diagnose AFlutter simply from the 12-lead tracing shown in Figure 02.19-2
(arrows).

02.21 FIGURE 02.21-1: Vagal Maneuvers to Confirm AFlutter

Confirmation of AFlutter as the rhythm diagnosis for Figure 02.19-1 was forthcoming following
application of a vagal maneuver (Figure 02.21-1).
Note transient slowing of the ventricular response after the large arrow (vagal maneuver)
revealing regular atrial activity at ~300/minute. The only rhythm that does this is atrial flutter.
Beyond-the-Core: Whether or not a vagal maneuver was truly needed in this case to confirm
AFlutter vs sufficient comfort in this diagnosis from simply reviewing the 12-lead ECG in
Figure 02.19-2 would depend on the experience level, expertise and practice preferences of
the treating clinician. Clinically We would be less inclined to use IV adenosine once we
know the rhythm is AFlutter (since adenosine wont convert AFlutter ) and more inclined to
treat with an AV nodal blocking agent ( diltiazem, beta-blocker) while contemplating more
definitive measures.

Figure 02.21-1: A vagal maneuver is applied (large arrow) to the rhythm initially shown in Figure
02.19-1. The vagal maneuver temporarily slows AV nodal conduction thereby revealing
underlying atrial activity at 300/minute (smaller red arrows ). The only rhythm that does this is

AFlutter.
02.22 FIGURE 02.22-1: Some KEY Aspects about AFlutter
Given the elusiveness of AFlutter We highlight some advanced special characteristics of this
rhythm by the 4 tracings shown in Figure 02.22-1:
How would you interpret each tracing in this Figure?
Which concept regarding recognition/differential diagnosis of AFlutter do you think is illustrated
by each example?

Figure 02.22-1 (Tracings A,B,C,D): How does each tracing relate to diagnosis or misdiagnosis of
AFlutter?
ANSWER to Tracing A (in Figure 02.22-1):
As noted in Section 02.18 there may be a variable ventricular response to AFlutter (Tracing
A). Despite irregular irregularity that would otherwise suggest AFib the diagnosis of
AFlutter is secure in Tracing A from the precisely regular sawtooth pattern of atrial activity
seen here at a rate just over 300/minute.

02.23 TRACING B: AFlutter with 3:1 AV Conduction

Figure 02.23-1: What is unusual about the example of AFlutter shown in Tracing B?
Answer to Tracing B:
The rhythm in Tracing B (initially seen as B in Fig. 02.22-1) is another example of
AFlutter, this time with 3:1 AV conduction. As noted in Section 02.18 odd conduction ratios
are extremely uncommon in AFlutter. That said they can be seen on occasion. The diagnosis
of AFlutter is secure in Tracing B from recognition of precisely regular atrial activity (arrows)
at a rate of ~300/minute. Nothing else does this. We count 3 flutter waves within each R-R
interval.

02.24 TRACING C: AFib-Flutter

Figure 02.24-1: Is the rhythm in Tracing C AFib or AFlutter?

Answer to Tracing C:
The rhythm in Tracing C (initially seen as C in Fig. 02.22-1) shows a slow, irregularly
irregular rhythm with narrow QRS and underlying atrial activity. Initially the rhythm looks like
AFlutter but toward the end of the tracing baseline undulations look more like AFib. Although
often referred to as AFib-Flutter the important clinical point is that the rhythm behaves as
AFib. Although technically this rhythm is best classified as very slow AFib We would also
accept interpretation as AFib-Flutter as a descriptive term that perhaps most accurately conveys
the ECG picture in Tracing C.

02.25 TRACING D: AFlutter vs Artifact

Figure 02.25-1: Is atrial activity in Tracing D real? What do you suspect the rhythm is? How might
you confirm this?
Answer to Tracing D:
The rhythm in Tracing D (initially seen as D in Fig. 02.22-1) is not AFlutter. Instead the
numerous small undulations that populate the baseline represent artifact. We know the rhythm in
Figure 02.25-1 is not AFlutter because: i) We can see regular underlying P waves ( arrows in
Figure 02.25-2) ; ii) These P waves are unaffected by the baseline artifact: iii) the artifact
undulations are too fast and irregular to be AFlutter; and iv) We looked at the patient ( who
manifested an obvious resting tremor).

Figure 02.25-2: Arrows highlight sinus P waves in Tracing D. These sinus P waves are
superimposed on baseline artifactual undulations.
02.26 Use of VAGAL Maneuvers (Carotid Massage, Valsalva)
Vagal maneuvers are commonly used to facilitate ECG diagnosis and/or to treat certain cardiac
arrhythmias. Vagal maneuvers work by producing a transient increase in parasympathetic tone
thus temporarily slowing conduction through the AV node. This was seen in Figure Figure 02.21-1
in which the vagal maneuver facilitated ECG diagnosis of AFlutter.
Carotid Sinus Massage (CSM) Always perform under constant ECG monitoring. Use the
right carotid first. Never press on both carotids at the same time. Remember that the carotid
sinus is located high in the neck at the angle of the jaw! (green arrow in Figure 02.26-1).

Figure 02.26-1: Carotid massage (See text).

Additional points to consider about CSM include:

Warn patient that the maneuver will be uncomfortable ( as very firm pressure is needed for
success). Apply enough pressure to indent a tennis ball.
Rub for no more than 3-5 seconds at a time.
IF no response may repeat CSM on the left side.
Don't do CSM if patient has a carotid bruit (as you may dislodge a carotid plaque).
Always monitor the patient on ECG! Mark the time you start carotid massage and the time
you stop (which provides hard copy of what occurred ). ECG changes with CSM may be quite
subtle (which is another reason to get a hard copy rhythm strip recording during the time
CSM is done).
Valsalva Have patient supine. Forcibly exhale (bear down) against a closed glottis (as if trying to
go to the bathroom) for up to 15 seconds at a time. If properly performed may be even more
effective than CSM!
02.27 FIGURE 02.27-1: Clinical Response to Vagal Maneuvers
Know the response you are looking for before beginning (Figure 02.27-1).
At times reapplication of a vagal maneuver after administration of an AV nodal blocking
drug (ie, diltiazem; a blocker) may work, whereas it didnt work before the drug was given.
A similar response as is described in Figure 02.27-1 would be expected with chemical
valsalva (from diagnostic/therapeutic use of Adenosine).

Figure 02.27-1: What to expect from CSM/Valsalva.

02.28 Using ADENOSINE = Chemical Valsava
Adenosine is an extremely useful drug for treatment of SVT. It will rapidly convert most PSVT
and it usually produces transient slowing of other SVT rhythms which may be diagnostic (as it is in
Figure 02.28-1).
Adenosine may also convert 5-10% of VT (Ventricular Tachycardia) rhythms especially
outflow track VT that is prone to develop in younger adults without underlying heart disease. For
this reason current ACLS Guidelines recommend trial of Adenosine early in the course of
treating either narrow or wide tachycardias of uncertain etiology.

Figure 02.28-1: Administration of Adenosine (chemical valsalva) was diagnostic of SVT

etiology in this patient (arrows reveal underlying AFlutter at ~300/minute ). But in so doing a
period of over 10 seconds ensued without a QRS complex. Marked bradycardia like this is not
uncommon following Adenosine. Bradycardia almost always resolves within 30-60 seconds (due to
the drugs ultra-short half-life ). Other transient side effects of Adenosine may include chest
pressure; flushing; bronchospasm; metallic taste; a feeling of impending doom. (Be sure to tell the
patient these effects are short-lived!).
NOTE: Fortunately Using Adenosine early in the treatment of a regular WCT (Wide-Complex
Tachycardia) of uncertain etiology is unlikely to be harmful (given the ultra-short half-life of the
drug). The good news is that doing so may convert many SVT rhythms it will be diagnostic
in others and it may even convert a small percentage of VT rhythms.
Beyond-the-Core: Adenosine is unlikely to work for VT with wide QRS in a patient with
ischemic heart disease. As a result we generally favor omitting it from the treatment protocol
of such patients.
Be aware that conversion of a regular WCT to sinus rhythm following use of Adenosine does
not prove a supraventricular etiology (since the drug may convert a small percentage of VT
rhythms).

02.29 PSVT/AVNRT
PSVT (Paroxysmal SupraVentricular Tachycardia) is a regular supraventricular tachycardia
that most often occurs at a rate between 150-to-240/minute (Figure 02.29-1). Atrial activity is usually
not evident although subtle notching or a negative deflection (representing retrograde atrial
activity) may sometimes be seen at the tail end of the QRS.

Figure 02.29-1: PSVT (regular SVT without sinus P waves at ~200/minute). Rate is calculated by
the every-other-beat method (See Section 02.31).

Mechanistically PSVT is a reentry tachycardia that involves at least some portion of the AV
node (Figure 02.29-2). This accounts for the other name for this rhythm = AVNRT (AV Nodal
Reentry Tachycardia).
PSVT is often initiated by a PAC ( which arrives early at the AV Node at a time when
conditions are just right to allow the reentry circuit to be set up ). Once set up the
impulse continues to circulate within the AV Node ( Figure 02-29-2) until the reentry
pathway is either interrupted (ie, by AV nodal blocking drugs or a vagal maneuver) or until
it stops spontaneously.
Of note, each time the impulse circulates around the AV Node it conducts a QRS down to the
ventricles and also conducts retrograde back up to the atria (Fig. 02.29-2).

Figure 02.29-2: PSVT. Schematic illustration of reentry involving a portion of the AV Node. Each
time the impulse circulates around the AV node it conducts a QRS down to the ventricles and also
conducts retrograde back up to the atria.
02.30 FIGURE 02.30-1: Retrograde Conduction with PSVT
Most of the time, atrial activity will not be seen during PSVT because the retrograde P wave will
be hidden within the simultaneously occurring QRS complex.
Beyond-the-Core: On occasion you will see notching in the terminal portion of the QRS
complex during PSVT (Figure 02.30-1). When present this retrograde atrial activity
indicates a reentry mechanism is operative as the mechanism of the SVT. Clinically reentry
SVT rhythms are more likely to respond to vagal maneuvers and/or use of Adenosine.
Beyond-the-Core: Confirmation that notching in the terminal portion of the QRS complex truly
represents retrograde atrial activity from a reentry SVT can be forthcoming by obtaining a
post-conversion 12-lead ECG. Once sinus rhythm has resumed this notching in the terminal
portion of the QRS should no longer be seen.

Figure 02.30-1: PSVT. Subtle notching is seen in the terminal portion of the QRS in several (but not
all) leads (arrows). Identification of such retrograde atrial activity during a regular SVT rhythm
indicates a reentry mechanism is operative.
02.31 The Every-other-Beat Method (for fast rates)
Accurate determination of heart rate is essential for assessment of the various SVTs
(SupraVentricular Tachycardias). When the rhythm is regular and the rate is fast calculating rate
is most easily accomplished using the "Every-other-Beat" Method (Figure 02.31-1):
The R-R interval of every-other-beat for the PSVT rhythm in Figure 02.31-1 is precisely 3
large boxes in duration.
Therefore half the rate will be 100/minute (300 divided by 3).
This means that the actual rate in Figure 02.31-1 must be twice this amount (= 100/minute X 2 =
200/minute).

Figure 02.31-1: PSVT (previously shown in Figure 02.29-1). Heart rate is estimated by the everyother-beat method. Since the R-R interval of every-other-beat is 3 large boxes in duration half
the rate = 100/minute (300/3). The actual rate is therefore twice this amount = 200/minute.
02.32 Junctional Rhythms
Junctional (or AV Nodal) rhythms are regular supraventricular rhythms in which atrial activity
reflects an AV Nodal site of origin ( Figure 02.32-1). As opposed to NSR (Normal Sinus Rhythm)
in which conduction begins in the SA Node and travels downward (left panel in Figure 02.32-1)
electrical activity begins in the AV Node with junctional beats or rhythm (right panel) and is
conducted backward (ie, retrograde) or away from Lead II. As a result, when a P wave is seen in
lead II with junctional beats or junctional rhythm it will be negative (since electrical activity is

traveling away from standard lead II in its path back to the atria).

Fig. 02.32-1: Anatomic site of origin for sinus rhythm (left) vs AV Nodal beats or AV Nodal
(junctional) rhythm (right). As shown in the inserts the P wave in lead II will be upright with
sinus rhythm (left insert) but negative when a P wave is seen with junctional rhythm (right insert).
02.33 Junctional Rhythms: P Wave Appearance in Lead II
The 3 possible scenarios for P wave appearance with junctional rhythms is best illustrated by
laddergram (Figure 02.33-1) . Relative speed of conduction backward (to depolarize the atria)
compared to forward speed of conduction (to depolarize the ventricles) will determine IF the P
wave in lead II is:
Negative before the QRS (Panel B of Figure 02.33-1) as would occur if it takes less time to
conduct back to atria than forward to ventricles.
Negative after the QRS (Panel D) as would occur if it takes more time to conduct back to
atria.
Absent completely as would occur IF it takes approximately equal time to conduct back to
atria as down to ventricles (such that the retrograde P wave is hidden within the QRS as
seen in Panel C).

Fig. 02.33-1: Laddergram of the 3 possibilities for P wave appearance in lead II with junctional beats
or junctional rhythm. Panel A illustrates the normal forward conduction of sinus rhythm. The
impulse originates in the SA Node travels through the atria slows down a bit as it passes
through the AV Node and is then transmitted down through the conduction system to the ventricles.
NOTE: With junctional beats (or junctional rhythm) the impulse originates from the AV Node .
It then travels back (retrograde) to the atria and down to the ventricles. As a result the P wave in
lead II may be negative appearing either before (Panel B) or after (Panel D) the QRS or no P

wave at all may be seen (Panel C). Clinically Situation C is most common, whereas it is rare to
see a P wave after the QRS (situation D).
02.34 Junctional Rhythms: Escape vs Accelerated
There are 3 basic types of junctional rhythms with the type determined by the rate of the rhythm
(Figure 02.34-1):
AV Nodal Escape Rhythm when the junctional rate in an adult is between 40-60/minute
(See Rhythm X in Figure 02.34-1). An AV Nodal escape rhythm arises because the SA Node
is either delayed or fails in its pacemaking function NOTE: This is not necessarily a
pathologic rhythm!
Accelerated Junctional Rhythm when the junctional rate speeds up to between 61-99/minute
(Tracing Y) at which point it takes over the pacemaking function from the SA Node.
Junctional Tachycardia when the rate exceeds 100/minute (Tracing Z).

Figure 02.34-1: Junctional rhythms. NOTE: Although we show no P wave in X and a negative P
wave (before and after the QRS) in Y, Z it is rate that determines the type of rhythm.
Clinical Notes: Junctional Rhythms T he KEY to assessing the clinical significance of a
junctional rhythm is appreciation of the setting in which it occurs:
Junctional escape (40-60/minute) may be seen on occasion in otherwise healthy young
adults without clinical consequence.
The same is true in children (and adolescents) for whom the normal escape rate is a bit
faster (50-80/minute).
In contrast accelerated junctional rhythms (in which the AV Node speeds up) typically
occur in a limited number of clinical situations (acute MI; post-operative state; congenital
heart disease; shock; digoxin toxicity). Recognition should prompt concern. The rhythm usually
resolves by treating the underlying condition.
PEARL: Regardless of the serum digoxin level Think Dig Toxicity until proven
otherwise whenever you see an accelerated junctional rhythm (albeit this is less common
nowadays given current reduced use of digoxin).
Final Note: Clinical implications of accelerated vs junctional tachycardia are the same (the

only difference is whether the rate is over or under 100/minute).

02.35 Low Atrial vs Junctional Rhythm?

Beyond-the-Core: Technically a rhythm with a negative P wave preceding each QRS complex
with fixed PR interval could be coming from a low atrial site instead of from the AV Node ( Figure
02.35-1):
Beats originating from either the AV Node (Point X in Panel A of Fig. 02.35-1) or from a low
atrial site (Point Y in Panel B) will both be perceived as moving away from lead II as they
conduct back to depolarize the atria. As a result a negative P wave may precede the QRS
complex in either case.
Practically speaking it does not matter whether a beat or rhythm is of junctional or low atrial
origin, because clinical implications are similar in each case.

Figure 02.35-1: The presence of a negative P wave before the QRS may also be seen with low atrial
as well as junctional beats or rhythm. Atrial depolarization moves away from lead II (red arrows )
when impulse origin is from either the AV node (X) or from a site low in the atria (Y).
02.36 VENTRICULAR (= wide QRS) Rhythms
With the exception of the chaotic variability of VFib (Ventricular Fibrillation) the sustained
ventricular rhythms are most often regular (or at least fairly regular) rhythms that originate from a
site in the ventricles.
The QRS complex is wide because the ventricular origin of these rhythms is outside the
conduction system. The QRS looks very different than sinus beats.
Ventricular rhythms may arise either as escape rhythms (if supraventricular pacemakers fail)
or as usurping rhythms (when the ventricular focus accelerates and takes over the
pacemaking function from the preexisting supraventricular pacemaker).
P waves with ventricular rhythms may be: i) absent; ii) unrelated to the QRS complex; or
iii) retrograde.

Types of Ventricular Rhythms: There are 3 basic types of ventricular rhythms with the type
determined by the rate of the rhythm:
Slow IVR (IdioVentricular Rhythm) Section 02.37.
AIVR (Accelerated IdioVentricular Rhythm) Section 02.38.
VT (Ventricular Tachycardia) Section 02.39.

02.37 Slow IdioVentricular Escape Rhythm

The term slow IVR is used to describe a regular (or at least somewhat regular) ventricular rhythm
(wide QRS; no conducting P waves) when the ventricular rate is between 20-40/minute. This is
the usual rate range of an intrinsic ventricular escape focus. As a result slow IVR is often referred
to as an IdioVentricular escape Rhythm (Figure 02.37-1):

Figure 02.37-1: Slow IVR. The ventricular rhythm is regular at a rate of ~38/minute (the R-R interval
= 8 large boxes; 300/8 ~38/minute). The QRS is wide. No P waves are seen.
Clinical Note: The occurrence of slow IVR is often an ominous finding that is commonly
seen during the course of cardiac arrest. It may also arise as a ventricular escape rhythm in a
patient with complete AV block.

02.38 AIVR
AIVR (Accelerated IdioVentricular Rhythm) is said to be present when the rate of the
ventricular rhythm is more than 40/minute but does not exceed 110-120/minute (Figure 02.38-1):
AIVR (also called slow VTach) is a relatively common escape rhythm that may be seen in
patients with acute MI and/or during reperfusion therapy. It may also occur as a rhythm of
cardiac arrest. No treatment is needed IF the patient is asymptomatic (as this rhythm typically
resolves on its own). Do not give antiarrhythmic drugs (the drugs may abolish the only escape
rhythm the patient has).

Figure 02.38-1: AIVR. The ventricular rhythm is regular at a rate of 75/minute (300/4). This is faster

than slow idioventricular escape but slower than VT. Otherwise the QRS is wide; there are no
P waves.
02.39 Ventricular Tachycardia
VT (Ventricular Tachycardia) is said to be present when the rate of the ventricular rhythm
exceeds 120-130/minute (Figure 02.39-1):
By definition VT is always a usurping rhythm, in that the ventricular focus accelerates
and takes over pacemaking from the preexisting supraventricular pacemaker. Prompt (if not
immediate) treatment is essential.

Figure 02.39-1: VT. The ventricular rhythm is regular at a rate of ~150/minute ( 300/2). The QRS is
wide; No P waves.
NOTE: There exists a gray zone in which the ventricular rhythm occurs at a rate between
110-to130/minute. This falls in between the rate range for fast VT (Section 02.39) and the rate
range for slow VT (Section 02.38).
02.40 ESCAPE Rhythms: ECG Recognition
IF for whatever reason sinus (or other atrial rhythm) fails an escape rhythm will hopefully arise
from either: i) the AV Node; or ii) the Ventricles (Figure 02.40-1).
The rate range for the various escape pacemakers is easy to remember because it steps
down sequentially from the lower limit of 60/minute for sinus rhythm (Figure 02.40-1).

Figure 02.40-1: Escape rhythms. AV Nodal Escape (Rhythm A) is recognized by the presence of
a narrow QRS rhythm; rate between 40-60/minute. Ventricular Escape (Rhythm B) is recognized

by the presence of a wide QRS rhythm; rate between 20-40/minute.

02.41 PRACTICE TRACINGS: What is the Rhythm?

Interpret the following 5 arrhythmias (Sections 02.42-thru-02.46) . All rhythm strips are obtained
from Lead II. The patient was hemodynamically stable in each case. Our answers follow after each
tracing.
Hint Use the Ps/Qs and 3R systematic approach for interpreting each rhythm (Section
02.1).

02.42 PRACTICE: Tracing A

Interpret the lead II rhythm strip in Figure 02.42-1. The patient is hemodynamically stable.

Figure 02.42-1: Practice Tracing A.

ANSWER to Tracing A: The rhythm is slightly irregular, with a rate between ~55-65/minute. The
QRS complex is narrow and is regularly preceded by an upright P wave with constant PR interval in
this lead II monitoring lead. This is sinus bradycardia and arrhythmia (Section 02.7).
Sinus arrhythmia is a common normal variant rhythm especially when seen in otherwise
healthy children or young adults.
Sinus arrhythmia is not always benign. Together with sinus bradycardia it may sometimes be
the initial manifestation of SSS (Sick Sinus Syndrome). Therefore History is everything! IF
the rhythm in Figure 02.42-1 was obtained from an otherwise healthy and asymptomatic young
adult no further follow-up or treatment is indicated.

02.43 PRACTICE: Tracing B

Interpret the lead II rhythm strip in Figure 02.43-1. The patient is hemodynamically stable.

Figure 02.43-1: Practice Tracing B.

ANSWER to Tracing B: The rhythm is regular at 75/minute (the R-R interval is 4 large boxes and
300 4 =75/minute). The QRS complex is narrow. It is not preceded by any P waves. Thus, this is
a n AV Nodal Rhythm, albeit one that is slightly accelerated over the usual 40-60/minute rate
expected for junctional escape in an adult (Sections 02.32-thru-02.34).
The fact that no P wave at all is seen in this lead II rhythm strip is abnormal. This means that the
impulse is not originating from the SA node.
It is important to know the age of this patient. The normal AV node escape rate in children is
between 50-80/minute. On occasion transient AV nodal escape may be seen in otherwise
healthy children. Therefore this tracing would not necessarily indicate any cardiac pathology
IF it was obtained from an otherwise healthy child.
Always consider the possible reasons why a patient may be in an AV nodal rhythm
especially when the escape rate is slightly accelerated (as it would be if the rhythm in Fig.
02.43-1 was obtained from an adult). If the patient is taking Digoxin Digitalis toxicity is
likely regardless of the serum digoxin level. Other clinical settings in which an accelerated
junctional rhythm is likely to be seen include: acute ischemic heart disease post-operative
state acutely ill patient congenital heart disease.

02.44 PRACTICE: Tracing C

Interpret the lead II rhythm strip in Figure 02.44-1. The patient is hemodynamically stable.

Figure 02.44-1: Practice Tracing C.

ANSWER to Tracing C: The rhythm is rapid and irregularly irregular. There are no definite P
waves. Although the QRS is wide this is not VT. Instead, the irregular irregularity and lack of
atrial activity define this rhythm as AFib, here with a rapid ventricular response (Section 02.14).
QRS widening is presumably from preexisting bundle branch block.
Note that there are several places in this tracing where it almost looks as if there may be P

waves. This is admittedly deceptive. Instead of P waves these are undulations in the
baseline that are commonly seen with atrial fibrillation (fib waves). Gross irregular
irregularity of the rhythm and lack of any repetitive P wave shape define this rhythm as AFib.
Confirmation could be forthcoming by obtained a 12-lead ECG with rhythm strip.
Beyond-the-Core: We suspect this patient has LAHB ( Left Anterior HemiBlock) because of
the markedly negative QRS in this lead II (Section 07.13). There may or may not also be
underlying RBBB. A 12-lead ECG would be needed to know for sure.

02.45 PRACTICE: Tracing D

Interpret the lead II rhythm strip in Figure 02.45-1. The patient is hemodynamically stable.

Figure 02.45-1: Practice Tracing D.

ANSWER to Tracing D: The rhythm is rapid and regular. The QRS appears to be narrow. We
estimate heart rate by the every-other-beat method (Section 02.31). The RR interval of
every-other-beat (ie, half the rate) is about 3 large boxes. This means that half the rate is
~100/minute (300/3). The actual rate is therefore twice this, or ~200/minute. The rhythm is PSVT
since a rate of ~200/minute is too fast for either sinus tachycardia in an adult or untreated
AFlutter (See List #2 Sections 02.52, 02.53).
Although children may manifest sinus tachycardia at rates over 200/minute the rapidity of the
rate in Fig. 02.45 virtually excludes sinus tachycardia in an adult.
Beyond-the-Core: A useful formula to keep in mind is that maximal heart rate = 220 age.
This formula is used prior to treadmill testing to estimate what the target heart rate should be
during the procedure (the usual goal being to attain at least 85% of maximal predicted heart
rate during exercise). Thus maximal estimated heart rate for a healthy 30-year old would be
220 30 = 190/minute. That said clinical sinus tachycardia in an adult (who is not
performing maximal exercise) rarely exceeds a rate of 160-170/minute. This is not to say that
you will never see sinus tachycardia rates faster than this but only to say the odds strongly
favor an etiology other than sinus tachycardia for a regular SVT >170/minute.

02.46 PRACTICE: Tracing E

Interpret the lead II rhythm strip in Figure 02.46-1. The patient is hemodynamically stable.

Figure 02.46-1: Practice Tracing E.

ANSWER to Tracing E: The rhythm is irregularly irregular. The R-R interval appears to vary
between 2 and 3 large boxes. The QRS is narrow. Despite the irregularity this is not AFib because
P waves are present. P wave morphology varies from beat-to-beat. This is MAT (Multifocal Atrial
Tachycardia Section 02.16).

It is important to distinguish MAT from AFib ( Section 02.17) . Both rhythms are irregularly
irregular. The difference is that no P waves are seen on any of the leads of a 12-lead ECG with
AFib. In contrast definite P waves are seen with MAT. As opposed to wandering pacemaker,
in which there is gradual transition from one P wave shape to another with MAT, P wave
variation is completely random and varies from one beat to-the-next (as in Fig. 02.46-1).
The KEY in management of MAT is to treat the underlying disorder. Most often this is either
pulmonary disease or a combination of multiple medical problems including sepsis, shock, acidbase disturbance, etc.

02.47 LIST #1: Regular WCT

NOTE: We have developed 6 Essential Lists to facilitate recall of important aspects of 12Lead/Arrhythmia interpretation. This is the first of our 6 Lists (Section 00.7).
The 1st priority in evaluating any tachycardia is to ensure that the patient is hemodynamically
stable. IF not immediately cardiovert! If the patient is unstable, it no longer matters what the
rhythm may be (ie, VT or SVT with aberrant conduction) since the need for immediate
synchronized cardioversion will be the same.
But IF the patient is STABLE hemodynamically an attempt can be made to determine the
etiology of the tachycardia before proceeding further.
IF the QRS during tachycardia is WIDE then by definition, the rhythm is a WCT
(Wide-Complex Tachycardia). Consider the causes = LIST #1 (Figure 02.47-1).

Figure 02.47-1: Causes of a Regular WCT. Always assume the rhythm is VT until proven otherwise
(See text).
02.48 List #1: KEY Points
Our reason for putting VT as the first 8 entities in LIST #1 is twofold: i) It is by far t he most
common cause of a regular (or almost regular) WCT in adults when sinus P waves are lacking; and
ii) It is the most serious cause! (Figure 02.48-1).

Figure 02.48-1: Regular monomorphic WCT rhythm without clear sign of atrial activity. The rate is
~170/minute. Presume VT until proven otherwise (See text).
We describe the WCT rhythm in Figure 02.48-1 as monomorphic since QRS morphology
stays the same during the tachycardia (vs polymorphic VT such as Torsades, in which QRS

morphology changes Section 06.6).

The likelihood that a WCT without P waves (as seen in Figure 02.48-1) is VT goes up even
more (to at least 90%) IF i) the patient in question is older and ii) the patient has underlying
heart disease (prior MI, cardiomyopathy, angina, heart failure ). This is true regardless of
whether the patient is alert and regardless of what the BP might be during the tachycardia
(VT can be present even if systolic BP exceeds 180 mmHg)!
Availability of a prior 12-lead ECG during sinus rhythm may be invaluable for assessing the
possibility of preexisting BBB. That said the clinical reality is that youll often have to
initiate treatment before knowing for certain what the WCT rhythm is

02.49 Suggested Approach to WCT/Presumed VT

Optimal management of WCT rhythms depends on the type of WCT. Assume VT until proven
otherwise.
As long as the patient remains stable Trial of medical therapy is reasonable. Be ready to
cardiovert IF at any time the patient becomes unstable.
Get a 12-lead ECG during tachycardia (Figure 02.49-1). This will confirm that the QRS is
truly wide as well as looking for atrial activity in other leads. We have found use of 3
Simple Rules (involving QRS morphology and axis during tachycardia) may facilitate
diagnosis (Section 02.50).
Consider early use of Adenosine (usually not harmful given its short half-life; may convert
SVT and 5-10% of VTs).
Consider antiarrhythmic (Amiodarone; Procainamide).
Be ready to cardiovert if/as needed.

Figure 02.49-1: 12-lead ECG for the rhythm in Fig. 02.48-1. This 12-lead tracing confirms that the
rhythm is VT (See Section 02.50).
02.50 Use of the 3 Simple Rules
We can statistically increase the chance that a regular WCT rhythm is VT to over 90% by applying 3

Simple Rules to the 12-lead ECG obtained during tachycardia:

Rule #1 Is there extreme axis deviation? The presence of mild or even moderate left or right
axis does not assist in distinguishing between VT vs SVT. But when there is extreme axis
deviation (such that the QRS in either lead I or aVF is virtually entirely negative) then VT
is almost certain!
Rule #2 Is Lead V6 all (or almost all) Negative? IF so then VT is highly likely. Use of
this lead V6 criterion is only helpful if there is no more than a tiny r wave in V6. If the R in V6
is 3mm this doesnt rule in or out VT.
Rule #3 Is the QRS Ugly? The uglier the QRS complex the more likely the rhythm is
VT. The reason for this is that aberrant conduction almost always manifests some variation of a
conduction defect (RBBB; LBBB; LAHB; LPHB or some combination thereof). In contrast
VT originates from outside the conduction system (and is therefore more likely to be wider and
far less organized = uglier in its conduction pattern).
Applying the 3 Simple Rules to Figure 02.49-1: If told that the rhythm in Figure 02.49-1 was
obtained from an older patient with underlying heart disease Wed estimate a ~90% likelihood of
VT based on the finding of a regular WCT rhythm without sinus P waves (Section 02.47). Use of the
3 Simple Rules allows us to increase the likelihood of VT to almost 100%:
There is extreme axis deviation in Figure 02.49-1 (the QRS complex is completely negative in
lead I of this tracing).
Lead V6 is almost entirely negative (at most a tiny r wave is present).
The QRS in Fig. 02.49-1 is very wide (almost 0.20 second) and formless. We say it is ugly
because QRS morphology does not resemble any form of BBB or hemiblock.

02.51 FIGURE 02.51-1: 12 Leads are BETTER than One

We present the lead II rhythm strip in Figure 02.51-1 to emphasize how 12 leads are better than
One. This rhythm strip was obtained from a patient who was hemodynamically stable and tolerating
the tachycardia. BP = 120/80 mmHg at the time this tracing was recorded.
As per the red arrow the rhythm in Figure 02.51-1 was interpreted as sinus tachycardia? Do
you agree?
How would you proceed?

Figure 02.51-1: Lead II rhythm strip obtained from a patient who was hemodynamically stable. Is

this sinus tachycardia?

Answer to Figure 02.51-1: There is a regular tachycardia at ~150/minute. Despite the arrow
suggesting sinus P waves we are uncertain about QRS width. Since the patient is
hemodynamically stable the KEY to management is to obtain a 12-lead ECG (Figure 02.51-2).
Some patients in sustained VT may remain alert and hemodynamically stable for extended
periods of time (sometimes for hours or even longer). Both short term and long term
management will be far more effective IF we can determine with certainty the rhythm diagnosis.
Obtaining a 12-lead ECG during tachycardia will often allow us to do so (Figure 02.51-2):

Figure 02.51-2: 12-lead ECG obtained during tachycardia. Does the red arrow in Figure 02.51-1
represent a sinus P wave or the initial part of the QRS complex? (See text).
Interpretation of Figure 02.51-2: It should now be apparent that there are no P waves on this
tracing. Instead the red vertical timelines show the QRS to be very wide. What was initially
perceived as a P wave in lead II (Figure 02.51-1) is in fact the initial part of the QRS complex.
By the 3 Simple Rules we can state with virtual certainty that the rhythm in Figure 02.51-2
is VT! This is because: i) there is extreme axis deviation (almost entirely negative QRS in lead
aVF); ii) the QRS in lead V6 is predominantly negative; and iii) the QRS is actually very wide
and ugly (amorphous, and not resembling any pattern of BBB/hemiblock).
BOTTOM Line: 12 leads are better than one. IF at all uncertain about the etiology of a tachycardia
and the patient is hemodynamically stable Get a 12-lead ECG. This will often clarify the clinical
picture.
VT may look like a narrow tachycardia if only a single monitoring lead is used. This is
because part of the QRS complex may sometimes lie on the baseline. Getting a 12-lead during
tachycardia will confirm QRS duration.

Some patients may remain alert and hemodynamically stable despite being in sustained VT for
extended periods of time.

02.52 LIST #2: Regular SVT

The 2nd of our 6 Lists also relates to assessment of tachycardia. We again emphasize that IF the
patient who is in tachycardia is unstable immediately cardiovert!
But IF the patient is STABLE hemodynamically an attempt can be made to determine the
etiology of the tachycardia before proceeding further.
IF the QRS during tachycardia is truly NARROW (i n all 12 leads) then by definition, the
rhythm is an SVT (SupraVentricular Tachycardia). One of the 3 entities in LIST #2 (Figure
02.52-1) is then likely to be the cause of ~90-95% of cases of a Regular SVT.

Figure 02.52-1: Common causes of a Regular SVT (See text).

Beyond-the-Core: It is theoretically possible for the QRS complex to be narrow despite ventricular
origin of the arrhythmia. That is VT (Ventricular Tachycardia) may on rare occasions originate
from a site in the Bundle of His or in one of the bundle branches. That said, for practical purposes
IF the QRS is truly narrow in all 12 leads the rhythm is supraventricular!
02.53 The Regular SVT: Differential Diagnosis?
The best way to illustrate practical utility of LIST #2 is through clinical example (Figure 02.53-1):
What is your differential diagnosis of the rhythm in Fig. 02.53-1?
Clinically How would you proceed?

Figure 02.53-1: Regular SVT at ~200/minute without sign of atrial activity. The patient is stable.
What is the rhythm?

Answer to Figure 02.53-1: The rhythm is regular. The QRS is narrow. By the every-other-beat
method (Section 02.31) the R-R interval of half the rate is 3 large boxes. Therefore half the
rate in Fig. 02.53-1 = 300/3 = 100/minute. This means that the actual rate = 100 X 2 = 200/minute.
There is no clear sign of atrial activity in Fig. 02.53-1. While one cannot rule out the possibility
that a P wave might be hidden within the ST segment this is highly unlikely (would require an
extremely long PR interval).
The differential diagnosis for this regular SVT without P waves is essentially that shown in
LIST #2 (Figure 02.52-1). While there are other types of SVT rhythms (ie, automatic atrial and
junctional tachycardias) these are far less common than the 3 entities we include in List #2.
NOTE: AFib is not a consideration in Figure 02.53-1 because this rhythm is regular!
To distinguish between the 3 entities on List #2 We begin by looking at the rate of this
regular SVT. IF the rate of a regular SVT is >160-170/minute then both sinus tachycardia
and AFlutter become far less likely. While sinus tachycardia may attain rates of 200/minute in
children excessively fast rates are unusual in nonexercising adults. Therefore, the rate of
~200/minute in Fig. 02.53-1 effectively rules out sinus tachycardia in this case.
AFlutter most often conducts at a ventricular rate that is close to 150/minute (usual range
~140-160/min). That said all bets are off regarding the rate range for flutter activity IF the
patient is on one or more antiarrhythmic drugs (which may slow the flutter rate).
BOTTOM Line: By the process of elimination the regular SVT at 200/minute in Figure 02.53-1 is
almost certain to be PSVT.
On the other hand IF the rate of this regular SVT would have been closer to 150/minute
then each of the 3 entities in List #2 would have to be considered.

02.54 Suggested Treatment Approach for a Regular SVT

Optimal management of the narrow tachycardia depends on the type of SVT. The good news is
that definitive diagnosis is not essential for appropriate initial management. As long as the patient
remains stable there is time to consider the following:
Get a 12-lead ECG during tachycardia. Verify that the QRS is truly narrow in all leads. You
may see sign of atrial activity in other leads (as was evident in Figure 02.19-2 and in Figure
02.30-1).
Fix any Fixables you can (low K+/Mg++; acidosis; hypoxemia; hypovolemia; ischemia;
heart failure, etc.).
Consider use of a vagal maneuver (Section 02.26).
Consider empiric use of Adenosine. This drug is well tolerated by most patients. It will convert
most PSVT and, it usually produces transient slowing of other SVT rhythms which may be
diagnostic (Figure 02.28-1).
Consider other AV-blocking drugs (-blockers; diltiazem).

02.55 FIGURE 02.55-1: Which SVT is present?

Interpret the rhythm for the 12-lead ECG and Lead II rhythm strip that appears in Figure 02.55-1:
What is your differential diagnosis?
What diagnostic maneuver might help in diagnosis?

Figure 02.55-1: Regular SVT at ~150/minute. Diagnosis?

Answer to Figure 02.55-1: The rhythm is regular at a ventricular rate that is close to 150/minute
(the R-R interval is ~2 large boxes in duration and 300/2 = 150/min). The QRS complex is
narrow (ie, not more than half a large box ). Normal atrial activity is absent since upright P
waves are not seen in lead II. Instead, there is suggestion of atrial activity having a negative
deflection in lead II (as well as in other inferior leads). There also appears to be a negative
notching in the ST segment in each of the inferior leads. Could this all represent atrial activity?
The answer is forthcoming with application of a vagal maneuver. The effect of Carotid Sinus
Massage (CSM) is illustrated in Figure 02.55-2. CSM was applied at the moment marked by the
large arrow.

Figure 02.55-2: Application of CSM (large red arrow ) to the rhythm previously shown in Fig.
02.55-1.
Interpretation of Figure 02.55-2: Application of carotid massage results in reduction in the AV
conduction ratio from the 2:1 ratio previously seen in Figure 02.55-1. Note slight lengthening of the
R-R interval following CSM during which the typical sawtooth pattern of AFlutter can be
readily recognized.
The differential diagnosis of the rhythm in Figure 02.55-1 was that of the causes of a Regular
SVT = List #2 (Section 02.52). CSM in this case proves that the rhythm is AFlutter.
Clinical NOTE: After lead II the next best lead to look for atrial activity in is lead V1. This is
because right-sided lead V1 lies anatomically in close proximity to the atria. Note that a flutter
sawtooth pattern is suggested in lead V1 on the 12-lead tracing in Figure 02.55-1.

In retrospect atrial activity was suggested in several leads in Fig. 02.55-1

(II,III,aVF;aVR,aVL,V1,V2,V5) but it was not seen in all leads. CSM confirmed the
diagnosis.
Bottom Line: The best way to avoid overlooking the diagnosis of AFlutter is to suspect
AFlutter until proven otherwise whenever confronted with a regular SVT at a rate close to
150/minute but without definite sinus P waves (Section 02.19).

02.56 Premature Beats

Premature Beats are QRS complexes that interrupt the underlying rhythm by occurring earlier
than expected. They are 3 basic types of early beats (Figure 02.56-1):
PACs (Premature Atrial Contractions) when the underlying rhythm is interrupted by an early
beat arising from somewhere in the atria other than the SA node. As a result the earlyoccurring P wave manifests a different shape (beat #4 in Fig. 02.56-1). Most often the impulse
is conducted with a narrow QRS complex that is identical in appearance to that of normal sinusconducted beats. This is because once the premature atrial impulse arrives at the AV Node
its path of conduction through the AV Node and down to the ventricles is the same as it is for
normally conducted sinus beats.
PJCs (Premature Junctional Contractions) when the underlying rhythm is interrupted by an
early beat arising from the AV Node. Most often the impulse is conducted with a narrow QRS
that is similar (if not identical) to normal sinus-conducted beats. The P wave in lead II is
negative or absent (beat #6 in Fig. 02.56-1; See also Sections 02.32-thru-02.35). Clinically
PJCs are much less common than PACs.
PVCs (Premature Ventricular Contractions) when the underlying rhythm is interrupted by an
early beat arising from the ventricles. PVCs are wide and have a very different appearance from
sinus beats. PVCs are not preceded by a premature P wave (beat #8 below). The reason PVCs
are wide is that the premature impulse arises from a site within the ventricles away from the
conduction system. It therefore takes more time for the premature impulse to be conducted
through the ventricles.

Figure 02.56-1: Sinus rhythm with premature beats. These differ from escape beats that occur late
(See text).
Beyond-the-Core: Although beat #6 in Figure 02.56-1 is labeled as a PJC it could be a low
atrial PAC instead. There is NO way to know for certain (Section 02.35). Management is the same
so clinically, it really does not matter whether beat #6 is a PJC vs a PAC arising from a low atrial
site (PACs are much more common than PJCs.)
PEARL Beyond-the-Core: Although the QRS complex of junctional beats is usually the
same as the QRS of sinus-conducted beats this is not always the case. At times there may
be slight variation in QRS morphology for early-occurring beats arising from the AV Node.

This is because junctional beats may arise from different locations within the AV Node
which may result in a slightly different path of conduction. Thus, the QRS complex will still be
narrow but the R wave may be a little taller or shorter; or the S wave a little bigger or
smaller. This is an advanced concept but it may assist in evaluating occasional complex AV
block tracings when it becomes important to determine IF certain beats are being conducted vs
representing AV nodal escape.

02.57 ESCAPE Beats: Timing is Everything

It is important to distinguish between early (premature) beats vs late beats. Early beats (PACs,
PJCs, PVCs) may be problematic especially if they precipitate runs of tachycardia (Tracing A in
Figure 02.57-1). In contrast late beats often reflect an escape phenomenon which may be
beneficial. Were it not for emergence of ventricular beats #5, 6 in Tracing B (Fig. 02.57-1) the
short pause (between beats #4-5) may have been much longer.
Unless accelerated the usual rate of ventricular escape is between 20-40/minute (AIVR
was covered in Section 02.38; Escape Rhythms in Section 02.40).

Figure 02.57-1: In Tracing A an early beat (PVC) precipitates a run of VT after beat #3. In
contrast beat #5 in Tracing B is not a PVC, because this beat is not premature. Instead beat
#5 in Tracing B occurs relatively late, and therefore reflects ventricular escape (See text).
02.58 Narrow-Complex Escape Beats
As highlighted by Figure 02.57-1 timing is the key parameter for distinguishing between
premature vs escape beats. Consider the events in the 2 tracings shown below in Figure 02.58-1:
What is beat #5 in both Tracing A and Tracing B of Figure 02.58-1?
Is the P wave that precedes beat #5 in Tracing B conducting?

Figure 02.58-1: Narrow-complex escape beats. Is the P wave that just precedes beat #5 in Tracing B
conducting? (See text).
Answer to Figure 02.58-1: The underlying rhythm in Figure 02.58-1 is sinus as determined by the
presence of regular upright P waves preceding each of the first 4 beats with a constant (and normal)
PR interval.
Beat #5 in both Tracing A and Tracing B of Figure 02.58-1 is late. As a result (by definition)
beat #5 can not be either a PAC or PJC, since it is not premature.
Instead beat #5 is an escape beat. The occurrence of beat #5 for each tracing in Figure
02.58-1 is a good thing! Sinus conduction fails after beat #4. If not for the escape beat (beat #5)
the pause in each case may have been much longer
Focusing first on Tracing A in Figure 02.58-1: The QRS complex of beat #5 is narrow. It is not
preceded by any P wave. As a result we know this escape beat must be arising from within the
conduction system. Possibilities include the AV Node, Bundle of His, or from one of the major
fascicles of the bundle branch system. Practically speaking precise location of the escape site does
not matter since initial clinical management will be the same regardless of the site of the escape beat.
Sinus rhythm resumes in Tracing A after slight delay with beat #6.
Beyond-the-Core: QRS morphology of escape beat #5 is similar but not quite identical to QRS
morphology of normal sinus beats (beat #5 is slightly taller than sinus beats and it has a
small narrow s wave that sinus beats dont ). As alluded to in the PEARL in Section 02.56
recognition of this slight difference in QRS morphology for beat #5 (compared to the QRS of
normal sinus beats) provides support that narrow-complex beat #5 is arising from a
supraventricular site other than the SA node.
Looking next at Tracing B in Figure 02.58-1: The QRS complex of beat #5 is again narrow. This
time beat #5 is preceded by a P wave albeit the PR interval preceding the QRS of beat #5 in
Tracing B is far too short to conduct.
The P wave preceding beat #5 in Tracing B is not a PAC because this P wave is not
premature.
We surmise instead that a brief sinus pause (of 7 large boxes =1.4 seconds) ensues after beat

#4. The sinus node finally recovers but before the P wave preceding beat #5 in Tracing B is
able to conduct to the ventricles, an escape beat occurs.
That the QRS complex of escape beat #5 in Tracing B is narrow tells us the escape focus must
be arising from a site within the ventricular conduction system. Possibilities again include the
AV Node, Bundle of His, or one of the major fascicles of the bundle branch system.
Beyond-the-Core: The R-R interval preceding escape beat #5 in Tracing B is 7 large boxes.
This corresponds to an escape rate of ~43/minute (300/7). Given that the normal AV nodal
escape rate range in adults is between 40-to-60/minute this 7-large-box long R-R interval is
consistent with the rate of AV nodal escape.
Normal sinus rhythm resumes in Tracing B after slight delay with beat #6.
Bottom Line: The complexities of trying to determine IF the site of narrow-complex escape beats or
rhythms originate from the AV Node, Bundle of His or fascicles of the bundle branch system are of
little clinical importance! What counts is that recognition of late beats with a narrow QRS (as
occurs in each tracing of Fig. 02.58-1) indicates an escape site from somewhere within the
ventricular conduction system.
02.59 PVC Definitions: Repetitive Forms and Runs of VT
Clinically the occurrence of repetitive PVCs (2 or more in a row) is of much more concern
than isolated PVCs. In addition to clinical assessment of the patient (ie, for underlying heart
disease; associated medical conditions; electrolyte imbalance; hypoxemia; etc.) one aims to
assess the relative frequency of PVCs QRS morphology (uniform or multiform) coupling
interval plus the rate and duration of any runs (Figure 02.59-1):
Tracing A: Following 3 sinus beats an isolated PVC occurs (beat #4). Beats #7,8
represent a ventricular couplet. Note that the coupling interval (distance between beat #6 and
beat #7) and QRS morphology of this couplet are the same as was seen for the isolated PVC
(beat #4). Beat #10 is another PVC. Since its shape is different, we say there are multiform
PVCs in Tracing A.
Tracing B: 3 sinus beats then a ventricular salvo (beats #4,5,6). Since the definition of
VT is 3 PVCs in a row this is a 3-beat run of VT. Beat #9 begins a longer run of VT. In
fact we have no idea of how long this run will last since Tracing B in Figure 02.59-1 is
cut off after beat #13. We describe beats #9- thru-13 as a 5-beat run of monomorphic VT at a
rate of ~150/minute.

Figure 02.59-1: Various forms of ventricular ectopy (See text).

02.60 Blocked PACs/Aberrant Conduction
Although most premature supraventricular beats (PACs or PJCs ) are conducted to the ventricles
normally (ie, with a narrow QRS) this is not always the case. Instead, PACs ( or PJCs) may
sometimes occur so early in the cycle as to be "blocked" (non-conducted) because the conduction
system is still in the ARP (Absolute Refractory Period = 2nd arrow in Figure 02.60-1).
At other times early beats may occur during the RRP (Relative Refractory Period) in
which case aberrant conduction (with a widened QRS) occurs (3rd arrow).

Figure 02.60-1: Blocked vs aberrantly conducted PACs.

NOTE: Whether a PAC will be blocked vs conducted normally or with aberrancy depends on
where in the cycle the PAC occurs (Figure 02.60-2). A PAC occurring at point X in Fig. 02.60-2 will
be blocked (corresponding to the PAC notching the T wave of beat #5 in Fig. 02.60-1 ). In contrast
a PAC that occurs after the RRP is over (point Z in Fig. 02.60-2) will be conducted normally
(corresponding to beat #4 in Fig. 02.60-1). It is when the PAC occurs within the RRP that aberrant
conduction is seen (corresponding to point Y in Fig. 02.60-2 = beat #7 in Fig. 02.60-1).

Figure 02.60-2: Whether a PAC ( or PJC) will be blocked conducted normally or conducted
with aberrancy will depend on where in the cycle the beat occurs (See text).
PEARL: The best way to diagnose PACs with aberrant conduction is when the abnormal beat is
clearly preceded by a PAC ( beat #7 in Fig. 02.60-1). That said, IF ever in doubt as to whether a
widened beat is an aberrantly conducted PAC vs a PVC Assume a beat is guilty (ie, a PVC)
until proven otherwise!
NOTE: Blocked PACs may be subtle and a challenge to detect. They will be found IF looked for
they'll often be hiding (notching) the preceding T wave (the PAC that occurs in the T wave
of beat #5 in Fig. 02.60-1 and the PAC marked by the 2nd arrow in Figure 02.60-3). The
KEY is to recognize blocked PACs ( and not misdiagnose the pause as a type of AV block).
Remember The commonest cause of a pause is a blocked PAC (and not AV block)!
Aberrant Conduction: Use of QRS Morphology
Aberrant conduction is most likely to take the form of some type of bundle branch block/hemiblock
pattern. RBBB aberration is the most common form because the right bundle branch generally has
a longer refractory period than other conduction fascicles. That said any BBB/hemiblock pattern
of aberrancy may be seen (RBBB; LBBB; isolated LAHB or LPHB; RBBB/LAHB; or RBBB/LPHB).
Attention to QRS morphology of the early-occurring beat may therefore help to distinguish between
aberrant conduction vs ventricular ectopy.
The rSR with taller right rabbit ear for beat #4 in Figure 02.60-3 is highly suggestive of
aberrant conduction.
The predominantly negative QRS deflection for beat #7 in Figure 02.60-1 is suggestive of
LAHB (Left Anterior HemiBlock) aberration.

Figure 02.60-3: The 1st PAC in this tracing is aberrantly conducted (1st red arrow that just
precedes beat #4) but the 2nd PAC is blocked ( 2nd red arrow that notches the T wave of beat
#7).

02.61 PRACTICE TRACINGS II: What is the Rhythm?

Interpret the following 5 arrhythmias (Sections 02.62-thru-02.66) . All rhythm strips are obtained
from Lead II. The patient was hemodynamically stable in each case. Our answers follow after each
tracing.
Hint Use the Ps/Qs and 3R systematic approach for interpreting each rhythm (Section
02.1).

02.62 PRACTICE: Tracing F

Interpret the lead II rhythm strip in Figure 02.62-1. The patient is hemodynamically stable.

Figure 02.62-1: Practice Tracing F.

ANSWER to Tracing F: The rhythm is regular at 75/minute. The QRS complex is wide. P waves are
present and upright in front of each QRS complex with a fixed PR interval. Thus despite QRS
widening this is a sinus rhythm.
QRS widening is due to preexisting BBB (Bundle Branch Block).
A 12-lead ECG would be needed to determine the type of BBB that is present.

02.63 PRACTICE: Tracing G

Interpret the lead II rhythm strip in Figure 02.63-1. The patient is hemodynamically stable.

Figure 02.63-1: Practice Tracing G.

ANSWER to Tracing G: The QRS is again wide and regular at 75/minute. However, no P waves

are seen in this Lead II. Thus, the rhythm is not sinus. In the absence of P waves QRS widening
suggests a ventricular site of origin. Because the rate is faster than usual for a ventricular escape
rhythm this is AIVR (Accelerated IdioVentricular Rhythm Section 02.38).
T he clinical setting is key for determining the approach to AIVR. This rhythm is often
surprisingly benign when it occurs in the setting of acute MI in a hemodynamically stable
patient. Its occurrence following PCI (PerCutaneous Intervention) may herald reperfusion
of the infarct-related artery. In contrast prognostic implications are much poorer when AIVR
is seen during the course of cardiopulmonary resuscitation.

02.64 PRACTICE: Tracing H

Interpret the lead II rhythm strip in Figure 02.64-1. The patient is hemodynamically stable.

Figure 02.64-1: Practice Tracing H.

ANSWER to Tracing H: The first 3 beats show NSR (Normal Sinus Rhythm) at a rate of 7075/minute. Beat #4 occurs early. It is wide, very different in morphology from sinus-conducted
beats, and is not preceded by a premature P wave. Beat #4 is a PVC. Since it is followed by another
PVC (beat #5) beats #4,5 form a ventricular couplet.
Beats #6 and 7 are normal sinus-conducted beats.
Beat #8 is early, narrow, of similar morphology to normal sinus beats and is preceded by a
different appearing premature P wave. Beat #8 is a PAC (Section 02.56).
Beyond-the-Core: There appears to be slight variation in the R-R interval of normal sinus beats
in this tracing (ie, the R-R interval between beats #1-2; 2-3; and 6-7 is slightly different). It is
difficult to determine IF this is due to underlying sinus arrhythmia vs some component of sinus
node suppression from the early-occuring beats. Clinically it does not really matter whether
sinus arrhythmia is present or not, as the primary rhythm abnormality relates to the PAC/PVCs.

02.65 PRACTICE: Tracing I

Interpret the lead II rhythm strip in Figure 02.65-1. The patient is hemodynamically stable.

Figure 02.65-1: Practice Tracing I.

ANSWER to Tracing I: The rhythm is rapid and regular at ~180/minute. The QRS appears to be
narrow, which makes this a Regular SVT. It is impossible to determine IF the upright deflection
between QRS complexes is a P wave, T wave, or both. The differential diagnosis is that of the 3
entities contained in List #2. These are: i) Sinus Tachycardia; ii) Atrial Flutter; or iii) PSVT (Section
02.52). The rapid rate of ~180/minute favors PSVT as the most likely diagnosis in this case.
Sinus Tachycardia rarely exceeds a rate of 160-170/minute in a non-exercising adult. This is
not to say that you can never have Sinus Tach at a rate of 180/minute in an adult but rather to
strongly suggest you consider other diagnostic possibilities as far more likely.
PSVT most commonly utilizes a reentry mechanism involving some portion of the AV Node to
sustain the tachycardia. As a result application of a vagal maneuver may be both diagnostic
and therapeutic (Sections 02.26, 02.27). If vagal maneuvers are ineffective administration of
an AV nodal blocking drug ( Adenosine; Diltiazem; a Blocker) stands an excellent chance of
converting the rhythm.
Beyond-the-Core: Assuming the patient continues to tolerate the tachycardia we favor
obtaining a 12-lead ECG during tachycardia. Doing so may provide additional clues to
etiology especially when compared to a post-conversion 12-lead tracing (ie, the thin s-wave
notch in the terminal portion of the QRS complex in Fig. 02.65-1 may represent retrograde
atrial activity during this reentry tachycardia similar to notching in the example of PSVT
seen previously in Figure 02.30-1).
Finally We note marked ST depression in Figure 02.65-1. That said the amount of ST
depression may be exaggerated by a rhythm strip. Never draw conclusions from ST segment
deviations (elevation or depression) on a rhythm strip. Obtaining a 12-lead ECG and
repeating the 12-lead after the tachycardia resolves is the best way to assess likely clinical
significance (if any) of ST depression seen during tachycardia.

02.66 PRACTICE: Tracing J

Interpret the lead II rhythm strip in Figure 02.66-1. The patient was hemodynamically stable during
the initial portion of this rhythm strip. Toward the end of the rhythm strip the pulse is lost.

Figure 02.66-1: Practice Tracing J.

ANSWER to Tracing J: The first 9 beats show a regular WCT (Wide-Complex Tachycardia) at a
rate of ~180/minute. No P waves are seen. Presume VT until proven otherwise (= List #1, reviewed
in Section 02.47). The rhythm then degenerates to VFib (Ventricular Fibrillation).

While List #1 does allow for the possibility of SVT with either preexisting BBB or aberrant
conduction VT should always be presumed until proven otherwise. Given deterioration of the
rhythm to VFib toward the end of the rhythm strip the first 9 beats are virtually certain to be
VT.
Confirmation that the chaotic electrical activity toward the end of the rhythm in Fig. 02.66-1
represents VFib is forthcoming from the fact that the pulse has been lost. The patient is in
need of immediate defibrillation!

02.67 AV Blocks / AV Dissociation

KEY Clinical Point: Diagnosis of the specific type of AV block is far less important than the clinical
context in which the conduction defect occurs. For example immediate treatment is not
necessarily needed for all patients with 3rd degree AV block!
Clearly a pacemaker is indicated for symptomatic bradycardia that is not readily reversible
(not due to drugs or some other treatable cause).
That said, a patient with 3rd degree AV block from acute inferior infarction may not necessarily
need a pacer IF the patient is asymptomatic with junctional escape at reasonable rate and a
normal BP (because AV block in this setting may resolve on its own).

02.68 Blocked PACs: Much More Common than AV Block

Before describing the AV Blocks it is well to emphasize the KEY clinical concept we introduced
in Section 02.60: The commonest cause of a pause is a blocked PAC. IF looked for blocked
PACs will be found much more often than any type of AV block.
We have already highlighted how to recognize blocked PACs by the notching (or other
deformity) they produce in the T wave at the onset of the pause (See the T waves of beat #5 in
Fig. 02.60-1; and of beat #7 in Fig. 02.60-3).
Consider the example in Figure 02.68-1. Despite two pauses and the presence of group beating
this rhythm does not represent any form of AV block. Do you see why not?

Figure 02.68-1: Despite 2 pauses and group beating this rhythm does not represent any form of
AV block. Why not?
Answer to Figure 02.68-1: Keeping in mind that the most common cause of a pause is a blocked
PAC we routinely look for blocked PACs whenever we see an unanticipated relative pause in the
cardiac rhythm.
Note that the T wave of all beats in Figure 02.68-1 is smooth and rounded except for the T
waves of the 2 beats at the onset of each short pause (= the T waves of beats #2 and #6). Instead
the T waves of beats #2 and #6 are both notched! This notching is the result of blocked PACs
that are hidden within these T waves (arrows in Figure 02.68-2).

As we will see momentarily (in Section 02.72) there are other reasons why the rhythm in
Figure 02.68-2 is not 2nd degree AV block of the Wenckebach type: i) the atrial rate is not
regular; and ii) the PR interval does not progressively increase within groups of beats.
Beyond-the-Core: Did you notice that the PR interval preceding beat #7 in Figure 02.68-1 is
shorter than the PR interval preceding all other beats? This is because beat #7 is a junctional
escape beat that occurs just before the sinus P wave preceding it has a chance to conduct to the
ventricles. We expand on this concept later in this chapter in our discussion on AV dissociation
(in Sections 02.77, 02.78).

Figure 02.68-2: Sinus rhythm with blocked PACs (arrows). There is no AV block in this tracing
because: i) the P-P interval is not regular (vertical red lines) ; and ii) the PR interval does not
progressively increase within groups of beats. The commonest cause of a pause is a blocked PAC.
02.69 The 3 Degrees of AV Block
Diagnosis of the different forms of AV block need not be difficult. Simply stated there are 3
degrees of AV block:
1st degree AV Block (Section 02.70) in which all impulses from above (ie, from the SA
node) are conducted to the ventricles. It is just that they take longer than usual to get there (ie,
more than 0.20 second in an adult).
2nd degree AV Block (Section 02.71) in which some sinus impulses get through the AV
node and are conducted to the ventricles, but others do not.
3rd degree or complete AV Block (Section 02.75) in which no sinus impulses get through.
NOTE: From a practical, clinical perspective (as we describe momentarily) the diagnosis of
both 1st degree and 3rd degree AV block is surprisingly easy!
Awareness of this important concept tremendously facilitates diagnosis of the AV blocks. That is
IF an AV block is present and the block is neither 1st degree nor 3rd degree then it must
be some form of 2nd degree AV block.

02.70 1st Degree AV Block

First degree AV block is diagnosed by the finding of a prolonged PR interval. This is defined as a
PR interval that clearly measures more than 0.20-0.21 second = clearly more than 1 large box in
duration on ECG grid paper (Figure 02.70-1).

Practically speaking 1st degree AV block is simply a sinus rhythm with a long PR interval.
T he isolated finding of 1st degree AV block (even if marked) is usually not clinically
significant (Figure 02.70-1). This is especially true when a prolonged PR interval is seen in an
otherwise healthy individual who does not have underlying heart disease. In contrast new 1st
degree AV block in a patient with acute evolving infarction (especially if associated with other
new conduction defects) is clearly cause for concern. Bottom Line: Clinical correlation is
everything!

Figure 02.70-1: Sinus rhythm with 1st Degree AV Block . Each QRS complex is preceded by an
upright P wave in this lead II rhythm strip with a fixed PR interval that clearly exceeds 1 large box in
duration.
Clinical NOTE: A PR interval that measures 0.20 second is normal. The PR interval must be
clearly more than this amount (ie, >0.21-0.22 second) to be prolonged.
Beyond-the-Core: Given the overall benign nature of isolated 1st degree AV block and the
clinical reality that otherwise healthy young adults may manifest slight PR interval prolongation
simply as a result of pronounced vagal tone (especially in well-conditioned athletic
individuals) our preference is not to call 1st degree AV block until the PR interval is
clearly 0.22 second. We also favor not using the term, borderline 1st degree when a PR
interval in the 0.19-to-0.21 second range is seen in an otherwise healthy individual. All the term
borderline PR means is that you almost have a finding that even if you had, would
clinically mean nothing. Instead our preference is to describe the PR interval as either being
normal or long (where long means at least 0.21 second in duration, if not 0.22 second).
Beyond-the-Core: Norms for the PR interval (as well as for QRS interval duration) are
different in children. Pediatric hearts are smaller. It therefore takes less time for the electrical
impulse to travel through the conduction system of a child. For example a PR interval of 0.18
second would be long for an infant. When in doubt about norms for a younger-aged patient
upper limits for the PR and QRS intervals should be looked up in an age-specific table.

02.71 The 3 Types of 2nd Degree AV Block

Second degree AV block is traditionally divided into two types ( Mobitz I and Mobitz II). That said
it is important to recognize that a third type of 2nd degree AV block also exists ( known as 2:1
AV block).
The distinguishing characteristic of the 2nd degree AV blocks is that some ( but not all) P
waves are conducted to the ventricles (Figure 02.71-1).

NOTE: The atrial rate should be regular (or almost regular) when there is AV block ( arrows
in Figure 02.71-1). It is common to see slight variation (known as ventriculophasic sinus
arrhythmia) in the setting of 2nd or 3rd degree AV blocks. However marked P wave
irregularity change in P wave morphology or prolonged sinus pauses all suggest some
phenomenon other than AV block is operative (ie, blocked PACs; escape rhythms without AV
block; sick sinus syndrome; sinus arrest).

Figure 02.71-1: Sinus rhythm with the 3 types of 2nd Degree AV Block . In each case the atrial
rhythm is regular and some (but not all) beats are conducted. Rhythm A Mobitz I 2nd degree AV
block with gradual prolongation of the PR interval until a P wave is dropped (Section 02.72).
Rhythm B Mobitz II with QRS widening and a fixed PR interval until sudden loss of conduction
with successive nonconducted P waves (Section 02.73). Rhythm C 2nd degree AV block with 2:1
AV conduction. It is impossible to be certain if 2:1 AV block represents Mobitz I or Mobitz II, since
we never see 2 conducted P waves in a row (Section 02.74).
02.72 Mobitz I 2nd Degree AV Block (= AV Wenckebach)
Mobitz I (AV Wenckebach ) is by far the most common type of 2nd degree AV block ( accounting
f o r more than 95% of cases in our experience) . Mobitz I is recognized by: i) Progressive
lengthening of the PR interval until a beat is dropped; ii) Group beating; iii) A regular ( or at least
fairly regular) atrial rate; and iv) The pause that contains the dropped beat is less than twice the
shortest R-R interval. These characteristics are known as the Footprints of Wenckebach. They
are all present in Figure 02.72-1:

Figure 02.72-1: Mobitz I 2nd Degree AV Block (= AV Wenckebach). The PR interval progressively
lengthens until a beat is dropped (See text).
Regarding the footprints of Wenckebach that are seen in Figure 02.72-1:

There is group beating. This takes the form of 2 groups encompassing beats #1,2,3 and beats
#4,5 (each group being separated by a pause of approximately equal duration between beats
#3-4 and between #5-6).
The P-P interval is regular (in this case at a rate of 100/minute).
Within groups the PR interval progressively lengthens until a beat is dropped. Note the PR
interval preceding beat #4 gets longer before beat #5 until the P wave after beat #5 is
nonconducted. The next cycle then begins as the PR interval shortens prior to beat #6.
Beyond-the-Core: Although AV Wenckebach is usually easy enough to diagnose simply by
recognition of progressive PR interval lengthening until a beat is dropped awareness of the
other footprints may be helpful confirming the diagnosis in less obvious cases. Not all
footprints are present in each case (ie, Wenckebach cycles may be atypical ). However, all of
the footprints are present in Figure 02.72-1. Note that in addition to group beating regular
atrial rate and progressive PR interval lengthening that the pause containing the dropped
beat is less than twice the shortest R-R interval. Thus, in the first group of beats in Figure
02.72-1 (beats #1,2,3) the shortest R-R interval is between beats #2-3. The pause that
contains the dropped beat (ie, the pause between beats #3-4) measures less than twice this R-R
interval between beats #2-3.
Clinical NOTE: Second degree AV block, Mobitz Type I usually occurs at the level of the AV
node. As a result the QRS complex with Mobitz I will usually be narrow.
Mobitz I is most often associated with inferior MI it often spontaneously resolves and it
often responds to Atropine (which works on the AV node).

02.73 Mobitz II 2nd Degree AV Block

Mobitz II 2nd degree AV block is recognized by QRS widening with a constant PR interval for
consecutively conducted beats until one or more beats are dropped (Figure 02.73-1).
Mobitz II occurs lower down in the conduction system. As a result the QRS complex is
usually wide. The problem with Mobitz II is its disturbing tendency to abruptly go from regular
conduction of P waves to nonconduction of multiple P waves in a row, sometimes leading to
ventricular standstill. This explains why pacing is almost always needed with true Mobitz II 2nd
degree AV block.
The features of Mobitz II are illustrated in Figure 02.73-1. Note that the QRS complex is wide.
The underlying atrial rate (P-P interval) is regular. Following normal conduction of the first 3
beats on the tracing there is nonconduction of multiple subsequent P waves.
Unlike Mobitz I the PR interval remains constant preceding all QRS complexes that do
conduct to the ventricles (beats #1,2,3; #4,5).
PEARL: The KEY for diagnosing Mobitz II is that the PR interval remains constant for
consecutively conducted P waves (seen for the PR interval preceding beats #1,2,3 in Figure
02.73-1).

Figure 02.73-1: Mobitz II 2nd Degree AV Block. The PR interval is constant preceding all QRS
complexes that do conduct to the ventricles. Note that the QRS complex is wide and that there are
consecutively conducted complexes early in the tracing prior to onset of AV block.
02.74 2-to-1 AV Block: Mobitz I or Mobitz II?
The 3rd type of 2nd degree AV Block occurs when there is 2:1 AV conduction in which
every-other P wave is conducted (Tracing C in Figure 02.71-1, which we reproduce below in
Figure 02.74-1). We can not be certain IF 2:1 AV block represents Mobitz I or Mobitz II because
w e never see 2 beats conducted in a row. Therefore we simply dont know if the PR interval
would progressively lengthen IF given a chance to do so.
NOTE: It is likely that the example of 2:1 AV Block seen in Figure 02.74-1 represents Mobitz I
because: i) Mobitz I is much more common than Mobitz II; and ii) the QRS is narrow. That said
We can not tell for sure (since we never see 2 conducted beats in a row in Figure 02.74.1).

Figure 02.74-1: 2nd Degree Block with 2:1 AV Conduction . Although we suspect this is Mobitz I
(since the QRS is narrow and Mobitz I is so much more common) we can not tell for certain
because we never see 2 consecutively conducted P waves.
Additional CLUES Suggesting Mobitz I: Serial tracings and the clinical setting may provide
additional clues in support of the diagnosis of Mobitz I for the rhythm in Figure 02.74-1:
Although possible it is rare for a patient to go back-and-forth between Mobitz I and
Mobitz II forms of AV block. Therefore, IF there is clear evidence elsewhere that this patient
manifested Mobitz I (from the patients chart; from ongoing telemetry monitoring) then it is
highly likely that the 2:1 AV conduction block seen in Figure 02.74-1 also represents Mobitz I.
Finally IF 2:1 AV block occurs in association with acute inferior infarction then Mobitz
I is far more likely (since occlusion of the right coronary artery commonly impedes blood
supply to both the inferior wall of the left ventricle and the AV nodal artery). In contrast
acute anterior infarction is much more likely to result in Mobitz II than Mobitz I AV block.

Clinical NOTE: Although there is 2:1 AV block in Figure 02.74-1 the ventricular rate is not
overly slow (the R-R interval is 6 large boxes; the ventricular rate is 50/minute). As a result
there is an excellent chance that this patient may be hemodynamically stable despite AV block.
Immediate treatment may therefore not be needed. IF the patient became hypotensive with the
rhythm shown in Figure 02.74-1 initial treatment with Atropine would be reasonable and
have reasonable chance to be effective given that the QRS complex is narrow.
FIGURE 02.74-2: Follow-Up Tracing to Figure 02.74-1
A little while after the rhythm in Figure 02.74-1 was recorded the follow-up tracing in Figure
02.74-2 is seen on the monitor.
Does this new rhythm labeled Tracing D in Figure 02.74-2 confirm our suspicion that the 2:1
AV block seen previously in Tracing C (Fig. 02.74-1) is the result of Mobitz I 2nd degree AV
block?

Figure 02.74-2: Tracing D is the follow-up rhythm strip obtained a short while after Tracing C
(Fig. 02.74.1) was recorded. Does tracing D confirm that the rhythm in Tracing C represents Mobitz
I?
Answer to Figure 02.74-2: The first 3 beats in Tracing D show a definite Wenckebach cycle
(progressively lengthening PR interval until the P wave after beat #3 is nonconducted). 2:1 AV
block then resumes with beat #4 in Tracing D. But because it is rare for 2nd degree AV block to
alternate between Mobitz I and Mobitz II it is virtually certain that the entire sequence of events
seen in Tracings C and D of Figure 02.74-2 represent 2nd degree AV block, Mobitz I.
02.75 3rd Degree (Complete) AV Block
Complete (or 3rd degree ) AV block is said to be present when none of the impulses from above
(P waves) are able to conduct to the ventricles. In this case there is complete AV Dissociation
because none of the P waves are related to any of the QRS complexes. The result is that 2
independent rhythms are going on. One of these rhythms will be from above (in the form of
regularly occurring sinus P waves). The other ongoing rhythm will be from below (in the form of
an escape rhythm originating either from the AV node, the His, or the ventricles ). Awareness of

these features facilitates recognition and understanding of diagnostic criteria for what 3rd degree AV
block is and what it is not:
With complete AV block none of the impulses from above (sinus P waves) are able to
penetrate the AV node to arrive at the ventricles. As a result there will be regular ( or almost
regular) atrial activity and a regular (or almost regular) ventricular escape rhythm (Figure
02.75-1).
There is complete AV dissociation in Figure 02.75.1 (ie, none of the P waves are related to
any QRS complexes). As a result P waves are seen to march through the QRS, occurring
a t all phases of the R-R cycle. This is most easily seen by focusing on each QRS complex in
both Rhythm A and Rhythm B in Fig. 02.75-1 and seeing that the PR interval immediately
preceding each QRS continually changes.

Figure 02.75-1: Anatomic levels of 3rd degree AV block. Rhythm A: Complete AV block at the
ventricular level. There is a regular atrial rhythm (arrows) and the QRS is wide with an
idioventricular escape rhythm at a rate between 20-40/minute. Rhythm B: Complete AV block at a
higher level (probably in the AV node ) as suggested by the presence of a narrow QRS escape
rhythm at a rate between 40-60/minute NOTE: White arrows in this Figure represent presumed P
waves that are hidden within the ST segment.
NOTE: The anatomic level of complete AV block may vary. Most commonly the level of block
will occur below the AV node with a resultant ventricular escape rhythm (Rhythm A in Figure
02.75-1). When this happens the QRS of the escape rhythm will be wide and the escape rate will
be between 20-40/minute.
The anatomic level of block may occur at a higher level within the conduction system (either
within the AV node or the Bundle of His). When this happens the QRS of the escape rhythm
will be narrow. IF the escape rhythm arises from the AV node the escape rate will typically
be between 40-60/minute (as seen in Rhythm B of Fig. 02.75-1).
Beyond-the-Core: IF the escape rhythm arises from the Bundle of His the QRS complex will
again be narrow, but the escape rate may be slower. One may therefore surmise the probable
anatomic level of block based on characteristics of the escape rhythm (QRS width and escape
rate) realizing that exceptions may exist in patients with preexisting conduction defects
and/or influence by medications, hypoxemia, acute ischemia/infarction, etc.

KEY Clinical Point: More important than the anatomic level of block per se in initial management is
the patients hemodynamic status. For example a hypotensive patient with altered mental status
and complete AV block associated with an escape rate of 40/minute will still be in dire need of
immediate treatment regardless of whether the escape rhythm manifests a wide or narrow QRS
complex.
Beyond-the-Core: Knowing that the escape rhythm QRS complex is narrow suggests greater
potential for reversibility and beneficial response to Atropine.

02.76 PEARLS for Recognizing/Confirming Complete AV Block

Most of the time IF the degree AV block is complete ( 3rd degree ) then the ventricular rhythm
should be at least fairly regular. This is because escape rhythms arising from the AV node, the His
or ventricles are usually fairly regular rhythms. Exceptions may occur during cardiopulmonary
resuscitation but even then, there will usually be a recognizable pattern of ventricular regularity.
If the ventricular rhythm in a tracing with AV block is not regular (or at least almost regular)
then it is likely that some conduction is occurring (ie, rather than 3rd degree there is
probably high-grade 2nd degree AV block ). Note that the R-R interval is regular for both
examples of complete AV block shown in Figure 02.75-1.
Confirmation of complete AV block requires that P waves fail to conduct despite being given
adequate opportunity to do so. Satisfying this requirement provides the evidence needed to
distinguish complete AV block from AV dissociation due to other causes. To do this one must see
P waves in all phases of the R-R cycle (ie, having opportunity to conduct but still failing to do
so).
For example, in Tracing A of Fig. 02.75-1 (which we reproduce below) the P wave hidden
within the T wave of beat #3 (white arrow) would not be expected to conduct to the ventricles
(because it occurs during the absolute refractory period). In contrast, virtually all other P
waves in Tracing A occur at points in the cardiac cycle that should allow opportunity to conduct
yet none of them do.

Tracing A from Figure 02.75-1: Complete AV block at the ventricular level.

Similarly, in Tracing B of Fig. 02.75-1 (which we reproduce below) the P wave that notches the
terminal portion of the T wave of beat #3 and the P wave hidden within the QRS complex of beat #4

each occur at a time when conduction is not expected (white arrows in Tracing B). However, all
other P waves in this tracing should have opportunity to conduct yet fail to do so.

Tracing B from Figure 02.75-1: Complete AV block at a higher level (probably in the AV node )
as suggested by the presence of a narrow QRS escape rhythm at a rate between 40-60/minute
KEY Clinical Point: In order to guarantee that P waves will have adequate opportunity to conduct
the rate of the escape rhythm should ideally not exceed 50/minute. Escape rates faster than this
often result in inopportune timing of P waves that mitigates against having an adequate opportunity to
conduct. In such instances (when the escape rate is well over 50/minute) a much longer period of
monitoring will be needed to ensure that the degree of AV block is complete. Note that the escape
rate is below 50/minute for both examples of AV block in Figure 02.75-1 further supporting our
conclusion that the degree of AV block is indeed complete in each case.
02.77 AV Dissociation
The term, AV dissociation simply means that for a certain period of time sinus P waves are not
related to neighboring QRS complexes. That is, the P waves preceding the QRS are not being
conducted to the ventricles.
AV dissociation may be intermittent, recurrent and short-lived or it may be persistent and
permanent, as occurs with complete AV block.
AV dissociation is never a diagnosis. Instead it is a condition caused by something else.
The task for the clinician is to figure out what the cause of AV dissociation is for any given
rhythm. This assignment is far more than academic since appropriate management depends
on figuring out the cause of AV dissociation. Active treatment may or may not be indicated. For
example optimal treatment of complete AV dissociation with an accelerated junctional
rhythm due to digitalis toxicity is simple: IF the patient is hemodynamically stable simply
stop digoxin! No pacemaker is needed despite that fact that none of the P waves on the tracing
may be conducting.
Complete AV dissociation is not the same as complete AV block ! This is one of the most
commonly misunderstood concepts in all of arrhythmia interpretation. Complete AV block is
just one of 3 possible causes of AV dissociation. As we will see momentarily patients with
complete AV dissociation may actually have no degree of AV block at all
Always try to determine which of the 3 Causes of AV Dissociation is operative. The 3 possible
causes are: i) AV block itself (either from 2nd or 3rd degree AV block ); ii) Usurpation in
which P waves transiently do not conduct because an accelerated junctional or ventricular
rhythm takes over the pacemaking function (ie, usurps the rhythm) ; and iii) Default in
which a junctional or ventricular escape rhythm takes over by "default" because the rate of the
sinus pacemaker has slowed down for whatever reason.

02.78 FIGURE 02.78-1: Is there any AV Block?

Consider the rhythm strip shown in Figure 02.78-1. Are the P waves that are seen in this tracing ( red
arrows) being conducted to the ventricles?
IF so Which one or two P waves are likely to be conducting?
Which P waves are clearly not conducting?
Is AV block present? If so what degree of AV block?
HINT: Do any of the P waves that are not conducting have a chance to conduct yet still fail
to do so?
Extra Credit: What is the correct interpretation of this rhythm?

Figure 02.78-1: Is there AV block? If so what degree of AV block is present? (See text).
Answer to Figure 02.78-1: Full interpretation of the rhythm strip shown here is problematic because:
i) We are not provided with information about the clinical setting; ii) The rhythm strip is short (just
over 4 seconds in duration); and iii) We do not get to see the immediately-preceding rhythm strips
that are likely to reveal what is truly going on. That said what can be stated about the rhythm in
Figure 02.78-1 is the following:
The underlying rhythm appears to be sinus as suggested by beat #1 which is preceded by an
upright P wave with reasonable PR interval (of 0.18 second) in this lead II monitoring lead.
The ventricular rhythm is regular at a rate just over 50/minute (the R-R interval is just under
6 large boxes in duration).
T he QRS complex is narrow. For practical purposes this means that the rhythm is
supraventricular (arising from either the SA node as in sinus rhythm or from the AV node).
The P waves preceding beats #3 and #4 in Fig. 02.78-1 are definitely not conducting. They
cant be since the PR interval preceding these beats is clearly too short to conduct.
The P wave preceding beat #2 is also probably not conducting. Although the PR interval
preceding beat #2 is not necessarily too short to conduct it is clearly less than the PR
interval preceding beat #1. Given that we know the P waves preceding beats #3 and #4 are not
conducting it is highly likely that the P wave preceding beat #2 is also not conducting.
The atrial rate (as defined by the P-P interval) is regular at 50/minute (the P-P interval is
precisely 6 large boxes in duration).
Regardless of whether the P wave preceding beat #2 is or is not conducting the theme of
the rhythm in Figure 02.78-1 is that there is initial sinus bradycardia (beat #1) at a rate of
50/minute followed by a period of AV dissociation ( since P waves preceding subsequent
beats are definitely not conducting). This is AV Dissociation by Default (ie, default from
sinus node slowing that allows emergence of an appropriate junctional escape rhythm at

52/minute).
KEY Clinical Point: There really is no evidence of any AV block at all in Figure 02.78-1. None of
the P waves that fail to conduct have any reasonable chance to conduct (since the PR interval is
simply too short before an appropriate junctional escape rhythm supervenes).
What occurs in Figure 02.78-1 is commonly seen among healthy adolescents and young adults
during sleep and/or undergoing anesthesia. The sinus rate temporarily slows and an
appropriate junctional escape rhythm arises to the rescue. There is no AV block. There is no
pathology. There is no need for acute intervention. Instead optimal treatment is benign
neglect (the clinician is perhaps better off not knowing that transient AV dissociation may be
occurring in such otherwise healthy and asymptomatic individuals).
BOTTOM Line: The correct diagnosis for the rhythm in Figure 02.78-1 is: Sinus bradycardia with
AV dissociation by default, resulting in an appropriate junctional escape rhythm at 52/minute .
Nothing more need be written in your interpretation.
Beyond-the-Core: Although we assumed that beat #1 in Figure 02.78-1 is conducting We
actually do not know for certain that this is true. This is because we never see 2 beats in a row
that conduct with the same PR interval. Therefore, it could be that the patients underlying
rhythm is sinus with marked 1st degree AV block and that beat #1 also manifests AV
dissociation. That said, regardless of whether or not beat #1 is conducting the theme of this
rhythm is still sinus bradycardia with AV dissociation by default. The need for clinical
correlation to guide management remains the same (ie, no immediate intervention is needed IF
the patient is asymptomatic and the setting benign).

02.79 SUMMARY: Complete AV Block vs AV Dissociation

We summarize the subject of AV Dissociation by Figure 02.79-1 in which all 3 the causes are
illustrated. Note the following:
Rhythm A in Figure 02.79-1: Although there is obvious AV dissociation ( since the PR interval
for several P waves is too short to conduct) there is not necessarily any AV block. We
interpret this rhythm as sinus bradycardia with AV dissociation by default resulting in an
appropriate junctional escape rhythm at 52/minute (See Answer to Fig. 02.78-1).
Rhythm B: There is AV dissociation by usurpation. Beats #1 and #2 are sinus conducted with a
normal PR interval. The PR interval then shortens. We know that P waves preceding beats #4
and #5 in Rhythm B are not conducting (the PR interval is clearly too short to conduct). No P
waves at all are seen after beat #5. The reason is that an accelerated junctional rhythm (at
78/minute) has usurped the pacemaking function from the SA node (that was beating at
75/minute). This situation is commonly seen in digitalis toxicity. Although the sinus P waves
preceding beats #4 and 5 in Rhythm B are not conducting (and the P preceding beat #3 is
probably also not conducting) none of these P waves have any reasonable chance to

conduct. Thus, despite nonconduction of P waves there is no evidence of any AV block. It is

likely that AV dissociation will spontaneously resolve once the cause of the accelerated
junctional rhythm is discovered and corrected.
Rhythm C: There is AV dissociation due to 3rd Degree AV Block . As opposed to Rhythm A
and Rhythm B, in which nonconducting P waves do not have any reasonable chance to conduct
P waves in Rhythm C occur at all points in the cardiac cycle. We would anticipate that
virtually all of the P waves indicated by solid red arrows in Rhythm C should have a chance to
conduct. Despite this none of these P waves conduct. Instead P waves march through
the QRS throughout Rhythm C. In addition the ventricular escape rhythm is less than
50/minute. Rhythm C therefore fulfills criteria for complete AV block as the cause of AV
dissociation.

Figure 02.79-1: The 3 causes of AV dissociation. Rhythm A AV dissociation by default of the

sinus pacemaker which has slowed; Rhythm B AV dissociation by usurpation of the rhythm by
another accelerated pacemaker (which in this case arises from the AV node ); and Rhythm C AV
dissociation due to AV block which could be either 2nd degree, or as in Rhythm C, a 3rd degree
AV block (See text).
02.80 High-Grade 2nd-Degree AV Block
A term is needed to describe the situation in Figure 02.80-1.
How would you interpret this rhythm?
Is there AV block? IF so Is the conduction disturbance likely to represent Mobitz I or Mobitz
II forms of AV block? Justify your answer.

Figure 02.80-1: Is the rhythm in this figure Mobitz I or Mobitz II AV block? What is high-grade
AV block?

Answer to Figure 02.80-1: As for assessment of any cardiac arrhythmia once you have ensured
that the patient is hemodynamically stable Watch your Ps, Qs and the 3Rs (Section 02.1):
P waves are present and regular (red arrows in Figure 02.80-2).
QRS complex is narrow (clearly less than half a large box).
The 3 Rs The atrial rate is 100/minute; the ventricular rhythm is irregular; some P waves
conduct others do not.
Impression: Some degree of AV block is present in Figure 02.80-2. We establish this by recognition
of: i) a regular atrial rate; and ii) the fact that some P waves conduct but others do not.
The conduction disturbance in Figure 02.80-2 is clearly not simple 1st degree AV block. We can
also recognize at a glance that this rhythm is not 3rd degree AV block because: i) the ventricular
rhythm is not at all regular (Section 02.76); and ii) some P waves are conducting. Therefore
the rhythm in Figure 02.80-2 must be a form of 2nd degree AV block.

Figure 02.80-2: Arrows have been added to Figure 02.80-1 to indicate regularly occurring P waves
throughout the tracing. Some P waves conduct but others dont . The rhythm is therefore 2nd
degree AV block (See text).
Which Form of 2nd-Degree AV Block ? There are features of each type of 2nd degree AV block in
Figure 02.80-2:
The first 3 beats are consistent with Mobitz I because: i) Mobitz I is far more common than
Mobitz II; ii) the QRS complex is narrow; and iii) the PR interval progressively increases from
beat #1 to beat #2 to beat #3. The P wave after beat #3 is nonconducted. The cycle then
resumes with shortening of the PR interval prior to beat #4.
There is 2:1 AV block for beats #4, 5 and 6 as every-other-P wave is conducted (confirmed
by the constant PR interval preceding the QRS complex of beats 4, 5, 6).
Two P waves in a row are nonconducted between beat #3 and beat #4. While on occasion,
multiple successive nonconducted P waves may be seen with Mobitz I 2nd degree AV block
this finding is much more suggestive of a more severe Mobitz II conduction disturbance
(Section 02.73).
Bottom Line: More important than determining the specific type of 2nd degree AV block for the
rhythm in Figure 02.80-2 are: i) the hemodynamic effect of the conduction defect; and ii) clinical
implications and potential need for a pacemaker. As a compromise to reflect our increased clinical

concern given successive nonconduction of P waves we favor use of the term high-grade AV
block for the conduction disturbance seen in Figure 02.80-2.
NOTE: There are many variations on the above theme in which the degree of AV block is
not quite complete and not necessarily conforming to either pure Mobitz I or Mobitz II yet
clearly of increased clinical concern due to nonconduction of multiple beats with resultant
overly slow ventricular rate.

02.81 Ventricular Standstill vs AV Block

Confusion sometimes arises in the terminology used to describe certain ventricular or arrest rhythms
related to complete AV block. The 4 rhythms illustrated in Figure 02.81-1 will hopefully clarify the
terminology used:
Rhythm A (repeated from Figure 02.75-1) represents complete AV block at the ventricular
level. There is a regular atrial rhythm (red arrows ) and a regular ventricular rhythm but
none of the P waves conduct to the ventricles. Instead P waves march through the QRS
complex with a continually changing PR interval. Note that the ventricular escape rate is slow
(well below 50/minute) and that P waves have more than adequate opportunity to conduct,
yet still fail to do so (Section 02.75).
Rhythm B represents ventricular standstill. Atrial activity continues (in the form of
regularly-occurring P waves) but no QRS complexes are seen. Clinical implications of this
rhythm are usually the same as for asystole. Patients with Mobitz II 2nd degree AV block
sometimes suddenly go from minimal nonconduction of beats to ventricular standstill (which is
why pacing is generally needed for patients with Mobitz II AV block).
Rhythm C represents a slow idioventricular rhythm seen here with an escape rate just
over 30/minute (Section 02.37). This is not a form of AV block because there are no P
waves. Instead following sinus arrest and failure of an AV nodal escape pacemaker to arise
there fortunately is appearance of a ventricular escape rhythm (without which there would
have been asystole).
Rhythm D represents asystole. There is no sign of any electrical activity (No P waves; No
QRS complexes).

Figure 02.81-1: Clarification of complete AV block ( Rhythm A) ventricular standstill (Rhythm

B) slow idioventricular escape (Rhythm C) and asystole in Rhythm D (See text).
02.82 Hyperkalemia vs AV Block
The incidence of Hyperkalemia has clearly increased in recent years. Reasons for this increase are
multiple but include the obesity epidemic with corresponding increase in the incidence of diabetes
and improved treatment of diabetes resulting in increased longevity. As a result many more
patients with diabetes now live long enough to develop complications associated with end-stage
kidney disease. Hyperkalemia is perhaps the most immediately life-threatening complication seen in
this group of patients.
Many more patients than ever before are now on dialysis. Hyperkalemia should always be
thought of in such patients whenever they present with either an unusual (or bizarre) 12-lead
ECG and/or a cardiac arrhythmia.
Chronic kidney disease patients who are not yet on dialysis may also develop hyperkalemia
especially if any of a number of predisposing situations are present. Among others, these
include: i) taking potassium-retaining medications (ACE-inhibitors; angiotensin-receptorblocking drugs; certain diuretics; potassium supplements) ; ii) dehydration; iii) acidosis; iv)
abrupt reduction in urine output; and v) cardiac arrest.
Hyperkalemia is notorious for its ability to mimic other ECG conditions (Section 11). Among
ECG changes produced by more severe degrees of hyperkalemia (common once serum
potassium exceeds 6-6.5 mEq/L) include: i) marked peaking of T waves in multiple leads; ii)
QRS widening; iii) reduced P wave amplitude sometimes with complete loss of P waves
(despite persistence of sinus conduction) ; iv) bizarre frontal plane axis shifts; and v) ST-T
wave changes that may mimic ischemia/acute infarction (ST elevation or depression; T wave
peaking and/or deep T wave inversion).

Relevance of the above information on Hyperkalemia to this Section on AV Block is highlighted by

the rhythm in Figure 02.82-1.
Should the patient whose rhythm is shown in Figure 02.82-1 be treated with Atropine and/or
pacing?
HINT: How might your answer to this question change IF told that this patient was alert and had
a history of chronic kidney disease?

Figure 02.82-1: Ventricular rhythm at ~40/minute. How should this patient be treated? (See text).
Answer to Figure 02.82-1: A regular ventricular ( wide QRS) rhythm is seen in this tracing at a rate
of ~40/minute. There are no P waves. While our initial impression is that of a ventricular escape
rhythm (as most commonly occurs in a setting of cardiac arrest) pending the need for additional
information, other possibilities should be entertained. For example IF told that this patient was
hemodynamically stable, alert and on longterm dialysis (or that he/she had a history of chronic
kidney disease) then a stat potassium value becomes essential for optimal management:
QRS widening the slow ventricular rate lack of P waves and suggestion of T wave
peaking in Figure 02.82-1 are all consistent with a possible diagnosis of hyperkalemia.
IF the diagnosis is hyperkalemia then immediate treatment would be very different than
treatment of slow ventricular escape in a patient with cardiac arrest whose serum potassium is
normal. As opposed to Atropine, use of a pressor agent and/or Pacing IV Calcium, Bicarb
and/or D50 plus Insulin may become the treatment(s) of choice.

02.83 FIGURE 02.83-1: Is there any AV Block at all?

We conclude this brief section on AV block with the rhythm in Figure 02-63. Is there AV block?
If so What type of AV block is present?

Figure 02.83-1: Is there AV block? If so What type? (See text).

Answer to Figure 02.83-1: Although it is tempting to interpret the rhythm in this tracing as 2:1 AV
block this is not what is happening!
Assuming the patient is hemodynamically stable We once again assess the 5 key parameters
for rhythm determination by the systematic Ps, Qs and 3R Approach: The QRS complex is
narrow. P waves are present and 2 P waves are seen for each QRS (blue and red arrows in
Figure 02.83-2) but P waves are not regular in this rhythm strip. This is the 1st clue that the
rhythm in Figure 02.83-2 does not represent a form of AV block (Section 02.71).

Figure 02.83-2: Red and blue arrows have been added to Figure 02.83-1 (See text).

Every-other-P wave in Figure 02.83-2 is conducting. We know this because the PR interval
preceding each QRS on the tracing is constant (blue arrows). Therefore the underlying
rhythm is sinus.
Every-other-P wave is early (red arrows ). Note P wave morphology of each early P wave is
different in shape (triphasic) than the biphasic P wave of sinus beats. Thus, the rhythm is atrial
bigeminy. Every-other-P wave is a PAC that occurs so early that it is blocked (red arrows).
Bottom Line: The rhythm in Figure 02.83-2 is a fitting way to end this Section on AV Blocks.
The most common cause of a pause is a blocked PAC. Blocked PACs are far more
common than any form of AV block. They will be found IF looked for. Remembering this clinical
reality (Section 02.68) and remembering to always assess each cardiac rhythm
systematically by the Ps, Qs & 3R Approach will facilitate recognizing AV block when it does
occur and help avoid misdiagnosis when instead one of the AV-block-mimics is present.

03.0 Doing an ECG / Technical Errors

The importance of correct lead placement and awareness of potential technical mishaps cannot be
overstated. We begin this Section with overview comments on lead derivation and placement. This
will enhance appreciation of the PEARLS we then present on recognizing artifact and lead placement
errors.
03.1 Limb Leads: Basic Concepts/Placement
A standard ECG is recorded by use of 10 electrodes, which results in a recording that shows 12
ECG leads. Four of these electrodes are limb lead electrodes which are placed on each of the 4
extremities (Figure 03.1-1). The other 6 electrodes are placed on the chest, as described in Section
03.6.

Figure 03.1-1: Limb lead electrodes are placed on each extremity (left panel). Derivation of the 3
standard limb leads (leads I,II,III) is shown in the right panel. NOTE: The 4th extremity electrode
is placed on the right leg (RL). This RL electrode had traditionally been used as a ground lead
though in modern ECG recording systems, it is now used more to reduce external interference.
Note on the left in Figure 03.1-1 that the 4 limb lead electrodes are shown placed on the 4
extremities but that on the right we schematically suggest a more proximal location for limb lead
electrode placement.
Depending on institution practice where you reside you are likely to encounter other slight
variations in such placement. The good news is that since (for the most part) the body
is a fairly homogeneous conductor of electricity there will usually be no more than minimal
(if any) variation in QRS morphology as a result of such variation in electrode lead placement.
That said Realize that there may on occasion be variation in QRST morphology because of
different limb lead electrode placement (Kligfield et al. AHA/ACC Recs. JACC 49:11091127, 2007). For example small Q waves may be present on one tracing and not on another.
This could potentially lead to misinterpretation of new or prior infarction. PEARL: Be
consistent! Do not change electrode placement at your site of practice from one day-to-the-next.

Ensuring that all who record ECGs in your site of practice use the same electrode lead
placement procedure will lead to consistency and enable effective use of comparison serial
tracings to establish that new findings are truly "new" (and not the result of different recording
technique).
Despite one's best efforts to be consistent in recording limb lead placement there may still on
occasion be instances when you'll need to deviate slightly from procedure. Examples include
patients with limb amputation and/or patients with significant tremor that impedes more distal
placement. The KEY in such instances is to note on the actual ECG what the problem is (ie,
marked tremor) and what the change in recording procedure is that you have made (ie, "used
more proximal lead placement, or other adjustment ). This way IF you encounter a change
in QRST morphology you'll know that altered technique may have had a contributing role in
producing that change.

03.2 Why 10 Electrodes but 12 Leads?

The reason there are only 10 electrodes (but 12 standard ECG leads) is that one of the electrodes
(on the right leg) is not used to derive ECG waveforms and the 6 limb leads are derived from the
remaining 3 extremity electrodes (on the right arm, left arm, and left leg). Together with the 6 chest
lead electrodes this makes a total of 1+3+6 = 10 electrodes used to record 12 ECG leads.
The theoretical basis of electrocardiography arose from the premise put forth by Willem
Einthoven, who in 1903 invented the first ECG machine. Einthoven stated that the heart lies in
the center of an equilateral electrical triangle (Figure 3.2-1) While anatomically, the heart is
not quite at the center of this triangle Einthovens original premise remains accurate
enough that more than 100 years later, this concept still explains many of the fundamental
principles of electrocardiography.
An ECG recording is simply the graphic representation of the hearts electrical activity. It is
nothing more and nothing less. This electrical activity is recorded by the 10 monitoring
electrodes and then displayed in a series of waveforms that make up the standard 12-lead
ECG.
NOTE-1: An electrical wavefront travels from a negative to positive recording electrode. A
wave of depolarization that is seen as approaching a monitoring electrode will write an
upward (positive) deflection on ECG in the lead it approaches. It will write a downward
(negative) deflection in the lead it moves away from.
NOTE-2: Einthoven arbitrarily selected the left shoulder (= LA or left arm) to be positive
when recording lead I. The groin (= LL or left leg) electrode was selected to be positive
when recording leads II and III. In this way a majority of QRS complexes in the limb leads
will be predominantly positive in most leads in the electrocardiograms of most individuals
(Figure 03.2-1).
NOTE-3: As will be discussed in Section 03.3 the ECG waveform that is seen on ECG for
the 3 standard limb leads (leads I,II,III) is derived from the difference in electrical potential
between 2 of the limb lead electrodes.

Figure 03.2-1: Electrically the heart lies near the center of an equilateral triangle (Einthovens
Triangle). Because each of the angles in an equilateral triangle has 60 degrees each of the
standard limb leads (leads I,II,III) are separated from each other by 60 degrees. The ECG
waveform for each of these limb leads is derived from the difference in electrical potential between
2 of the limb lead electrodes (See text).
Beyond-the-Core: In 2007 an esteemed group of electrocardiography experts put forth an
ACC/AHA/HRS Scientific Statement of Recommendations for Standardization and Interpretation of
the ECG (Kligfield et al. JACC 49:1109-1127, 2007 ). The stated goal of this consensus report
was to reassess the relation of the resting ECG to its technology. Among the many insightful
conclusions arising out of this publication (many of which are described in this Section 3) is that
the term, unipolar should no longer be used.
In the past it was said that 3 of the 12 leads on a standard ECG were bipolar (= leads
I,II,III) and the other 9 leads (aVR,aVL,aVF; and V1-thru-V6) were unipolar. No longer!
The ACC/AHA/HRS Consensus Report emphasized that all leads are effectively bipolar.
In the past derivation of the 3 augmented leads (aVR,aVL,aVF) was determined from the
difference in electrical potential between the respective anatomic recording site minus a central
null vector. This process is no longer used. Instead all 12 leads now use a derived electrode
to serve as the opposing electrode for any lead pair.
Chest leads use Wilsons central terminal as the opposing derived electrode (Section 03.6). In
contrast the 3 augmented leads (aVR,aVL,aVF) use the Goldberger central terminal. The
central terminal previously used during the early days of electrocardiography was derived from
the mean potential of RA, LA and LL electrodes. As a result the amplitude of complexes
recorded from these extremity leads was low because the potential from the recording site was
part of the central terminal. Thus, the recording potential was partially subtracted from the total
potential displayed on the ECG. By removing the potential of the lead being recorded from the
central terminal Goldberger was able to augment the amplitude of recording complexes by
50%.
Abbreviations of Societies contributing to the Consensus Report:
ACC American College of Cardiology.
AHA American Heart Association.
HRS Heart Rhythm Society.

03.3 Derivation of the Standard Limb Leads (Leads I,II,III)

As stated the ECG waveform in the 3 standard limb leads is derived from the electrical
difference between 2 of the standard limb lead electrodes. From Figure 03.2-1 it can therefore be
seen that the electrical potential of standard lead I is a result of the electrical difference between the
LA and RA recording electrodes. Since the electrical wavefront travels from negative to positive
positive Lead I is directed toward the left arm in a horizontal plane that corresponds to an angle of
zero degrees. As we will see momentarily (in Section 03.5) zero degrees is our starting point in
the Hexaxial Lead System
It follows (from Fig. 03.2-1) that the electrical potential of standard Lead II is the difference
between the LL and RA electrodes.
Lead III is derived from the difference between the LL and LA electrodes.

Reproduced Figure 03.2-1: Einthovens triangle. The ECG waveform for each of the 3 standard
limb leads (I,II,III) is derived from the difference in electrical potential between 2 of the limb lead
electrodes (See text).
Beyond-the-Core: The 4 limb lead electrodes (placed on the RA,LA,LL and RL extremities)
serve to define the 6 frontal plane limb leads.
T he RL (Ri ght Leg) electrode serves as an electronic reference that helps attenuate
unwanted noise (interference). This RL electrode (which is not shown in Fig. 03.2-1) is not
used in the derivation of any of the limb leads.
This leaves 3 pairs of electrodes to generate the ECG waveforms of the 6 limb leads. Within
each pair one electrode is established as the positive end of the lead whereas the other
electrode of the pair is deemed the negative end. For example (as seen in Figure 03.2-1)
Lead I is derived from the electrical difference between the LA minus the RA electrodes (LARA), whereby the LA electrode is positive and the RA electrode is negative.
Since the sum of voltage gains and voltage drops within the closed circuit of the 3 standard limb
leads is equal to zero (according to Einthovens Law) the potential of lead II = the potential
of lead I + lead III at any instant of time in the cardiac cycle.

KEY Point: Because the potential of Lead II = Lead I + Lead III any of the 3 standard limb
leads can be mathematically derived from the other 2 leads. Therefore the 3 standard limb
leads contain only 2 independent pieces of information (Kligfield et al. JACC 49:1109-1127,
2007).

03.4 The 3 Augmented Leads (Leads aVR,aVL,aVF)

In addition to the 3 standard limb leads (I,II,III) there are 3 augmented limb leads. These are
Le ad aVR Lead aVL and Lead aVF. These 3 extremity leads record the difference in
electrical potential between the respective extremity lead site and the Golderberger reference central
terminal (Section 03.2). For practical purposes the orientation for each of these 3 augmented
leads (aVR,aVL,aVF) can be thought of as an outwardly directed line extending from the electrical
center of the heart to the particular electrode site on the right arm; left arm; or left leg (outwardly
directed red arrows in Figure 03.4-1).
NOTE: As discussed in Section 03.2 Leads aVR, aVL and aVF are known as the
"augmented" leads (which accounts for the little a preceding VR, VL and VF). The reason
for this a is that these extremity leads normally produce a relatively small electrical
potential. This smaller electrical potential is magnified (ie, augmented) by approximately 50%
through use of the Goldberger central reference system. Doing so results in comparable relative
size for the QRST complex in all 12 leads of a standard ECG.

Figure 03.4-1: Hexaxial lead system with lead orientation in number of degrees displayed for the 6
limb leads. Electrical orientation for the 3 standard limb leads (I,II,III) is depicted by outwardly
directly yellow arrows at 0, +60 and +120 degrees. Orientation for the 3 augmented leads
(aVR,aVL,aVF) is depicted by outwardly directly red arrows. Lead aVR is in the upper right
quadrant; lead aVF is vertical at +90 degrees; lead aVL is in the upper left quadrant at -30
degrees (See text).
Beyond-the-Core: As alluded to in Section 03.2 the Goldberger central terminal is now used as
the opposing electrode for each of the extremity leads instead of Wilsons central terminal that was

used in the past. The Goldberger central terminal is derived by dividing the sum of the electrical
potential of the other 2 extremity leads by two. That is, for lead aVR this value is (LA + LL)/2; for
lead aVL it is (RA + LL)/2; and for lead aVF it is (RA + LA)/2.
KEY Point: It is not important to try to memorize these hard-to-remember relationships! What
IS important is to appreciate that the ECG waveform for each of the 3 augmented leads can
be derived simply from knowing the ECG appearance of any 2 of the 3 standard limb leads!
Thus, from a mathematical standpoint there is much redundancy of information. Among the
12 standard leads that make up an ECG there are only 8 independent pieces of information
(because 1 of the 3 standard limb leads and all 3 of the augmented leads are derived from the
other 2 limb leads)!
BOTTOM Line: The AHA/ACC/HRS Consensus Report wants clinicians to recognize the
derived and redundant nature of the 6 limb leads. Technically only 2 leads are needed to
reproduce all ECG waveforms in these 6 leads (Kligfield et al. AHA/ACC Recs. JACC
49:1109-1127, 2007 ). That said all 6 limb leads are retained because their use facilitates
understanding and clinical interpretation (ie, it would seem far more difficult and contrived to
contemplate diagnosis of acute inferior MI from only seeing lead I and lead II although
this theoretically is possible).

03.5 The Hexaxial Lead System

Figure 03.4-1 puts together lead orientation for the 6 limb leads. This composite makes up what is
known as the Hexaxial Lead System.
Lead I is a lateral (leftward) monitoring lead that views the heart's electrical activity from a
horizontally oriented vantage point defined as 0 degrees. This is our starting point in the
Hexaxial Lead System.
In contrast to lead I standard Lead II and Lead III are inferior leads that respectively view
the heart's electrical activity from vantage points angulated at +60 and +120 degrees relative to
the heart's electrical center.
Lead aVL is another lateral (leftward) monitoring lead (Figure 03.4-1). It records the
heart's electrical activity from a vantage point that looks down at the heart from the patient's left
shoulder (from a position that corresponds to an angle of -30 degrees with respect to the
heart's electrical center).
Lead aVF is an inferior monitoring lead. The recording electrode is placed on the patient's
left lower extremity and the heart's electrical activity is viewed from a vantage point that
looks directly up at the heart from the patient's feet. This provides a perpendicular vantage point
(that corresponds to an angle of +90 degrees).
Lead aVR is the last of the augmented leads. It is the most distant recording electrode. Lead
aVR views the heart from afar looking down from the patient's right shoulder. Because the
heart sits in the left side of the chest the hearts electrical activity will generally be directed
away from this right-sided and most distant recording electrode. As a result, for practical
purposes QRST morphology in lead aVR usually contributes little to interpretation of most

tracings (with notable exception when there is lead misplacement or dextrocardia ) . PEARL:
There are some additional important clinical situations in which lead aVR may provide
invaluable information to assist our interpretation (We cover this concept in detail in Sections
09.31thru-through 09.40 devoted to How to Use Lead aVR).

03.6 Precordial Lead Placement

In addition to 3 limb and 3 augmented leads 6 more leads are routinely included in a standard
12-lead ECG. These are the precordial chest leads which view the hearts electrical activity in
the transverse (horizontal) plane. These 6 precordial leads are positioned according to anatomic
landmarks (Figure 03.6-1). As opposed to the 3 augmented limb leads (aVR,aVL,aVF) which are
connected within a closed electrical loop the 6 precordial chest leads are independent of each
other (ie, they are based on electrical activity assessed from their specific recording site and
cannot be derived from other electrodes as the 6 limb leads can).
The electrical recording from each chest lead is derived from the difference in potential
between the respective anatomic recording site and a reference central terminal. For the chest
leads the central terminal used is the one first derived by Wilson in the 1930s. This central
terminal is equal to mean potential from the RA, LA and LL electrodes ( roughly corresponding
to the center of Einthovens equilateral triangle).
BOTTOM Line: Each of the 6 precordial (chest) leads provides independent information based
on electrical activity recorded from its respective anatomic site (as shown in Figure 03.6-1)
minus the potential from a central reference terminal. Clinically the viewpoint of each
precordial lead on a 12-lead tracing correlates with the anatomic area of the heart that lies
below it.

Figure 03.6-1: Anatomic landmarks for precordial lead placement (See text).

03.7 Use of Additional Leads

Most of the time the 12 viewpoints provided by a standard 12-lead ECG convey adequate
information to appropriately evaluate and manage the patient. That said there are occasions when
use of additional leads may be helpful. Most commonly, these extra viewpoints include one or more
right-sided leads (especially lead V4R) and/or use of posterior leads (V7,V8,V9,V10).
The goal of considering additional leads is to facilitate recognition of acute RV ( Right
Ventricular) and/or posterior infarction. This objective has resulted in preference by some for a
15-lead ECG (addition of V4R, V8, V9 to the standard 12 leads).
Lead V4R: same placement as lead V4, but on the right chest.
Lead V8: placed in the back at the tip of the left scapula at the same horizontal level of lead
V6.
Lead V9: placed in the back in the left paraspinal area in between the scapula and posterior
spine, level with V6.
Our Bias: We prefer to start with 12 leads. Most of the time 12 leads are all that are needed to
determine optimal initial management. That said it is good to be aware of those situations for
which use of additional leads may be helpful (We return to this concept in Section 10.31 on acute
RV MI and in Section 10.36 on diagnosis of posterior MI).
BOTTOM Line: Opinions vary regarding need for 12 vs 15 leads. Clearly, a balance must be
struck between urgency of the situation How Long it will take to obtain additional leads
and whether this time is really worth what youll actually learn from getting more leads.

03.8 Technical Errors: Angle of Louis and Lead V1

Accurate placement of precordial leads on the chest is essential. Placing a precordial lead as little
as one IC (Intercostal Space) either too high or too low can dramatically alter QRS morphology and
amplitude.
The KEY to determining correct placement of precordial leads is to first identify the Angle of
Louis. This can be done by lowering your finger from the manubrial notch (in the midline at
the upper edge border of the sternum) until it comes to lie on a small horizontal ridge. The
2nd intercostal space lies just below this point (Figure 03.8-1).
Drop down 2 additional intercostal spaces (to the 4th intercostal space) and move just to
the right of the sternum to locate the reference position for Lead V1 (Figure 03.6-1 and Figure
03.8-1).

Figure 03.8-1: Anatomic landmarks (Angle of Louis).

Clinical NOTE: Amazingly inaccurate placement of lead V1 remains one of the most
common technical errors committed. From description of precordial lead placement in Figure
03.6-1 it should be obvious that IF the wrong intercostal space is used for placement of lead
V1 that all precordial leads will be inaccurately placed!

03.9 Technical Mishaps: Important Caveats

Be aware of the following caveats:
In women recording electrodes should be placed under the left breast to avoid precordial
lead placement errors. This is especially problematic in women with large breasts. That said
consensus is lacking as to optimal electrode placement in women because of inconsistent
literature results on the effect lead placement has on ECG waveforms. The amount of voltage
attenuation by breast tissue appears to be variable and reproducibility of precordial lead
placement is often precarious, depending on experience of the technician; breast size, shape and
adiposity; and small changes in patient position. BOTTOM Line: The AHA/ACC/HRS
Consensus Statement still recommends electrodes be placed under the breast at this time but
this recommendation may change pending additional study (Kligfield et al. AHA/ACC Recs.
JACC 49:1109-1127, 2007 ). Until that time the KEY is consistency of lead placement in any
given patient!
Lead V5 and lead V6 should both be placed level with lead V4. This is preferred to the 5th
intercostal space, which was the previously recommended reference point (Kligfield et al.
AHA/ACC Recs. JACC 49:1109-1127, 2007 ). The reason for recommending placement of leads
V5 and V6 at the same horizontal level as lead V4 is that the course of each intercostal space
is variable.
Definition of lead V5 as midway between V4 and V6 is a more reproducible landmark than the
anterior axillary line especially in cases when body habitus precludes accurate identification
of the anterior axillary line (Kligfield et al. AHA/ACC Recs. JACC 49:1109-1127, 2007).
Chest wall abnormalities are a common source of placement errors. These include pectus
excavatum or carinatum (hollow or pigeon breast) severe emphysema and large body
habitus, among others. Making a small mark on the chest where the leads were placed will
hopefully clarify lead placement and promote consistency with serial tracings.

Is the Bed Flat? Often overlooked is the effect that inclination of the bed may have on the
12-lead ECG recording. Patients with acute dyspnea (as is common with acute heart failure,
COPD, pulmonary embolism) may simply not be able to lie flat when first seen. Inclination
of the bed by 20-30 degrees may either produce Q waves or make Q waves disappear
(especially in the limb leads). Be sure to note the angle of the bed when the ECG is recorded if
it is not flat. This will hopefully resolve the problem of inferior Q waves coming and going as
the patient gets better or worse.
Comparing Serial Tracings Remember to take into account the effect that a change in axis
or precordial lead placement may have on the QRS and on ST-T waves. IF the mean QRS axis
has changed between one tracing and the next then the reason for a new Q wave seen on a
subsequent tracing may be the change in axis (and not necessarily the result of infarction).
Similarly a change in precordial lead placement may dramatically alter QRS amplitude and
morphology. The task of determining whether differences are due to a true ECG change vs axis
shift/placement may be challenging!
Arm Leads should ideally be placed between shoulders and the wrists, away from bony
prominences. Leg Leads should be placed between hips and ankles, away from bony areas.
IF for whatever reason more proximal lead placement (of limb leads on the trunk) is used
this should be noted on the tracing. Consistency is key.

03.10 Important Concepts: Lead Misplacement/Dextrocardia

Although we include technical mishaps discussed in this Section 03 at an early point in this ECG
ePub many of these concepts are advanced. Youll want to return to this section often
QUESTIONS on KEY Concepts:
What might be wrong technically in Panel A and Panel B of Figure 03.10-1?
How could you verify the cause for the unexpected appearance in each case?

Figure 03.10-1: Which technical mishaps do you suspect? (See text).

Answer to Panel A in Figure 03.10-1: The most common error in lead placement is mixing up left

and right arm electrodes. Suspect this (or dextrocardia) IF there is: i) global negativity in lead I
(negative P, QRS and T wave ); ii) an upright QRS complex in lead aVR and iii) a negative P
wave in lead II. All 3 of these findings are present in Panel A:
Normally the QRS in left-sided Lead I will be upright (assuming the heart lies in the left
side of the thorax). Lateral infarction may produce a Q in lead I but usually there is at least
some R wave. You should never see global negativity in lead I (unless there is dextrocardia
or lead reversal).
Lead aVR should normally show a negative QRS complex. The hearts electrical activity
normally moves toward the left or away from right-sided lead aVR. About the only time you
wont see global negativity in lead aVR is with marked RVH ( unless there is dextrocardia
or lead reversal).
Lead II should always show an upright P wave IF the rhythm is sinus. The path of electrical
activity from the SA Node to the AV Node is virtually parallel to the +60 degree angle of lead II
(Section 02.3). Therefore IF the P wave in lead II is not upright then the rhythm is not
sinus (unless there is dextrocardia or lead reversal).
Panel B: We reproduce Panel B from Figure 03.10-1 below in Figure 03.10-2. Which technical
mishap do you suspect? Explain your answer.

Figure 03.10-2: Which technical mishap do you suspect from the schematic precordial lead sequence
shown here? (See text).
Answer to Figure 03.10-2: Lead V2 in the precordial lead sequence in Panel B simply does not
make sense. There is not only loss of r wave from lead V1 to V2 but an upright T wave is also
seen between negative T waves in neighboring leads V1 and V3. Suspect an error in precordial
lead placement!
Key Point: Unusual R wave progression (ie, abrupt transition; sudden loss or gain of R wave
that only lasts for a single lead) should suggest precordial lead misplacement. IF ever in
doubt Repeat the ECG!

03.11 Dextrocardia: ECG Recognition

Dextrocardia is rare but it does occur. The average clinician will see no more than a handful of
cases in his/her lifetime. Dextrocardia typically produces the same ECG picture in the limb leads as
right-to-left arm lead reversal. That is lead I looks like aVR should look (there is global
negativity) and lead aVR looks like lead I should look with a positive QRS complex (Panel A in
Figure 03.11-1).
QUESTION on Recognizing Dextrocardia:
IF the limb leads in Panel A of Figure 03.11-1 were the result of dextrocardia Would you
expect the precordial lead sequence to look more like Panel C or Panel D?
Which precordial lead sequence would you expect IF the limb leads were the result of limb
lead reversal?

Figure 03.11-1: Limb lead appearance in Panel A is consistent with either limb lead reversal or
dextrocardia. Which precordial lead sequence (C or D) would you expect if the patient had
dextrocardia?
Answer to Figure 03.11-1: Panel C in Fig. 03.11-1 shows normal R wave progression in the
precordial leads. Note gradual (progressive) increase in R wave amplitude as one moves from lead
V1-toward-V4 with transition (where the R wave becomes taller than the S wave is deep)
occurring at normal location between V3-to-V4 (Section 09.5).
IF the limb leads shown in Panel A were accompanied by the precordial lead sequence in
Panel C this would suggest simple lead reversal (because R wave progression is normal as
expected when the heart lies in the left hemithorax).
On the other hand We would suspect Dextrocardia IF the limb leads in Panel A were
accompanied by the precordial lead sequence in Panel D because reverse R wave
progression is seen. That is, the R wave is tallest in lead V1 of Panel D and becomes
progressively smaller as one moves across the left precordium. This is as one would expect IF
the heart was in the right hemithorax.
Confirmation of Dextrocardia is easy: i) Listen to the heart (heart sounds will be heard on the
right); ii) Chest X-Ray will show a right-sided heart shadow; and/or iii) Repeat the ECG with
precordial leads placed on the right and you will now see normal R wave progression.
Beyond-the-Core: There are many potential variations of dextrocardia, each with its own
particular characteristics. Thus, the heart may lie on the right but the atria and ventricles may

be arranged normally (dextroversion). Alternatively the heart may be a mirror image of

normal, with the atria and ventricles reversed. The great vessels and other visceral organs may
or may not be reversed. The P wave in lead II may or may not be negative depending on the
nature of associated anatomic abnormalities. Regardless of P wave appearance in lead II a
form of dextrocardia should be suspected IF ever you see global negativity in lead I with QRS
positivity in lead aVR. Confirmation can then be forthcoming by: i) listening on the right for
heart sounds; ii) Chest x-ray; and/or iii) Repeating the ECG with precordial leads placed on the
right (which will now show normal R wave progression).

03.12 PRACTICE: Identifying Technical Errors

Consider the following series of tracings (Sections 03.13-thru-03.23). In each case Identify the
likely technical mishap. Our answers follow after each tracing.
Be Aware: An example of dextrocardia is included.
Acknowledgements: My appreciation to the following people for allowing me to use their tracings
that appear in the following Figures:
David Richley (of Scarborough in North Yorkshire, UK ) Figures 03.16-1; 03.16-2; 03.17-1;
03.18-1; 03.21-1.
Dawn Altman (of the ECG Guru) Figures 03.19-1; 03.19-2.
Jenda Enis Stros (of Liberec, CzechRepublic) Figures 03.20-1; 03.22-1.

03.13 PRACTICE: Tracing A

The rhythm in Tracing A was diagnosed as atrial flutter. Do you agree?

Figure 03.13-1: Practice Tracing A.

Answer to Tracing A: At first glance it looks like there are flutter waves in lead II, as well as in
several other leads on this tracing. That said the rhythm is not AFlutter because: i) The
undulations we see in lead II and elsewhere are not nearly regular enough to represent the 300/minute
consistent sawtooth pattern of atrial flutter; and ii) We can see regular underlying P waves ( red
arrows in Figure 03.13-2).
Note that the P waves highlighted by red arrows in Figure 03.13-2 are unaffected by the
baseline artifact!
Clinically one look at the patient confirmed that the baseline activity was artifact from a
marked resting tremor. PEARL: Be aware that the rate of a Parkinsonian resting tremor is
often close to the rate of AFlutter.
NOTE: We have already seen the lead II rhythm strip from this patient (Section 02.25).

Figure 03.13-2: Arrows have been added to Figure 03.13-1 to highlight underlying sinus P waves.
Baseline undulations are artifact from tremor.

03.14 PRACTICE: Tracing B

Beats #6 and #7 were diagnosed as a ventricular couplet (2 PVCs in a row) followed by 2 more
PVCs (beats #10,12) later on in the tracing. Do you agree?

Figure 03.14-1: Practice Tracing B.

Answer to Tracing B: At first glance it looks like there are multiple PVCs on this tracing. This is
especially true for beat #6 which is wide and perfectly placed where one might expect a PVC to
occur. That said we know that there are no PVCs on this tracing. Instead there is artifact. We say
this because:
There are baseline undulations seen throughout the tracing especially during the last half of
the tracing. Recognition that these coarse short vertical irregularities represent artifact should
heighten awareness that other unexpected undulations might also represent artifact.
The timing of beat #7 is impossible for this beat to be a real. IF beat #7 was a PVC there is
no way that beat #8 could conduct (since it would doubtlessly fall within the absolute
refractory period of beat #7). Knowing beat #7 is the result of artifact tells us that other
similar-looking deflections (ie, #6,10,12) must also be artifact.

03.15 PRACTICE: Tracing C

The rhythm in Tracing C was diagnosed as atrial flutter. Do you agree?

Figure 03.15-1: Practice Tracing C. (NOTE: Lead MCL-1 is a right-sided monitoring lead that
provides similar perspective as lead V1 on a 12-lead tracing).
Answer to Tracing C: As was the case for Tracing A ( Figure 03.13-1) the rhythm in Tracing C
initially looks like AFlutter. That said this rhythm is unlikely to be AFlutter because:
A true sawtooth pattern is absent. Instead we see irregularly occurring short vertical spikes at a
rate significantly greater than 300/minute. This strongly suggests that these short vertical spikes
represent artifact.
NOTE: We are not at all certain what the rhythm in Figure 03.15-1 is. A 12-lead ECG would be
needed to comment further as this will reveal IF flutter or other atrial activity is seen in other
leads. What can be said from Tracing C in Fig. 03.15-1 is the following: i) The rhythm looks to
be supraventricular (narrow QRS in this MCL-1 lead) ; ii) The rhythm is almost but not
completely regular (slight but definite variation in R-R intervals of some beats when measured
with calipers); iii) No definite P waves are seen (although we cant be sure if atrial activity is
or is not present elsewhere without a 12-lead tracing); and iv) Artifact appears to be present.
Pending results of a 12-lead ECG We suspect the rhythm is probably AFib (Atrial
Fibrillation) given lack of P waves and slight-but-definite irregularity in the rhythm.

03.16 PRACTICE: Tracing D

What might be wrong?

Figure 03.16-1: Practice Tracing D.

Answer to Tracing D: There is global negativity in lead I (of the P wave, QRS and T wave). This
should virtually never occur normally. The most likely causes of global negativity in lead I are: i)
LA-RA (Left Arm-Right-Arm) lead reversal; and ii) Dextrocardia (Sections 03.10 and 03.11).
In addition to global negativity in lead I Note that the P wave, QRS complex and T wave in
lead aVR are not negative as they usually are under normal circumstances. This is consistent
with either lead reversal or dextrocardia.
R wave progression is normal in Tracing D (with transition occurring between lead V3-toV4). This defines the problem as limb lead reversal and not dextrocardia (Section 03.11).
The diagnosis of LA-RA limb lead reversal was confirmed by repeating the ECG after
verifying correct limb lead placement (Figure 03.16-2). Note in Fig. 03.16-2 that the P wave,
QRS and T wave in lead I are now all upright and that there is now global negativity in lead
aVR as is normally expected.
Clinical Note: The P wave in lead II will often (but not always) be negative when there is
either lead reversal or dextrocardia. That said the P wave in lead II of Figure 03.16-1 is
upright despite limb lead reversal. The P wave is even more upright with correct lead
placement (Figure 03.16-2).

Figure 03.16-2: The ECG from Figure 03.16-1 has been repeated. Note that the P, QRS and T wave
i n lead I are now positive and that global negativity has been restored in lead aVR. R wave

progression is normal and unchanged from Fig. 03.16-1. This confirms that the unusual picture
initially seen in Figure 03.16-1 was due to LA-RA limb lead reversal (and not dextrocardia).
Acknowledgement: My appreciation to David Richley (of Scarborough in North Yorkshire,
UK) for allowing me to use these tracings.

03.16.1 ADDENDUM: Prevalence/Types of Limb Lead Errors

There are many possible ways to misconnect the 4 limb lead electrodes. Of the estimated 300 million
ECGs obtained annually worldwide as many as 6 million ECGs (~2% of the total) are thought to
manifest some technical mishap (Rowlands DJ: J Electrocardiology 41:84-90, 2008). Awareness of
how to recognize technical mishaps when they occur is therefore essential!
There are 6 ways to commit a single limb lead misconnection (RA-LA; RA-RL; RA-LL; LA-RL;
LA-LL; and RL-LL). The number of possible errors increases if multiple lead mix-ups are
included among the possibilities. Recall of the specific ECG pattern likely to be seen by each of
these technical mishaps is challenging even for the advanced interpreter. Fortunately it is not
necessary to recall each particular ECG pattern as long as you recognize that one or more leads
are misconnected.
NOTE-1: The most common form of lead misconnection is the easiest to recognize. This is LARA (Left Arm-Right Arm) limb lead reversal in which the ECG waveform in lead I looks
like aVR, and vice versa (Sections 03.10, 03.11 and Figure 03.16-1).
NOTE-2: Lead misconnections as well as anatomic errors in placement may also occur in
precordial leads. We address precordial lead errors later in this section (Sections 03.20-thru03.23).

03.16.2 ECG Findings that Suggest Limb Lead Misconnection

As stated limb lead reversal is surprisingly common. Its occasional occurrence is an almost
inevitable consequence of the quantity of ECGs that are ordered. Clinically A possible limb lead
misconnection should be suspected IF any of the following findings are present:
Global negativity in lead I.
A predominantly positive QRS complex in lead aVR.
A negative P wave in lead II.
A null vector (completely flat line) in any of the limb leads.
BOTTOM Line: It is prudent to suspect possible lead misplacement on recognition of any of the
above findings. The good news is that it is usually easy to check out IF your suspicion is
accurate: Simply repeat the ECG to see if the abnormal finding goes away.
Apply these concepts to the ECG examples we show in Sections 03.17-thru-03.19.

03.17 PRACTICE: Tracing E

What might be wrong?

Figure 03.17-1: Practice Tracing E.

Answer to Tracing E: A null vector (totally flat line) is seen in lead III. This should virtually
never occur normally. The most likely cause of a null vector in lead III, but an otherwise fairly
normal tracing is LA-RL (Left Arm-Right Leg) limb lead reversal.
As emphasized in the beginning of this Section (in Figure 03.1-1) the RL (Ri ght Leg)
electrode serves as a zero electrical potential (ground lead) reference point.
Lead misconnections involving the RL electrode typically produce a predictable ECG pattern.
With LA-RL lead reversal Leads I and II look the same; leads aVL and aVF look the same
and lead III records a null vector. This is precisely the pattern we see in Figure 03.17-1.
Note that precordial lead R wave progression in Fig. 03.17-1 is normal (with transition
occurring between V3-to-V4).
IF on the other hand, there was RA-RL lead reversal Leads I and aVL will look the same
(with a negative QRS); leads aVR and aVF look the same (with a positive QRS) and it will
be lead II that records a null vector (Figure 03.18-1).
BOTTOM Line: Many brain cells are required to commit the expected specific ECG patterns of
LA-RL and RA-RL lead reversal to memory. This is not needed clinically because all that counts
is recognition that some type of lead misconnection is possible. Awareness of the 4 easy-toremember ECG findings cited in Section 03.16.2 should be all that is needed to recognize most
clinically significant lead misconnections. Look for one or more of the following: i) Global negativity
in lead I; ii) A predominantly positive QRS complex in lead aVR; iii) A negative P wave in lead II;
and/or iv) A null vector (completely flat line) in any of the limb leads.
Beyond-the-Core: The electrical potential recorded from the RL electrode is virtually identical
to that recorded from the LL electrode (zero in each case). As a result RL-LL
misconnection does not change the relationships in Einthovens triangle because both RL
and LL electrodes record a similar zero electrical potential. This means you will not be able to
recognize RL-LL misconnection based on ECG appearance. That said this does not matter,
because the 12-lead ECG will be essentially unchanged if RL and LL electrodes are
inadvertently misconnected.

Acknowledgement: My appreciation to David Richley (of Scarborough in North Yorkshire,

UK) for allowing me to use this tracing.

03.18 PRACTICE: Tracing F

What might be wrong?

Figure 03.18-1: Practice Tracing F.

Answer to Tracing F: A null vector (totally flat line) is seen in lead II. This should virtually never
occur normally. The most likely cause of a null vector in lead II is RA-RL (Right Arm-Right Leg)
limb lead reversal.
In Section 03.17 We discussed the ECG pattern expected with LA- RL lead reversal (Tracing
E = Figure 03.17-1). In this case the overall ECG looks relatively normal with exception of a
null vector in lead III.
In contrast the null vector in Figure 03.18-1 is seen in lead II. This suggests that the
misconnection is the result of RA-RL lead reversal. Other features of RA-RL misconnection are
that: i) Leads I and aVL look the same (and manifest a negative QRS) ; and ii) leads aVR and
aVF look the same (and manifest a positive QRS). Note that precordial lead R wave
progression in Fig. 03.18-1 is normal (with transition occurring between V3-to-V4).
BOTTOM Line: Once again recall of the specific features that distinguish RA-RL lead reversal
from other limb lead misconnections is far less important than recognizing that some type of lead
misconnection is likely. Recognition of a technical mishap is easy for the ECG shown in Figure
03.18-1 because: i) there is global negativity in lead I; ii) lead aVR is positive; and iii) there is a null
vector in one of the limb leads (seen here in lead II).
Confirmation that limb lead reversal is the cause of the ECG picture in Figure 03.18-1 is
readily attained by verifying lead placement and repeating the ECG. The abnormal findings in
Fig. 03.18-1 (null vector in lead II; global negativity in lead I; positive R wave in aVR)
should no longer be seen once an ECG with correct lead placement is obtained.
Acknowledgement: My appreciation to David Richley (of Scarborough in North Yorkshire,
UK) for allowing me to use this tracing.

03.19 PRACTICE: Tracing G

What might be wrong?

Figure 03.19-1: Practice Tracing G.

Answer to Tracing G: There are several distinctly unusual findings on the 12-lead ECG seen in
Figure 03.19-1. These include:
Very negative P wave with deep Q wave in lead I. This is not the obvious global negativity
appearance that we have previously seen in Figure 03.16-1 and Figure 03.18-1 in which we
knew something was wrong. But the P wave in left-sided lead I is usually not decidedly
negative when the P wave is positive in lead II as it is here. In addition the Q wave in lead I
is clearly too deep to be a normal septal q wave. While possible the Q waves in leads I and
aVL represent prior high lateral infarction the possibility of a technical mishap should be
considered.
Both the P wave and QRS complex in lead aVR are positive. This shouldnt normally be if all
leads are correctly placed unless there is marked underlying structural abnormality.
Impression of Figure 03.19-1: In addition to the unusual appearance of leads I and aVR overall
QRS amplitude in Fig. 03.19-1 is greatly reduced (with the largest QRS complex surprisingly being
recorded in lead V1) there is marked frontal plane axis deviation and precordial R wave
progression is reversed. Bottom Line: Something is very wrong here.
Our first reaction to seeing the ECG in Figure 03.19-1 is to find out more about the patient.
Are there symptoms? Any history of heart disease or prior infarction?
Is there a prior ECG?
What does physical examination show? Are heart sounds heard on the left side of the chest?
Is there a chest x-ray?
What does a repeat ECG look like after verifying that all leads are correctly placed?
Follow-Up to the Case: Heart sounds were heard on the right side of the chest. The ECG was
repeated with precordial leads placed on the right (Panel B in Figure 03.19-2). The patient had
dextrocardia.

As discussed in Sections 03.10 and 03.11 there are many potential forms of dextrocardia.
The common theme on ECG is that the appearance of leads I and aVR is reversed with
dextrocardia from what you would normally expect. This is indeed the case in Figure 03.19-1.
It is easy to confirm dextrocardia (Section 03.11): i) Heart sounds are heard on the right; ii)
Chest x-ray shows a right-sided heart shadow; and iii) Repeat ECG with precordial leads
placed on the right at least partially normalizes R wave progression. While admittedly, R wave
progression in Panel B of Figure 03.19-2 is not normal (since a predominant R wave is never
seen) right-sided placement of precordial leads clearly results in an increase in positive
forces, as would be expected if the heart was situated on the right side of the chest.

Figure 03.19-2: Comparison between the original precordial lead sequence seen in Figure 03.19-1
(Panel A) with the precordial lead sequence on repeat ECG with precordial leads now placed in
comparable anatomic location, but on the right side of the chest (Panel B). Note that while a
predominant R wave is never attained in Panel B there is nevertheless a decided increase in
positive QRS amplitude that supports the diagnosis of dextrocardia.
Acknowledgement: My appreciation to Dawn Altman (of the ECG Guru) for allowing me to use
these tracings.

03.20 PRACTICE: Tracing H

Beat #5 was interpreted as either a PVC or an aberrantly conducted PAC. Do you agree?

Figure 03.20-1: Practice Tracing H.

Answer to Tracing H: At first glance beat #5 looks like a legitimate early beat, especially in
leads I, II and aVR. That said beat #5 is not real. Instead, it is artifact. We know this because:
Beat #5 lacks a T wave.
There is absolutely no effect of the waveform labeled #5 on the underlying rhythm that continues
undisturbed at the same R-R interval.
The waveform labeled #5 looks like artifact.
There is evidence elsewhere on this tracing of similar artifactual distortion. Note the small
geometric spike in the T wave of beat #1 in leads II and aVR as well as a similar small spike
artifact occurring just past the midpoint of the R-R interval between beats #3-to-4 in leads I, II
and aVR.
Bottom Line: The deflection labeled #5 in Figure 03.20-1 is not real. We can dismiss it as artifact
without need for further attention.
Acknowledgement: My appreciation to Jenda Enis Stros (of Liberec, CzechRepublic) for
allowing me to use this tracing.

03.21 PRACTICE: Tracing I

The precordial lead sequence seen in Panel A and Panel B of Figure 03.21-1 was obtained moments
apart from the same patient.
Can you guess what changed from one tracing to the next?

Figure 03.21-1: Practice Tracing I.

Answer to Tracing I: The precordial lead sequence in Panel A was obtained with incorrect high
placement of several chest lead electrodes. The effect this may have on the ECG recording is
obvious when compared to the repeat ECG performed on this patient a short while later with
verified correct lead placement (Panel B).
Note loss in amplitude of the initial r wave in leads V1 and V2 when chest leads are placed too
high (Panel A). In addition an rSr (incomplete RBBB) pattern with T wave inversion was
seen in both leads V1,V2 in Panel A but is no longer seen in Panel B when the ECG is
repeated with correct chest lead placement.
Clinical Note: The importance of correct chest lead placement cannot be overstated (Sections 03.6
and 03.7). Erroneous placement of lead V1 at a location that is 1 or 2 interspaces too high will
result in erroneous placement of the remaining 5 precordial leads. Potential consequences include:
Misinterpretation of LAA (Le f t Atrial Abnormality) since inadvertent high chest lead
placement may result in deepening of the negative component of the P wave in lead V1.
Inaccurate diagnosis of incomplete RBBB with associated ST-T wave abnormality ( Panel A in
Fig. 03.21-1). This could result in confusion with Brugada syndrome variants that are really not
present (Section 05.XXXX)
Inaccurate interpretation of R wave progression in the precordial leads leading to overcall
or undercall of prior anteroseptal infarction.
Inaccurate representation of true precordial lead amplitude (leading to inaccurate diagnosis of

LVH).
False impression that there has been a change in ECG appearance when either the prior
tracing(s) or current tracing was unknowingly obtained with inaccurate chest lead placement.
Acknowledgement: My appreciation to David Richley (of Scarborough in North Yorkshire,
UK) for allowing me to use this tracing.

03.22 PRACTICE: Tracing J

What might be wrong?

Figure 03.22-1: Practice Tracing J.

Answer to Tracing J: The precordial lead appearance of lead V2 makes no sense:
The initial small r wave that was seen in lead V1 has been lost. Instead there is now a smallbut-definite Q wave in lead V2. This is associated with a disproportionately tall R wave as
well as some ST segment elevation.
Equally abrupt change in QRST appearance between leads V2-to-V3 as was seen between
leads V1-to-V2.
Bottom Line: Something just looks wrong. The solution is easy: Repeat the ECG, being sure to
verify correct precordial lead placement. Only in this way can we determine IF the ST elevation seen
in lead V2 of Figure 03.22-1 is likely to be real and of concern, or a consequence of inaccurate chest
lead placement.
Acknowledgement: My appreciation to Jenda Enis Stros (of Liberec, CzechRepublic) for
allowing me to use this tracing.

03.23 PRACTICE: Tracing K

What might be wrong?

Figure 03.23-1: Practice Tracing K.

Answer to Tracing K: While overall the ECG in Figure 03.23 appears to be fairly unremarkable
lead V6 simply does not make sense.
We interpret the ECG in Fig. 03.23-1 as showing normal sinus rhythm; normal intervals and axis;
no chamber enlargement; no more than a tiny q wave in lead III; normal R wave progression
(with transition between leads V3-to-V4) and some baseline artifact (especially in lead V5)
but no acute ST-T wave changes. That said it does not make sense for the S wave that
disappeared after lead V4 to abruptly reappear with a predominant S>R wave in lead V6.
Instead it would make much more sense if the waveform currently seen in lead V6 was
recorded in lead V4 (with the current V4 and V5 recordings being instead from V5 and V6).
Bottom Line: Simply repeating the ECG after verifying chest lead placement is an easy way to
know for certain what the true precordial lead ECG appearance in Tracing K should be.

04.0 Intervals (PR/QRS/QT)

04.1 What are the 3 Intervals in ECG Interpretation?

As per the Systematic Approach introduced in Section 01.1 after assessing a 12-lead ECG for
Rate and Rhythm one then looks to determine the 3 ECG Intervals (Figure 04.1-1):
The PR interval is defined as the period that extends from the onset of atrial depolarization
(beginning of the P wave) until the onset of ventricular depolarization (beginning of the
QRS complex).
The QRS complex itself (discussed more in Section 05.1).
The QT interval the period from the onset of the QRS complex until the end of the T wave
(See Section 06.1).

Figure 04.1-1: The 3 ECG Intervals (= the PR QRS QT intervals). Measure intervals in the lead
where the interval looks longest. Precise determination of an interval is usually not necessary if it
falls within the normal range.
04.2 The PR Interval: What is Normal?
The best lead to assess the PR interval in is usually lead II. The P wave should be upright in lead II
if the rhythm is sinus. In adults the PR interval is considered normal if it measures between 0.12
and 0.20 second (See Panel A in Figure 04.2-1).
The PR interval is "short" if it measures less than 0.12 second in duration in lead II (Panel
B). One cause of a short PR interval is WPW (Wolff-Parkinson-White) syndrome in which an
AP (Accessory Pathway) exists that bypasses the AV node, thereby requiring less time for the
impulse to arrive in the ventricles (See Section 05.37). NOTE: Not all patients with a short PR
interval (0.12 sec.) have WPW. Instead the PR interval may sometimes be short because it is

anatomically small or conduction is fast. Beyond-the-Core: The chance that a patient has an AP
becomes greater when the PR interval is very short (ie, 0.10 second).
The PR interval is long if it measures more than 0.20-0.21 second. One can tell at a
glance if the PR interval is long by looking to see IF it is clearly more than 1 large box in
duration (Panel C in Fig. 04.2-1).

Figure 04.2-1: Limits of the PR interval. Panel A The PR interval is normal (between 0.12-0.20
second in adults). Panel B the PR interval is short (less than 0.12 second). Panel C the PR
interval is long (clearly more than one large box in duration).
04.3 The PR Interval: Clinical Notes
When the PR interval is long We say there is 1st-degree AV block. Given that the isolated finding
of 1st degree AV block ( even if marked) is usually not clinically significant (Section 02.70) we
generally undercall this finding. Our preference is to accept a PR interval = 0.21 second as normal
(and not to call 1st degree until the PR interval is 0.22 second = definitely more than 1 large
box). The PR interval in Panel C of Figure 04.2-1 is clearly more than 1 large box in duration (We
estimate the PR interval in Panel C to be ~0.26 second).
We prefer not to use the term, borderline 1st degree since all this really says, is that you
almost have a finding that even if present would not be clinically important. Instead, our
preference is to say the PR interval is either normal (0.21 second) or long (>0.21 second).
Precise determination of a PR interval that falls within the normal range is not necessary.
Clinically it does not matter IF the PR is 0.16, 0.17 or for that matter 0.19 second. Instead, it
suffices to simply say the PR interval is normal".
Norms for children for the PR and QRS intervals are slightly different because the pediatric
heart is smaller than the adult heart. Specific normal limits for the various intervals are agedependent. For example a PR interval of 0.18 second may be prolonged for a young child,
whereas it would be normal for a young adult. For the purposes of this ePub it suffices to be
aware that interval duration may differ slightly because of the smaller heart of a younger patient.

04.4 Memory Aid: How to Recall the 3 ECG Intervals

An easy way to recall the upper limits of normal for the 3 ECG intervals is simply to think of the
numbers 1 and 2 :
The PR interval is long (in adults) IF it is clearly more than 1 large box (>0.20-0.21
second in duration).
The QRS is long IF it measures more than 1/2 a large box (>0.10 second in duration).
The QT interval is long IF it comprises more than 1/2 the R-R interval.

05.0 Bundle Branch Block/IVCD

05.1 The QRS Interval: What is Normal QRS Duration?

The QRS interval represents the time it takes for ventricular depolarization to occur. With sinus
rhythm in adults the process of ventricular activation should normally be complete in no more
than 0.10 second. This means that IF the QRS complex is longer than half a large box in duration
that the QRS is wide (Figure 05.5-1):

Figure 05.1-1: The QRS is wide IF it measures more than 0.10 second (which is more than
half a large box in duration).
Clinical Notes: QRS duration can be measured from any of the 12 leads of a standard ECG. Select
the lead in which the QRS complex appears to be longest.
Practically speaking all that matters is whether the QRS is normal or wide. Precise
measurement of QRS duration for a complex that is clearly within the normal range is not
necessary. Given that 0.10 second is the upper normal limit for QRS duration in adults the
QRS is said to be wide IF it measures more than half a large box in duration (Figure
05.1-1).
These limits for QRS interval duration do not hold true for children (for whom lesser degrees of
QRS prolongation may be abnormal).

05.2 IF the QRS is Wide: What Next? (BBB Algorithm)

IF the QRS complex is wide We suggest that you STOP! At this point Short-circuit your usual
sequence. Instead of your usual systematic approach We suggest the following:
First Ensure that the patient is stable! This is because IF the patient is unstable (and the
rhythm is VT = Ventricular Tachycardia) you may need to immediately shock (Section
02.47).
But IF the QRS is wide and the rhythm is supraventricular the next step in your ECG
interpretation approach should be to proceed according to the Algorithm shown in Figure 05.21:

Figure 05.2-1: Algorithm for how to proceed IF the rhythm is supraventricular (ie, not WPW or
VT) and the QRS is wide. You should be able to determine the type of conduction defect in no more
than a few seconds (See text).
KEY Point: IF the QRS is Wide and the rhythm is supraventricular (ie, sinus, AV nodal) then
determine WHY the QRS is wide before proceeding further with your interpretation. Practically
speaking (and assuming we are not dealing with VT or WPW) there are only 3 reasons for QRS
widening with sinus rhythm:
There is typical RBBB (Right Bundle Branch Block).
There is typical LBBB (Left Bundle Branch Block).
The QRS is wide but neither typical RBBB nor typical LBBB is present. In this case, the reason
the QRS is wide will be IVCD (IntraVentricular Conduction Delay).
The good news (as discussed on the next few pages) is that use of the Algorithm in Figure
05.2-1 allows accurate diagnosis of the type of conduction defect (BBB or IVCD) in less than 5
seconds!
The reason we can accurately diagnose the type of conduction defect so quickly is that: i)
There are only 3 possible answers (typical RBBB; typical LBBB; or IVCD) ; and ii) We only
need to look at 3 leads to make the diagnosis. NOTE: With experience Youll look at all 12
leads for finer aspects of ECG interpretation. But only 3 leads are needed to diagnose the type of
conduction defect.
The 3 KEY leads (and the only 3 leads needed) to determine the type of conduction defect
(RBBB, LBBB, or IVCD) are leads I, V1, and V6. NOTE: We key in on 2 left-sided leads
(leads I,V6) and 1 right-sided lead (lead V1) when using Figure 05.2-1 to diagnose the type
of conduction defect:

Remember Use of the algorithm in Fig. 05.2-1 implies that the rhythm is supraventricular
(and not VT or WPW).

05.3 FIGURE 05.3-1: Why the Need for the BBB Algorithm?
The reason you want to recognize conduction defects before you get too far in the interpretation
process is that criteria for axis, LVH, RVH, ischemia and infarction are all different when there is
BBB or IVCD! Consider the example in Figure 05.3-1, obtained from a hemodynamically stable
patient with a history of heart failure:
Has this patient had an anterior MI (slanted red arrows) at some point in the past?
Is there ongoing lateral ischemia (red circle) in lead V6?

Figure 05.3-1: 12-lead ECG obtained from a stable patient with a history of heart failure. The rhythm
is sinus (vertical arrow in lead II insert) and the QRS is wide. What next? Has there been
anterior infarction (slanted arrows)? Is there lateral ischemia (red circle in lead V6)?
Answer to Figure 05.3-1: The patient is hemodynamically stable. The rhythm is sinus (vertical
arrow in the lead II insert) and the QRS complex is wide. Thus, although one might be tempted to
call anterior MI (slanted arrows in V1,V2,V3) and ongoing ischemia (red circle in lead V6) the
Algorithm in Figure 05.2-1 advises us to first STOP and diagnose WHY the QRS is wide (?) before
proceeding further.
As we will discuss momentarily the reason for QRS widening in Figure 05.3-1 is complete
LBBB (See Section 05.6). As a result the deep anterior QS complexes and lateral ST-T
wave changes are simply expected consequences of LBBB and not indicative of prior infarction
or ischemia.
BOTTOM Line: Had we not STOPPED at an early point in the interpretation process to assess
the reason for QRS widening we would have spent needless time thinking the patient had
potentially active ischemia/infarction when in reality there is no evidence of acute change on
this ECG.

05.4 Typical RBBB: Criteria for ECG Recognition

The 12-lead appearance of typical complete RBBB in the 3 KEY leads (leads I,V1,V6) is
schematically shown in Figure 05.4-1. ECG criteria for diagnosis of complete RBBB include the
following:
QRS widening to at least 0.11 second.
An rSR' or rsR' in right-sided lead V1.
A wide terminal S wave in lead I and lead V6. The QRS complex is usually predominantly
positive in these left-sided leads with RBBB. There may or may not be an initial small q wave.
The KEY to confirming the diagnosis of RBBB is the wide terminal S wave in leads V1,V6
(Figure 05.4-1).

Figure 05.4-1: Schematic ECG of typical complete RBBB in the 3 KEY leads. Note the rsR in lead
V1 and wide terminal S waves in leads I,V6. Memory Aid Think of RBBB and the "R's" in
that there is an rSR' complex with a taller Right rabbit ear (the R) in a Right-sided lead (= lead
V1).
Clinical Example of Complete RBBB: We illustrate application of the criteria for diagnosis of
complete RBBB by our sequential approach to the 12-lead ECG shown in Figure 05.4-2:
The rhythm in this ECG is sinus tachycardia at a rate just over 100/minute (arrow in lead II
indicating upright sinus P wave).
The QRS complex is wide (0.11 second). QRS duration is best assessed from a lead where the
QRS is well defined and its duration appears to be longest. Despite seemingly normal QRS
duration in several leads on this tracing (leads aVL,V3,V4) there is little doubt that the QRS
is clearly more than half a large box in duration in lead V1.
Identification of a sinus rhythm with QRS widening is indication to STOP our systematic
approach and branch to the Algorithm in Figure 05.2-1. We focus on the 3 KEY leads (leads
I,V1,V6). As shown in the inserts in Figure 05.4-2 complete RBBB is diagnosed by the
typical rSR in V1 (with taller right rabbit ear) and the wide terminal S wave in leads I,V6.

Figure 05.4-2: 12-lead ECG showing complete RBBB (See text).

05.5 RBBB: Clinical Notes
The upper normal limit for QRS duration in adults is 0.10 second (half of a large box). Anything
more than 0.10 second is long (Section 05.1).
Complete RBBB may occur with a QRS of 0.11 second. This differs from the situation for
LBBB for which the QRS must attain 0.12 second (Section 05.6). The RV ( Right Ventricle)
is much thinner than the LV so RBBB may be complete with a QRS complex that is not as
wide as it needs to be when there is complete LBBB (conduction through nonspecialized
myocardial fibers in the blocked right ventricle may be complete within 0.11 second
whereas it will take 0.12 second to get through the thicker LV when there is LBBB).
An incomplete RBBB is said to be present IF QRS morphology is typical in leads I,V1,V6
but the QRS is not prolonged to at least 0.11 second (See Section 05.18).
RBBB is a terminal delay. It does not affect the initial part of ventricular activation (during
which time the septum is activated and during which time Q waves are written). As a result
Q waves may still be written despite RBBB. This differs from LBBB which alters septal and
initial vector activation (thereby hiding most Q waves! See Sections 05.7, 05.8). Note that
despite the complete RBBB present in Figure 05.4-2 inferior Q waves (in leads II,III,aVF)
are still seen (which may be indicative of inferior infarction of uncertain age).
The terminal delay of RBBB may account for the fact that: i) the R in V1 may be quite tall ( the
LV has already depolarized so the small RV is unopposed as it depolarizes ) ; and ii) the
terminal S wave in leads V1,V6 is wide (conduction through the blocked RV is slow due to the
RBBB).
RBBB is a relatively common conduction defect that is not necessarily associated with
underlying pathology (especially if seen in an otherwise healthy adult with a normal physical
exam and no history of heart disease). IF doubt exists about possible underlying heart disease
an Echo could be obtained (though an Echo is not necessarily needed on a routine basis).
In contrast new RBBB in a patient with acute MI is clearly cause for concern (suggests a
larger infarct and more worrisome course).
In contrast to RBBB (which may be a relatively benign finding in otherwise healthy adults)
the finding of complete LBBB is almost always associated with some significant underlying
cardiac pathology.

05.6 Typical LBBB: Criteria for ECG Recognition

The 12-lead appearance of typical complete LBBB in the 3 KEY leads (leads I,V1,V6) is
schematically shown in Figure 05.6-1. ECG criteria for complete LBBB include the following:
QRS widening to at least 0.12 second (whereas complete RBBB can occur with a QRS = 0.11
second).
An upright (monophasic) QRS complex in leads I and V6 that may (or may not) be notched.
But there should not normally be any q wave in either lead I or V6.
A predominantly negative QRS complex in lead V1. There may (or may not) be an initial small
r wave in lead V1 (lead V1 may show either a QS or rS complex).

Figure 05.6-1: Schematic ECG of typical complete LBBB in the 3 KEY leads. NOTE: there
should never normally be a Q wave in a left-sided lead (lead I,V6) with typical LBBB unless there
has been prior infarction (Section 05.28).
05.7 FIGURE 05.7-1: LBBB alters Septal Activation
Normally the very first part of the ventricles to depolarize (after the impulse passes through the
AV node and Bundle of His) is the left side of the ventricular septum. As a result septal
depolarization normally moves from left-to-right (arrow pointing left-to-right in Panel A of Figure
05.7-1).
Since the RBB (Right Bundle Branch) travels down the right side of the septum this initial
left-to-right direction of septal depolarization does not change when there is RBBB because the
left side of the septum remains intact and still initiates septal depolarization (Panel B).
In contrast, with LBBB the normal left-to-right direction of septal activation will change.
This is because the block with LBBB prevents the initial vector of septal activation from starting
on the left (Panel C). As a result ventricular activation with LBBB moves almost entirely
from right-to-left. Thus, the initial part of the QRS complex (during which time Q waves are
written) is altered by LBBB that changes the direction of septal depolarization.

Figure 05.7-1: Sequence of normal septal activation in which there is left-to-right septal
depolarization (arrow in Panel A). This left-to-right direction is preserved with RBBB (Panel B)
but becomes right-to-left with LBBB (arrow in Panel C).
It is this altered direction of initial septal activation that accounts for many of the ECG findings of
LBBB:
Because septal activation with LBBB moves right-to-left the small septal q waves that
are often normally present in one or more lateral leads (I,aVL,V6) should not be seen. IF a Q
wave (even a small one) is seen in a lateral lead (I, aVL or V6) in a patient with LBBB that
patient has had a prior infarction.
Following right-to-left septal activation (arrow in Panel C of Figure 05.7-1) ventricular
activation continues to the left and posteriorly, as the large LV is depolarized. This results in the
totally upright complex (R wave) seen in left-sided leads (I,V6) with LBBB. There may or may
not be a notch = RR in leads I,V6 (Figure 05.6-1).
Right-to-left septal activation, followed by continued leftward depolarization (as the rest of the
LV is activated) results in a predominantly negative complex (QS or rS) in right-sided lead
V1 with LBBB. Neighboring anterior leads (V1,V2,V3) often manifest a QS complex with
LBBB without this indicating prior MI (Figure 05.8-1 in the next Section).

05.8 FIGURE 05.8-1: Clinical Example of Complete LBBB

We illustrate application of the criteria for diagnosis of complete LBBB by our sequential approach
to the 12-lead ECG shown in Figure 05.8-1:
The rhythm in this ECG is sinus tachycardia at a rate of ~100/minute (arrow in lead II
indicating upright sinus P wave).
The QRS complex is wide (at least 0.12 second in duration).
Identification of a sinus rhythm with QRS widening is indication to STOP our systematic
approach and branch to the Algorithm in Figure 05.2-1. We focus on the 3 KEY leads (leads
I,V1,V6). As shown in the inserts in Figure 05.8-1 complete LBBB is diagnosed by the
predominantly negative QRS complex in lead V1 and the monophasic upright R wave in leads
I and V6.
Note that the R wave is notched in lead I of Fig. 05.8-1 but not in lead V6. R wave notching
in one or more lateral leads may or may not be seen with LBBB. No definite clinical

implications are conveyed by its presence or absence.

Note also that there are QS complexes in leads V1-thru-V3 and there is ST-T wave
depression in several lateral leads (I,V5,V6). Both of these findings are common with LBBB,
and do not convey any information regarding possible ischemia/infarction. In addition the
slight (but not marked) ST elevation seen in anterior precordial leads is common and an
expected finding with LBBB.
Beyond-the-Core: We also draw attention to the QS complex seen in leads III and aVF of Figure
05.8-1. Because LBBB changes the sequence of initial ventricular activation (during which time
Q waves are written) the presence of Q waves in leads other than the lateral leads is not
indicative of infarction when there is LBBB. Bottom Line: All we can say about the ECG in
Figure 05.8-1 is that there is complete LBBB. There is no evidence of any acute change.

Figure 05.8-1: 12-lead ECG showing complete LBBB (See text).

05.9 LBBB: Clinical Notes
The ECG finding of LBBB is virtually always associated with significant underlying heart disease
(ie, cardiomyopathy, longstanding hypertension with LVH, heart failure, coronary artery disease,
valvular or congenital heart disease). It is rare in adults (or in children) to find isolated benign
LBBB.
The diagnosis of other conditions (ischemia, infarction, ventricular hypertrophy ) will
always be more difficult when there is BBB. This is especially true for LBBB which
changes the direction of initial septal activation (Section 05.7). That said diagnosis of other
conditions is not impossible on certain occasions (See Sections 05.24-through-05.32).
The reason no septal q wave should be seen with typical LBBB in either lead I or lead V6
is that LBBB causes the septum to be activated from right-to-left. As a result left-sided
leads (I,V6 and for that matter aVL and V5) see the initial activation vector as coming toward
instead of moving away from the left (Panel C in Figure 05.7-1). IF on the other hand, there has
been septal MI you may then see a small q wave in one or more lateral leads despite the
LBBB.

05.10 Incomplete LBBB: Does it Exist?

There is an entity known as incomplete LBBB. That said incomplete LBBB is very uncommon,
difficult to diagnose, and usually not clinically important to distinguish from nonspecific IVCD. This
differs from the situation with incomplete RBBB which is very common and easy to diagnose (See
Section 05.18).
Complicating diagnosis of incomplete LBBB is uncertainty about when LBBB is truly
complete. IF for example, the QRS continues to widen over a period of months-to-years (say,
from 0.12 to 0.14 to 0.16 second) at what point was the LBBB complete? Recognition of
incomplete LBBB is also made more difficult by the fact that other conditions (ie, LAHB, LVH)
may slightly widen the QRS in a similar-appearing pattern.
Practically Speaking the diagnosis of incomplete LBBB is really a retrospective one. It is
only over time that you can know with certainty that a prior ECG with some QRS widening was
in fact one stage in an evolving process that ultimately led to more QRS widening that finally
became complete LBBB. BOTTOM Line: While nice to be aware of the controversy and lack
of consensus regarding the definition of incomplete LBBB this diagnosis is difficult to
prove and usually of little clinical benefit. We therefore suggest not to worry about trying to
distinguish between incomplete LBBB vs slight QRS widening due to a nonspecific IVCD
pattern.

05.11 IVCD: Criteria for ECG Recognition

The ECG appearance of IVCD (IntraVentricular Conduction Delay or Defect) is difficult to
characterize. This is because IVCD is often the end result of a number of different pathophysiologic
processes rather than a discrete defect in the conduction system (as usually occurs with RBBB or
LBBB).
Examples of conditions that may lead to IVCD include myocardial infarction, cardiomyopathy
with ventricular fibrosis, chamber enlargement and/or any combination of these (with or
without an associated component of BBB).
A schematic example of IVCD is shown in Figure 05.11-1. ECG diagnostic criteria for IVCD
include the following:
QRS widening to at least 0.11 second.
Neither typical RBBB nor typical LBBB is present.

Figure 05.11-1: Schematic example of IVCD. QRS morphology is not typical here for either RBBB
or LBBB in all 3 of the KEY leads (leads I and V1 are consistent with RBBB but lead V6
suggests LBBB). Clearly many forms of IVCD are possible in addition to the one shown here.
05.12 IVCD: Clinical Notes
The term IVCD is used to describe the entity in which there is sinus rhythm with QRS widening
but QRS morphology in the 3 KEY leads (I,V1,V6) is not typical for either RBBB or LBBB.
This use of the term IVCD is magic as it tremendously simplifies (and expedites) the
diagnostic process. Once we rule out VT and WPW We know QRS widening in a
supraventricular rhythm will be due to either RBBB, LBBB or IVCD (See Algorithm in Figure
05.2-1).
IF criteria for RBBB and LBBB are not met (in each of the 3 KEY leads) then IVCD is the
reason for the wide QRS. End of process! We illustrate this concept in the clinical example of
IVCD shown below (Figure 05.13-1).
NOTE: It will often be difficult (if not impossible) with IVCD to assess for LVH/RVH; prior MI; or
acute ST-T wave changes.
As is the case for RBBB and LBBB the clinical significance of IVCD depends greatly on the
setting in which it occurs. Slight QRS widening (of up to 0.10-to-0.11 second) is
occasionally seen in otherwise healthy young adults (in which case, this slight QRS widening
of IVCD is most often of no clinical significance).
IF doubt exists about the presence of underlying structural heart disease an Echo could be
obtained (although an Echo is not necessarily needed on a routine basis).
In contrast IVCD in an older adult with chest pain or heart failure may carry similar
implications as would LBBB (ie, coronary artery disease, infarction, cardiomyopathy ).
Clinical correlation is everything!

05.13 FIGURE 05.13-1: Clinical Example of IVCD

We illustrate application of the criteria for diagnosis of IVCD by our sequential approach to the 12lead ECG shown in Figure 05.13-1:
The rhythm in this ECG is AFib (Atrial Fibrillation) because it is irregularly irregular

without P waves.
The QRS complex is wide (at least 0.12 second).
Identification of a supraventricular rhythm with QRS widening is indication to STOP our
systematic approach and branch to the Algorithm in Figure 05.2-1. We focus on the 3 KEY
leads (leads I,V1,V6). As shown in the inserts in Figure 05.13-1 IVCD is diagnosed because
QRS morphology does not resemble either RBBB or LBBB in each of the 3 key leads. That is,
the QRS complex in lead I of Fig. 05.13-1 looks like LBBB but not in leads V1,V6 (which if
anything look more like RBBB) . Bottom Line: One cant say much else about this tracing
beyond AFib with a controlled ventricular response plus QRS widening due to IVCD.

Figure 05.13-1: 12-lead ECG showing IVCD (See text).

05.14 ST-T Wave Changes: What Happens with BBB?
RBBB and LBBB each alter the sequence of ventricular depolarization. This is why they produce the
alterations in QRS morphology discussed in this Section. As a direct result of this altered sequence of
activation these conduction defects also alter the sequence of ventricular repolarization, which
leads to development of secondary (2) ST-T wave changes (Figure 05.14-1).
The ST-T wave changes shown in Fig. 05.14-1 are called secondary because they are the
direct result of (ie, they are secondary to) the conduction defect itself. That is We expect to
see this pattern of ST-T wave response shown in Figure 05.14-1 as a normal part of RBBB or
LBBB.

Figure 05.14-1: The expected ST-T wave response to either typical RBBB or typical LBBB is ST
opposition. That is the ST segment and T wave should be oppositely directed to the last QRS
deflection (red and yellow arrows ) in each of the 3 KEY leads (= leads I,V1,V6). Deviation from
this pattern is abnormal and indicates a primary (1) ST-T wave change (that suggests ischemia
or infarction).
KEY Points: The beauty of the ST opposition rule in Figure 05.14-1 is that it allows you to
assess ST-T morphology with BBB within 2-3 seconds!
Although we do look at all 12 leads with BBB, when applying the ST-T wave opposition
principle Look only in the 3 KEY leads (= leads I,V1,V6). Once you have done so You can
refine your interpretation by looking at ST-T wave changes in the remaining leads ( See Section
05.15).
NOTE: The ST opposition rule works for RBBB and LBBB but not for IVCD (which is
why it is often quite difficult to assess for acute changes with IVCD).

05.15 FIGURE 05.15-1: Assessing ST-T Wave Changes with BBB

Apply the ST opposition rule to the examples of RBBB and LBBB shown in Figure 05.15-1 (in
which we reproduce the ECGs previously shown in Figure 05.4-2 and Figure 05.8-1). Are the ST-T
waves in the 3 KEY leads doing what they should for bundle branch block seen in each case?

Figure 05.15-1: Are ST-T changes as expected for the examples of typical RBBB (Top tracing) and
LBBB (Bottom tracing) seen here?
Answer to Figure 05.15-1: Sinus rhythm with QRS widening is seen for both tracings shown here.
Focus on the 3 KEY leads (I,V1,V6) allows rapid diagnosis of complete RBBB (top tracing) and
complete LBBB (bottom tracing). It should now take no more than seconds to establish that ST-T
waves (white arrows) are oppositely directed to the last QRS deflection (red arrows ) in each of
the 3 key leads. Looking at this in more detail:
TOP Tracing Recognition of the rSR ( with taller right rabbit ear) in V1 and wide terminal
S waves in leads I,V6 define the conduction defect as RBBB. The last QRS deflection in lead
V1 is upward (the R = red arrow in V1 ) so the ST-T wave is appropriately negative (white
arrow). Terminal S waves in leads I,V6 inscribe a downward deflection ( red arrows in these
leads) so the T wave is appropriately upright in both lead I and V6 (white arrows).
BOTTOM Tracing Recognition of a monophasic upright R wave in left-sided leads I,V6 and
a predominantly negative QRS complex in lead V1 defines the conduction defect as LBBB. The
only QRS deflection in leads I,V6 is upward (the monophasic R wave = red arrows in I,V6)
so the ST-T wave is negative in these leads ( white arrows). Lead V1 manifests a predominantly
negative QRS deflection (red arrow in V1) so the ST-T wave is appropriately upright in this
lead (white arrow).
NOTE: Neighboring leads may or may not manifest ST-T wave opposition to the last QRS
deflection. For example, there is ST-T wave opposition for anterior leads V2,V3 in the bottom
tracing (negative QRS with upright T wave) but not necessarily for all of the other leads. For
this reason Our focus in on looking at the 3 KEY leads = leads I, V1 and V6.

05.16 RBBB Equivalent Patterns

The shape of the QRS complex in lead V1 may vary greatly with RBBB. It will not always show a
"neat" rSR ( or rsR') in this lead. Instead, any of the patterns shown for lead V1 in Figure 05.16-1
qualify for diagnosis of RBBB as long as the QRS complex is widened (to 0.11 second) and
as long as there is a wide terminal S wave in left-sided leads I and V6.

Figure 05.16-1: RBBB Equivalent Patterns in lead V1. Despite lack of a taller-right-rabbit-ear
rSR pattern in lead V1 RBBB is still present IF: i) the QRS is wide ( 0.11 second) ; ii) an
upright QRS complex similar to one of the patterns shown here is seen in lead V1; and iii) a wide
terminal S wave is seen in lead I and lead V6.
KEY Points: Normally the QRS complex in lead V1 is predominantly negative. This is because
this right-sided lead (V1) sees electrical activity as moving away from V1 (or toward the left
ventricle). The finding of predominant positive activity (ie, a tall R wave) in right-sided lead V1 is
not normal.
IF the rhythm is sinus and the QRS is wide with an RBBB-Equivalent pattern in lead V1
then the conduction defect is RBBB as long as there are wide terminal S waves in leads I
and V6 (Figure 05.16-1).
Reasons why the typical triphasic (rsR; taller right rabbit ear) complex in V1 may be lost in
some patients with RBBB include scarring (as may occur with cardiomyopathy) and/or
infarction (which would be especially suggested by a qR pattern in lead V1).

05.17 FIGURE 05.17-1: Is this RBBB?

The schematic tracing in Figure 05.17-1 shows sinus rhythm and QRS widening.
What type of BBB is seen in Figure 05.17-1?

Figure 05.17-1: What type of conduction block is present?

Answer to Figure 05.17-1: Lead II shows the rhythm is sinus. The QRS is wide and upright in lead
V1 but not in the usual rSR (taller right rabbit ear) pattern for typical RBBB. Instead, the left
rabbit ear is taller. This qualifies as an RBBB Equivalent pattern (Figure 05.16-1). Since wide
terminal S waves are seen in the lateral leads (I,V6) this tracing satisfies criteria for RBBB. ST-T
wave changes are appropriate (opposite the last QRS deflection in the 3 key leads) so there are
no acute changes.
05.18 Incomplete RBBB: How is it Diagnosed?
As discussed in Section 05.5 IRBBB (Incomplete Right Bundle Branch Block) is diagnosed when
QRS morphology is consistent with RBBB (Section 05.4) but QRS duration is less than 0.11 second
(Figure 05.18-1):

Figure 05.18-1: ECG showing IRBBB (Incomplete Right Bundle Branch Block) obtained from a
healthy young adult. An rSr is seen in lead V1 with S waves in leads I,V6 but QRS duration is
0.11 sec (not more than half a large box). Note that the S waves seen in leads I,V6 are narrow.
KEY Points about IRBBB: Patients with IRBBB run the gamut from common occurrence in up to
~5% of otherwise healthy young adults (in which case it is benign) to IRBBB serving as an ECG
sign of RVH/COPD; acute pulmonary embolus; or acute conduction system damage seen with acute
MI. Clinical correlation is everything!
An rSr in lead V1 (and/or in leads III or V2 ) is a common benign finding in healthy young
adults (due to normal late depolarization of the RV outflow track) . IF, as is seen in Figure
05.18-1 there is also an S wave in leads I and V6 then we define this as IRBBB. If S

waves are missing We simply say, an rSr is present in lead V1.

Note that the ST-T wave in lead V1 of Figure 05.18-1 is inverted. This is an expected finding
given the IRBBB pattern in V1 (See Section 05.14 on the ST opposition rule).
Beyond-the-Core: Be aware that placing chest leads V1 and V2 an interspace too high is a
technical mishap that may misleadingly induce an rSr pattern in these leads (Section 03.21).

05.19 PRACTICE: Bundle Branch Block

Interpret the following 2 schematic and 2 real tracings (Sections 05.20-thru-05.23). Sinus rhythm is
present in each tracing but the QRS is wide. What type of conduction defect is present? Is there
indication of possible ongoing ischemia/infarction in any of these tracings?
Our Answers follow each case.
Hint: Feel free to refer back to Figures 05.2-1; 05.4-1; 05.6-1; 05.11-1; and 05.14-1 while
formulating your answers.

05.20 PRACTICE: Tracing A

In schematic Tracing A (Figure 05.20-1) there is sinus rhythm with QRS widening.
What type of BBB is present? Is anything else going on?

Figure 05.20-1: Practice Tracing A. What type of BBB is present?

ANSWER to Tracing A: There is sinus rhythm with QRS widening. QRS morphology is consistent
with the pattern of complete LBBB in each of the 3 key leads (Section 05.6). However, a Q wave is
present in Lead V6. This is not normally seen with typical LBBB. The finding of a Q wave in a
lateral lead (I, aVL,or V6) with LBBB indicates prior infarction.
There are also abnormal (ie, primary) ST-T wave changes in the 3 key leads As emphasized
in Section 05.14 (Figure 05.14-1) the T wave with typical LBBB should not be upright in
lead I. The T wave should also not be negative in lead V1 with uncomplicated LBBB.
Bottom Line: We interpret schematic Tracing A as showing LBBB with primary ST-T wave
changes. This suggests infarction has taken place at some point in the past. Clinical history and
comparison with prior tracings would be needed to determine if the changes seen are new,
recent or old.

Beyond-the-Core: Rather than lateral infarction the Q wave in lead V6 indicates prior
septal infarction. As discussed and illustrated in Section 05.7 LBBB changes the direction of
septal activation (from left-to-right to right-to-left). Thus, development of a Q wave in a
lateral lead with LBBB indicates further disturbance with the process septal activation,
presumably due to septal infarction.

05.21 PRACTICE: Tracing B

In schematic Tracing B (Figure 05.21-1) there is sinus rhythm with QRS widening.
What type of conduction defect is present?

Figure 05.21-1: Practice Tracing B. What type of conduction defect is present?

ANSWER to Tracing B: There is sinus rhythm with QRS widening. That said QRS morphology
is not consistent with either RBBB or LBBB in each of the 3 key leads. That is the monophasic R
wave in lead I looks like LBBB; the wide terminal S wave in V6 is consistent with RBBB; and the
R=S pattern in V1 looks like neither LBBB nor RBBB.
By the process of elimination we interpret the conduction defect in Figure 05.21-1 as IVCD
(Section 05.11).
STT wave morphology is difficult to interpret with IVCD. This is because the ST Opposition
Rule does not necessarily work with IVCD (Section 05.14). As a result ST-T waves are not
necessarily directed opposite to the last QRS deflection in the 3 key leads. It may therefore not
be possible to assess for ischemia/infarction when there is IVCD (unless ST-T wave changes
are extreme).

05.22 PRACTICE: Tracing C

There is again sinus rhythm with QRS widening in Tracing C (Figure 05.22-1).
What type of BBB is present? Is anything else going on?

Figure 05.22-1: Practice Tracing C. What type of BBB is present? Is anything else going on?
ANSWER to Tracing C: The rhythm is sinus bradycardia at ~50/minute. The QRS complex is wide
in a pattern consistent with complete RBBB (Section 05.4). That is there is an rSR ( with taller
right rabbit ear) in lead V1 with wide terminal S waves in both leads I and V6.
NOTE-1: ST-T waves are not as expected for uncomplicated BBB (Section 05.14). That is
ST-T waves in Figure 05.22-1 are not oppositely directed to the last QRS deflection in each of
the 3 KEY leads. Instead there is ST flattening in leads I,V1 and T wave inversion (instead of
an upright T wave) in lead V6. Thus there are primary ST-T wave changes on this tracing
which suggests possible recent or ongoing ischemia/infarction.
NOTE-2: The ECG in Figure 05.22-1 provides an excellent example of how we use the
concept of neighboring leads to refine our interpretation. Thus, the ST Opposition Rule (Figure
05.14-1) allows us to quickly determine that ST-T wave depression in lead V6 is not normal
for typical RBBB. We therefore should not expect neighboring leads (ie, leads V4,V5) to
manifest the deep symmetric T wave inversion that is seen in Fig. 05.14-1. This suggests that in
addition to RBBB there is a wider area of lateral ischemia.
Finally there are relatively larger-than-expected Q waves in the lateral leads (leads I, V5,
V6, and especially aVL). Especially in the context of RBBB and primary ST-T wave changes
these Q waves (particularly the relatively deep Q in lead aVL) may well reflect infarction
of uncertain age.
Bottom Line: We interpret the ECG in Tracing C as showing sinus bradycardia with
complete RBBB. There are lateral Q waves of uncertain significance and primary ST-T wave
changes that suggest possible infarction/ischemia of uncertain age in addition to RBBB. This
could be acute. Clinical correlation is needed.
Beyond-the-Core: The question often arises as to how far over in the anterior leads ST-T wave

depression from RBBB may be seen? We expect to see ST-T wave depression in leads V1,V2
with RBBB as part of the normal secondary ST-T wave changes of BBB. This was seen in the
12-lead ECG example of typical RBBB shown in Figure 05.4-2. Sometimes anterior ST-T
depression with typical RBBB may carry over as far as lead V3 but it should usually not go
beyond this! It should be clear that ST-T wave appearance in Figure 05.22-1 is not normal
because: i) the ST-T wave should be upright in lead V6 ( as well as in leads V4,V5); and ii) the
ST segment becomes coved in lead V3 and the amount of T wave inversion in V3 is
increased compared to V2 (whereas with simple RBBB we would expect a decrease in amount
of ST-T wave change from V2-to-V3).

05.23 PRACTICE: Tracing D

A final example of sinus rhythm with QRS widening is seen in Tracing D (Figure 05.23-1).
What type of conduction defect is present?

Figure 05.23-1: Practice Tracing D. What type of conduction defect is present?

ANSWER to Tracing D: There is sinus rhythm with QRS widening. There is a PAC ( the 4 beat
occurs early). QRS morphology is not consistent with either RBBB or LBBB in each of the 3 key
leads. That is the negative QS complex in lead V1 is consistent with LBBB but, if anything the
wide terminal S waves in the tiny complexes seen in leads I and V6 are consistent with RBBB.
By the process of elimination we interpret the conduction defect in Figure 05.23-1 as IVCD
(Section 05.11).
As stated STT wave morphology is difficult to interpret with IVCD because the ST
Opposition Rule is not necessarily followed (Section 05.14). We would interpret ST-T wave
changes seen here as nonspecific. Clinical correlation is needed to determine the likely
significance of the conduction defect seen.

05.24 Diagnosing BBB + Acute MI

Diagnosis of ischemia/infarction is always more challenging when there is underlying BBB (Bundle
Branch Block). That said suspicion of old or acute events will surprisingly often be possible.
The goal of Sections 05.24-thru-05.29 is to briefly review key considerations for assessing
the patient with a conduction defect for possible ischemia/infarction.

05.25 Begin with the ST Opposition Rule

While not infallible, the ST opposition rule (Sections 05.14, 05.15) is a good place to start when
assessing patients with RBBB or LBBB for possible ischemia/infarction. In Figure 05.25-1 we
reproduce the ST-T wave changes to look for:
Normally with LBBB/RBBB the ST-T wave will be oppositely directed to the last QRS
deflection in the 3 KEY leads (leads I,V1,V6).
NOTE: With IVCD the ST opposition rule does not consistently work (reliability for
ischemia/infarction is more limited).

Figure 05.25-1: The expected ST-T wave response to either typical RBBB or typical LBBB is ST
opposition. That is the ST segment and T wave should be oppositely directed to the last QRS
deflection (red and yellow arrows ) in each of the 3 KEY leads (= leads I,V1,V6). Deviation from
this pattern is abnormal and indicates a primary (1) ST-T wave change (that suggests ischemia
or infarction).
05.26 RBBB: You Can See Q Waves!
Clinically it will usually be easier to diagnose ischemia/infarction when there is underlying

RBBB than when there is LBBB. This is because RBBB does not alter the initial direction of septal
depolarization as LBBB does (Section 05.7).
As the initial part of the QRS complex Q waves are written at an early point during the
process of ventricular activation. Because the conduction defect of RBBB does not alter the leftto-right direction of normal septal activation (since the right bundle branch goes down the
right side of the septum) the presence of RBBB will usually not prevent inscription of Q
waves. This is in contrast to LBBB that does change the direction of initial septal activation
(Section 05.28). KEY Point: Much (most) of the time You can see infarction Q waves even
when complete RBBB is present (Figure 05.26-1). You may or may not see acute changes.

Figure 05.26-1: Sinus tachycardia with complete RBBB. Despite RBBB Q waves are seen in
leads II,III,aVF; and V5,V6. This suggests inferolateral infarction has occurred at some point in the
past. ST-T wave appearance suggests that the infarct is less likely to be acute (See text).
05.27 Underlying RBBB: How to Diagnose Acute MI?
As stated in Section 05.24 Diagnosis of ischemia/infarction is always more challenging when
there is underlying BBB. This is because the typical secondary ST-T wave changes that result from
BBB (Figure 05.25-1) may mask ST-T wave changes due to ischemia/infarction. That said it is
important to carefully scrutinize the ECG, because chronic (and even acute) changes may at times be
seen.
Realize that it will always be more difficult to diagnose ischemia/infarction with LBBB than
with RBBB. But sometimes youll be surprised! (as we illustrate in Section 05.29).
Consider the case of complete RBBB seen in Figure 05.27:
The rhythm in Figure 05.27 is regular and the QRS complex is wide. Although we do not see
upright P waves in lead II the mechanism of this rhythm is clearly supraventricular as
evidenced by upright P waves with fixed PR interval that are seen to regularly occur in
simultaneously recorded leads V1,V2,V3.

Figure 05.27-1: Supraventricular rhythm with complete RBBB. Despite RBBB there is evidence
of infarction that may be acute (See text).
Analysis of the ECG in Figure 05.27-1: Although uncertain about the precise mechanism of this
rhythm unmistakable P waves in simultaneously recorded leads V1,V2,V3 define the rhythm to be
supraventricular. Perhaps artifact undulations in the baseline of lead II prevent sinus P waves from
being seen or perhaps this is a low atrial rhythm? Regardless We proceed by assessing the reason
for QRS widening according to the Algorithm put forth at the beginning of this Section on BBB
(Figure 05.2-1).
A predominantly upright wide QR complex is seen in lead V1. This qualifies as an RBBB
equivalent pattern (Section 05.16).
The diagnosis of complete RBBB is secured by noting the presence of wide terminal S waves in
both leads I and V6.
Q waves are seen in several leads of this tracing. The q wave in lead I is small, and of
uncertain significance. However, the qrS pattern in lead aVL is distinctly abnormal and highly
suggestive of lateral infarction. In addition the QR pattern in lead V1 in the setting of RBBB
is virtually diagnostic of prior anterior (or anteroseptal) infaction.
ST-T waves are not normal for RBBB. Although the small amplitude upright T wave in lead
I is consistent with the S T opposition rule (Fig. 05.25-1) ST depression in lead V6 and
subtle-but-real ST elevation in lead V1 are both contrary to what one normally expects with
RBBB.
By the concept of neighboring leads We see similar ST depression with shallow T
inversion extending from V6 to V4,V5 and ST coving with slight elevation not only in V1, but
also in V2,V3.
Bottom Line: Despite RBBB We are strongly suspicious of previous and perhaps recent (if
not acute ongoing) infarction in Figure 05.27-1. History and comparison with prior tracings
would be invaluable for clarifying what is likely to be new vs old.

05.28 Underlying LBBB: How to Diagnose Acute MI?

Special considerations are needed to assess for ischemia/infarction when there is LBBB. These are
highlighted in the schematic tracings shown in Figure 05.28-1.

Diagnosis of LBBB is confirmed in Panel A of Fig. 05.28-1 by the finding sinus rhythm with
QRS widening showing a negative QRS complex in lead V1 and a monophasic upright R wave
in leads I,V6 (Section 05.6).
Note in this schematic example of typical LBBB (Panel A) that there are QS complexes and
ST elevation in leads V1,V2,V3 that simulate anterior infarction and that ST-T wave
depression in lateral leads simulates ischemia. All of these findings are commonly seen with
LBBB.
Key Point: There is no ECG evidence of ischemia/infarction in Panel A of Figure 05.28-1.
Instead All one can say is that there is LBBB.

Figure 05.28-1: Schematic illustration of typical LBBB (Panel A) and of LBBB with ECG signs
of acute STEMI (Panel B).
Clinical Considerations: The main thing one cares about in assessing a patient with LBBB who
presents to the ED (Emergency Department) with new-onset chest pain is whether there is acute
coronary occlusion (ST Elevation Myocardial Infarction-equivalent) necessitating immediate
intervention (cath lab activation; angioplasty/stenting).
Overall less than 5% of patients with LBBB and new-onset chest pain have acute coronary
occlusion. Although insensitive the finding of primary ST elevation is highly specific for
acute coronary occlusion. This is seen in leads II,III,aVF of Panel B in Figure 05.28-1.
Further support of likely acute coronary occlusion may be forthcoming IF there is excessive
discordance. That is IF in leads V1,V2, or V3 you can see a clear J point where the QRS
ends and the ST segment begins and IF the J point of the ST segment is up or down >20%
of QRS amplitude then there is excessive discordance (by the Smith-modified Sgarbossa
criterion). This criterion is satisfied in lead V3 of Panel B (J-point elevation = 6; S wave
depth = 24 and 6/24>20%). CAVEAT it may be difficult to know where the J-point is if
anterior ST elevation with LBBB is of smooth contour (in which case you wont be able to use
this criterion).
NOTE: Debate continues as to whether the ECG finding of LBBB of uncertain age in a patient with
new-onset chest pain is sufficient to justify acute cath lab activation.

Most such patients do not have acute coronary occlusion. Some may have troponin elevation
(that satisfies the definition of acute MI) but overall, initial management of patients without
acute ECG changes will be similar to that of patients admitted to the hospital with a rule out
MI diagnosis.
Awareness of the need to look for primary ST elevation and excessive discordance in chest pain
patients with LBBB will hopefully help to identify the important minority likely to have acute
coronary occlusion.
Analysis of Other Leads in Panel B: In addition to the excessive discordance described above
there are findings in other leads in Panel B that strongly suggest acute ischemia/infarction (Figure
05.28-2):
How many of these other findings can you identify?

Figure 05.28-2: In addition to excessive discordance for the ST segment in lead V3 What other
findings strongly suggest acute ischemia/infarction?
ANSWER to Panel B in Figure 05.28-2: Assessment of the schematic tracing in Panel B
summarizes essential points covered thus far:
QRS morphology in the 3 key leads is consistent with LBBB (upright QRS in leads I,V6;
negative QRS in lead V1).
Look next at ST opposition in the 3 key leads. ST-T waves are oppositely directed to the last
QRS deflection (as they should be) in leads I,V1,V6.
There should never normally be lateral q waves with LBBB (Section 05.6). Finding a Q wave
i n lead I, aVL, V5, or V6 means an infarct has at some point occurred. Note the Q wave in
leads I and aVL in Panel B.
Although not common primary ST elevation is the most reliable indicator of acute STEMI
with LBBB. This is seen in leads II,III,aVF of Panel Panel B. Therefore, despite LBBB the

schematic ECG seen in Figure 05.28-2 (= Panel B) is diagnostic of acute inferior STEMI.
In addition to excessive discordance for the amount of anterior ST elevation there may also
be excessive discordance for the amount of lateral ST depression. That said primary ST
elevation in the inferior leads of this tracing is far more reliable as an indicator of acute STEMI
with LBBB.

05.29 FIGURE 05.29-1: Acute STEMI despite LBBB/RBBB?

We conclude this section on assessing patients with RBBB and LBBB for ECG evidence of acute
ischemia/infarction with a series of 4 ECGs, beginning with the 2 tracings shown in Figure 05.291.
Both of the ECGs in Figure 05.29-1 were obtained from patients with new-onset chest pain and
known LBBB. Despite underlying LBBB Is there ECG evidence of acute STEMI on either
tracing? Should the cath lab be activated?

Figure 05.29-1: ECGs obtained from 2 patients with baseline LBBB and new-onset chest pain. Is
there evidence of acute MI in either tracing?
ANSWER to Figure 05.29-1: Sinus rhythm with LBBB is present in both ECGs shown above.
Despite Q waves in leads III,aVF; and in V1,V2,V3 there is no evidence of acute STEMI in the
Top ECG. Instead, ST-T waves are appropriately opposite (Figure 05.25-1) and there is no
excessive discordance. The Q waves that are seen in leads V1,V2,V3 are expected with LBBB, and
those that are seen in leads III and aVF are not necessarily abnormal given the presence of this
conduction defect.

Bottom ECG shows LBBB with acute STEMI! Note primary ST elevation in leads
II,III,aVF; and especially in leads V5,V6. Activate the cath lab!
Now consider the example of RBBB shown in Figure 05.29-2. This tracing was obtained from a
patient with new-onset chest pain. In addition to complete RBBB Is there also evidence of an
acute STEMI?
How certain are you of your diagnosis?

Figure 05.29-2: ECG obtained from a patient with new-onset chest pain. In addition to complete
RBBB Is there also evidence of an acute STEMI? (See text).
ANSWER to Figure 05.29-2: The rhythm is sinus arrhythmia. Complete RBBB is diagnosed by QRS
widening with an rSR in V1 plus wide terminal S waves in leads I,V6.
There is subtle-but-real ST coving and elevation in lead V1 that should not be. Support that
this finding is real is forthcoming from slight-but-definite ST segment coving and elevation
in lead III (and to a lesser extent in aVF) plus reciprocal ST depression in lead aVL.
A deep Q wave is already present in lead III.
We interpret this tracing as sinus arrhythmia; RBBB; and probable acute ongoing inferior
STEMI.
Beyond-the-Core: We suspect acute proximal RCA (Ri g h t Coronary Artery) occlusion,
possibly with acute right ventricular MI (given subtle ST elevation in lead V1 in the setting of
acute inferior infarction).
Finally, consider the conduction defect shown in Figure 05.29-3 obtained from a patient with
chest pain. Despite LBBB/IVCD Is there evidence of an acute STEMI?
How certain are you of your diagnosis?

Figure 05.29-3: ECG obtained from a patient with new-onset chest pain. In addition to the conduction
defect Is there also evidence of an acute STEMI? (My appreciation to Ben Beuchler for allowing
me to publish this ECG)
ANSWER to Figure 05.29-3: The rhythm is sinus at ~75/minute. The QRS complex is wide.
Although the anterior precordial leads look like LBBB (deep QS complexes) R wave amplitude
in lead I is tiny, and there is a terminal S wave in V6. Our preference would be to call the conduction
defect = IVCD (IntraVentricular Conduction Defect) though we would accept either IVCD or
LBBB as correct interpretations. In either case the anterior QS complexes seen are not diagnostic
of prior infarction given the conduction defect.
Regardless of the terminology used (LBBB or IVCD) the important clinical point is that
interpretation of acute ischemia/infarction is more difficult in the setting of this type of
conduction defect. Thus, the ST segment elevation seen in leads V1-through-V4 of Figure 05.293 is not a reliable predictor of acute anterior infarction, since LBBB commonly manifests
anterior ST elevation comparable in shape and amount to that seen here.
On the other hand there should not be ST elevation in the inferior leads (Figure 05.29-4).
Note J-point ST elevation is present in each of the inferior leads (red arrows in blow-up inserts
of Fig. 05.29-4). In support that this inferior ST elevation is real is mirror-image shape
reciprocal ST depression in lead aVL (red circle ). In addition it looks like a Q wave has
already formed in lead aVL. Therefore this ECG strongly suggests acute inferior STEMI
despite the presence of underlying LBBB/IVCD.

Figure 05.29-4: Addition of blow-up inserts to Figure 05.29-3, from this patient with chest pain. We
would accept either IVCD or LBBB as explanations for the conduction defect. While no conclusions

can be drawn from the ST elevation seen in anterior precordial leads acute STEMI can be
diagnosed from the ST elevation seen in each of the inferior leads (red arrows ) with a Q wave and
mirror-image reciprocal ST-T wave changes in lead aVL (See text).

05.30 Diagnosing BBB + LVH

ECG Diagnosis of ventricular chamber enlargement becomes difficult in the presence of conduction
defects (RBBB, LBBB, IVCD). Criteria for LVH/RVH are based on the normal sequence and
progression of ventricular activation. All of this changes in the presence of bundle branch block.
Instead of near-simultaneous left and right ventricular activation there will be delay in
activation of that part (or those parts) of the ventricles served by the nonfunctioning conduction
fascicle(s). This alteration in time sequence of the relative contribution of left and right
ventricular forces invalidates numeric and morphologic criteria for chamber enlargement that
were derived during sinus rhythm with intact ventricular conduction.
BOTTOM Line: Traditional ECG criteria for assessment of ventricular chamber enlargement should
not be used when there is BBB/IVCD. One never quite knows how much of the increase in QRS
amplitude seen is a result of ventricular hypertrophy vs scarring, prior infarction and/or alteration in
sequence (and therefore relative contribution) of ventricular depolarization forces.
On the other hand criteria for LAA/RAA are unchanged by BBB/IVCD (Sections 08.14through-08.22).
Clinically IF you really need to know about atrial or ventricular chamber dimensions Get
an Echocardiogram!
NOTE: What follows in Sections 05.31 and 05.32 constitutes advanced material that may be
Beyond-the-Core for the usual provider. We accept a preference by some to simplify ECG
interpretation and skip the step of assessing ventricular enlargement when there is BBB because of the
difficulty validating ECG criteria in the presence of conduction defects.
That said, for those with an interest in going Beyond-the-Core Read on! There are ways with
high reliability to diagnose probable LVH despite the presence of LBBB or RBBB.

05.31 LBBB: What Criteria to Use for LVH/RVH?

Most patients with LBBB have underlying heart disease. IF there is longterm hypertension,
cardiomyopathy or heart failure and LBBB the prevalence of LVH is ~80%, even before one
looks at the ECG.
The probability that a patient with LBBB has LVH goes up to >90% IF with LBBB there are
very deep S waves (25-30mm) in V1,V2 or V3 (Figure 05.31-1).
The likelihood of LBBB plus LVH also increases IF the patient has LAA (Le f t Atrial
Abnormality) as evidenced by a deep negative component to the P wave in lead V1.

Figure 05.31-1: Sinus rhythm with LBBB plus probable LVH because: i) the deep negative
component to the P wave in lead V1 suggests LAA (circle) and ii) the S wave in lead V2 is very
deep (>25mm). NOTE: Either LAA or the deep S wave in V1,V2,V3 alone would have been enough
to increase likelihood of LVH.
Semantic Point: We favor use of the terminology, probable LVH for the ECG picture seen in
Figure 05.31-1, in which there is LBBB plus a very deep S wave in lead V2. Although statistical
likelihood that this patient has LVH is at least 90% (actually more since there is also LAA) the
ECG diagnosis of LVH is based more on prevalence than on specific ECG voltage criteria. Use of
the modifier probable acknowledges the uncertainties of diagnosing LVH in the presence of this
conduction defect.
How Deep the S Wave? Note that we cannot tell from Figure 05.31-1 how deep the S wave in
lead V3 would be since the bottom of the S wave in this lead has been cut off.
Clinical Notes: Consider the following additional points:
The presence of LBBB may mask and mimic other conditions. Weve already discussed special
considerations for assessing ischemia/infarction with LBBB (Section 05.28). For example
despite the QS complex in leads V1,V2,V3 of Figure 05.31-1 We can not diagnose prior
anterior infarction. This is because the patient has complete LBBB. Anterior precordial QS
complexes with poor R wave progression are an expected accompaniment of complete LBBB
(Section 05.8).
In addition We can not comment on the possibility of LV strain in the presence of LBBB.
As highlighted by the ST Opposition Rule (Section 05.25) lateral ST-T wave depression is
an expected finding in LBBB. Its presence or absence says nothing about whether or not there is
associated LV strain. Thus, even though we would interpret the ECG in Figure 05.31-1 as
suggestive of probable LVH ( because of the deep S in V2 plus LAA) the ST-T depression
seen in leads I,aVL,V5,V6 of this tracing is of no support to our interpretation. All we can say is,
LBBB with probable LVH.

Finally Realize that it is virtually impossible to diagnose RVH when there is LBBB. The
LBBB simply masks right ventricular events.

05.32 RBBB: What Criteria to Use for LVH/RVH?

ECG diagnosis of ventricular chamber enlargement is equally challenging when there is RBBB. Once
again difficulty arises because the altered sequence of ventricular activation leaves us uncertain
as to how much any increase in QRS amplitude might be due to ventricular hypertrophy vs delay (and
therefore nonopposition) of right ventricular depolarization forces. Realizing the imperfection
inherent with any proposed ECG criteria for chamber enlargement when there is BBB We make
the following points:
Complete RBBB is a terminal delay (Sections 05.4; 05.5). As such it does not affect the
initial parts of ventricular activation (during which time the septum and then left ventricle are
activated). As a result the process of LV activation is virtually intact when there is RBBB
with the exception that the larger left ventricle will no longer be opposed by smaller RV forces
that are delayed. Bottom Line: ECG voltage criteria for LVH in the presence of complete
RBBB are probably not that different in certain leads compared to voltage criteria when there is
no conduction defect.
Suspect LVH (despite RBBB) IF the R wave in lead aVL is 12, or the R wave in lead V5
or V6 is 25.
Depth of the S wave in leads V1,V2 is no longer of assistance for assessing LVH when there is
RBBB because the rSR in lead V1 essentially precludes S wave formation.
Consider the ECG in Figure 05.32-1. There is a low atrial rhythm with QRS widening consistent with
complete RBBB (rSR in V1; wide terminal S waves in leads I,V6).
Is there ECG evidence of ventricular enlargement in Figure 05.32-1?

Figure 05.32-1: Low atrial rhythm with complete RBBB. Is there ECG evidence of ventricular

enlargement? (See text).

Answer to Figure 05:32-1: ECG criteria for the diagnosis of LVH are covered in detail in Sections
08.1-through-0.8.13. S wave depth typically increases in leads V1,V2 with LVH reflecting an
increase in LV forces moving away from these right-sided leads. That said the presence of
complete RBBB in Figure 05.32-1 negates formation of S waves in leads V1,V2. Other leads must
therefore be used to assess the possibility of LVH.

R wave amplitude is not increased in leads V5,V6 of Figure 05.32-1.

On the other hand the R wave in lead aVL does attain at least 12mm in height, and therefore
satisfies criteria for probable LVH in this patient with RBBB.
NOTE: We qualify our assessment in Figure 05.32-1 with the term, probable LVH to
acknowledge reduced specificity of voltage criteria for LVH in the presence of complete RBBB.
We simply dont know how much of the increase in R wave amplitude in aVL is due to anatomic
LV enlargement vs nonopposition of LV depolarization forces due to the conduction defect.

Is there RVH in Figure 05.32-1? By definition ECG diagnosis of RVH in the presence of RBBB
is problematic. This is because the presence of this conduction defect totally changes the sequence
and nature of RV depolarization. RV depolarization with RBBB is delayed and unopposed by LV
depolarization that will usually be complete by the time the activation wavefront finally makes its
way into the right ventricle. As a result the tiny right ventricle may sometimes generate a
surprisingly tall R deflection in lead V1 ( because there no longer is opposition from LV forces ).
KEY Point: The height of the R deflection in lead V1 with complete RBBB is not necessarily
related to the size/thickness of the right ventricle.

Realize that some electrocardiographers cite R amplitude of >10mm ( or >15mm) in lead V1 as

a criterion for diagnosing RVH in the presence of RBBB. We are not in favor of this practice
because it will result in false positive diagnosis of RVH in many cases.
Our Preference is to undercall RVH in the presence of RBBB. We generally do not
indicate probable RVH in the setting of RBBB unless in addition to a very tall R component
in lead V1 (of >10-15mm) there is also RAA (Right Atrial Abnormality) in a patient known
to have longstanding pulmonary disease. BOTTOM Line: While we acknowledge that some
interpreters may say RVH is present in Figure 05.32-1 because of the tall R component in lead
V1 We would not do so because: i) No history of pulmonary disease is given; and ii) there is
no sign of RAA.

05.33 Brugada Syndrome

First described in 1992 the Brugada Syndrome is important to recognize because of an associated
ver y high risk of sudden death in otherwise healthy young or middle-aged adults who have
structurally normal hearts.
The prevalence of Brugada Syndrome in the general population is ~1/2,000. The syndrome has
become a leading cause of sudden death in young adults (under 40 years of age).
Given heightened awareness and recent increased attention directed toward early recognition
We suspect the estimated prevalence for Brugada syndrome will continue to increase in the
years-to-come.

05.34 ECG Recognition: Distinction Between Type I and II

Distinction is made between 2 types of Brugada ECG patterns:
Type I (seen in Panel A of Figure 05.34-1) is diagnostic of Brugada Syndrome because
it shows 2mm coved ST elevation with sharp downslope plus T wave inversion in 2 anterior
leads. This is not RBBB.
Type II (i n Panel B) is not diagnostic of Brugada Syndrome unless the saddleback
anterior ST elevation with positive T wave (seen here in leads V2,V3) at some time later
converts to a Type I tracing. Most often this concave up ST elevation is due to benign early
repolarization (assuming no syncope, arrhythmia or familial history of sudden death at an
early age).

Figure 05.34-1: Leads V1,V2 in Panel A are diagnostic of Brugada Syndrome. The saddleback
pattern in leads V2,V3 of Panel B is not.
CAVEAT: Type I or Type II Brugada ECG patterns may be induced by a variety of factors. A partial
list includes the following:

Certain drugs (antiarrhythmics; calcium channel blockers; -blockers; antianginals;

psychotropic medications; alcohol; cocaine; other drugs).
Acute febrile illness.
Variations in autonomic tone.
Hypothermia.
Electrolyte imbalance (hypokalemia).
Ischemia/infarction.
Cardioversion/defibrillation.
Bradycardia.
Repositioning precordial leads (recording leads V1,V2 from the 2nd or 3rd intercostal space).
NOTE: Whether clinical implications of a transient induced Brugada pattern (Type I or Type II
ECG) are the same as with its spontaneous occurrence is uncertain and probably depends on
associated clinical parameters. Thus, transient induction of a Type II ECG pattern would seem less
likely to be important if only briefly seen during acute febrile illness in an otherwise healthy young
adult with negative family history. In contrast induction of longer-lasting Type I ECG changes in
an older patient with syncope and positive family history is unquestionably of great concern.
Definitive answers regarding clinical implications have not yet been worked out for all situations
so judgment is needed in clinical decision-making.
05.35 WHAT to DO? - when a Brugada Pattern is Found?
The clinical question that arises is the following: What to do? IF you encounter a patient with a
Type I or Type II tracing?
Patients found to have a Type I ECG (even if asymptomatic) should probably be referred to
a cardiologist. EP (ElectroPhysiologic) study is clearly indicated when there are symptoms
(seizure; syncope or presyncope; arrhythmia) or for positive family history of sudden death at
an early age (below 50). An ICD (Implantable Cardioverter Defibrillator) is indicated IF the
patient has inducible VT (Figure 05.35-1).
Follow-up with a knowledgeable primary care clinician (but without necessarily referring to
cardiology) may be appropriate IF a non-diagnostic pattern is seen in an otherwise healthy
adult with normal exam and negative family history (Figure 05.35-2).
IF in doubt about What to Do? for a patient you encounter who has a Brugada-type ECG it
is prudent to err on the side of caution. This entails consulting a clinician experienced in
diagnosis and management of Brugada syndrome, its variants and its mimics.

Figure 05.35-1: ECG obtained from a young adult with syncope. Even without a positive family
history for sudden death at an early age the Type I Brugada pattern seen here in leads V1,V2 is
enough to justify prompt referral to an EP (ElectroPhysiology) cardiologist for consideration of ICD
placement. Note J-point ST elevation of 2-3mm in lead V1 and more than 5mm in V2 followed by
convincingly steep ST downslope into inverted T waves (comparable to Panel A in Fig. 05.34-1).
This ECG is diagnostic for Brugada Syndrome.

Figure 05.35-2: ECG obtained from an asymptomatic young adult. An rSr pattern is seen in lead V1
with saddleback ST elevation in lead V2. This ECG is consistent with a Type II Brugada pattern.
Although more than is usually seen with simple incomplete RBBB or early repolarization the ECG
pattern in this figure is not diagnostic of Brugada syndrome. Referral and ICD placement are not
necessarily needed especially if this asymptomatic young adult has a negative family history.
Bottom Line: Judgment and clinical correlation are needed for optimal evaluation and management.
Not all answers are yet in. Each case should be individualized (See text).

05.36 WPW (Wolff-Parkinson-White)

In the setting of normal sinus rhythm the only exception to the simplified Algorithm for assessment
of QRS Widening (Section 05.2) is the Wolff-Parkinson-White (WPW) Syndrome.
Although admittedly uncommon (~2 per 1,000 in the general population) WPW occurs just
often enough to cause problems for the unwary. The importance of WPW is twofold: i) It is
the great mimic and may simulate other conditions (such as ischemia/infarction,
hypertrophy and/or conduction defects) IF it is not recognized; and ii) The presence of one
or more accessory pathways predisposes the patient to a number of potentially important
cardiac arrhythmias.

05.37 WPW: Pathophysiology / ECG Recognition

WPW is a syndrome in which one or more accessory pathways exist that allow an alternate route
for transmission of the electrical impulse from atria to ventricles. Thus, with WPW sinus impulses
bypass the AV node via an AP (Accessory Pathway) and therefore arrive early in the ventricles
(Panel A in Figure 05.37-1).

Figure 05.37-1: With WPW impulses bypass the AV node via AP conduction. Although the AP
shown in Panel A is right-sided it could be left-sided, anterior or posterior and at times there is
more than a single AP. The 3 ECG signs of WPW are seen in Panel B i) a delta wave (which
may be positive or negative); ii) QRS widening; and iii) a short PR interval (See text).
ECG Recognition of WPW: It is usually easy to recognize WPW on a baseline 12-lead ECG when
conduction completely utilizes the AP (Accessory Pathway). There are 3 ECG features to look for
(Panel B in Figure 05.37-1):
Delta waves.
A short PR interval.

QRS widening.
Delta Wave: The delta wave is recognized as a distortion of the initial portion of the QRS complex.
It is due to the fact that the electrical impulse bypasses the AV node and arrives at the ventricles
directly via conduction over the accessory pathway.
Delta waves may be upright (positive) or downward (negative) depending on where in the
heart the AP is located. When delta waves are negative they may simulate the Q wave of
myocardial infarction (Panel B in Fig. 05.37-1):
Even when conduction is entirely over the AP delta waves will not always be seen in every
lead. Moreover, delta waves may come and go since conduction over the AP may be
intermittent. At times conduction may simultaneously occur over both the normal and
accessory pathway. When this happens the ECG characteristics of WPW may be subtle
because the contribution from conduction over the normal AV nodal pathway may predominate
(and thereby mask) ECG features of pre-excitation.
Short PR Interval: The reason the PR interval is short with WPW is that the AV node is
bypassed. With normal conduction in sinus rhythm the electrical impulse slows down as it passes
through the AV node on its way to the ventricles. As a result most of the PR interval normally
consists of the time it takes for the impulse to traverse the AV node. The electrical impulse arrives at
the ventricles sooner with WPW because the usual relative delay that occurs when passing through
the AV node is avoided by conduction over the AP.
QRS Widening: The QRS widens with WPW because after the impulse arrives at the ventricles
(via conduction over the AP) it must travel over nonspecialized myocardial tissue until such time
that it attains whatever distal portion of the conduction system that has not yet depolarized. Thus the
delta wave may extend for 0.04 second or more (reflecting slow conduction over nonspecialized
myocardial tissue). When the delta wave deflection is added to the rest of the QRS complex the
result is a widened complex.
Bottom Line Regarding ECG Recognition: Many variations exist on the above theme. Remember
the following:
WPW is not common in the general population but it does occur (and you will see it)!
When a patient with WPW is conducting over their accessory pathway you can diagnose
WPW by recognition of the following 3 ECG features in at least several of the 12 leads of an
ECG: i) QRS widening; ii) a delta wave; and iii) a short PR interval.
Preexcitation (ie, WPW conduction over an AP) can be intermittent. There may be no
indication on ECG that a patient has WPW if conduction is entirely (or almost entirely) over the
normal AV nodal pathway at the time the tracing is recorded.

05.38 WPW: The Great Mimic of other Conditions

As already emphasized an essential reason for recognizing WPW is so that it is not confused with
other conditions. This point is well illustrated by the schematic tracing shown in Figure 05.38-1:

Note in Fig. 05.38-1 that delta waves are not always present in all leads. For example, they
are completely missing in leads I,aVL and V4,V5 of Figure 05.38-1.
Negative delta waves are present in leads II,III,aVF and simulate inferior infarction.
The tall R wave in lead V1 simulates RBBB.
The tall, monophasic R wave in lead V6 simulates LBBB.
ST-T wave depression in lead V6 simulates ischemia.
BOTTOM Line: It is easy to overlook WPW if one does not routinely use a Systematic Approach.
This is especially true IF conduction goes down both the AP and the normal AV nodal pathway at
the same time (in which case the delta wave may be subtle and the QRS may be no more than
minimally widened).

Figure 05.38-1: Schematic example of WPW. Known as the great mimic the ECG picture of
WPW may resemble infarction, ischemia, chamber enlargement and/or bundle branch block as it
does here (See text).
05.39 FIGURE 05.39-1: Recognizing WPW on a 12-Lead
Primary care care and emergency clinicians will not always have the luxury of a baseline 12-lead
ECG at the time a patient with WPW-associated tachycardia is initially seen. However, with luck
a baseline 12-lead ECG with telltale features of WPW may occasionally be found in the patients
chart thereby confirming the diagnosis. We show such a tracing with overt WPW in Figure 0539-1. Note the following:
Suggestion of WPW is readily apparent from initial inspection of lead II in which all 3 ECG
features are seen: i) short PR interval; ii) delta wave (red arrow) ; and QRS widening. The
diagnosis of WPW is confirmed by recognition of definite delta waves in other leads (III,aVF;
V4,V5,V6).
Negative delta waves are seen in leads aVR and aVL (blue arrows). The negative delta wave
in lead aVL may simulate high lateral infarction.
NOTE: Delta waves are not prominent in every lead. The delta wave is subtle in leads I and V2
and completely absent in lead V1. The QRS complex does not appear wide in these leads.
Depending on the relative contribution from normal AV nodal pathway conduction and AP
(Accessory Pathway) conduction more or less leads may manifest delta waves, and the QRS
complex may be obviously wide or only minimally prolonged.
Clinically One can not diagnose LVH, ischemia or infarction from the ECG shown in Figure

05.39-1 despite the tall inferior R waves, deep Q wave in lead aVL, and ST-T wave changes
in V1,V2,V3 since the patient has WPW.
Bottom Line: It should be apparent from Figure 05.39-1 that the diagnosis of WPW could be easily
overlooked IF one was not systematic in their approach. At first glance the QRS complex does not
look overly wide. That said there is no mistaking the lead II findings of a short PR interval with
upward delta wave (red arrow) that when added to the remaining portion of the QRS results in
QRS widening. Confirmation of WPW is forthcoming from recognition of delta waves in most (but
not all) of the other leads on the tracing.

Figure 05.39-1: 12-lead ECG showing sinus rhythm with WPW. Note the short PR, delta wave and
QRS widening in lead II (red arrow). Delta waves are negative in leads aVR and aVL (blue
arrows). Delta waves are subtle in leads I,V2 and no delta wave at all is seen in lead V1 (See text).
05.40 FIGURE 05.40-1: Recognizing WPW
Another 12-lead ECG example of WPW is provided below in Figure 05.40-1. It would be easy to
misdiagnose this tracing as showing LVH and/or anterior infarction IF one failed to recognize the
short PR interval with delta waves in many leads (red arrows).
The purpose of our sequential Systematic Approach to ECG interpretation is to avoid
overlooking entities such as WPW that is easy to do if your attention jumps first to QRS
morphology before assessing intervals. As emphasized in our ECG Crib Sheet (Section 00.6.3)
the 3 Intervals (PR/QRS/QT) should be assessed early in the process. Doing so should alert
you to the short PR interval and wide QRS complex in Figure 05.40-1. We need to determine the
cause of these abnormal intervals before proceeding further. Knowing the patient has WPW
tells us that assessment for infarction, ischemia, conduction defects and chamber enlargement
will not be reliable.

Figure 05.40-1: 12-lead ECG showing sinus rhythm with a short PR interval. The QRS is wide and
delta waves are present in multiple leads (arrows). Note negative delta waves in V1,V2,V3 simulate
anterior infarction. Increased QRS amplitude in V5,V6 simulates LVH. QRS morphology in leads
I,V1,V6 simulates LBBB. This is WPW.

05.41 FIGURE 05.41-1: Atypical RBBB or WPW?

We present one more 12-lead ECG to illustrate the challenge of distinguishing between bundle branch
block and WPW (Figure 05.41-1).
Doesnt the upright and widened QRS complex in lead V1 of Figure 05.41-1 resemble RBBB?

Figure 05.41-1: QRS widening with an upright QRS complex in lead V1. What is this due to? (See
text).
Answer to Figure 05.41-1: As stated there is obvious QRS widening in this tracing. Approaching
this ECG systematically the QRS complex in lead II appears to begin very soon after completion
of the P wave in this lead. Admittedly the PR interval does not seem overly short in every lead on
this tracing. However, suspicion of a short PR interval should alert you to look closer at the QRS
complex:
Slurring on the upstroke of the initial part of the QRS complex is present in a number of leads
(leads II, aVF, and V1-thru-V6 ). These are delta waves and they confirm that the reason for
QRS widening is WPW. There is no RBBB.
As we will see in Section 10 when we discuss LIST #6 (Section 10.47) WPW is one of the
important causes of a tall R wave in lead V1.

05.42 WPW Addendum #1: How to Localize the AP?

Beyond-the-Core: Delta wave morphology and orientation on 12-lead ECG may assist in
surprisingly accurate localization of the AP ( Accessory Pathway) in the patient with WPW. This is
of more than academic interest to the EP cardiologist as it facilitates and expedites localization of
the AP during EP (ElectroPhysiology) study. In addition it helps in planning the procedure as well
as in patient discussion, since risks of catheter ablation and likely success rates are based in part on
localization of the AP.
We emphasize that ECG localization of the AP is an advanced topic that clearly extends beyond
clinical needs of the non-EP-cardiologist. Practically speaking it suffices to recognize WPW
and IF there is need for referral. That said ECG localization of the AP is a fascinating topic
that is not necessarily difficult if certain basic parameters are followed.
The choice is YOURS! Feel free to SKIP OVER this Addendum #1 on localizing the AP with
WPW (Sections 05.42-thru-05.46) if you prefer not to get into this aspect of ECG
interpretation. I avoided this topic for the first 30 years of my academic career and my ECG
interpretation ability was none the worse for it. BUT if youd like to be let in on a most userfriendly approach Ive encountered for AP localization Read on! I wager youll be
pleasantly surprised at how easy approximate AP localization can be from a few well spent
seconds analyzing the 12-lead ECG using the step-by-step approach I outline below (Clinical
examples discussed in Sections 05.44, 05.45, and 05.46).
M y Suggested Approach is based on my synthesis of material primarily from the following 2
references:
Das MK, Zipes DP: Electrocardiography of Arrhythmias A Comprehensive Review (ePub
book). Elsevier-Saunders, Philadelphia, 2012.
Fitzpatrick AP Gonzales RP Scheinman MM, et al: Algorithm for the Localization of Accessory
Atrioventricular Connections Using a Baseline Electrocardiogram. J Am Coll Cardiol
23:107-116, 1994.

05.43 WPW: The Basics of AP Localization

ECG localization of the AP is not perfect. Accuracy of ECG localization is clearly suboptimal if
there is less than maximum preexcitation as may occur when the QRS is minimally widened
because a substantial portion of ventricular activation is occurring by transmission of the impulse
over the normal AV nodal pathway.
Approximate distribution of AP sites is the following: i) Lateral (Left Ventricular) Free Wall
~50% of APs; ii) Right or Left PosteroSeptal Area ~20%; iii) RV ( Right Ventricular)

Free Wall ~20%; and iv) AnteroSeptal Area ~10%.

On occasion more than a single AP may be present in a given patient. Together with variation
in the relative amount of AP vs normal pathway conduction this may account for changing
delta wave morphology that can sometimes be seen from one ECG to the next in a given patient.
As a general rule IF the delta wave (first ~40msec of the QRS) is upright (positive) in lead
V1 (RBBB pattern) then there is a LEFT-sided AP (as in Step A-1).
IF the delta wave is downward (negative) in lead V1 (LBBB pattern) then as a general rule
there is a RIGHT-sided AP (The major exception to this is when transition occurs between
leads V1-to-V2 as described in Step B-1).
Step A-1: IF the QRS in Lead V1 is UPRIGHT
When the QRS complex is upright in lead V1 then there is a RBBB pattern. In this case
transition (where the R wave becomes taller than the S wave) is said to occur before or by lead V1.
This defines a LEFT-sided AP. Proceed as follows:
Measure the sum of delta wave polarities in the 3 inferior leads (II,III,aVF) giving a score
of +1 if the delta (first 40msec of the QRS) is positive; 0 if the delta is isoelectric; and -1 if the
delta is negative.
IF Sum of inferior lead Polarities is +2 or +3 = AnteroLateral LV Free Wall AP.
IF Sum of inferior lead Polarities is less than +2 then the AP is posterior.
IF Sum of inferior lead Polarities is -2 or -1 and the R wave in lead I is at least 0.8mV (8
mm) more than the S wave in lead I = PosteroSeptal AP. Otherwise = there is a PosteroLateral
LV Free Wall AP.
Step A-2: IF Transition Occurs Between Lead V1-to-V2:
IF the R wave in lead V1 is less than the S wave in V1 but by lead V2 the R wave becomes taller
than the S wave in V2 (ie, IF transition occurs between V1-to-V2) then the AP could be either
left or right-sided. Proceed as follows:
IF the R wave in lead I is less than 1.0mV (10 mm) greater than the S wave in lead I = then there
is a LEFT-sided AP. In this case Proceed as above (Step A-1) for when the QRS is
UPRIGHT (beginning by measuring sum of delta polarity in the inferior leads to determine if
the AP is anterolateral posteroseptal or posterolateral).
But IF the R wave in lead I is at least 1.0mV (10 mm) more than the S wave in lead I = then
there is a RIGHT-sided AP. In this case Proceed as described in Step B-1.
Step B-1: How to Tell IF the AP is RIGHT-sided?
When the QRS complex is downward (negative) in lead V1 and transition (where the R wave
becomes taller than the S wave) occurs after lead V2 then there is a RIGHT-sided AP.
As stated above there can also be a RIGHT-sided AP IF transition occurs between V1-to-V2
and the R wave in lead I is at least 1.0mV (10 mm) more than the S wave in lead I.

Step B-2: When the AP is RIGHT-sided:

Localization of a right-sided AP will depend on where transition occurs. There are 3 possibilities.
Transition may be: i) by or before V2-to-V3 (Step B-3) ; ii) between V3-to-V4 (Step B-4) ; or iii)
after V4 (Step B-5).
Step B-3: Right-Sided AP: Transition by or before V2-to-V3:
IF the AP is right-sided with transition by or before lead V2-to-V3 then the AP is Septal. To
determine which septal area is involved Proceed as follows:
Measure the sum of delta wave polarities in the 3 inferior leads (II,III,aVF) giving a score
of +1 if the delta (first 40msec of the QRS) is positive; 0 if the delta is isoelectric; and -1 if the
delta is negative.
IF Sum of inferior lead Polarities is -2 or -3 = PosteroSeptal AP.
IF Sum of inferior lead Polarities is -1, 0 or +1 = MidSeptal AP.
IF Sum of inferior lead Polarities is +2 or +3 = AnteroSeptal AP.
Step B-4: Right-Sided AP: Transition between V3-to-V4:
IF the AP is right-sided with transition between lead V3-to-V4 then the AP is either septal or
right ventricular free wall. To determine which Proceed as follows:
Measure delta wave amplitude (first ~40msec of the QRS) in lead II.
IF the delta wave in lead II is at least 1.0mV (10mm) = Septal AP. To then find out which septal
area is involved Proceed as above for when transition is between V2-to-V3 (Step B-3).
IF the delta wave in lead II is less than 1.0mV (10mm) = RV Free Wall AP. To determine IF the
AP is located on the anterolateral or posterolateral RV Free Wall Proceed as below for
when transition is after V4 (Step B-5).
Step B-5: Right-Sided AP: Transition after Lead V4:
IF the AP is right-sided with transition after lead V4 then the AP is located in the RV Free Wall.
To determine IF the AP is located on the anterolateral or posterolateral RV Free Wall Proceed
as follows:
Measure the delta wave frontal axis (looking at delta wave polarity in leads I and aVF).
IF the delta wave frontal axis is positive (= more than 0 degrees ) = Anterolateral RV Free
Wall AP.
But IF the delta wave frontal axis is negative (= less than 0 degrees) then look at the R wave
in lead III.
IF delta wave frontal axis is negative and the R wave in lead III is net positive =
AnteroLateral RV Free Wall AP.
IF delta wave frontal axis is negative and the R wave in lead III is net negative =
PosteroLateral RV Free Wall AP.

05.44 FIGURE 05.44-1: Where is the AP?

Lets apply the above approach for AP localization to the ECG shown in Figure 05.44-1 (this ECG
was previously seen in Figure 05.40).Where is the AP likely to be?

Figure 05.44-1: Sinus rhythm with WPW. Where is the AP?

Answer to Figure 05.44-1: We begin by looking to see IF the QRS complex in lead V1 of this tracing
is upright or negative:
Since the QRS in V1 is negative we skip over Step A-1.
Transition (where the R wave in precordial leads becomes taller than the S wave ) is not
between V1-to-V2 therefore we also skip over Step A-2.
According to Step B-1 the AP is RIGHT-sided (because the QRS is negative in V1 and
transition occurs after lead V2).
Transition occurs between V3-to-V4. Therefore we skip to Step B-4. We are asked to measure
delta wave amplitude in lead II. Realizing that it is not always easy to distinguish the precise
end of slurring from the delta wave vs the point of transition to the remaining portion of the QRS
it looks like there is a markedly positive delta wave (of at least 10mm) in lead II. This
suggests a Septal location for the AP.
To determine the likely part of the septum that is involved We are asked to return to Step B3. Delta wave polarities are clearly positive in each of the inferior leads therefore we
suspect an AnteroSeptal AP location.

05.45 FIGURE 05.45-1: Where is the AP?

Localize the AP for the example of WPW shown below in Figure 05.45-1 (this ECG was previously
seen in Figure 05.41-1).Where is the AP likely to be?

Figure 05.45-1: Sinus rhythm with WPW. Where is the AP?

Answer to Figure 05.45-1: We begin again by looking to see IF the QRS complex in lead V1 of Fig.
05.45-1 is upright or negative:
Since the QRS complex in lead V1 is upright we begin with Step A-1. Because the QRS is
positive in lead V1 we already know we are dealing with a LEFT-sided AP.
The sum of delta wave polarities is at least +2 (decidedly positive delta waves in leads II,aVF
though no more than minimally positive in III, if not isoelectric in this lead). Therefore
we suspect an AnteroLateral LV Free Wall AP.

05.46 FIGURE 05.46-1: Where is the AP?

Localize the AP for the example of WPW shown below in Figure 05.46-1 (this ECG was previously
seen in Figure 05.39-1).Where is the AP likely to be?

Figure 05.46-1: Sinus rhythm with WPW. Where is the AP?

Answer to Figure 05.46-1: We begin again by looking to see IF the QRS complex in lead V1 of Fig.
05.46-1 is upright or negative:

Since the QRS complex in V1 is negative we skip over Step A-1.

Transition (where the R wave in precordial leads becomes taller than the S wave ) is not
between V1-to-V2 therefore we also skip over Step A-2.
According to Step B-1 the AP is RIGHT-sided (because the QRS is negative in V1 and
transition occurs after lead V2).
Transition occurs between V2-to-V3. Therefore we skip to Step B-3. We are asked to measure
the sum of delta wave polarities in the inferior leads. Given that delta wave polarities are
decidedly positive in each of the inferior leads we suspect an AnteroSeptal AP location.

05.47 Addendum #2: Arrhythmias with WPW

We have already emphasized how conduction of the sinus impulse in patients with WPW may be: i)
via the normal (AV nodal) pathway; ii) down the AP ( Accessory Pathway) ; or iii) it may alternate
between the two. The same 3 possibilities for conduction exist when a patient with WPW develops a
supraventricular tachyarrhythmia. In these next few sections we briefly review key points to
consider when the patient with WPW develops an SVT (SupraVentricular Tachycardia).
Patients with WPW are prone to SVT rhythms in which a reentry circuit is set up between the
normal AV nodal pathway and the AP. Assuming there is no preexisting bundle branch block
whether or not the QRS complex will be wide during the tachycardia in a patient with WPW
will depend upon whether the reentrant pathway goes up or down the AP (Figure 05.47-1).

Figure 05.47-1: SVT pathways with WPW. Conduction of the impulse from atria to ventricles during
WPW-associated tachycardia may either be: i) as in Panel A = orthodromic (down the normal AV
nodal-His-Purkinje system and back up the AP) as commonly occurs with PSVT; or ii) as in
Panel B = antidromic (first down the AP and then back up the normal pathway) as commonly
occurs with AFib or AFlutter and only rarely with PSVT. Assuming there is no underlying bundle
branch block the QRS will be narrow with orthodromic conduction (Panel A) and wide with
antidromic conduction (Panel B).
05.48 PSVT with WPW: When the QRS During Tachycardia is Narrow
When PSVT occurs in a patient with WPW the tachycardia is almost always orthodromic (down
the normal AV nodal-His-Purkinje system and back up the AP = Panel A in Figure 05.47-1).
Because conduction goes down the normal AV nodal pathway the QRS is narrow during the
tachycardia. As a result the usual AV nodal blocking drugs (Verapamil-Diltiazem--

Blockers) can be used and are usually effective.

A delta wave will not be seen during the tachycardia. The presence of WPW may only be
suspected in a patient with narrow-complex PSVT IF an ECG showing delta waves is found in
the medical chart or obtained following conversion of the tachycardia.
PSVT is by far the most common tachyarrhythmia observed in patients with WPW. It is often
well tolerated.
Beyond-the-Core: A surprising number of patients with PSVT actually have one or more
concealed accessory pathways. That is a conduction pathway exists between atria and
ventricles that only allows orthodromic (but not antidromic) conduction. Since forward
conduction down the AP is not possible a delta wave is never seen. However, ready
availability of an AP reentry pathway may predispose such patients to frequent episodes of
PSVT. While acute treatment considerations are similar to those for treatment of any other
narrow-complex PSVT awareness of this entity may lower ones threshold for EP referral
after the episode if PSVT episodes are frequent and/or difficult to control with medication.
Ablation of the AP may be curative.
Way-Beyond-the-Core: Taking the last advanced information bullet one step further You may
at times be able to suspect the presence of an AP in some WPW patients with narrow complex
PSVT even without seeing a delta wave IF you see a negative P wave with long R-P interval
reflecting retrograde conduction back to the atria during the reentrant cycle. When retrograde
conduction is seen during AVNRT in a patient without WPW the RP is very short (most often
seen as a notch at the tail end of the QRS complex) reflecting short distance travel within the
AV node. The RP tends to be longer ( negative P usually seen midway within the ST segment)
for a patient in whom the reentry circuit runs down the AV node and back up an AP lying outside
the AV node. Technically this type of PSVT in a patient with accessory pathways is known as
AVRT (AtrioVentricular Reciprocating Tachycardia). Distinction in the ECG picture between
AVNRT vs AVRT ( when an AP is present) is an advanced concept that generally does not
impact on acute treatment. We often will simply not know if a narrow-complex PSVT rhythm
involves AV node vs AP in its reentry circuit.
Final Way-Beyond-the-Core Point: Adenosine may shorten the refractory period of atrial tissue
which could initiate AFib in a predisposed individual. As a result Adenosine should be
used with caution in patients with known WPW, given theoretic possibility of inducing AFib
(which could have significant consequence in a patient with accessory pathways). That said
we often will not know at the time treatment is needed IF the patient with a narrow-complex
PSVT has a concealed AP and even if they do, giving Adenosine to such a patient will rarely be
problematic.
BOTTOM Line = What to Remember!
Most of the time PSVT in a patient with WPW will conduct with a narrow QRS complex (as in
Panel A in Figure 05.47-1).
Practically speaking you do not have to worry in the immediate acute setting IF a patient with
narrow-complex PSVT has WPW or not. Initial treatment measures are the same. These include:
i) A vagal maneuver; and/or ii) Adenosine; and/or iii) Other AV nodal blocking agent
(Diltiazem, -Blocker).

With regard to longterm management awareness that a significant percentage of patients with
narrow-complex PSVT have a concealed AP ( even when they never show overt WPW on their
ECG) should lower our threshold for EP referral if PSVT episodes recur despite medical
therapy.

05.49 Very Rapid AFib with WPW

In contrast to the situation for PSVT with WPW the occurrence of AFib in a patient with WPW
almost always manifests a wide QRS during the tachycardia. This is because the path of conduction
for AFib with WPW is almost always antidromic (first down the AP and then back up the
normal pathway = Panel B in Figure 05.47-1).
Because of the short RP (Refractory Period) of the accessory pathway there may be 1:1
conduction of atrial impulses (at times resulting in a ventricular response that may exceed
250/minute!). As might be anticipated these rapid rates are not always well tolerated (may
deteriorate to VFib).
It is recognition of the ECG picture of exceedingly rapid AFib (over 220/minute in parts of the
tracing) in conjunction with QRS widening and marked variability in regularity of the tracing
that clues the clinician into the almost certain diagnosis of WPW with very rapid AFib. This is
the case for the rhythm in Figure 05.49-1.

Figure 05.49-1: WPW with very rapid AFib. Even without benefit of a 12-lead ECG an almost
certain diagnosis of WPW can be made from this single rhythm strip because: i) there is QRS
widening with marked irregular irregularity showing far more variation in rate than is seen with VT;
and ii) parts of the rhythm show a rate between 250-300/minute, which is far too fast for AFib
conduction over the normal AV nodal pathway. Thus, the rhythm must be AFib and conduction
must be bypassing the normal AV nodal pathway in a patient with WPW who has an AP ( Accessory
Pathway).
Treatment Considerations: WPW with Very Rapid AFib
The importance of recognizing that the example of very rapid AFib seen in Figure 05.49-1 is from a
patient with WPW is that treatment considerations are very different than they are for the much
more common usual AFib patient.
AV Nodal Blocking Drugs that are regularly used to treat the common form of rapid AFib
are contraindicated. This includes Verapamil-Diltiazem-Digoxin and possibly -Blockers.

By impeding conduction down the normal AV nodal pathway all of these agents may
inadvertently facilitate forward (antidromic) conduction of AFib impulses down the AP
(Accessory Pathway), thereby accelerating the rapid AFib even more. This may precipitate
deterioration to VFib.
Realizing that Adenosine is often used as a diagnostic measure during assessment of various
WCT (Wide-Complex Tachycardia) rhythms it is best to avoid Adenosine whenever
possible IF very rapid AFib with WPW is suspected (since Adenosine may likewise accelerate
AP conduction in a patient with WPW). That said the ultra-short half-life of Adenosine is
muc h less likely to be deleterious compared to other AV nodal blocking drugs if it is
inadvertently given.
Drugs of Choice: The 3 drugs that have most commonly been recommended for antiarrhythmic
treatment of hemodynamically stable very rapid AFib (or AFlutter) with WPW are i)
Procainamide; ii) Amiodarone; and iii) Ibutilide. There are pros and cons for use of each of these
agents that extent beyond the scope of this ePub on ECG interpretation. Each drug has its
advocates. All in theory reduce forward transmission of impulses down the accessory pathway.
KEY Point: IF at any time during the treatment process the patient becomes hemodynamically
unstable then cardiovert!

05.50 Atrial Flutter with WPW

When AFlutter occurs in a patient with WPW the tachyarrhythmia is also antidromic (first down
the AP and then back up the normal pathway = as in Panel B of Figure 05.47-1).
As with AFib the QRS is wide in AFlutter with WPW. There may be 1:1 AV conduction of
atrial impulses (so that the ventricular response may be 250-300/minute)!
Very fast AFlutter with WPW is seen even less often than AFib (but clinical manifestations and
treatment are similar).

05.51 PSVT with WPW: When the QRS is Wide

In rare instances PSVT may be antidromic (ie, travel first down the AP and then back up the
normal pathway = as occurs in Panel B of Figure 05.47-1).
In these rare instances the QRS will be wide and the PSVT rhythm may be indistinguishable
from VT.
It may only be after conversion to sinus rhythm that telltale delta waves of WPW can be
identified. Fortunately the vast majority (~95%) of PSVT episodes with WPW are
orthodromic (with narrow QRS) . Synchronized cardioversion will be the usual treatment of
choice for episodes of a regular WCT (Wide-Complex Tachycardia) in which one suspects
antidromic PSVT in a patient with WPW as the etiology.

05.52 FIGURE 05.52-1: VT or WPW? What to Do?

We complete our discussion of arrhythmias in the patient with WPW by the 12-lead ECG shown in
Figure 05.52-1 obtained from a hemodynamically stable young adult who presented to the ED
(Emergency Department) with new-onset palpitations.
What is the rhythm? What does this patient have?
How should the patient be treated?
Which drugs should not be given?

Figure 05.52-1: 12-lead ECG from a young adult with palpitations. What is the rhythm? (See text).
Answer to Figure 05.52-1: The rhythm in this hemodynamically stable young adult is an irregularly
irregular WCT (Wide-Complex Tachycardia). No P waves are seen in any of the 12 leads of this
tracing. This defines the rhythm as AFib. That said the ventricular response is exceedingly rapid
(attaining a rate of nearly 300/minute in some parts of the tracing). In addition there is marked
variability in rate of the ventricular response (seen best in leads aVF and V3).
This 12-lead ECG is virtually diagnostic of very rapid AFib in a patient who has WPW. VT
(Ventricular Tachycardia) may at times be slightly irregular but it should not be as
irregularly irregular as seen here throughout the tracing.
The rapidity of the rate (nearly 300/minute in certain parts of the tracing) suggests AP
conduction until proven otherwise (Section 05.49). Treatment considerations are as described in
Section 05.49 (IV Amiodarone, Procainamide or Ibutilide if the patient remains stable with
immediate cardioversion at the first sign of instability).
The patient should be referred to an EP cardiologist after resolution of the acute tachycardia for
consideration of an ablative procedure that may be curative.

06.0 QT Interval / Torsades de Pointes

06.1 How to Measure the QT

The QT interval is the period that extends from the beginning of ventricular depolarization
until the end of ventricular repolarization (Figure 06.1-1). For practical purposes, the QT is
prolonged IF it clearly measures more than half the R-R interval. The principal exception to this
rule is when the heart rate is rapid (>90-100 /minute) in which case it becomes more difficult to
measure the QT and determine its clinical significance.
To Measure the QT Select a lead where you can clearly see the end of the T wave. Select
that lead in which the QT appears to be longest.
NOTE: If there is no q wave in the QRS complex Measure from the beginning of the R
wave (Figure 06.1-1).

Figure 06.1-1: Provided that heart rate is not overly fast (ie, 90-100/minute) the QT is normal if
it is not more than half the R-R interval. There are 3 possibilities: i) Left Panel The QT is
clearly normal; ii) Middle The QT is borderline, as it is approximately half the R-R interval
(or at most, slightly more than half the R-R interval); or iii) Right The QT is clearly prolonged.
06.2 LIST #3: Causes of QT Prolongation
Clinically We want to know IF the QT is normal or long. This is usually easy to tell by the
eyeball method (ie, Is the QT more than half the R-R interval?) provided that the heart rate is
not excessively fast (>90-100/minute).
Practically speaking one only cares IF the QT interval is normal, borderline, or long. Patients
with a long QT interval are at increased risk of developing the potentially life-threatening
arrhythmia Torsades de Pointes (Section 06.6).
Beyond-the-Core: Hypercalcemia produces QT shortening. That said Hypercalcemia is
difficult to recognize on ECG, and is usually only seen with very high serum calcium values (of
>12 mg/dL).

Causes of a Long QT:

The common causes of a long QT interval can be divided into 3 categories: i) Drugs; ii) Electrolyte
disorders; and iii) CNS catastrophes. We consolidate this information in our LIST #3 (Figure 06.21):
KEY Point: The NOTE at the bottom of List #3 reminds us that other conditions (ie,
ischemia/infarction/BBB) may also prolong the QT. Clinically We pay less attention to
the QT interval when the ECG picture is dominated by other findings. But IF the only thing
wrong (beyond nonspecific changes) is a long QT Think Drugs/Lytes/CNS as the cause!

Figure 06.2-1: List #3 = Common Causes of a Long QT Interval.

06.3 A Closer Look at LIST #3: Drugs Lytes CNS
We expand on the causes of QT prolongation in LIST #3 ( Figure 06.2-1) by emphasizing the
following points:
DRUGS An ever increasing number of drugs (in addition to those in List #3) may either
affect the QT interval directly and/or produce p450 system drug interactions that increase
Torsades risk if taken together with other QT-lengthening drugs. Clinically it is usually not a
problem in an otherwise healthy adult to take any single drug that may affect the QT. But the
amount of QT prolongation (and the risk of Torsades ) may be additive IF more than one QTlengthening drug is taken especially if circumstances or other condition predisposing to
Torsades is present (Section 06.4).
LYTES 3 electrolyte disorders should be kept in mind when assessing a patient with QT
prolongation: i) Hypokalemia is characterized by ST flattening/depression; development of
U waves; and QT lengthening (Section 11.7); ii) Hypomagnesemia produces identical ECG
and clinical effects as hypokalemia (Section 11.8) ; and iii) Hypocalcemia which if other
electrolytes are normal, tends to produce a normal T wave after a prolonged QT interval
(Section 11.1).
NOTE: Rather than QT lengthening it is really the QU interval that is prolonged with
hypokalemia and/or hypomagnesemia (as T and U waves tend to fuse as the U wave becomes

bigger with more profound electrolyte depletion).

CNS catastrophes (ie, coma, stroke, trauma, seizure, bleed) are known to produce some of
the most bizarre ST-T wave abnormalities (and some of the longest QT intervals). Resultant
ST segment elevation that may be seen with CNS catastrophes can at times mimic the changes of
acute MI. The reason for ST-T wave abnormalities with CNS disorders is uncertain but is
thought to relate to disturbance of autonomic tone.

06.4 Conditions Predisposing to a Long QT/Torsades

Be aware of circumstances that increase the risk of QT prolongation and therefore of developing
Torsades de Pointes. These include:
Female sex (women are more predisposed to Torsades!).
Electrolyte disorders (low K+/low Mg++).
Bradycardia (usually 50/minute) since a long preceding R-R interval (as seen with
bradycardia) sets up prolongation of the QT interval for the following beat.
Structural heart disease (heart failure; marked LVH; cardiomyopathy; ischemia; prior
infarction).
Significant renal or hepatic dysfunction.
Baseline QT prolongation if the QTc is >450 msec. ( especially if >500 msec. Section
06.5).

06.5 The QTc: Corrected QT Interval

Up to now We have focused on the eyeball method for determining IF the QT interval is normal
or long:
IF the QT is less than half the R-R then the QT is normal.
But IF the QT is more than half the R-R the QT is long (Figure 06.1-1).
In either case, more precise determination of the QT interval is usually not necessary since for
practical purposes, the main thing we are concerned with is whether the QT is normal or long. That
said at times it will be important to more precisely determine the QT. This is especially true when
it is not readily apparent from inspection whether the QT interval is normal or long.
Tables exist for precise determination of the QT based on the age, sex and heart rate.
Accounting for difference in heart rate results in a QTc where the little c indicates
correction of the QT for heart rate.
Beyond-the-Core: The formula for determining QTc = the QT that you measure divided by
the square root of the R-R interval. The good news is that at a heart rate of 60/minute the
R-R interval = 5 large boxes (= 1.0 second) and the square root of one is one! This means
that at a rate of 60/minute the QTc is the QT interval that you measure.

KEY Point: The computerized interpretation will accurately calculate the QTc for you! In
general the upper normal for the QTc is ~450msec. More than this suggests QT
prolongation. Definite concern about QT prolongation increases once the QTc exceeds 480 msec
(especially if >500 msec)!

06.6 Torsades: WHY Care about QT Prolongation?

Why Care about the QT interval? The answer is to hopefully prevent the rhythm seen in Figure 06.61. Cardiopulmonary resuscitation was ongoing at the time this tracing was obtained.

Figure 06.6-1: Irregular WCT rhythm obtained during cardiopulmonary resuscitation. What is the
rhythm? What to do next? (See text).
Answer to Figure 06.6-1: After 2 sinus beats the rhythm dramatically changes. This is
polymorphic VT as defined by constantly varying QRS morphology throughout the rest of the
tracing.
Torsades de Pointes is defined as polymorphic VT that occurs in association with a
prolonged QT interval on baseline ECG. The very rapid irregular WCT seen in Figure 06.6-1
manifests the shifting QRS polarity around the baseline (twisting of the points) that is
characteristic of Torsades.
NOTE: There appears to be a prolonged QT interval for the first 2 sinus beats in Figure 06.6-1
(ie, the QT looks to be more than half the R-R interval) in which case the rhythm would be
Torsades. That said it is difficult to be certain where the T wave (and therefore the QT
interval) ends in this tracing. Clinically It will simply not always be possible to assess QT
duration during polymorphic VT.
Clinical Reality When we either do not have access to a prior baseline 12-lead ECG on the
patient or cannot accurately assess the QT interval from the rhythm strip we will be unable to
distinguish whether the rhythm is PMVT (PolyMorphic Ventricular Tachycardia) or
Torsades (which is simply PMVT with baseline QT prolongation).
Treatment of Figure 06.6-1: Regardless of whether this irregular WCT rhythm is PMVT or
Torsades initial treatment measures are the same: i) Defibrillation if the rhythm persists; ii)
Magnesium Sulfate (1-2 gm IV which often needs to be repeated up to 4-8 gm); and iii) Try to find
and fix the underlying cause of PMVT/Torsades. Potential additional measures for resistant cases (ie,
overdrive pacing, isoproterenol) extend beyond the scope of this ePUb on ECG diagnosis.
Beyond-the-Core: There are some differences in etiology and response to treatment between
Torsades vs PMVT without QT prolongation that are worthy of mention. While IV Magnesium
Sulfate is the drug of choice for both disorders PMVT tends to respond less well to this

treatment than when there is Torsades with QT prolongation. Rather than being drug or
electrolyte induced PMVT with a normal QT more often has an ischemic etiology
(occasionally due to Brugada Syndrome). Efforts addressed at treating acute ischemia may
therefore be helpful. IV Amiodarone and/or -blockers may reduce recurrence and should be
considered if IV Magnesium is ineffective.

06.7 FIGURE 06.7-1: Torsades vs PMVT vs Something Else?

Would you treat both of the rhythms in Figure 06.7-1 with defibrillation and IV Magnesium?
What additional information is essential for answering this question?

Figure 06.7-1: Torsades vs PMVT vs something else? (See text). HINT: Timelines for determining
heart rate are shown by the square boxes in each tracing (corresponding to a large box on ECG grid
paper in each case).
Answer to Figure 06.7-1: At first glance, it appears that both of these rhythm strips represent
PMVT/Torsades. While superficially they do the devil is in the details ( in this case the rate of
the rhythm).
Note in Rhythm A of Fig. 06.7-1 that there are at certain points in the tracing two vertical
deflections for each large box. This corresponds to a rate of ~500-to-600/minute, or too fast for
Torsades. This is artifact. We do not see any normal beats on this tracing but instead just see
very straight line, excessively fast deflections suggestive of artifact.
The rate in Rhythm B is also fast but much closer to ~300/minute (~1 complex per each
large box) which clearly falls within the appropriate rate range for PMVT/Torsades. The
rhythm begins and ends by a few normal (narrow) sinus beats. Given the rapid rate it is
difficult to determine if the QT is or is not prolonged. Therefore, we can not be certain if
Rhythm B is PMVT or technically qualifies as Torsades. As emphasized in Section 06.6
initial treatment measures are the same regardless of whether or not there is baseline QT
prolongation.

K E Y Point: Awareness of clinical context is an essential component of clinical ECG

interpretation. The diagnostic dilemma of whether Rhythm A in Figure 06.7-1 is real might be
easily resolved IF we knew that the patient was alert and hemodynamically stable (which would
confirm artifact). Loose lead connections, tremor, scratching, shivering, and seizure activity are but a
few of the possible causes of artifact-related deflections that might simulate a tachyarrhythmia.
06.8 FIGURE 06.8-1: Is the QT Long?
Comment on the QT interval for the 12-lead ECG shown in Figure 06.8-1. What clinical conditions
are likely to account for findings on this ECG?

Figure 06.8-1: Is the QT interval prolonged? If so What is the likely cause(s)?

Answer to Figure 06.8-1: The rhythm is sinus tachycardia at a rate just over 100/minute. The PR
interval and QRS duration are both normal. However the QT interval is long:
As emphasized in Section 06.1 the QT interval should be measured in a lead where you can
clearly see the end of the T wave and in which the QT appears to be longest. As a result a
lead such as aVL should not be used, since the end of the T wave is not well defined in this lead
(red question mark in Fig. 06.8-1).
On the other hand it is much easier to determine the limits of the T wave in other leads. This
is especially true for lead V2 in which the QT interval is obviously more than half the R-R
interval. NOTE: Although the eyeball method for assessing QT interval duration is admittedly
less accurate when heart rate exceeds 90-100/minute (Section 06.2) QT duration in Figure
06.8-1 is so much more than half the R-R interval, that the QT is undoubtedly prolonged despite
the fact that the heart rate is relatively rapid.
Regarding assessment of the rest of the ECG in Figure 06.8-1 the most remarkable finding is
deep, symmetric T wave inversion in most precordial leads.
IMPRESSION: Sinus tachycardia marked QT prolongation and diffuse symmetric T wave
inversion. In addition to ischemia (which is suggested by this symmetric T wave inversion) Think
Drugs/Lytes/CNS as the categories of entities to consider in your differential diagnosis for the
markedly prolonged QT interval seen here (LIST #3 in Figure 06.2-1). Clinical correlation is
needed to comment further on the most likely causes.

Beyond-the-Core: The reason we say the QT interval is markedly prolonged is that the QT
literally makes up more than 2/3 of the R-R interval (See insert of leads V2,V3 in Figure 06.81). Thus despite the relatively rapid rate and the possibility of ischemia strong consideration
should be given to drug-induced QT prolongation severe hypokalemia/hypomagnesemia
and/or CNS catastrophe as contributing causes (List #3).

06.9 FIGURE 06.9-1: Is the QT Long?

We conclude this segment on assessment of the QT interval with one more 12-lead tracing ( Figure
06.9-1). The rhythm is sinus tachycardia at a rate of ~150/minute. There is diffuse ST segment
depression. Comment on the QT interval.

Figure 06.9-1: Sinus tachycardia at ~150/minute. There is diffuse ST depression. Comment on the
QT interval (See text).

Answer to Figure 06.9-1: As stated there is sinus tachycardia and diffuse ST segment depression.
Clearly a heart rate of ~150/minute is too fast to accurately apply the eyeball method for QT
assessment. That said a look at multiple leads in Figure 06.9-1 suggests that the QT interval
makes up as much as ~80% (if not more) of the R-R interval.
While numerical determination of a QTc is not realistic for the ECG in Figure 06.9-1 (because
the rate is too fast) we strongly suspect the QT is significantly prolonged. Clinically We
again consider Drugs/Lytes/CNS as possible contributing causes.

06.10 QTc Addendum: Using/Calculating the QTc

Beyond-the-Core: As emphasized in Section 06.5 the computerized interpretation will

automatically generate a QTc value for you that takes into account the patients baseline heart rate.
The computer-calculated QTc is usually quite accurate. As a result a perfectly appropriate
approach is to first estimate QT interval duration yourself by the eyeball method (the QT should
not be more than half the R-R interval) and, to then check this out with the QTc value provided
by the computer:
The upper normal limit for the QTc is ~450msec. QTc values greater than this suggest QT
prolongation.
Clinically concern about QT prolongation increases once the QTc exceeds 480 msec
(especially if >500 msec)!
An advantage of incorporating the computer-calculated QTc value is that doing so facilitates
serial comparison of QT duration in a given patient. For example slight prolongation of the QTc
from a baseline of 430 msec to 445 msec in a patient started on Sotalol (an antiarrhythmic agent
known to significantly increase QT duration when used in higher doses) would not necessarily
mandate stopping the drug or even lowering the dose. However, continued progressive QT
prolongation (say, from 430 msec to 445 msec to 470 msec ) would clearly require
reassessment of the treatment regimen.
06.11 BEYOND-the-Core: Estimating the QTc Yourself
For those providers with a desire to quickly estimate the QTc on their own without need to use the
computer-calculated value We propose the following:
The formula for determining QTc = the QT that you measure divided by the square root of
the R-R interval. The good news is that at a heart rate of 60/minute the R-R interval = 5
large boxes (= 1.0 second) and the square root of one is one! This means that at a rate of
60/minute the QTc is the QT interval that you measure.
At heart rates faster than 60/minute the QTc will be more than the QT that you measure
(because QTc varies inversely with the square root of the R-R interval and the R-R interval
for rates faster than 60/minute is less than one).
Determining the square root for any R-R interval other than an R-R interval of exactly 1.0
second is complex. This is why a computer is needed for precise QTc calculation. That said
We have devised a simple correction factor that can be used to rapidly approximate QTc
duration.
Use of Our Proposed Correction Factor for QTc Estimation:
Determine the heart rate. Measure the QT interval in a lead where you can clearly see the end of the T

wave and in which the QT interval appears to be longest. Then multiply the QT interval you measure
by the correction factor corresponding to your estimation of heart rate:
Multiply by 1.0 for a heart rate of ~60/minute.
Multiply by 1.1 for a heart rate of ~75/minute.
Multiply by 1.2 for a heart rate of ~85/minute.
Multiply by 1.3 for a heart rate of ~100/minute.
Applying the QTc Correction Factor:
Lets assume that the QT interval you measure is 0.40 second (= precisely 2 large boxes in
duration). IF the heart rate was ~60/minute then the QTc = the QT you measure = 0.40 second.
IF on the other hand, the heart rate was 75/minute then we can estimate the QTc by
multiplying the QT we measure (= 0.40 second) by the correction factor of 1.1 = ~0.44 second.
IF instead the heart rate was ~85/minute then the QTc would be 0.40 X 1.2 = ~0.48 second.
IF instead the heart rate was ~100/minute then the QTc would be 0.40 X 1.3 = ~0.52 second.
Accuracy for QTc estimation decreases with rates substantially faster than 100/minute so we
do not offer additional correction factors beyond this rate.
Practically speaking there is no need to correct the QT for rate when there is bradycardia
(since change in the QTc is relatively small at rates below 60/minute).

06.12 FIGURE 06.12-1: Approximate the QTc

The 12-lead ECG in Figure 06.12-1 shows normal sinus rhythm at a rate just over 75/minute (since
the R-R interval is just under 4 large boxes in duration).
Assess the QT by the eyeball method. Is the QT interval likely to be normal or prolonged?
Estimate the QTc by applying the appropriate correction factor from Section 06.11 that
corresponds to a heart rate just over 75/minute.

Figure 06.12-1: Sinus rhythm at a rate just over 75/minute. Assess the QT interval. Approximate the

QTc (See text).

Answer to Figure 06.12-1: As stated there is sinus rhythm at a rate just over 75/minute.
We select lead V2 to measure the QT because we can clearly see the end of the T wave in
this lead. Alternatively We could have measured the QT in a number of other leads (ie, leads II,
V3,V4,V5).
By the eyeball method the QT appears to be normal (since the QT is not more than half
the R-R interval).
As shown in Figure 06.12-1 We measure the QT to be ~0.38 second (just a bit less than 2
large boxes in duration).
Given the heart rate close to 75/minute We use a correction factor of 1.1. Multiplying 0.38
X 1.1 is approximately 0.42 second = the QTc. Since 420 msec is clearly less than normal
upper limit of 450 msec (Section 06.10) we know that the QTc is normal even without
referring to the computer-calculated value.

06.13 FIGURE 06.13-1: Approximate the QTc

The 12-lead ECG in Figure 06.13-1 shows sinus tachycardia at a rate of ~100/minute (since the R-R
interval is ~3 large boxes in duration). The QRS complex is narrow.
Assess the QT by the eyeball method. Is the QT interval likely to be normal or prolonged?
Estimate the QTc by applying the appropriate correction factor from Section 06.11 that
corresponds to a heart rate of ~100/minute.

Figure 06.13-1: Sinus tachycardia at ~100/minute. Assess the QT interval. Approximate the QTc
(See text).
Answer to Figure 06.13-1: As stated there is sinus tachycardia at a rate of ~100/minute. The QRS
complex is narrow so any QT widening that may be seen is not the result of bundle branch block
or other conduction defect.

We again select lead V2 to assess the QT. By the eyeball method the QT appears to be
markedly prolonged. Although heart rate is faster than is optimal for QT assessment the QT
takes up more than 2/3 of the R-R interval. There is therefore no doubt that the QT is prolonged.
As shown in Figure 06.13-1 We measure the QT to be ~0.48 second (easily more than 2
large boxes in duration).
Given the heart rate = 100/minute We use a correction factor of 1.3. Multiplying 0.48 X 1.3
comes to a QTc of over 600 msec! Therefore we know that the QTc is dangerously
prolonged without having to refer to the computer-calculated value.
BOTTOM Line: This QTc Addendum ( Sections 06.10-thru-06.13) is written solely for those
wanting additional insight into clinical use of more precise QTc determination, including a userfriendly method for rapid estimation of the QTc on your own without need to refer to the computercalculated value. We emphasize that this is advanced material.

Most of the time it suffices to simply use the eyeball method covered in Sections 06.1 and
06.2 for QT assessment.
Awareness that computerized interpretations automatically provided you with a fairly accurate
QTc value corrected for heart rate helps take QT interval assessment one step further. The
normal upper limit for QT duration is ~450 msec. QTc values greater than this amount indicate
QT prolongation. Clinical concern about QT prolongation increases with QTc intervals that
exceed 480-500 msec. Serial QTc assessment may provide additional insight when progressive
increase in QT duration is subtle.
For those who want more Try out our proposed method for rapid QTc estimation in Section
06.11.

07.0 Determining Axis / Hemiblocks

07.1 Overview: Limb Lead Location

The mean QRS Axis may be defined as the average direction of the hearts electrical activity. A
standard ECG is recorded by viewing the heart's electrical activity from 12 leads. Each lead records
the heart's electrical potential from its own particular vantage point (Figure 07.1-1).
As discussed in detail in Sections 03.1-thru-03.5 the three standard limb leads are I, II, and
III. Because electrical derivation of these leads is based on the premise of Einthoven's
equilateral triangle each of these leads is separated from each other by 60, starting with
lead I (at 0) followed by lead II (at +60) and lead III (60 further away at +120).
The augmented limb leads are each separated from each other by 120 and as such form a
"Mercedes-Benz" triangle (dotted lines in Figure 07.1-1) beginning with vertical lead aVF
(at +90) lateral lead aVL (at -30) and distant lead aVR (which we can usually ignore
in axis determination and need not recall its degree location).

Figure 07.1-1: Limb lead location for calculation of axis.

Clinical Reality: Although axis determination is essential for diagnosis of the hemiblocks (Section
07.9) and may contribute to diagnosing RVH; pulmonary embolus; dextrocardia; and lead
misplacement most of the time, calculation of axis provides only limited clinical information.
07.2 AXIS: The Quadrant Approach
Mean QRS axis is calculated in the frontal plane. The 2 KEY leads that are used for axis
determination are lead I and lead aVF:
Think of Lead I as the "starting" point. As such, it is easy to remember that this horizontal
lead is oriented toward 0 (Figure 07.2-1).
Lead aVF is oriented perpendicular to lead I (ie, looking straight up from the Feet). Lead
aVF is therefore 90 away from lead I (or at +90).

Figure 07.2-1: Axis quadrants. A normal axis is defined by the borders of leads I and aVF (ie, a
normal axis lies between 0-to-90).
KEY Point: It is easiest to define axis by Quadrants:
A normal axis (See Figure 07.2-1) is defined as lying within the limits of lead I (at 0) and
lead aVF (at +90).
LAD (Left Axis Deviation) lies between -1 to -90.
RAD (Right Axis Deviation) lies between +91 to +180.
A n indeterminate axis lies between +180 and +270 (or between -90 and -180). This
quadrant is the furthest away from the heart and is often referred to as the northwest
quadrant or No-mans land.
Clinical Note: Although by the Quadrant Approach we describe an axis of +95 as RAD and an
axis of -10 as LAD we emphasize that this minimal amount of axis deviation is not of clinical
consequence. It is rarely important to be more precise than within 20-to-30 of the actual axis.
07.3 AXIS: The Concept of Net QRS Deflection
Determination of the mean axis quadrant can be made at a glance by inspection (and
comparison) of the net QRS deflection in lead I vs lead aVF. To determine the net QRS
deflection in any given lead Mentally subtract negative deflections from positive ones (Figure
07.3-1). It is net area that counts. For example:
Panel A (in Figure 07.3-1) is all positive.
Panel B is predominantly positive (compared to the R wave, the s wave is small).
Panel C is predominantly positive (with a small q wave and a small s wave but a tall R
wave).

Panel D is positive (albeit with no more than a small R wave).

NOTE: The reason we use both small-case and large-case letters in describing Q, R and S wave
deflections is to convey relative size. While we are not aware of any official distinction between
small- vs large-case We favor use of 3 mm (3 little boxes) as our defining characteristic:
Q, R, and S waves all manifest an amplitude of at least 3 mm.
The amplitude of q, r and s waves is 3 mm or less. We generally use a small-case designation
for 3 mm deflections that are narrow vs large-case designation for a 3 mm deflection that is
wider. Thus, we describe the complex in Panel C of Fig. 07.3-1 as a qRs deflection.

Figure 07.3-1: Illustration of how to assess net QRS deflection. Each of the examples shown here
manifest a net positive deflection (See text).
07.4 FIGURE 07.4-1: How to Rapidly Determine Axis Quadrant
We can determine the quadrant in which the axis lies within seconds by 2 simple steps: Step #1:
Assess the net QRS deflection in leads I and aVF; and Step #2: Use the Table in Figure 07.4-1:

Figure 07.4-1: Rapid determination of the axis quadrant based on the net QRS deflection in leads I
and aVF. For example IF net QRS deflection is positive in both leads I and aVF then the axis is
normal (between 0-to-90).
07.5 AXIS: Refining the Quadrant Approach
Using the Table in Figure 07.4-1 allows near instant determination of the axis quadrant. We can
refine our estimate for axis by considering the following:
IF the net QRS deflection in lead I (at 0) is about the same as that for lead aVF (at +90)
then the axis should lie midway between these leads (= close to +45 ).
Instead IF the net QRS deflection in lead I is positive but clearly exceeds the net deflection in
lead aVF then the mean QRS axis lies closer to lead I (ie, between 0 and +40).
In contrast the axis lies closer to lead aVF (between +50 and +90) IF the net QRS
deflection in lead aVF is greater than it is in lead I.
The axis is perpendicular to (ie, 90 away from) a lead where the QRS complex is isoelectric
(equal parts positive and negative to the QRS).
All you are doing is approximating. Axis calculation need not be exact as long as your
estimate is within 20-to-30 of the actual axis. As a result we often provide an axis range
for our answer (ie, The axis lies between +40 to +50).
Realize that you can further refine your estimate of axis by looking at net QRS deflection in
other limb leads. That said this is usually not clinically needed, as will soon be apparent in
review of the axis examples that follow.
Final Note: The computerized interpretation is usually quite accurate for determination of
heart rate, intervals and axis. IF you prefer you can almost always depend on the axis
calculated by the computer.

07.6 FIGURE 07.6-1: What is the Axis?

Based on the net QRS deflection in leads I and aVF Estimate the mean QRS axis in Panels A and
B of Figure 07.6-1.
In which of the 4 Quadrants does the axis lie? (Feel free to refer back to Sections 07.4 and 07.5
in formulating your answer).

Figure 07.6-1: Estimate the axis for Panels A and B. In which of the 4 quadrants does the axis lie?
Answer to Figure 07.6-1: We can tell at a glance that the axis is normal (between 0-to-90) in both
A and B because the net QRS deflection in both leads I and aVF is positive in each case. Use of a
quadrant diagram allows us to refine our estimate for axis (Figure 07.6-2):
Panel A (in Figure 07.6-1) We estimate the axis at between +30-40. The net deflection for
both I and aVF is positive. The R wave in lead I is clearly taller than it is in lead aVF. As a
result the axis must lie closer to lead I (or between 0-to-45). We illustrate this in Panel A of
Figure 07.6-2.
Panel B (in Figure 07.6-1) We estimate the axis at between +60-75. The net QRS
deflection is decidedly more positive in aVF (Panel B in Fig. 07.6-2).

Figure 07.6-2: Quadrant diagram illustrating axis location (black arrows) for Panels A and B from
Fig. 07.6-1.
07.7 FIGURE 07.7-1: What is the Axis?
Estimate the mean QRS axis in Panels C and D of Figure 07.7-1:

Figure 07.7-1: Estimate the axis for Panels C and D. In which of the 4 quadrants does the axis lie?
Answer to Figure 07.7-1: We can tell at a glance that the axis is normal for C (positive deflection
in I and aVF) but not normal in D (negative deflection in one of these leads). Use of a quadrant
diagram allows a closer look (Figure 07.7-2):
Panel C (in Figure 07.7-1) We estimate the axis at between +10-20. Relative positivity of
the net deflection in lead I compared to aVF is even more marked than it was for Panel A in
Figure 07.6-1. The axis in Panel C must therefore lie very close to lead I (as shown in Panel C
of the quadrant diagram in Figure 07.7-2).
Panel D (in Figure 07.7-1) There is at least slight LAD (Left Axis Deviation) since net
QRS deflection is negative in lead aVF. As we will see momentarily in discussion of
hemiblocks (Section 07.9) use of lead II will be needed to determine if the amount of LAD is
more or less than -30. We illustrate slight leftward axis for Panel D in the corresponding
quadrant diagram shown in Figure 07.7-2.

Figure 07.7-2: Quadrant diagram illustrating axis location (black arrows) for Panels C and D from
Fig. 07.7-1.
07.8 FIGURE 07.8-1: What is the Axis?
Estimate the mean QRS axis in Panels E and F of Figure 07.8-1:

Figure 07.8-1: Estimate the axis for Panels E and F. In which of the 4 quadrants does the axis lie?
Answer to Figure 07.8-1: We can tell at a glance that the axis is not normal for E or F because
net QRS deflection is not positive in both leads I and aVF. Use of a quadrant diagram allows a
closer look (Figure 07.8-2):

Panel E (in Figure 07.8-1) There is RAD (Ri ght Ax i s Deviation) since net QRS
amplitude in lead I is clearly negative (the S in lead I is deeper than the R wave is tall). We
estimate mean QRS axis to be between +100-to-110. We illustrate this in Panel E of the Figure
07.8-2 quadrant diagram. Clinical NOTE: It is sometimes difficult to accurately determine the
specific number of degrees with right axis deviation. That said it is not overly important
whether the axis is +105, or for that matter +120. What counts clinically is that there is
definite RAD.
Panel F (in Figure 07.8-1) The axis is indeterminate since the net QRS deflection is
negative in both leads I and aVF. Clinically it no longer matters how many degrees the axis
is. All that counts is that axis location is in the upper right (indeterminate) quadrant (Panel F in
the Figure 07.8-2 quadrant diagram) . PEARL: The most common clinical conditions
associated with an indeterminate axis are: i) RVH; ii) COPD; and iii) Large body habitus.

Figure 07.8-2: Quadrant diagram illustrating axis location (black arrows) for Panels E and F from
Fig. 07.8-1.

07.9 Hemiblocks: LAHB and LPHB

07.10 Hemiblocks: Anatomic Considerations

As seen below in Figure 07.10-1 after the electrical impulse arrives at the AV Node it travels
down the Bundle of HIS. From there, the ventricular conduction system divides into the slender
Right Bundle Branch and the much thicker Common Left Bundle Branch.
T h e Common Left Bundle Branch divides into 2 parts: the Anterior and Posterior
Hemifascicles. Development of a hemiblock simply entails a defect in conduction over
one of these hemifascicles.
Note in Figure 07.10-1 that the posterior hemifascicle is anatomically much thicker than the
anterior hemifascicle. This is one reason why LPHB is uncommon. The other reason is a richer
(dual) blood supply compared to the anterior hemifascicle. As a result it is rare to see
LPHB as an isolated defect in a patient without significant heart disease. Most patients with
LPHB have bifascicular block (RBBB/LPHB See Sections 07.20, 07.21).

Figure 07.10-1: The ventricular conduction system. Note how much thicker the left posterior
hemifascicle is compared to the anterior hemifascicle and the right bundle branch.
KEY Clinical Point: The anatomic diagram in Figure 07.10-1 is simplified. In reality there are
millions of fibers in the ventricular conduction system with many potential anatomic variants on the
arrangement shown. That said, most of the time conduction fibers to the left ventricle are arranged
in two large groups (hemifascicles) one of which is situated slightly in front (anterior) of the
other.
The benefit of accepting the arrangement in Figure 07.10-1 as the general anatomic model, is that
it greatly simplifies diagnosis of the hemiblocks!

07.11 Advanced Concept: LSFB (a 3rd type of Fascicular Block)

Beyond-the-Core: In a significant percentage of patients a 3rd (septal) hemifascicle appears to
exist (not shown in Fig. 07.10-1). The collection of fibers that make up this septal hemifascicle is
thinner, more variable in distribution than are fibers in the anterior and posterior hemifascicles, and
generally manifests a shorter refractory period. As its name implies fibers from the septal
hemifascicle contribute to early activation of a portion of the ventricular septum in certain patients.
As a result a 3rd type of partial LBBB conduction block (in addition to LAHB and LPHB)
may occur = LSFB (Left Septal Fascicular Block).
LSFB is not commonly recognized on ECG. This is because of several reasons: i) the
existence of this 3rd hemifascicle is not well appreciated; ii) LSFB is uncommon; and iii) ECG
manifestations of LSFB when it does occur are often masked by simultaneous occurrence of
other conduction defects. Practically speaking Do NOT be concerned about recognizing
LSFB unless you are a student of advanced arrhythmia interpretation.
BOTTOM Line: Our reason for mentioning the existence in some patients of a septal
hemifascicle and therefore a potential 3rd type of fascicular block is twofold: i) to shed light on
the otherwise unexplained coming-and-going of septal q waves (or of the initial small r wave
in V1,V2) that is sometimes seen in some challenging arrhythmias (may be due to intermittent
LSFB aberrant conduction); and ii) to emphasize that the anatomic arrangement presented in
Figure 07.10-1 is a simplification. This simplification works well for understanding the general
anatomic pattern of the ventricular conduction system and it allows rapid diagnosis of the
hemiblocks (Section 07.12).

07.12 Hemiblocks: An Approach to Rapid ECG Diagnosis

Agreement among experts is lacking regarding diagnostic criteria for hemiblock. Some experts
specify a certain number of degrees in axis deviation whereas others favor QRS morphology
change rather than axis criteria. Fortunately ECG diagnosis of hemiblocks can be simplified into
an equally accurate yet user-friendly approach that allows classification in less than 5 seconds. This
approach is based on the following concepts:
There are 2 hemiblocks that we need to concern ourselves with: anterior and posterior. Life is
simpler (and no less accurate in the overwhelming majority of cases) if we do not initially
concern ourself about the infrequent, difficult-to-diagnose 3rd type of conduction deflect =
LSFB (Section 07.11).
Of the 2 types of hemiblock that we do need to concern ourselves with Le f t Posterior
HemiBlock (LPHB) is rare! As already emphasized (Section 07.10) the reason LPHB is
so uncommon is that the posterior hemifascicle is much thicker anatomically and it has a dual
blood supply (from the left and right coronary arteries); the anterior hemifascicle does not.
Even experts often do not agree on the ECG diagnosis of LPHB. As a result You are
probably none the worse if you never diagnose LPHB. On those uncommon occasions when
LPHB does occur it will almost always be seen in association with RBBB (See Section
07.21 and 07.25).

In contrast diagnosis of LAHB (Left Anterior Hemi-Block) is far more common (>98%
of hemiblocks in our experience). ECG diagnosis of LAHB becomes easy IF you accept as
your criterion for diagnosis recognition of a pathologic left axis (Section 07.13).

07.13 LAHB: ECG Diagnosis = pathologic LAD

Expert electrocardiographers do not agree on how to define LAHB. Some define it by the number of
degrees (be this requiring a leftward axis more negative than -30, -45, or -60). Others maintain
that rather than axis it is QRS morphology in the limb leads that defines LAHB. Life is simpler
(and equally accurate) IF you equate pathologic LAD = LAHB. Consider the following:
Some LAD (ie, -10 to -20) is common and not necessarily abnormal.
We define a pathologic LAD as a left axis more negative than -30. It is easy to tell IF
pathologic LAD is present. You only need to look at lead II (Figure 07.13-1):

Figure 07.13-1: Diagnosis is simplified by defining LAHB as a pathologic left axis (= a net
deflection in lead II that is more negative than positive).
KEY Summarizing Point: For practical purposes We equate the ECG diagnosis of LAHB with
the finding of pathologic LAD (which we define as a mean QRS axis more negative than -30).
Assuming lead I is positive (as it almost always is) then the amount of LAD is pathologic
IF the net deflection in Lead II is negative (See Lead II Appearance in the lower right
portion of Figure 07.13-1).

07.14 FIGURE 07.14-1: Is there LAD? IF so Is there LAHB?

Apply the quadrant approach to determine the axis for the 12-lead ECG shown in Figure 07.14-1:
Is there LAD? If so Is there also LAHB?
Which lead should be used to determine if LAHB is or is not present in Figure 07.14-1?

Figure 07.14-1: Estimate the axis. Is there LAD? If so Is there also LAHB? (See text).
Answer to Figure 07.14-1: It is easy to determine the axis for the 12-lead ECG shown in Fig. 07.141 by use of the quadrant approach:
The net QRS deflection in lead aVF is negative. It is positive in lead I.
By the Table in Figure 07.4-1 LAD is therefore present. The situation is similar to the
example illustrated by Panel D in Section 07.7, which we reproduce below in Figure 07.14-2.
Once established that there is LAD We determine IF the amount of LAD is pathologic by
looking at lead II.
Pathologic LAD is clearly present in Figure 07.14-1 since the net QRS deflection in lead II
is decidedly more negative than positive. Therefore there is LAHB in Figure 07.14-1. We
estimate the mean QRS axis in this tracing to be at least -40.

Figure 07.14-2: We reproduce Panel D from Section 07.7. The situation is similar to that shown in
Figure 07.14-1. There is LAD because the net QRS deflection is positive in lead I and negative in
lead aVF. We would need to see lead II in order to determine IF the amount of LAD was
pathologic (ie, more negative than -40).
07.15 SUMMARY: ECG Diagnosis of LAHB in 3 Seconds
Panels G and H in Figure 07.15-1 summarize how to tell within seconds IF there is LAHB:

Panel G By the quadrant approach, the more-negative-than-positive deflection in lead aVF

defines there to be LAD. However the lead II deflection is not more negative than positive.
Therefore the axis is not more negative than -30 in Panel G, which means there is LAD but not
LAHB. In fact the isoelectric appearance in lead II means that the axis is virtually
perpendicular to (90 away from) lead II or precisely at -30.
Panel H The once again more-negative-than-positive deflection in lead aVF defines there to
be LAD. This time the lead II deflection is more negative than positive. Therefore the LAD is
sufficiently leftward to qualify as LAHB. We estimate the mean QRS axis to be at least -40.

Figure 07.15-1: Panels G and H both show LAD. There is LAHB in H but not in G (because net
QRS deflection is negative in lead II for H, but not in G).

07.16 Bifascicular Block

07.17 Definition/Types of Bifascicular Block

The term bifascicular block implies that more than a single major branch of the ventricular
conduction system is not functioning. The defect in conduction may be transient or permanent.
Practically speaking there are 2 Types of Bifascicular Block:
RBBB/LAHB = RBBB plus LAHB.
RBBB/LPHB = RBBB plus LPHB.
Clinical Note: Semantically complete LBBB is also a type of bifascicular block since
there is implication of failed conduction (by definition) in both anterior and posterior hemifascicles
when there is LBBB. That said We generally do not think of LBBB as bifascicular block. This
leaves us with the 2 types of hemiblock cited above (RBBB + either LAHB or LPHB).
07.18 RBBB/LAHB: ECG Recognition
By far the most common form of bifascicular block is the combination of RBBB/LAHB. The
schematic tracing in Figure 07.18-1 shows the typical ECG appearance of this conduction defect.
Note the underlying rhythm is sinus (upright P wave in lead II) and the QRS looks to be wide. We
focus attention on the 3 key leads for diagnosing BBB (leads I,V1,V6 Section 05.2) plus on
lead II.
RBBB is recognized by its characteristic appearance in the 3 key leads (rSR with taller
right rabbit ear in V1; wide terminal S wave in leads I,V6).
That there also is LAHB is seen from the negative net deflection in lead II (Section 07.13).

Figure 07.18-1: RBBB/LAHB. RBBB is diagnosed by the rSR in lead V1 with wide, terminal S
waves in I,V6. LAHB is diagnosed by the decidedly more-negative-than-positive deflection in
lead II (See text).

07.19 The Meaning of Axis when there is RBBB

The concept of axis in the setting of RBBB is problematic. Calculation of axis is based on the
average direction of the hearts electrical activity in the frontal plane. In the presence of RBBB
electrical activity first goes left-to-right (as the septum is depolarized) then right-to-left (as the
left ventricle is depolarized) and then left-to-right again as the blocked right ventricle is finally
activated via slow myocardial conduction through nonspecialized fibers. So in the setting of RBBB
the average direction of the hearts electrical activity does not reflect the actual zig-zag path of
the depolarization impulse.
Bottom Line: Dont worry about axis when RBBB is present!
All we care about when there is RBBB is which of these 3 possible settings is operative: i)
RBBB and nothing else; ii) RBBB plus LAHB; or iii) RBBB plus LPHB.
The ECG picture of RBBB/LAHB is easy to recognize. In addition to RBBB We can tell at a
glance IF LAHB is also present by a look at lead II to see IF the net QRS deflection is
predominantly negative (Figure 07.18-1).

07.20 Clinical Implications of Bifascicular Block

The clinical significance of virtually any conduction system defect depends on the setting in which it
occurs. Isolated RBBB may sometimes occur in otherwise healthy individuals without underlying
heart disease in which case RBBB is unlikely to have any adverse prognostic implications
(Section 05.5). In contrast a new finding of RBBB in the setting of acute evolving MI implies
ongoing conduction system damage (suggesting a larger infarct size and possible need for a
pacemaker).
Bifascicular block clearly implies a more important conduction defect than isolated RBBB.
That said IF the patient is otherwise asymptomatic, t he n bifascicular block from
RBBB/LAHB may n o t necessarily convey any adverse prognostic implications. Combined
RBBB/LAHB is seen surprisingly often as an incidental finding in an otherwise asymptomatic
older individual.
On the other hand IF new RBBB/LAHB develops in the setting of acute coronary syndrome
the extent of damage is probably large (and the patient may soon need a pacemaker).
Clinical context is everything!
The other form of bifascicular block = RBBB/LPHB is much less common. As previously
stated (Section 07.10) the reason LPHB is so uncommon relates to its anatomy (much thicker
fascicle) and dual blood supply. As a result, IF RBBB/LPHB does occur it implies a more
extensive conduction system defect (with potentially more severe prognostic implications).

07.21 RBBB/LPHB: ECG Recognition

The uncommon form of bifascicular block is the combination of RBBB/LPHB. The schematic
tracing in Figure 07.21-1 shows the typical ECG appearance of this conduction defect. Note the
underlying rhythm is sinus (upright P wave in lead II) and the QRS looks to be wide. We focus

attention on the 3 key leads for diagnosing BBB (leads I,V1,V6 Section 05.2) plus on lead II.
RBBB is recognized by its characteristic appearance in the 3 key leads (rSR with taller
right rabbit ear in V1; wide terminal S wave in leads I,V6).
That there also is LPHB is seen from the presence in lead I of a de e p straight initial
descent of the S wave in this lead. In support of the diagnosis of RBBB/LPHB is the
presence of a qR pattern in lead II with a relatively tall R wave in this lead.
NOTE: Leads II, III and aVF all typically manifest a similar ECG appearance when there is
RBBB plus LPHB (ie, a qR pattern with relatively tall R wave). That said We can simplify
the process of recognizing RBBB/LPHB by focusing attention on QRS appearance in the 3 key
leads (I,V1,V6) plus on lead II as is done in Figure 07.21-1.

Figure 07.21-1: RBBB/LPHB. RBBB is diagnosed by the rSR in lead V1 with wide, terminal S
waves in I,V6. LPHB is diagnosed by the very steep initial descent of the S wave in lead I. In
addition Note the qR pattern in lead II with relatively tall R wave (See text).
07.22 RBBB/LPHB: Finer Points on ECG Recognition
The experts often do not agree on the diagnosis of bifascicular block from RBBB/LPHB. The KEY to
recognizing this form of bifascicular block is that once complete RBBB is identified Focus
attention on S wave descent in lead I.
As emphasized in Section 05.4 a wide terminal S wave in lateral leads I,V6 is part of the
expected QRS morphology seen with complete RBBB (Panel A in Figure 07.22-1). That said
the initial (straight portion) of the S wave in lead I is not nearly as steep with isolated
RBBB as it is when LPHB is also present (red arrow in Panel B of Fig. 07.22-1).

Figure 07.22-1: RBBB by itself (Panel A) compared to bifascicular block when there is RBBB
plus LPHB (Panel B). Note the very steep initial descent of the S wave (red arrow) in lead I when
LPHB is also present (See text).
Beyond-the-Core: Because the posterior hemifascicle lies not only posterior, but also inferior and
rightward (in 3 dimensions) with respect to the anterior hemifascicle the blocked portion of the
QRS deflection in lead I is directed inferior and to the right. This is the reason for the steep negative
S wave descent in lead I and the predominant positive R wave in leads II, III, and aVF (Panel B in
Fig. 07.22-1).
Typically there will also be a slender initial r wave in lead I and a small narrow q wave in
the inferior leads (II,III,aVF) when there is RBBB/LPHB. This is because the initial direction
of left ventricular depolarization with RBBB/LPHB is toward that part of the LV supplied by the
intact left anterior hemifascicle. Given the relative leftward and superior orientation of the left
anterior hemifascicle (compared to the relative rightward and inferior orientation of the
posterior hemifascicle) initial electrical activity with RBBB/LPHB tends to produce a small
r in lead I and a small q in inferior leads (Panel B in Figure 07.22-1). That said these subtle
ECG features might be altered if in addition to RBBB/LPHB there has been prior scarring or
infarction.
Bottom Line: Remember that bifascicular block from RBBB/LPHB is uncommon in clinical
practice. ECG diagnosis is often challenging and encompasses an advanced subject area about
which cardiologists do not always agree. You are probably none the worse if you never
diagnose this entity. Our goal is merely to highlight the ECG features we find helpful for
recognizing RBBB/LPHB when it is present. Realize that once you do identify this form of
bifascicular block it is almost certain that your patient has extensive underlying heart
disease.

07.23 FIGURE 07.23-1: Is there Bifascicular Block?

Assess the ECG in Figure 07.23-1 for the presence of conduction defects.
Is there bifascicular block?

Figure 07.23-1: Sinus rhythm with RBBB/LPHB (See text).

Answer to Figure 07.23-1: The rhythm is sinus. The QRS complex is wide.
RBBB is recognized by its characteristic appearance in the 3 key leads (rSR with taller
right rabbit ear in V1; wide terminal S wave in leads I,V6).
In addition, there is LPHB as diagnosed by the presence in lead I of a deep straight initial
descent of the S wave in this lead. In support of the diagnosis of RBBB/LPHB is the
presence of a qR pattern in leads II,III,aVF with a relatively tall R wave in these leads
(especially in lead III). Thus, there is bifascicular block (RBBB/LPHB).

07.24 FIGURE 07.24-1: Is there Bi- or Tri-Fascicular Block?

Assess the ECG in Figure 07.24-1 for the presence of conduction defects.
Is there bifascicular block?
What is trifascicular block?

Figure 07.24-1: Sinus rhythm with RBBB/LAHB. Is there trifascicular block? (See text).
Answer to Figure 07.24-1: The rhythm is sinus (upright P wave in lead II, as shown by the red
arrow). The PR interval is prolonged (clearly more than a large box in duration) so there is 1st
degree AV block (Section 02.70).

The QRS complex is wide. Blowup inserts from the 3 key leads (I,V1,V6) confirm RBBB
(rSR in V1; wide terminal S waves in leads I and V6). NOTE: Even though the S wave in lead
I is not deep it is relatively wide, and this satisfies criteria for RBBB (Section 05.4).
LPHB is clearly not present in Figure 07.24-1 because the S in lead I is small without a steep
descent.
On the other hand LAHB is present, because the QRS deflection in lead II is predominantly
negative (Section 07.18). Therefore there is bifascicular block (RBBB/LAHB).
Beyond-the-Core: The term, trifascicular block implies impaired conduction in all 3 of the major
conduction fascicles: i) the right bundle branch; ii) the left anterior hemifascicle; and iii) the left
posterior hemifascicle.
Clinically Diagnosis of trifascicular block is usually not possible from the surface ECG. We
simply cannot tell IF PR interval prolongation in a patient with bifascicular block (as in Figure
07.24-1) is due to AV nodal disease or disease in the remaining conducting fascicle. Therefore
We would interpret this ECG as showing bifascicular block (RBBB/LAHB) plus 1st degree
AV block.

07.25 FIGURE 07.25-1: Isolated LPHB vs Right Axis Deviation?

We conclude our discussion on hemiblocks and bifascicular block with the 12-lead ECG shown in
Figure 07.25-1 obtained from an otherwise healthy young adult male seen in the office for an
insurance physical. The rhythm is sinus (probable sinus arrhythmia) and the QRS complex does
not appear to be prolonged.
RAD (Right Axis Deviation) is clearly present as determined by a predominantly negative
QRS in lead I with an upright QRS in lead aVF.
Does this patient have LPHB?

Figure 07.25-1: 12-lead ECG obtained from an otherwise healthy 30-year-old man. There is RAD.

Does the patient have LPHB? (See text).

Answer to Figure 07.25-1: Although there is marked RAD We would not interpret this tracing as
showing LPHB because: i) LPHB is rarely seen as an isolated conduction defect; and ii) The patient
is an otherwise healthy 30-year-old man which is a distinctly unusual setting for LPHB to occur.

We would interpret this ECG as showing sinus arrhythmia; RAD; and peaked T waves with
some J-point ST elevation that is most suggestive of an early repolarization pattern.
Given the considerable amount of RAD seen here the possibility of RVH ( Right Ventricular
Hypertrophy) should be contemplated. Assuming no murmur was heard on auscultation the
decision of whether or not to obtain an Echo could be made clinically.
Perhaps if new RAD to this degree was seen in a patient with ongoing acute infarction the
cause might be LPHB (as occurs in Figure 10.43-1). However, given the setting described here
this is highly unlikely.
On occasion otherwise healthy adolescents and young adults may present with RAD not due
to RVH or other underlying structural heart disease. We suspect this is the situation here.

08.0 LVH: Chamber Enlargement

The unfortunate clinical reality is that the ECG is just not very accurate as a diagnostic tool for
determining chamber enlargement. Even in the best of hands the sensitivity of ECG for detecting
LVH does not exceed 60% (although specificity may approach 90 to 95% when certain criteria
are met). Diagnostic accuracy for determining RVH (Right Ventricular Hypertrophy) and atrial
enlargement is even less (See Sections 08.14-through-08.22; and 08.23-through-08.33).
Echocardiography is far superior to the ECG for diagnosing enlargement of any cardiac
chamber.
Therefore IF you truly need to know Get an Echo!

08.1 ECG Diagnosis of LVH: Simplified Criteria

There are more than 50 sets of criteria in the literature for ECG diagnosis of LVH. None are optimal.
The simplified criteria for LVH we favor as providing what we feel is the best balance between
sensitivity and specificity are shown in Figure 08.1-1.

Figure 08.1-1: Simplified ECG criteria for LVH (See text).

KEY Points: The beauty of Figure 08.1-1 is that these simplified criteria only require recall of 2
numbers = 35 and 12. In our experience these 2 criteria almost always allow diagnosis
whenever it is possible by ECG to determine that there is LVH.
Only one voltage criterion (ie, 35 or 12) needs to be satisfied for ECG diagnosis of LVH.
Note that voltage criteria for LVH may not be valid for younger patients. This is because
younger adults (in their 20s ) often manifest increased QRS amplitude without true chamber
enlargement. We suggest not using the voltage criteria in Figure 08.1-1 for patients less than 35
years old.
The accuracy (specificity) for the ECG diagnosis of LVH can be greatly increased IF in
addition to satisfying one or more voltage criteria, ST-T wave changes of "LV strain" are also
present (Section 08.9).
The Clinical History helps in assessing for LVH. For example, it is important to appreciate

even before looking at the ECG itself that the chance of true chamber enlargement is greatly
increased IF the tracing is obtained from a middle-aged, African-American man with longterm
hypertension. KEY POINT: A history of underlying heart disease (heart failure,
hypertension, cardiomyopathy, valvular disease, coronary artery disease ) clearly
increases the likelihood of LVH in any given patient.

08.2 LVH: Physiologic Rationale for Voltage Criteria

The physiologic rationale for derivation of virtually all voltage criteria for LVH is simple. We
illustrate this concept in Figure 08.2-1:
Normal LV (Left Ventricle) activation is directed away from right-sided leads (ie, V1,V2)
and toward left-sided leads (aVL; V5,V6). As a result leads V1,V2 normally manifest a
predominant S wave.
Since the LV is situated to the left and posteriorly in the thorax normal LV activation
generally results in a predominant R wave in left-sided leads aVL,V5,V6 (Panel A in Fig. 08.21). With LVH there is more LV mass ( large red arrow in Panel B). As a result the S
wave in V1,V2 becomes deeper; and the R wave in aVL and/or V5,V6 becomes taller.

Figure 08.2-1: Rationale for derivation of LVH voltage criteria. There is deepening of the S wave in
right-sided leads = V1,V2; and/or an increase in R wave amplitude in left-sided leads (ie, V5,V6,
aVL).
08.3 LVH: ECG Diagnosis using Lead aVL
In Section 03 We discussed localization of lead aVL in the hexaxial lead system (looking down at
the heart from the left shoulder at an angle of approximately -30 degrees ). We then specified
anatomic landmarks used for precordial lead placement when recording an ECG (Section 03.6).
Awareness of this relative position of unipolar lead aVL (looking down at the heart from the left
shoulder) allows us to envision how lead aVL views the hearts electrical activity from a higher
perspective than precordial leads (ie, V1,V2; V5,V6) that are placed on the chest.
As a result Use of the criterion for R wave amplitude in lead aVL 12mm is likely to be
most helpful when there is a leftward axis (this aVL criterion may satisfy voltage for LVH
despite sometimes minimal QRS size in V1,V2 and V5,V6).

Remember Only 1 voltage criterion (35 or 12) is needed to satisfy voltage for LVH.
Figure 08.3-1: LVH using Lead aVL
We illustrate use of lead aVL for making the diagnosis of LVH by voltage in Figure 08.3-1. This ECG
was obtained from an older adult with hypertension. R wave amplitude in lead aVL is clearly
increased (more than 3 large boxes or greater than 15 mm ). However there is no indication at
all of voltage for LVH from assessment of QRS amplitude in the precordial leads (deepest S in
V1,V2 + tallest R in V5,V6 is very much less than 35 mm).
Since only 1 voltage criterion is needed the presence of a tall R wave in lead aVL (12 mm)
in Figure 08.3-1 satisfies voltage criteria for LVH.
Note there is LAD as is evident from the predominantly negative QRS in lead aVF with
positive QRS in lead I. This supports the premise that lead aVL tends to be most helpful as a
voltage criterion for LVH in the presence of a leftward axis.

Figure 08.3-1: ECG obtained from an older adult with hypertension. Voltage criteria for LVH are
satisfied by the tall R wave in lead aVL (12 mm) despite relatively low voltage in the precordial
leads (See text).
08.4 FIGURE 08.4-1: Is there Voltage for LVH?
The ECG in Figure 08.4-1 was obtained from an otherwise healthy 29-year old man who was seen in
the office for an insurance physical.
Is there LVH?
HINT: Feel free to review the simplified criteria for LVH in Figure 08.1-1 before answering.

Figure 08.4-1: ECG from a 29-year old man. Is there LVH?

Answer to Figure 08.4-1: The ECG shows sinus arrhythmia and is essentially normal. There is no
LVH because this patient is less than 35 years old. Note that ST-T waves are unremarkable. There
is no indication of LV strain.
We illustrate how to assess for voltage by the blow-up of the 4 key precordial leads shown in
Figure 08.4-2. As per the criteria detailed in Figure 08.1-1 one adds the deepest S wave in
leads V1,V2 plus the tallest R wave in V5,V6. The sum = 43 (ie, 20 + 23=43) but since the
patient is under 35 years of age voltage for LVH is not present (Section 08.7).

Figure 08.4-2: Blowup of selected precordial leads from Figure 08.4-1 to illustrate how QRS
amplitude is counted. The deepest S wave in V1,V2 is 20 (in lead V1) + the tallest R wave in V5,
V6 (= 23 in lead V5) is >35 BUT because the patient is less than 35 years of age voltage for
LVH is not present.
08.5 Standardization Mark: Is Standardization Normal?
Most of the time the ECG will be set to normal standardization. Confirmation that this is the case
is easily achieved by recognition of the standardization mark at the very beginning or end of the 12lead recording (black arrow at the onset of lead III in Figure 08.4-1).

Normal standardization is designated by a rectangular standardization mark that is 10 mm (=2

large boxes) tall.
On occasion ECG complexes may be extremely large and extend beyond the space provided
for one or more leads on the tracing. Selection of half standardization reduces waveform
amplitude by half with result that the entire complex in each lead will again fit on the ECG
recording paper and be seen.
These concepts are illustrated in Figure 08.5-1 in which the Top Panel is a blow-up of leads
III and aVF from Figure 08.4-1.
IF instead, this ECG was recorded at half standardization actual QRS amplitude would be
twice that shown = 10 vs 5 in lead III; and 26 vs 13 in lead aVF (Lower Panel in Fig. 08.5-1).

Figure 08.5-1: Blowup of Figure 08.4-1 to illustrate the appearance of a normal (top) and half
(bottom) standardization mark. Actual voltage is twice that shown when the ECG is recorded at
half standardization.
08.6 LVH: Additional Voltage Criteria
No single voltage criterion will identify all patients with LVH. As a result we occasionally turn to
additional voltage criteria. We favor any of the following:
A deep S wave (20-25 mm) in lead V1 or V2.
A tall R wave (25 mm in V5 or 20 mm in V6).
An R wave 20 in any inferior lead (II, III, or aVF).
Cornell Criteria LVH is present IF sum of R wave in lead aVL + S wave in lead V3 is
20mm (female) or 28mm (male).
Bottom Line: In our experience, IF all you remember are the numbers 35 and 12 for LVH voltage
criteria then ~90% of the time when it is possible to diagnose LVH on the ECG of an adult, you
will be able to do so!
Satisfying any of the above additional criteria should help to pick up most of the remaining

~10%.
Incorporating Clinical History and looking for strain or a strain equivalent pattern
(Section 08.13) will further refine and increase accuracy (specificity) of your diagnosis.
Keep in mind that competing conditions (ie, hyperkalemia, acute infarction, conduction
defects, pulmonary disease) may mask ECG diagnosis of LVH.
IF you really need to know about chamber size Get an Echo. The ECG is simply not
optimally accurate.

08.7 LVH: Voltage Criteria for Patients Less than 35

Young adults often have increased amplitude not due to true chamber enlargement. As a ballpark
estimate for LVH voltage criteria when the patient is 35 years old We use sum of the deepest S
wave in V1,V2 + tallest R wave in V5,V6 53. This number 53 can be easily remembered
because it is the reverse of the number 35.
Look at the selected precordial lead sequence shown in Figure 08.7-1 (previously shown in Fig.
08.4-2). Sum of the deepest S wave in V1,V2 (20) + tallest R wave in V5,V6 (23) = 43 mm.
We were initially told ( in Section 08.4) that these leads were obtained from a 29-year old
man. In this case voltage criteria for LVH would not be met (the patient is under 35 and
the voltage sum is less than 53).
On the other hand, IF this patient was over 35 then voltage criteria for LVH would be
satisfied (since the voltage sum is more than 35).

Figure 08.7-1: Selected precordial leads reproduced from Fig. 08.4-2. Is there voltage for LVH ( See
text).
KEY Point: There is no magic per se about becoming 35 years old and suddenly satisfying voltage
criteria for LVH. The age cutoff is far from precise. That said, it is helpful to be aware that more
often than not when a healthy adult under 35 manifests increased QRS amplitude but without ST-T
wave changes of strain most of the time there is not true chamber enlargement.

08.8 FIGURE 08.8-1: Which Leads for What with LVH?

In an attempt to expedite ECG recognition of LVH We suggest use of Figure 08.8-1. This figure
highlights our two favored LVH voltage criteria (Section 08.1):
LVH by 35 We look for deepest S wave in V1,V2 + tallest R wave in V5,V6. If 35 =
LVH.
LVH by 12 If the R wave in lead aVL 12 = LVH.
We then look for LV strain or a strain equivalent (Section 08.13) in one (or more) of
the left-sided leads = I,aVL; V4,V5,V6.
For LAE Look at lead II (notched P wave) and/or lead V1 (deep negative component to the
P in V1).
For RAE (not shown on this Figure) Use lead II (Sections 08.19).

Figure 08.8-1: Chamber Enlargement: Which leads for what?

08.9 LV Strain: ECG Recognition
It is difficult to define strain. We conceptualize the ECG picture of strain as a pattern of
asymmetric ST-T depression (Figure 08.9-1). Perhaps strain simply reflects that point of anatomic
ventricular enlargement at which increased demand (from chamber thickening) outstrips blood
supply with resultant ST-T wave repolarization changes from suboptimal perfusion. Or perhaps
not. That said What counts clinically is ECG recognition of a strain pattern.
Note how downslope of the ST segment in Figure 08.9-1 is slower with strain (arrow in
Panel C) compared to the more rapid return of the ST segment to baseline.

Figure 08.9-1: ST-T wave appearance of normal ( A) vs strain (C) or a strain equivalent (B)
vs ischemia (D).
Pattern Recognition: The concept of pattern recognition is essential to ECG diagnosis. Consider
the following:
With ischemia (seen in Panel D of Figure 08.9-1) there will often be symmetric T wave
inversion in two or more leads in a general lead area.
NOTE: As one traces the path in Figure 08.9-1 from a normal ST-T wave ( seen in Panel A)
to the asymmetric ST-T wave typical of LV strain (seen in Panel C) one passes through
an intermediate stage, where the ST-T wave flattens with beginning ST depression (Panel B).
We designate this intermediate stage as a strain equivalent.
Terminology: In general, when we use the term strain We are referring to LV strain that
develops in response to Left Ventricular Hypertrophy (LVH).
There is also RV strain that typically develops in association with marked RVH or in
response to acute pulmonary embolus. For now Think LV strain when we use the
unspecified designation of strain (RV strain is discussed in Sections 08.28, 08.29).
Which are the Leads that may show LV Strain?
We expect to see LV strain in leads that look at the left ventricle. These include one (or more) of
the lateral leads I,aVL; and V4,V5,V6 (highlighted by green boxes in Figure 08.8-1).
Less often a typical LV strain pattern (with asymmetric ST-T wave depression ) may also
be seen in the inferior leads especially if the patient has a relatively vertical (inferior) axis.
LV strain is generally not seen in anterior leads (V1,V2,V3). In contrast, RV strain (as
may occur with RVH or acute pulmonary embolus) typically is seen in either anterior or
inferior leads (See Section 08.29).
FIGURE 08.9-2: Which Leads Show LV Strain?
The ECG in Figure 08.9-2 was obtained from a patient with longstanding hypertension. There is
obvious voltage for LVH (very deep S wave in V2 + very tall R wave in V6).
Which of the 5 lateral leads manifest ST-T wave changes consistent with strain?
Explain the ST-T wave depression seen in each of the inferior leads (II,III,aVF).

Figure 08.9-2: ECG from a patient with longstanding hypertension. Which leads show ST-T wave
changes consistent with LV strain? (See text).
Answer to Figure 08.9-2: The rhythm is sinus. As stated there is obvious voltage for LVH ( very
deep S wave in V2 + very tall R wave in V6).
ST-T wave changes consistent with LV strain are clearly seen in lead V6 of Figure 08.9-2.
We would interpret the flat ST segment with slight T inversion in lead V5 as a strain
equivalent (Section 08.13) . Neither aVL nor lead V4 manifest strain (upright T wave in
these leads). The nonspecific ST-T wave flattening in lead I might be a strain equivalent
albeit minimal QRS amplitude in this lead makes this supposition less convincing.
NOTE: Asymmetric ST-T wave depression in each of the inferior leads (II,III,aVF) in this
tracing looks typical for LV strain (closely resembles Panel C in Fig. 08.9-1). Given the
relatively vertical axis (about +75 degrees) it is far more likely that these inferior ST-T
wave changes reflect LV strain rather than ischemia ( especially if the patient is not having
new or recent chest discomfort). Thus, the ECG in Fig. 08.9-2 appears to represent an example
of the occasional occurrence of LV strain in inferior as well as lateral leads.
Beyond-the-Core: NOTE in Figure 08.9-2 that the ST segment is elevated in leads V2,V3.
Is this likely to reflect an ACS (Acute Coronary Syndrome)?
Answer: As will be discussed in detail in Sections 09 and 10 ST segment deviations (elevation
or depression) are most often judged with respect to the preceding PR segment baseline. With this in
mind there unmistakably is at least 2 mm of ST elevation in leads V2,V3. That said it is highly
unlikely that this anterior ST elevation represents ACS because:
There is no mention of chest discomfort in this patient with longstanding hypertension.

In patients with LVH and strain there will often be several mm of ST elevation in anterior
leads as a mirror-image reflection of lateral precordial strain. Note that IF you flipped over
the ECG complex in lead V6 of Figure 08.9-2 (very tall R wave; ST-T changes of strain) that
the result would be identical to what is seen in leads V2,V3 (very deep S wave; mirror-image
ST-T wave appearance of what was seen in V6).
BOTTOM Line: In addition to ST-T wave depression that may be seen in one or more of the
lateral leads with LV strain slight ST elevation (with mirror-image appearance to the
ST-T wave in lateral leads) may also be seen in anterior leads.

08.10 LV Strain: Voltage for LVH vs True Chamber Enlargement

The reason it is important to recognize strain is that this finding greatly increases the accuracy
of the ECG diagnosis of LVH.
The presence of increased voltage without strain has low specificity (50%) for true
chamber enlargement (especially if the patient is otherwise healthy and without underlying
heart disease). We interpret the finding of increased voltage without ST-T wave changes of
strain as Voltage for LVH . This designation serves to acknowledge that despite an increase
in QRS amplitude statistical likelihood of true chamber enlargement is low.
NOTE: On occasion there may be typical ST-T wave changes of LV strain but without
voltage for LVH. The ECG is simply not that sensitive for demonstrating increased QRS
amplitude in patients with anatomic LV chamber enlargement. While we do not advise making a
definitive ECG diagnosis of LVH in the absence of voltage criteria We may nevertheless
suspect LVH rather than ischemia in the presence of asymmetric ST depression IF: i) the history
does not sound like there is cardiac chest pain; and ii) the patient has one or more conditions
predisposing to LVH. Clearly Clinical correlation is needed.
Assess the ECG in Figure 08.10-1 for LVH. We previously encountered this tracing in Figure 08.4-1
at which time we were told that it came from a 29-year old man. Despite sum of deepest S wave in
V1,V2 + tallest R wave in V5,V6 being >35mm the patients age (ie, less than 35 years old)
meant that voltage criteria for LVH were not fulfilled.
BUT What IF instead of a 29-year old man, this ECG had been obtained from a 40-year old
man? Would there now be voltage for LVH?
NOTE: ST-T waves are normal in all lateral leads in Figure 08.10-1 such that there is no
indication of LV strain.

Figure 08.10-1: ECG previously seen in Fig. 08.4-1. Is there voltage for LVH? (See text).
Answer to Figure 08.10-1: IF instead of being 29, the patient was 40 then the ECG in Fig. 08.101 would meet voltage criteria for LVH. That said the absence of any ST-T wave indication of
strain means that the chance of true chamber enlargement is still low. This is especially true if this
40-year old man was previously healthy with normal blood pressure.
08.11 FIGURE 08.11-1: Is there True Chamber Enlargement?
Contrast the ECG just shown in Figure 08.10-1 with the 6 precordial leads in Figure 08.11-1.
These precordial leads were obtained from an older adult with longstanding hypertension.
Is there LVH? What is the likelihood of true chamber enlargement?

Figure 08.11-1: Precordial lead sequence obtained from an older adult with longstanding
hypertension. What is the likelihood of true chamber enlargement?
Answer to Figure 08.11-1: QRS amplitude is markedly increased in the 6 precordial leads shown

easily satisfying voltage criteria for LVH (Section 08.1). In addition note ST-T wave changes
consistent with LV strain in leads V4,V5,V6. Specificity for LVH has got to be close to 100%.
KEY Point: Once strain and voltage are both present specificity for true chamber enlargement
goes way up (to ~90% and >95% if the patient has underlying heart disease). This is seen in
Figure 08.11-1.
ECG diagnosis of LVH plus strain is not a trivial one. The Framingham study demonstrated
up to an 8-fold increased morbidity/mortality in patients with longstanding hypertension when
there was evidence of LVH with strain on their office ECG tracing.

08.12 Can there be both LV Strain and Ischemia?

Clinically both ischemia and strain may exist at the same time. Patients with LVH from
longstanding hypertension may also have coronary disease. If anything such patients are at greater
risk of ischemia/infarction.
The ECG changes of either ischemia or strain may mask the other. In some patients
symmetric T wave inversion may predominate. In others J-point depression with asymmetric
ST segment sagging may be more prominent. Distinguishing between acute ischemia vs strain
may be extremely challenging (if not impossible) from review of a single ECG tracing.
NOTE: When history and ST-T wave appearance suggest that both LV strain and ischemia
are present We often write the following on our interpretation: LVH and strain and/or
ische mia. Suggest clinical correlation. This is precisely what we would write for
interpretation of the precordial lead sequence shown in Figure 08.12-1.

Figure 08.12-1: Precordial lead sequence obtained from an older adult with a history of coronary
disease. We would write the following for our interpretation: LVH and strain and/or ischemia
(See text).

Figure 08.12-1: Additional Points of Interest

Note that standardization is normal in Fig. 08.12-1 (arrow at the end of V4 indicating the
rectangular standardization mark is 2 large boxes tall as it should be).
Note slight variation in S wave depth in lead V2. Such slight variation is common. We
sometimes adjust for it by taking an average for amplitude in a given lead.
Note overlap (within the red circle ) of the S wave from V4 with the R wave in V5. We could
have eliminated this by recording the tracing at half standardization. That said most of the
time we prefer normal standardization. The point to emphasize is that caution is needed in
determining true R wave amplitude in lead V5 of Figure 08.12-1.
KEY Points: Comparing Figs. 08.11-1 and 08.12-1:
Our interpretation of ST-T wave appearance in Figure 08.12-1 contrasts with that from Fig. 08.11-1.
The best way to highlight this contrast is by side-to-side comparison of both tracings (Panels A and
B in Figure 08.12-2):
In both Panel A and Panel B deepest S wave in V1,V2 + tallest R wave in V5,V6 easily
satisfy voltage criteria for LVH.
In Panel A ST-T wave appearance in leads V5,V6 strongly suggests LV strain (there is
asymmetric ST depression with slow sagging downslope).
In contrast, for Panel B ST segments are coved in V3-through-V6. In addition, there is 1-2
mm of J-point ST depression (below the PR segment baseline) in leads V4,V5,V6 with T
wave inversion that is deep and appears to be much more symmetric (especially in leads
V4,V5). This appearance is more suggestive of ischemia.
In particular lead V3 in Panel B looks ischemic (pure LV strain virtually never produces
ST coving and symmetric T inversion this far anterior).
Lead V6 in Panel B has an intermediate appearance between strain and/or ischemia.
Given that this patient is older and has a history of heart disease and decidedly meets voltage
criteria for LVH We would interpret this tracing as, LVH and strain and/or ischemia.
Clinical correlation and comparison with prior tracings would be needed to determine IF an
acute ischemic process might be ongoing.

Figure 08.12-2: Comparison of the precordial lead sequence from Figure 08.11-1 (Panel A) with
that from Figure 08.12-1 (Panel B). Voltage criteria for LVH are easily satisfied in each tracing. STT wave changes in Panel B are much more suggestive of LVH with ischemia and/or strain (See
text).
Return to Panel A in Figure 08.12-2. Note that the J-point appears to be slightly depressed in leads
V4-through-V6, and that there is subtle ST coving in the depressed ST segment in V4. Thus, although
the overall picture in Panel A is clearly more suggestive of LVH with strain We can not exclude
the possibility of some component of ischemia.
Clinical correlation is needed.
Availability of prior tracings on this patient would help to determine whether J-point depression
i n Panel A is new or old. In the meantime Interpreting ST-T wave changes in Panel A as
consistent with strain and/or ischemia with need for clinical correlation is appropriate.

08.13 Strain Equivalent Patterns: Clinical Implications

As discussed in Section 08.9 an intermediate strain equivalent stage exists, in which the ST-T
wave is not completely normal but does not yet manifest full appearance of the asymmetric
sagging ST segment characteristic of strain. We expand on this concept in Figure 08.13-1:
Clinical implications of LVH voltage plus a strain equivalent (any of the 3 examples shown
below in Figure 08.13-1) are the same as they are for the fully developed pattern of strain
(=greatly increased specificity for LVH and a worse longterm prognosis).

Figure 08.13-1: Examples of strain equivalent patterns (See the illustrative ECG shown below in
Figure 08.13-2).
FIGURE 08.13-2: Is there LVH with Strain?
Apply the concept of recognizing an ST-T strain equivalent pattern to the precordial lead sequence
shown in Figure 08.13-2, taken from a middle-aged man with hypertension.
Are ECG criteria for LVH satisfied? If so What is the likelihood of true chamber enlargement
in Fig. 08.13-2?

Figure 08.13-2: Precordial lead sequence from a patient with hypertension. Is there LVH? What is
the likelihood of true chamber enlargement? (See text).
Answer to Figure 08.13-2: Voltage criteria for LVH are satisfied as sum of deepest S wave in
V1,V2 + tallest R wave in V5,V6 is >35 (ie, 17 + 21 = 38).
The ST-T wave segment in lateral leads V4,V5,V6 is not normal. Instead there clearly is
flattening of the ST segment and T wave, with a hint of ST depression. That said a fully
developed pattern of LV strain is not seen.
Impression: The ST-T wave in leads V4,V5,V6 of Figure 08.13-2 closely resembles the 3rd

strain equivalent pattern shown in the lower panel of Figure 08.13-1. In view of the history
(hypertension) and more than adequate voltage for LVH we would write LVH (not just
voltage for LVH) on our interpretation. The likelihood of true chamber enlargement is high.

08.14 Atrial Enlargement

The ECG is neither sensitive nor specific for atrial enlargement (Echo is far more accurate). That
said there are times when the ECG may provide suggestive clues which clinically are very helpful
(Figure 08.16-1):
Recognition of LAA (Left Atrial Abnormality) may support the ECG diagnosis of LVH
(especially in the presence of underlying BBB).
Recognition of RAA (Right Atrial Abnormality) in association with other ECG signs may
strongly suggest RVH (and/or pulmonary hypertension). It may also suggest acute pulmonary
embolus.
ECG signs of multichamber enlargement (at least LVH, LAA, RAA and possibly also RVH)
when seen in a patient with underlying heart disease suggests cardiomyopathy.

08.15 Terminology: Enlargement vs Abnormality?

Many clinicians use LAA/RAA and LAE/RAE interchangeably. We prefer the terms, LAA and
RAA (where the A stands for Abnormality) in acknowledgement that an abnormal-looking P
wave on ECG does not always mean true atrial chamber enlargement. It simply means a differentthan-usual P wave appearance.
Other Reasons for Abnormal P Waves include body habitus (tall, peaked P waves may be
seen in slender individuals with a vertical axis); increased atrial pressure (ie, from heart
failure) and intra-atrial conduction defects.
Clinical context will usually suggest whether RAA/LAA is likely to reflect true atrial
enlargement or something else.
IF we know true atrial chamber Enlargement is likely (because of marked LVH or RVH on ECG
in a patient with underlying heart disease) then we may switch to the LAE or RAE
designation. Otherwise we generally prefer to use the terms LAA or RAA.
NOTE: The atrial do not hypertrophy, in that their walls dont thicken. Instead the atria
enlarge (dilate).

08.16 FIGURE 08.16-1: ECG Criteria for RAA/LAA

ECG Criteria for the diagnosis of RAA and LAA are summarized pictorially in Figure 08.16-1. Note
that the 2 leads used to assess for atrial abnormality are lead II and lead V1.
We explore the physiologic rationale for these ECG criteria in Section 08.17.
We discuss specific ECG findings suggesting RAA and LAA in detail in Sections 08.18-through08.20.

Figure 08.16-1: ECG signs of atrial abnormality/enlargement (See text).

08.17 Physiologic Rationale for Normal P Wave Appearance
Physiologic rationale for the ECG signs of atrial enlargement is based on: i) anatomic location of
lead V1 (the V1 electrode lies over the RA = right atrium) and ii) relative direction of RA
and LA depolarization with respect to the SA node (Figure 08.17-1).
With NSR (Normal Sinus Rhythm) the impulse begins in the SA Node which lies in the
upper part of the right atrium (Panel A in Fig. 08.17-1). Activation of the RA will therefore be
seen as approaching lead V1 whereas activation of the LA will be seen as moving away
from lead V1 (red arrows in Panel B). This explains why in theory the P wave in lead V1
should normally be biphasic, with an initial positive component (as the RA is depolarized)
followed by a negative component (as the LA is depolarized).
In Practice the normal P wave in lead V1 may be positive, negative or biphasic (as is shown
under NSR in Fig. 08.16-1).
The reason the P wave is normally upright in lead II with sinus rhythm is shown in Panel C of
Figure 08.17-1. Summation of RA and LA activation is seen as moving toward lead II at +60
degrees (red arrows in Panel C).

Figure 08.17-1: Physiologic basis for why with NSR (Normal Sinus Rhythm) the P wave in lead
V1 may be positive, negative or biphasic (Panel B) whereas in lead II, the normal P wave will be
upright (Panel C).

08.18 A Closer Look: The P Wave with Normal Sinus Rhythm

Appreciation of the concepts illustrated in Figure 08.17-1 facilitates an understanding of normal sinus
P wave appearance in leads II and V1 as well as an understanding of what happens to P wave
appearance in these same leads with RAA/LAA.
With NSR (Normal Sinus Rhythm) the P wave in lead II should be upright (Figure 08.18-1).
However the P wave may normally be upright, negative or biphasic in lead V1.
Realize that IF there are 2 components to the P wave in lead V1 the 1st component (which
will be positive) represents RA depolarization (since the sinus node is in the RA). The 2nd
component (which is negative) represents LA activation. It is this 2nd (negative) component
that gets larger when there is LAA (Section 08.20).
KEY Point: The finding of a negative P wave in lead V1 is not abnormal. It does not
necessarily mean the left atrium is large IF this negative component to the P wave is relatively
small (Section 08.20).
Clinical Note: Be aware that minor deviation from correct lead placement may alter P wave
appearance in lead V1. Despite best intentions the clinical reality is that precordial lead
misplacement is relatively common.

Figure 08.18-1: ECG appearance of the normal P wave in leads II and V1. Note that with sinus
rhythm the normal P wave in lead V1 may be upright, negative or biphasic.
08.19 ECG Diagnosis of RAA: P Pulmonale
RAA (Right Atrial Abnormality) is diagnosed by the finding of tall Peaked and Pointed P waves
in the Pulmonary leads (Figure 08.19-1). Because patients with COPD often have low diaphragms
(and therefore an inferior axis ) we think of the inferior leads (II,III,aVF) as the pulmonary
leads.
The P wave should be half a large box tall (=2.5mm) in at least one of the inferior leads for
RAA.
IF the P wave in one or more inferior leads looks uncomfortable to sit on Think RAA! =
P Pulmonale.
Most of the time Lead V1 will not be helpful in ECG diagnosis of RAA.
Beyond-the-Core: On occasion RAA may be suggested by P wave appearance in lead V1 IF
the positive component of the P wave is pointed. This is true even if this pointed positive
component is not quite 2.5 mm tall.

Figure 08.19-1: ECG criteria for RAA (P pulmonale). Most commonly ECG diagnosis of RA is
made from P wave appearance in lead II (tall, peaked and pointed P wave at least 2.5 mm tall). The
P wave looks, uncomfortable to sit on. On occasion RAA may be suggested by the finding of a
pointed positive component to the P wave in lead V1.

08.20 ECG Diagnosis of LAA: P Mitrale

LAA (Left Atrial Abnormality) is diagnosed by finding an m-shaped (notched) and widened P
wave (0.12 second) in a "mitral" lead (I,II,aVL ) and/or a deep negative component to the P
wave in lead V1 = P Mitrale (Figure 08.20-1).
The reason the P wave becomes wider with LAA is that the left atrium is activated after the right
atrium (since the SA Node is in the RA). It is addition of this LA component to the P wave that
produces the notch/extra hump to form the M in lead II.
The best ECG sign of LAA is the finding of a deep, negative component to the P wave in lead
V1 that is at least 1 little box deep or wide.
We generally undercall LAA because of the overall poor specificity the ECG has for atrial
enlargement. Remember that some negativity to the P wave in lead V1 is a normal finding!
Therefore, it is best not to even contemplate an ECG diagnosis of LAA unless the negative
component to the P wave in lead V1 is definitely at least 1 little box deep and/or wide.

Figure 08.20-1: ECG criteria for LAA (P mitrale) in lead II and lead V1. Look for a notched
(longer) P wave in lead II and a deep negative component to the P wave in lead V1 (that is at
least 1 little box deep and/or wide). It is best to undercall the ECG diagnosis of LAA (See text).
08.21 FIGURE 08.21-1: Is there ECG Evidence of RAA/LAA?
Assess the ECG in Figure 08.21-1 for RAA and LAA. Keep in mind that this tracing was obtained
from an otherwise healthy and asymptomatic 27-year old man who was seen in the office for an
insurance physical.

Figure 08.21-1: ECG obtained from a healthy 27-year old man. Is there ECG evidence for
RAA/LAA? (See text).
Answer to Figure 08.21-1: There is sinus arrhythmia. All intervals (PR/QRS/QT) are normal. The
axis is vertical but still within the normal range of zero to +90 degrees. Given the near isoelectric
QRS complex in lead I (which manifests no more than a minimal net positive deflection) We
estimate the mean QRS axis to be about +80 degrees.
There is no LVH as the patient is less than 35 years of age (Section 08.7).
There is RAA (tall peaked and pointed P waves in the pulmonary leads with the P wave
in lead II 2.5 mm).
There is no LAA as the P wave is not notched, and there is no negative component to the P
wave in lead V1.
Regarding QRST Changes: There are small septal q waves in multiple leads; transition occurs
between lead V2-to-V3 (which is normal); and ST-T wave changes are unremarkable.
Impression: This ECG is probably not abnormal given that it was obtained from an otherwise
healthy and asymptomatic 27-year old man. Use of the term, RAA allows us to indicate that the
P wave is larger than is normally seen without labeling this patient as having right atrial pathology.
Instead it is much more likely that the vertical axis and peaked inferior P waves seen here reflect a
normal variant in an otherwise healthy young adult with a vertical ECG axis and an anatomically
normal right atrium.
08.22 FIGURE 08.22-1: Is there ECG Evidence of RAA/LAA?
The ECG in Figure 08.22-1 was obtained from an older adult with heart failure. Assess this tracing
for ECG evidence of chamber enlargement.
What clinical diagnosis is suggested by the ECG picture shown here?

Figure 08.22-1: ECG obtained from an older patient with heart failure. Which cardiac chambers are
enlarged? (See text).

Answer to Figure 08.22-1: The rhythm is sinus. The PR, QRS and QT intervals are normal. There is
RAD (Right Axis Deviation) as diagnosed by the markedly negative net deflection of the QRS in
lead I (Section 07.4).

There is RAA (tall peaked and pointed P waves in the pulmonary leads with the P wave
in lead II at least half a large box tall).
There is LAA (deep negative component to the P wave in lead V1).
There is LVH (very deep S waves in V1,V2 + very tall R waves in V5,V6). ST-T wave changes
are consistent with LV strain and/or ischemia (Section 08.12).
There is also probable RVH (marked RAD + RAA).
PEARL: The presence of multichamber enlargement (at least 3 chambers) in a patient with
heart failure is strongly suggestive of cardiomyopathy.

08.23 RVH/Pulmonary Disease

Detection of right ventricular enlargement in adults by ECG criteria is often exceedingly difficult.
This is because the LV ( Left Ventricle) is normally so much larger and thicker than the RV ( Right
Ventricle) in adults that it masks even moderate increases in right ventricular chamber size. As a
result, many patients with RVH (Right Ventricular Hypertrophy) will not be identified IF
assessment for chamber enlargement is limited to obtaining an ECG (an Echo is needed to know for
sure).
NOTE: In contrast to adults ECG diagnosis of RVH is often surprisingly easy in children
with congenital heart disease (because relative size of the RV compared to the LV is not nearly
as different as it is in adults).

08.24 ECG Diagnosis of RVH: Simplified Criteria

Development of RVH may lead to a number of ECG findings. We list these in Figure 08.24-1. None
of these findings alone will accurately predict anatomic RV enlargement. Instead Several criteria
are needed.
Think of the ECG diagnosis of RVH as similar to making a "detective" diagnosis. No single
clue solves the mystery. With regard to ECG interpretation No single finding in Figure
08.24-1 is diagnostic. Instead determination of RVH is made by deduction (ie, from
identifying a combination of the ECG findings listed in Fig. 08.24-1):

Figure 08.24-1: ECG criteria for RVH. A combination of at least several of these criteria is needed
for accuracy (See text).
Clinical NOTE: Pulmonary disease without frank RVH is common in longterm smokers. Progression
to cor pulmonale (in which there is frank RVH) represents a relatively late stage in the process.
Careful search for the ECG findings in Figure 08.24-1 may provide clues to either longterm
pulmonary disease and/or associated RVH:

Consider Pulmonary Disease IF you see 2 or more of the first 5 criteria listed in Figure
08.24-1 (especially IF the patient is a known smoker or has other known lung problems).
Suspect pulmonary disease plus RVH IF in addition you also see a tall R wave in lead V1
(with or without ST-T wave changes of RV strain).
By Definition By the time you see clear ECG evidence of RVH in an adult the extent of
RVH is usually marked (the patient almost always has end-stage COPD and/or pulmonary
hypertension).

08.25 ECG Diagnosis: Review of Specific RVH Criteria

While no single finding in Figure 08.24-1 by itself is enough to diagnose RVH seeing several
criteria on a single tracing is very suggestive of RVH especially when seen in a likely clinical
setting (ie, COPD, longterm asthma, right-sided heart failure, pulmonary hypertension). Over the
next few sections We review specific ECG criteria for RVH:
RAD (Right Axis Deviation) is highly suggestive of RVH when seen in a likely clinical
setting and in association with other criteria listed in Figure 08.24-1. Few other conditions
produce RAD. This is why we strongly suspect RVH is also present in the patient with
cardiomyopathy whose ECG was shown in Figure 08.22-1. In the clinical context of heart
failure with evidence of multi-chamber enlargement on ECG (RAA/LAA/LVH) the markedly
negative QRS complex in lead I of Fig. 08.22-1 (which we reproduce below in Figure 08.25-1)
suggests there is also enlargement of the 4th cardiac chamber (= RVH).
RAA It is usually easy to recognize the tall, peaked, pointed P waves of RAA (Section
08.19). PEARL: Only one condition produces RAA without at the same time producing RVH ( =
tricuspid stenosis). Therefore identifying RAA on ECG is an indirect sign that RVH is very
likely. This was the case for the patient with cardiomyopathy whose ECG was shown in Fig.
08.22-1 (reproduced below in Figure 08.25-1).

Figure 08.25-1: This ECG is reproduced from Fig. 08.22-1. The patient has a history of heart failure.
The ECG shows RAA (tall, peaked P wave in lead II); LAA (deep negative component to the P in
V1) ; and LVH with strain and/or ischemia (markedly increased QRS amplitude in precordial
leads with ST-T wave changes in V3-through-V6 ). We strongly suspect a cardiomyopathy with
enlargement of the 4th cardiac chamber (= RVH) because in addition to LAA/LVH: i) RAA is also
present; and ii) there is otherwise unexplained marked RAD (See text).
08.26 RVH: Review of Additional Criteria
Some findings in Figure 08.24-1 are more suggestive of RVH and/or pulmonary disease than others.
The findings we describe below are less specific when seen in isolation but they may be
diagnostic when they occur in combination (as we demonstrate in the next few sections). Remember
Not all findings are seen in every patient.
Indeterminate Axis Alterations in lung volume with emphysema often lead to rightward and
posterior axis deviation. As a result net QRS deflection in both leads I and aVF may become
negative. PEARL: IF ever you see an indeterminate axis Think RVH/COPD/Obesity
(Section 07.8).
IRBBB (rSr in V1) The presence of an r (r prime) in lead V1 suggests that terminal
electrical activity is directed toward the right. While this ECG sign is often benign and
commonly seen as an isolated finding in otherwise healthy individuals (Section 05.18) it
supports the diagnosis of pulmonary disease/possible RVH if seen in association with other
suggestive findings.
Persistent S Waves R wave amplitude normally increases as one moves across the
precordial leads (as electrical activity moves toward the left where the larger LV lies ). R
wave amplitude usually peaks (is tallest) in V4 or V5 and then drops off (in V5,V6).
Normally, there is not any S wave at all in V5,V6 since by this time in the depolarization
process all electrical activity is traveling leftward. IF more than tiny S waves are still present
i n V5,V6 this implies significant rightward activity is still ongoing (Think
RVH/COPD/large body habitus). That said this finding is not present in Figure 08.25-1
(although a ~5mm S wave is seen in lead V5 no S wave at all is seen in lead V6).
Low Voltage Air is not a good conductor of electricity. The large emphysematous chest of a
patient with COPD dampens (reduces) voltage. Technically low voltage is defined as QRS
amplitude 5 mm (ie, 1 large box) in all 6 limb leads (I,II,III; aVR,aVL,aVF). That said
we also use low voltage as a relative term when overall QRS amplitude subjectively
appears to be reduced. When you see low voltage Think COPD (although low voltage
may also be seen in hypothyroidism; obesity; pneumothorax; pericardial effusion; or as a
normal variant).
NOTE: Using the above definition for low voltage (ie, the QRS being 5 mm in all 6 limb leads)
this ECG finding is not all that common. When low voltage is seen it is a nonspecific finding.
That said IF low voltage is noted in the presence of other criteria for RVH, this finding adds
support to the diagnosis of probable pulmonary disease (especially in a patient with a history of
smoking).

08.27 Schamroths Sign for RVH: A Null Vector in Lead I

Beyond-the-Core: We draw attention to an interesting, uncommon finding known as Schamroths
Sign. This is the presence of a null vector (or very small QRS complex) in lead I that is not due to
technical error/lead misplacement (Figure 08.27-1). When seen in the right clinical setting (ie, a
patient with COPD/pulmonary disease) then this ECG finding is highly suggestive of advanced
pulmonary disease with probable RVH (especially if other findings in Figure 08.24-1 are also
present).

Figure 08.27-1: Schamroths sign. Note the null vector in lead I. RAA is also present (tall,
peaked P wave in lead II). When seen in a patient with pulmonary disease and not due to technical
error Schamroths sign suggests disease is severe and that there is probable RVH ( See also
Section 08.33).
08.28 RVH: Tall R Wave in V1; RV Strain
The 2 findings in Figure 08.24-1 that best distinguish between pulmonary disease with vs without
associated RVH are: i) presence of a tall R wave in lead V1; and ii) presence of RV strain.
Tall R Wave in Lead V1 Lead V1 is a right-sided lead. As a result, the QRS is normally
negative in lead V1 (electrical activity moves toward the larger LV and away from V1). IF the
R wave is taller than the S wave in lead V1 this means rightward forces are increased
(which may be an important sign of RVH). Clinically by the time a tall R wave is seen in
lead V1 in an adult with pulmonary disease the extent of RVH is usually marked (ie, the
patient is likely to have end-stage COPD and/or pulmonary hypertension). This is the case in
schematic Figure 08.29-1 shown below.
RV Strain Just as LV strain is a sign of true LVH seeing strain in one or both of
the right-sided lead areas (II,III,aVF and/or V1,V2,V3) strongly supports a diagnosis of
RVH (Figure 08.29-1).

08.29 Schematic FIGURE 08.29-1: Example of RVH + RV Strain

Most of the ECG criteria for RVH are present in schematic Figure 08.29-1. Note the following:
Marked RAD (negative net deflection in lead I; positive QRS in lead aVF).
RAA (tall, peaked P wave that looks uncomfortable to sit on in II,III,aVF).
Tall R Wave in lead V1 (Section 08.28).

Persistence of deep S waves in V5,V6 (Section 08.26).

Fnally there is "RV strain". Typically RV strain is seen in inferior and/or anterior
leads (both of which are present here ). PEARL: Inferior and/or anterior ST-T wave changes
as seen in Figure 08.29-1 will often not be due to ischemia but rather to RVH or pulmonary
embolus. The presence of RAD; RAA; persistent precordial S waves; and tall R wave in lead
V1 all suggest that the inferior and anterior ST-T wave changes seen in Fig. 08.29-1 are the
result of pulmonary disease.

Figure 08.29-1: Schematic example of RVH + RV strain. This ECG picture with virtually all
criteria from Figure 08.24-1 is uncommon in adults and usually indicates significant RVH/ endstage COPD and/or pulmonary hypertension.
08.30 Schematic FIGURE 08.30-1: Example of Pulmonary Disease
Pulmonary disease (such as COPD) without frank RVH may sometimes be suggested by ECG.
Specifically we look for the presence of at least 2 of the first 5 findings from Figure 08.24-1. This
concept is illustrated in schematic Figure 08.30-1. Note the following:
An indeterminate axis (negative QRS deflection in both leads I and aVF).
RAA (tall, peaked P wave that looks uncomfortable to sit on in II,III,aVF).
rSr in lead V1 (Section 08.26).
Persistence of deep S waves throughout all precordial leads (Section 08.26). Transition never
occurs (the R wave never becomes taller than the S wave in the precordial leads).

Figure 08.30-1: Schematic ECG that strongly suggests pulmonary disease. Low voltage is not seen

 but the other 4 criteria from Figure 08.24-1 are seen (Note the axis is indeterminate; there is
RAA; an rSr in V1; and persistence of precordial S waves).
Clinical Note: There is no definitive ECG sign that proves a patient has pulmonary disease.
Instead We use this descriptor as a qualitative term that may help to explain a combination of
ECG findings that are likely to be seen in a group of patients with longstanding/severe pulmonary
disorders. As stated the point at which pulmonary disease crosses over to cor pulmonale with
frank RVH is often elusive and not detectable by ECG. An Echo would be far more informative
regarding true right-sided chamber size, function and pressures.
We suspect pulmonary disease when a longtime smoker presents with an ECG manifesting at
least 2 or 3 of the first 5 findings in Figure 08.24-1.
Given the presence of 4 of these first 5 findings in schematic Figure 08.30-1 it is certainly
possible that such a patient might have frank RVH that simply is not yet manifesting a
predominant R wave in lead V1. The ECG is simply not sensitive enough to reliably pick up all
cases of RVH.
Remember that the adult LV is about 3 times as thick as the RV. In 3 dimensions LV mass may
normally be up to 10 times greater than normal RV mass. Development of RVH in an adult to the
point that it becomes evident on ECG (by a predominant R wave in lead V1 as in Figure
08.29-1) is therefore a late sign.

08.31 Pediatric RVH: A few Brief Thoughts

Beyond-the-Core: Interpretation of pediatric 12-lead ECGs is a specialty unto itself (well beyond
the scope of this ePub). Most providers are only infrequently called upon to interpret pediatric
ECGs. We therefore limit our comments here to discussion of a few basic concepts:
ECG criteria for determining atrial abnormality (RAA, LAA) in children are similar to criteria
that are used in adults (Sections 08.19, 08.20).
Ve r y different criteria must be used for determining ventricular enlargement in pediatric
patients. Depending on the age of the child being assessed voltage criteria will vary greatly.
Detailed tables of pediatric norms are found in textbooks on this subject. Suffice it to say that
QRS amplitude is often normally increased in the pediatric patient. Technical problems relating
to accuracy of chest lead placement on the tiny chest of a small child when ECGs are recorded
by nonpediatric providers are common. Determining whether QRS amplitude exceeds limits for
age and satisfies pediatric ECG criteria for LVH is far from a simple matter. Practically
Speaking the child with symptoms and/or a murmur will be referred if there is any suspicion
of chamber enlargement.
KEY Point: As opposed to the difficulty for the nonpediatric provider in determining LVH
suspected RVH is often far easier to surmise on ECG. In contrast to the situation just described for
adults (in which LV mass is normally up to 10 times greater than RV mass ) RV mass is
comparable to LV mass at birth, and tends to remain so for the first few years of life. As a result a
proportionately smaller increase in RV size is much more likely in children to produce a noticeable

change in net electrical activity between the two ventricles. RVH is therefore much easier to
diagnose in young children than it is in adults. Be aware of the following:
Some degree of RAD is common in young children.
The R wave may normally be taller than the S wave is deep in lead V1 up to about age 5. By
the time a child is 6 years old the S wave in lead V1 will usually be deeper than the R wave
in this lead is tall.
It is common to see anterior T wave inversion on the ECG of otherwise healthy children. This
ECG phenomenon is known as a juvenile T wave variant. Symmetric T wave inversion may
extend to as far as lead V3 or V4 as a normal phenomenon in a young child or early adolescent.
Clinical correlation is essential to avoid mistaking this normal T wave variant as a pathologic
pattern (Section 01.4).
IF in doubt about norms Refer to age-specific tables! Have a low threshold for consulting
with someone having expertise in pediatric ECG interpretation.
Pediatric ECGs: Is RVH Likely?
Imagine the schematic ECGs shown in Figure 08.31-1 and Figure 08.31-2 were each obtained from a
2-year old child. Is RVH likely?

Figure 08.31-1: Schematic ECG from a young child. Although there is a predominant R wave in lead
V1 this may normally be seen up to 5 years of age. Lack of other findings suggests this 2 year old
probably does not have RVH.

Figure 08.31-2: Schematic ECG from a young child. RVH is suggested by a combination of findings
including RAD; RAA; tall R wave in lead V1 with RV strain; and persistent deep S waves in
V5,V6 (See text).

08.32 FIGURE 08.32-1: Is there RVH?

The ECG in Figure 08.32-1 was obtained from an older adult with new-onset shortness of breath
thought to be due to congestive heart failure.
What else do you suspect?

Figure 08.32-1: ECG from a patient with heart failure. Is this ECG what you would expect from a
patient with left-sided heart failure? (See text).
Answer to Figure 08.32-1: The rhythm is sinus tachycardia at ~115/minute. The QRS is narrow. As
opposed to the usual picture of left-sided heart failure (in which one expects to see LVH with strain)
there is no sign on this ECG of LVH. Instead the tracing strongly suggests severe pulmonary
disease (if not frank RVH):
There is marked RAD (predominantly negative QRS complex in lead I; positive QRS in lead
aVF).
RAA is present (tall, peaked, uncomfortable-to-sit-on P wave in inferior leads that in lead
II is clearly >2.5mm).
An incomplete RBBB is seen (rsR in lead V1; S waves in leads I,V6). Note that the r in lead
V1 is relatively tall.
Deep S waves persist through to V5,V6.
There are nonspecific ST-T wave abnormalities albeit not quite RV strain ( and no acute
changes).
Bottom Line: ECG Impression The combination of marked RAD, definite RAA, IRBBB and
persistent precordial S waves all point to a diagnosis of RVH for the ECG shown in Figure 08.32-1.
Clinical Impression: This ECG should make one rethink the premise of left-sided heart failure
as the primary cause of this patients new-onset shortness of breath. Instead
longstanding/severe pulmonary disease is likely given the combination of ECG findings.

Depending on the history (and comparison with prior ECGs on this patient) acute
pulmonary embolism might also be considered as a possible diagnosis (See Section 08.34).
Beyond-the-Core: There is also LAA in Figure 08.32-1 (very deep negative component to the
P wave in lead V1). Whether this reflects anatomic enlargement vs increased LA pressure is
uncertain.

08.33 FIGURE 08.33-1: Is there RVH?

We conclude this section on RVH with the ECG shown in Figure 08.33-1. We have previously seen
this tracing (in Figure 02.17-1).
Does this ECG suggest pulmonary disease?
Is there RVH?

Figure 08.33-1: ECG reproduced from Figure 02.17-1. Is there evidence of pulmonary disease? Is
RVH likely?
Answer to Figure 08.33-1: This patient undoubtedly has severe pulmonary disease (if not frank
RVH). We note the following findings:
The rhythm is MAT (Sections 02.16, 02.17) as determined by the irregular irregularity with
multiple different P wave morphologies that change from beat-to-beat. The presence of MAT is
most often associated with severe pulmonary disease.
Several of the P wave forms that are seen in lead II are highly suggestive of RAA (tall, peaked
and pointed P waves in this lead).
There is persistence of fairly deep S waves in lateral precordial leads.
Schamroths Sign is present as suggested by the very low amplitude r wave with flat ST-T
wave in lead I (Section 08.27).
Clinical Impression: The ECG in Figure 08.33-1 was obtained from a patient known to have COPD.
The combination of ECG findings noted above should provide insight that the degree of pulmonary

disease is severe, if not already associated with RVH and increased pulmonary pressures.

08.34 Acute Pulmonary Embolus

The ECG is usually not a good tool for diagnosing acute pulmonary embolism (acute PE). That said
there are times when an ECG may strongly suggest the diagnosis before V/Q scan or chest CT can
be done. Acute PE should be considered IF:
IF the clinical setting is right (new-onset dyspnea pleuritic chest pain predisposing
risk factors or previous history of PE or deep venous thrombosis).
IF the patient has sinus tachycardia (usually seen with large PE, albeit clearly nonspecific for
the diagnosis).
Two or more ECG signs of acute right-heart strain. These include: i) RAD; ii) RAA; iii)
IRBBB or RBBB; iv) Tall R wave in lead V1; and v) Deep S waves in leads V5,V6 (Section
08.24).
RV strain as suggested by asymmetric ST-T wave depression in inferior and/or anterior
leads (ie, leads II,III,aVF and/or V1,V2,V3). Alternatively there may only be nonspecific
ST-T wave changes (ST flattening; slight ST depression).
New-onset A Fib (a common but nonspecific finding with acute PE).
History and the ECG are similar to that presented in Section 08.32.
Possibly with an S1-Q3-T3 pattern (Section 08.36).

08.35 Acute PE: Key Clinical Points

From a clinical perspective Acute PE is increasingly overdiagnosed! Many small
(subsegmental) PEs unlikely to be of clinical consequence are being identified by overuse of Chest
CT ordered on lower-risk patients with atypical symptoms.
The ECG is unlikely to identify patients with smaller PEs. Dont expect to see anything on the
ECG of these patients (this may be a blessing in disguise).
Overall sensitivity of the ECG for picking up acute PE is poor. Failure to see any of the ECG
signs in Section 08.34 does not rule out the possibility of acute PE IF history and clinical
features suggest the diagnosis. Chest CT is needed.
Sensitivity of the ECG for suggesting the possibility of acute PE is better with larger
(especially submassive) PEs. One should at the least see sinus tachycardia in such patients
often with nonspecific ST-T wave changes . Large acute PE is commonly associated with other
ECG signs but these may be subtle and are generally nondiagnostic.
Be aware of the clinical significance of RV strain. The finding of anterior T wave inversion
(in leads V1,V2,V3) in an adult with new-onset dyspnea or pleuritic (or atypical) chest pain
will much more often be due to acute PE than to ischemic heart disease. This is especially true
IF there is also inferior T wave inversion (in II,III,aVF) as seen in Figure 08.35-1.

Figure 08.35-1: Schematic ECG illustrating a series of ECG findings that taken together are highly
suggestive of acute PE (Pulmonary Embolism) especially when seen in a patient with new-onset
dyspnea. Note RV strain in the form of asymmetric ST-T wave depression seen here in both
inferior and anterior leads (II,III,aVF; and V1,V2,V3). In addition there is RAD (the QRS in lead
I is markedly negative) RAA (tall, peaked P wave in inferior leads) incomplete RBBB (rSr
in V1; S waves in I,V6) and persistent precordial S waves that remain deep up to leads V5,V6.
08.36 FIGURE 08.36-1: Should You Look for an S1-Q3-T3?
Over the years much attention has been focused on the diagnostic utility of recognizing an S1-Q3T3 pattern as an ECG indicator of acute PE. While important to be aware of what a positive S1Q3-T3 pattern is We feel this ECG sign is highly overrated. Our reasons for stating this are
given below.
What is a Positive S1-Q3-T3 Sign?
We define an S1-Q3-T3 pattern as the presence of: i) an S wave in lead I; ii) a Q wave in lead III;
and iii) T wave inversion in lead III (Figure 08.36-1):
In order to be valid all 3 of these ECG indicators must be present! That is lead III must
show both a Q wave and an inverted T wave! The presence of only 2 ECG indicators does not
qualify as a positive S1-Q3-T3 pattern.

Figure 08.36-1: S1-Q3-T3 Pattern as recognized by the presence of: i) an S wave in lead I; ii) a Q
wave in lead III; and iii) T wave inversion in lead III. To be valid all 3 of these ECG indicators
must be present.
The S1-Q3-T3 Pattern: Pros and Cons
By itself one can not rely on a positive S1-Q3-T3 sign as an ECG indicator of acute PE. This is
because even in the best of studies both sensitivity and specificity of a positive S1-Q3-T3 sign for
acute PE is poor. That is Failure to see this sign in NO way rules out the possibility of acute PE.
More often than not you will not see an S1-Q3-T3 sign despite even large acute PE.
We have seen the S1-Q3-T3 sign many times in completely healthy and asymptomatic adults!
Clearly these patients do not have acute PE.
BOTTOM Line: Recognition of a positive S1-Q3-T3 pattern may help in the diagnosis of
acute PE IF the positive S1-Q3-T3 pattern is present in association with other suggestive
ECG signs and the right clinical history. But a positive S1-Q3-T3 is not helpful by itself
and absence of a positive S1-Q3-T3 on ECG rules out nothing.

08.37 FIGURE 08.37-1: The Cause of Anterior T Inversion?

Imagine the ECG in Figure 08.37-1 was obtained from an adult with new-onset atypical chest
discomfort and shortness of breath.
Given this clinical scenario How would you interpret the symmetric T wave inversion seen
in leads V1, V2, V3?

Figure 08.37-1: ECG obtained from a patient with atypical chest pain and new-onset dyspnea. How
would you interpret the anterior T wave inversion (arrows) seen here? Note that an S1-Q3-T3
pattern is not present (there is an S1-Q3 but no T3 as highlighted by the blue-white circle).
Answer to Figure 08.37-1: The rhythm is sinus. There is RAD (the QRS complex in lead I is

predominantly negative) RAA (tall, peaked and pointed P wave in lead II) and fairly deep,
symmetric T wave inversion is seen in leads V1,V2,V3 (arrows in Figure 08.37-1).
The finding of symmetric T wave inversion in a patient with chest discomfort should always
prompt consideration of ischemia (which we would do in this case). That said one should
especially consider acute PE in this case because: i) The patient also has new-onset dyspnea;
and ii) there are other signs suggestive of acute RV strain on this tracing ( marked RAD; RAA).
As a result Acute PE would be our 1st diagnosis!
NOTE: An S1-Q3-T3 is not present in Figure 08.37-1 because the T wave is not inverted
in lead III (blue-white circle seen in the lead III blow-up). That said lack of an S1-Q3-T3
pattern should never be used alone to rule in or out acute PE. While possible ischemia must be
considered the history of new-onset dyspnea and this ECG showing anterior T wave
inversion plus marked RAD and RAA makes acute PE our working diagnosis until proven
otherwise.

08.38 FIGURE 08.38-1: Is there Acute Anterior STEMI?

The ECG in Figure 08.38-1 was obtained from a patient who presented with syncope, shock, and
acute hypoxemia. In addition to RBBB (QRS widening with an rSR in V1 and S waves in I,V6)
there is ST coving in V1,V2,V3 and slight-but-definite ST elevation in leads V1,V2.
In view of this clinical scenario Is this ECG suggestive of acute STEMI (ST Elevation
Myocardial Infarction)?
Should you activate the cath lab based on this tracing?

Figure 08.38-1: ECG obtained from a patient who presented with syncope, shock and acute
hypoxemia. Is this ECG suggestive of acute anterior STEMI?
Answer to Figure 08.38-1: This ECG needs to be interpreted as the sum of its parts in context
with the clinical history. Remarkably absent from the history in this patient who presented with
syncope, shock and acute hypoxemia is any mention of chest pain. ECG findings in Figure 08.38-1
include:

Sinus tachycardia (rate ~ 100/minute).

RBBB (QRS widening to at least 0.11 second; rSR in lead V1; wide S in lead I; subtle-butpresent s wave seen in lead V6).
Diffuse ST-T wave changes (See below).
Presence of an S1-Q3-T3 pattern as a supportive ECG sign (Figure 08.38-2). Although the q
wave and T inversion in lead III are admittedly subtle each component of the S1-Q3-T3
pattern is present (red arrows in Fig. 08.38-2).

Figure 08.38-2: We have added red arrows to Fig. 08.38-1 to highlight the presence of an S1-Q3-T3
pattern. Other ECG findings suggestive of acute PE given the history include: i) Sinus tachycardia;
ii) RBBB; iii) diffuse ST-T wave changes; and iv) ST elevation in lead aVR (See text).

Clinical Impression of Figure 08.38-2: We emphasize that one can not rule out the possibility of
acute anterior STEMI from the ECG shown in Figure 08.32-2. That said virtually all facets of the
history and this ECG can be explained by one unifying diagnosis = acute PE:

Patients with submassive acute PE commonly present with syncope, shock and/or acute
hypoxemia. IF these symptoms were the result of acute STEMI We would expect far more
extensive ST elevation than is seen in Figure 08.38-2.
In the overall clinical context of this case the symmetric anterior T wave inversion with
diffuse ST depression elsewhere (in inferior and lateral precordial leads ) is perfectly
consistent with acute RV strain.
As expected sinus tachycardia is present.
RBBB is another common sign of acute RV strain.
A limited number of conditions produce ST elevation that is most marked in lead aVR but
minimal or nonexistent elsewhere, with possible exception of lead V1 (See Sections 09.31through-09.40). One of these conditions is acute PE (Section 09.33). Note that there is marked
ST elevation in lead aVR of Figure 08.32-2 (red blow-up box) with ST elevation otherwise
limited to lead V1 and no more than a trace in lead V2.
BOTTOM Line: Putting all clues together acute PE should be assumed until proven
otherwise. This patient was found to have a large saddle embolus.

09.0 Q-R-S-T Changes

09.1 FIGURE 09.1-1: Assessing Q-R-S-T Changes

The "heart" of ECG interpretation resides with assessing the tracing for QRST Changes. The purpose
of this mnemonic Q-R-S-T is to ensure a systematic approach so that nothing is left out.
The most common mistake that occurs when a systematic approach is not closely followed is to allow
more dramatic ST-T wave changes to consume one's attention while subtler ( but equally
important) findings go unnoticed. Examples of such alltoo-easy-to-overlook findings include
failure to recognize non-sinus rhythms; a dominant R wave in lead V1; poor R wave progression
and subtle ST-T wave changes.
BOTTOM Line: Always use a Systematic Approach. This not only prevents overlooking
important ECG findings but also saves time by streamlining and organizing your approach
(Figure 09.1-1):

Figure 09.1-1: Systematic approach for assessing Q-R-S-T Changes (See text).
LEAD aVR: Largely ignored in the past Use of lead aVR is now increasingly appreciated as an
invaluable adjunct to ECG interpretation. We fully explore this advanced concept in Sections 09.31through-09.40. In the meantime We suggest not being overly concerned about the ECG appearance
in lead aVR:
For the most part assessment of lead aVR is not essential to the basics of ECG interpretation
(assuming the leads are on correctly and there is no dextrocardia).
Beyond-the-Core: ECG appearance in lead aVR may assist in assessing not only technical
errors but also narrow and wide-complex tachycardias; acute coronary syndrome from
multivessel or left main disease; pericarditis; pulmonary embolism; and more (See Sections
09.31-through-09.40).

09.2 Septal Depolarization: Reason for Normal Septal Q Waves

In Section 05.7 We introduced the concept of normal septal activation. Normally the very first
part of the ventricles to depolarize (after the impulse passes through the AV node and Bundle of
His) is the left side of the ventricular septum. As a result septal depolarization normally
moves from left-to-right (red arrow pointing left-to-right in Panel A of Figure 09.2-1).
As a result of this initial left-to-right direction of septal depolarization left-sided leads
(I,aVL; V4,V5,V6) normally see initial ventricular activation as moving away which is why
small septal q waves are often normally seen in one or more of the lateral leads (Panel A).
In contrast right-sided leads (V1,V2) normally view initial ventricular activation as coming
toward the site on the chest where these leads lie. This explains why a small initial r wave is
commonly seen in leads V1, V2 (See lead V1 in Panel A). This initial small r wave represents
septal depolarization. It is lost when there is septal infarction (See Figure 09.3-1 in Section
09.3).

Figure 09.2-1: Normal septal activation (A) vs LBBB (B). Septal activation normally begins on the
left side of the septum and travels left-to-right (red arrow in Panel A). As a result one
normally sees a small r wave in right-sided leads (V1,V2) and small, narrow q waves in one or more
of the lateral leads (I,aVL; V4,V5,V6). RBBB does not change these findings (since the right bundle
branch travels down the right side of the septum). In contrast LBBB reverses the direction of
septal activation (red arrow in Panel B). As a result one should never normally see a septal q
wave in a lateral lead with LBBB, unless there has been septal infarction (See text).
What Happens with BBB?
Since the RBB (Right Bundle Branch) travels down the right side of the septum the initial left-toright direction of normal septal depolarization does not change when there is RBBB (Section 05.7).
In contrast with LBBB, the normal left-to-right direction of septal activation will reverse
because the block with LBBB prevents the initial vector of septal activation from starting on the
left (Panel B in Figure 09.2-1). As a result ventricular activation with LBBB moves almost
entirely from right-to-left. This explains why septal q waves should not normally be seen with
LBBB in lateral leads (Sections 05.6-through-05.9).

09.3 Precordial Lead Appearance: What is Normal?

In Figure 09.3-1 We illustrate normal precordial lead appearance by means of a schematic crosssectional (transverse) view of the heart within the thorax:
The small black arrow in Figure 09.3-1 schematically depicts the direction of normal septal
depolarization (which moves from left-to-right).
The large red arrow depicts the general direction of LV (Le f t Ventricular) depolarization
(which as seen in Fig. 09.3-1 is to the left and posteriorly).
The smaller RV (Right Ventricle) predominantly sees electrical activity as moving away
from the right (and toward the larger and thicker left ventricle ). This explains why the QRS
complex in right-sided precordial leads (V1,V2) is normally predominantly negative
whereas the QRS in left-sided leads (V5,V6) is generally positive.

Figure 09.3-1: Transverse (cross-sectional) view of the heart illustrating precordial lead
appearance in leads V1-through-V6. Note that transition occurs between lead V2-to-V4. There is
overlap between leads viewing septal anterior and lateral precordial areas. Septal
depolarization normally moves left-to-right (small black arrow). The major component of ventricular
activation moves to the left and posteriorly (large red arrow ) which reflects the relative size and
anatomic position of the left ventricle.
FIGURE 09.3-1: Key Clinical Points
Note that there is overlap in Figure 09.3-1 between leads viewing septal anterior and
lateral precordial lead areas. That is lead V2 is both a septal and anterior lead; lead V4 is
both an anterior and lateral lead.
Septal depolarization (the small black arrow in Figure 09.3-1) goes left-to-right. The normal
small initial positive deflection (r wave) in leads V1,V2 results from septal activation coming
toward these right-sided leads. With septal infarction this small initial r wave in leads
V1,V2 is lost.
Small normal septal q waves are commonly seen in one (or more) of the lateral leads

(I,aVL; V4,V5,V6). This makes sense since the left-to-right direction of septal activation
moves away from left-sided leads (and therefore writes a small q wave).
The area where the R wave becomes taller than the S wave (Transition) occurs normally in
Figure 09.3-1. That is the QRS is predominantly negative in lead V2 it is isoelectric in
V3 and positive in V4 (so transition occurs between leads V2-to-V4, which is normal).

09.4 Basic Lead Groups: Which Leads look Where?

It is essential to know which leads view which areas of the heart. The trained eye keys into
specific Lead Groups (Figure 09.4-1):
In Sections 03 and 07 we introduced derivation and anatomic correlation for the 6 limb leads
in the frontal plane. This includes the 3 inferior leads (II,III,aVF) the 2 high-lateral leads
(I,aVL) and the most remote (right-sided) lead, which is lead aVR. We expand on these
relationships in Figure 09.4-1.
Think of the electrical viewpoint of lead aVL as looking down at the heart from perspective of
the left shoulder. Thus, lead aVL views the hearts electrical activity from higher perspective
than precordial leads that are placed on the chest. Bipolar lead I at horizontal perspective
(corresponding to 0 degree placement in Einthovens triangle ) also views the hearts
electrical activity from higher perspective than is seen from precordial leads. This is why leads
I and aVL are designated high lateral leads to be distinguished from lower lying lateral
precordial leads (V4,V5,V6).
In contrast Think of the electrical viewpoint of lead aVF as looking straight up from the Feet
(perpendicular in the frontal plane axis at +90 degrees). The other 2 inferior leads are lead II
(at +60 degrees) and lead III (at +120 degrees).
The remaining 6 leads are the precordial leads. Anatomic localization of these 6 chest leads is
best understood by reviewing the landmarks used for performing an ECG (Section 03.6) in
context with the horizontal plane view just discussed in Figure 09.3-1. This should explain
septal (V1,V2) anterior (V2,V3,V4) and lateral (V4,V5,V6) precordial lead viewpoints
for these unipolar leads that view the hearts electrical activity from perspective of their
placement site on the chest.

Figure 09.4-1: Basic Lead Groups. As suggested in Fig. 09.3-1 there is overlap in the precordial
lead areas (lead V2 reflects both septal and anterior events; lead V4 reflects both anterior and
lateral events).

About Lead aVR: The most remote of the 12 standard leads is lead aVR. This right-sided lead
views the hearts electrical activity from the distant perspective of the right shoulder. Lead aVR is
unique for providing a view that assesses the basal part of the interventricular septum. It is also
unique in providing a mirror-image view of ongoing electrical activity throughout the rest of the
heart.
Note that we do not assign a specific number of degrees to the vantage point for lead aVR
(Figure 09.4-1). Instead it suffices to think of this lead as providing a remote right-sided
view. Lead aVR may show reciprocal changes to what occurs in other areas of the heart.
Diffuse ST depression in multiple leads from subendocardial ischemia in a patient with severe
coronary disease may therefore manifest mirror-image ST elevation that is only seen in
lead aVR (This concept discussed in detail in Section 09.40).

09.5 R Wave Progression: Where is Transition?

The R of our suggested Q-R-S-T memory aid serves to remind us to assess each tracing for R
Wave Progression. A typical sequence of R wave progression across the 6 precordial leads is
illustrated in Figure 09.5-1, which is a close-up view taken from the lower part of Figure 09.3-1.
Normally the R wave becomes progressively taller as one moves across the precordial leads.
The R wave often (but not always) tops out in lead V5 and then drops off in amplitude by
lead V6. These relationships are shown in Figure 09.5-1.
The easiest way to quickly describe evolution of the QRS waveform from a predominantly
negative complex in V1,V2 to a predominantly positive complex in more lateral precordial
leads is by commenting on the point of Transition, which indicates the leads between
which the QRS becomes more positive than negative. Transition normally occurs between lead
V2-to-V3 or between V3-to-V4. In Figure 09.5-1 Transition occurs between leads V2-toV4 (since the QRS is predominantly negative in V2 isoelectric in V3 and clearly positive
by V4).

Figure 09.5-1: Close-up of the cross-sectional view shown in Figure 09.3-1 in which progression

of QRS complexes in the precordial leads is shown. Note the small r wave in lead V1 and that there
are small septal q waves in leads V5,V6. R wave amplitude tops out in V5; Transition is normal
(occurs between leads V2-to-V4).
Where is Transition?
Determining the point of transition is easy. It is a highly reproducible determination and not
subject to inter-interpreter variability (Figure 09.5-2). In contrast there is great variation in the
way different interpreters evaluate an ECG for the adequacy of R Wave Progression (Section 09.7).
Transition is said to be Normal IF it occurs between leads V2-to-V4 (Panel B in Figure
09.5-2). Regardless of r wave amplitude in the first few precordial leads the R wave
becomes taller than the S wave is deep by lead V3 or V4. In Panel B transition occurs
between leads V3-to-V4.
Transition is said to be Early IF the R wave becomes taller than the S wave is deep by lead
V2. This is the case in Panel A in which transition occurs between leads V1-to-V2.
Transition is said to be Late IF the point at which the R wave becomes taller than the S wave
is deep is delayed to after lead V4. This is the case in Panel C in which transition occurs
between leads V4-to-V5.

Figure 09.5-2: Transition in the precordial leads. Normal transition occurs between leads V2-to-V4
(Panel B) vs Early (A) or Late (C) transition.
KEY Clinical Points: There is no doubt about where transition occurs for each of the 3 precordial
lead sequences shown in Figure 09.5-2. Subjectivity does not enter into the definition.
NOTE: The point of transition is a descriptive finding. The clinical significance of normal,
early or late transition will depend on other ECG parameters (as will be discussed shortly).
Our purpose for routinely including assessment of R wave progression and the point of
transition in our Systematic Approach (= the R of Q-R-S-T Changes) is not to overlook
the finding of a disproportionately tall R wave in lead V1. Careful assessment of precordial
lead morphology should also pick up: i) any r that might be present in lead V1; and ii) any Q
waves or loss of r wave that might occur in precordial leads (Section 09.8).

09.6 Old Terminology: R Wave Progression CW, CCW Rotation

ECG description of precordial lead QRS appearance has evolved over time. In the past the term
R Wave Progression was universally used to convey progressive increase (or lack thereof) of
QRS amplitude as one successively views the precordial leads.
R Wave Progression was said to be normal IF the R wave gradually and progressively
became taller as one moved across the precordial leads (at least until leads V4,V5).
PRWP (Poor R Wave Progression) was said to be present IF the R wave in lead V1 through
to leads V3-V4 either did not become taller, or only increased slowly in size.
Abnormalities in the way the R wave did or did not progress were described by rotation
direction. CCW (CounterClockWise) rotation was said to exist in the transverse plane IF
the zone of transition occurred before lead V3 vs CW (ClockWise) rotation IF transition
occurred after lead V4.
Old vs New Terminology: Use of the ECG designations of clockwise and counterclockwise
rotation is outdated. These terms are no longer actively used. We find these terms confusing
because they are based on the unexpected premise of an observer standing at the feet of the patient
looking upward to envision precordial lead progression of R wave amplitude. We suggest you
ignore the terms clockwise and counterclockwise rotation, which do not contribute to
meaningful ECG interpretation.
In contrast We have kept the term R Wave Progression (RWP) in our ECG vocabulary,
because this term remains ingrained in the minds of many ECG interpreters.
Clinical Perspective: It is better to determine precordial lead Transition than to worry
about R wave progression. The point of transition much more reproducibly describes what
occurs in the transverse plane (Section 09.5).

09.7 FIGURE 09.7-1: Poor R Wave Progression

Given continued reference by clinicians to R wave progression as a component of ECG
interpretation it is essential to appreciate what is meant by the term, PRWP.
PRWP (Poor R Wave Progression) is said to exist IF the R wave does not progressively
increase as one moves across the precordial leads. A number of conditions may be associated
with PRWP. We list these in Figure 09.7-1. The problem is that many of the entities on this list
are clinical opposites (ie, RVH vs LVH; normal variant vs myocardial infarction). Clinical
utility of a term that fails to distinguish between opposites is limited.
Clinical Perspective: The term PRWP is clearly suboptimal. That said, despite its
shortcomings the designation PRWP remains in active use. Specific indication of which
precordial leads manifest Q waves (or QS complexes) and noting the area of transition is far
better. Nevertheless Youll want to be aware of the entities commonly associated with PRWP

(Figure 09.7-1):

Figure 09.7-1: Common causes of PRWP which is said to exist if the R wave does not become
progressively taller as one moves across the precordial leads (See text).
09.8 FIGURE 09.8-1: Anterior MI vs Lead Placement Error?
Technical mishaps and lead placement errors were reviewed in Section 03. Awareness of these
technical pitfalls is especially relevant in assessing precordial lead R wave progression. For
example Examine the precordial lead sequence shown in Panel A of Figure 09.8-1.
Does the precordial lead sequence in Panel A make sense? If not What might be the cause of
the problem?
HINT: Be sure to look not only at R wave progression but also at T wave progression in the
precordial leads shown in Panel A.

Figure 09.8-1: Precordial lead R wave progression in Panel A does not make sense because
there is abrupt loss and return of r wave between V1-to-V3. Note also what happen to T wave
morphology as one moves from V1-to-V2-to-V3 in Panel A (See text).
Answer to Figure 09.8-1: When R wave progression is normal there is gradual increase in R
wave amplitude as one moves across successive precordial leads. This is not seen in Panel A of
Figure 09.8-1:

A relatively tall initial R wave is seen in lead V1.

There is loss of R wave amplitude between lead V1-to-V2.
R wave amplitude in Panel A returns by lead V3.
Although possible that abrupt loss and return of r wave in Panel A could be the result of
isolated anterior infarction it is far more likely to represent an error in lead placement.
Loss and return of R wave amplitude is usually not nearly so abrupt when due to infarction.
Further support of lead placement error is forthcoming from assessment of changes in T wave
morphology. T wave progression from lead V1-to-V3 in Panel A also does not make sense.
Normally the T wave may be negative, flat (isoelectric), or upright in lead V1. The T wave
should not go from positive in lead V1 to negative in lead V2 to positive once more in
lead V3 as it does in Panel A.
Putting It All Together: The precordial lead sequence in Panel A would make much more
sense IF lead V2 was really lead V1 and lead V1 was really lead V2. This technical lead
placement error is in fact the cause of the unusual (and unrealistic) R wave and T wave
progression seen in Panel A. Correct lead placement is shown in Panel B. R wave and T wave
progression is now normal with transition between lead V3-to-V4.
PEARL: Another reason for routinely including assessment of transition, R wave progression
and precordial lead appearance in our Systematic Approach (the R in Q-R-S-T Changes)
is to avoid overlooking technical lead placement errors like the one in Figure 09.8-1.

09.9 FIGURE 09.9-1: What is the Cause of PRWP?

As we have emphasized the designation PRWP (Poor R Wave Progression) lacks specificity.
That is many conditions may account for relatively low anterior r wave amplitude (Figure 09.7-1).
The purpose of Section 09.9 and Section 09.10 is to illustrate how integration of the overall ECG
picture facilitates determining which of the entities listed in Figure 09.7-1 is likely to be operative.
The schematic precordial lead sequences in both Panel A and Panel B of Figure 09.9-1 qualify
as manifesting PRWP. Contemplate WHY we label Panel A as suggestive of COPD and
Panel B as suggestive of lead placement error.

Figure 09.9-1: PRWP due to COPD vs placement error (See text).

Answer to Figure 09.9-1: PRWP is clearly present in the schematic 12-lead ECG shown in Panel A.
No more than a tiny initial r wave is seen in leads V1,V2 and R wave amplitude remains small
through to lead V6. Transition never occurs (ie, the R wave never becomes taller than the S wave is
deep).
The reason the schematic ECG in Panel A is strongly suggestive of COPD is that several
additional ECG signs of pulmonary disease are present. These include: i) RAD (Right Axis
Deviation); ii) RAA (Right Atrial Abnormality); and iii) persistent precordial S waves that are
still deep in V5,V6 (See Section 08.30 for Review of ECG findings with pulmonary disease).
NOTE: Despite PRWP for the precordial lead sequence in Panel A anterior infarction is
far less likely because: i) an r wave (albeit a small r wave) is present in all precordial leads;
and ii) the overall ECG picture in Panel A strongly suggests COPD.
In contrast to Panel A the 6 precordial leads in Panel B strongly suggest le ad placement
error. Abrupt loss and return of r wave from V1-to-V3 is not a logical sequence for normal R
wave progression especially given rapid development of a predominant R wave by lead V4.
Confirmation of technical error should be easy to establish by verifying chest lead placement and
then repeating the ECG.

09.10 FIGURE 09.10-1: QS in V1,V2 vs Anterior MI?

Two final examples of PRWP are shown in Panels B and C of Figure 09.10-1. For comparison we
begin with an example of normal R wave progression in Panel A.
Why do we label Panel B as suggestive of anterior MI?
Is the precordial lead sequence in Panel C also indicative of septal and/or anterior infarction?
If so How likely is it that prior infarction has occurred?

Figure 09.10-1: Normal RWP ( R Wave Progression) is seen in Panel A. This is in comparison with
precordial lead sequences suggestive of anterior MI (Panel B) vs an indeterminate pattern showing
a QS complex in leads V1,V2 but not in V3 (Panel C).

Answer to Figure 09.10-1: With normal R wave progression (Panel A) there is progressive
increase in R wave amplitude across successive precordial leads until transition occurs. In Panel A
the R wave tops out in lead V5 and transition occurs between V3-to-V4.
Normally the QRS complex in lead V1 is predominantly negative, because ventricular
depolarization is traveling away from this right-sided lead. There may (or may not) normally be
a small upright initial r wave in lead V1. Thus, the fact that a QS (entirely negative) complex is
seen in lead V1 of Panel A is completely consistent with normal ventricular depolarization.
Although tiny a small r wave (positive initial deflection) is seen by lead V2 of Panel A.
In contrast, in Panel C a QS pattern is seen in both lead V1 and V2. This may or may not be
a normal finding. Instead, it could indicate: i) a technical lead placement error; or ii) septal
infarction. Since there may not be any reliable way to distinguish between normal variant vs lead
placement error vs prior septal infarction We simply acknowledge, QS in V1,V2; Suggest
clinical correlation in our interpretation.
Statistically the odds are far greater (approximately 4-to-1) that either normal variant or
lead placement error rather than septal infarction are the reason for a QS complex in V1,V2 but
not V3 (as seen in Panel C).
It is only when no r wave at all is seen in V1,V2 and V3 that prior anterior (or anteroseptal)
infarction becomes more likely (Panel B).
Additional support that the precordial lead sequence in Panel B indicates prior anteroseptal
infarction is the finding of a small-but-definite q wave in lead V4 but not in leads V5,V6. If
the initial negative deflection in lead V4 was a septal q wave We would also expect to see
similar small septal q waves in leads V5,V6.
NOTE-1: The above comments regarding clinical implications of a QS complex in leads
V1,V2,V3 hold true only when the QRS complex is narrow. QRS widening due to LBBB
commonly produces QS complexes in anterior leads that are simply the result of the conduction
defection and are not indicative of anterior infarction (Section 05.8).
NOTE-2: There are 2 other potential reasons for PRWP with a narrow QRS complex that are
not the result of prior infarction. These are: i) LVH; and ii) LAHB. Usually at least some r wave
will be seen by lead V3 with these other conditions though not always. Bottom Line: It is
sometimes extremely difficult to know with certainty the cause of PRWP when R waves in leads
V1,V2,V3 are either very small or absent. Clinical correlation is essential.
Beyond-the-Core: It is insightful to appreciate the physiologic reason why R wave progression is
often poor in the presence of LVH and/or LAHB.
LVH (Left Ventricular Hypertrophy) produces an increase in leftward and posterior forces.
When marked these leftward and posterior forces may totally predominate over initial
rightward and anterior forces seen in leads V1,V2,V3. The result is reduction in r wave
amplitude in anterior leads. At times there may even be elimination of any r wave at all in
V1,V2,V3.
LAHB (Left Anterior HemiBlock) The bundle of conduction fibers in the LAH (Left Anterior
Hemifascicle) lies slightly in front of (anterior to) fibers in the LPH (Le f t Posterior
Hemifascicle). As a result block in the LAH (as occurs with LAHB) results in an initial

posterior direction for electrical activity that is first conducted over the intact LPH. The result
may once again be reduction in r wave amplitude in the anterior leads.

09.11 FIGURE 09.11-1: PRWP from LVH vs Anterior MI?

Examine the 2 precordial lead sequences shown in Figure 09.11-1. PRWP with delayed transition
(between V4-to-V5) is seen in both Panel A and Panel B.
What is the difference between these 2 precordial lead sequences?
Is anterior infarction likely in either case?
Does LVH explain all ECG findings?
Beyond-the-Core: Comment on the ST elevation seen in leads V2,V3 (short red horizontal
lines in leads V2,V3 in Panel B).

Figure 09.11-1: LVH with PRWP. Red arrows and circles highlight the difference in R wave
progression between Panel A and Panel B. Is there evidence of anterior infarction in one or both
cases? Does LVH explain all ECG findings? (See text).
Answer to Figure 09.11-1: QRS amplitude is markedly increased in both Panel A and Panel B
easily satisfying criteria for LVH (deepest S in V1,V2 + tallest R in V5,V6 >35mm). In addition
ST-T wave changes of LV strain are seen in lead V6.
Both precordial lead sequences in Figure 09.11-1 manifest a QS complex in leads V1,V2 (red
arrows). The difference is that a QS complex is also present in lead V3 of Panel B (red
arrow) whereas a small initial positive deflection (r wave) is seen in lead V3 of Panel A
(red circle).
As emphasized in Section 09.10 the ECG picture in Panel A (QS in V1,V2 but not in lead

V3) is far more likely not to be due anterior infarction. We would therefore write the following
as our interpretation: LVH and strain; QS in V1,V2 of uncertain significance; Suggest
clinical correlation.
In contrast the ECG picture in Panel B (QS in V1,V2 and in lead V3) makes it more likely
that anterior infarction has occurred. That said QRS amplitude is so greatly increased, that
loss of r waves in V1,V2,V3 could be the result of marked LVH. We simply can not know for
sure on the basis of this single ECG tracing. We would therefore write the following as our
interpretation: LVH and strain; QS in V1,V2 and V3; possible prior anterior infarction;
Strongly suggest clinical correlation.
Final Point: A subtle-but-real additional finding in Figure 09.11-1 is the presence of at least 2mm of
ST elevation in leads V2,V3 in both Panel A and Panel B (short red horizontal lines in Panel B).
This ST elevation should be noted. That said We strongly suspect this ST elevation is not
indicative of acute injury because: i) Shape of the ST elevation is concave up = smiley vs ST
coving that is far more predictive of acute injury; and ii) the ECG picture in the anterior leads is
the reciprocal (mirror-image) of what is seen in lead V6. This mirror-image picture of
concave-up ST elevation in one or more anterior leads is often seen simply as a reflection of
LVH in patients without acute infarction.
BOTTOM Line: R wave progression is a descriptive finding. There are many potential causes of
PRWP ( which we listed in Figure 09.7-1). Some of these causes are benign. Some are not. Clinical
correlation in context with the overall ECG picture is needed to determine likely clinical
implications when PRWP is noted.
09.12 FIGURE 09.12-1: Normal Q Waves; Normal T Inversion
Among the most challenging tasks for the ECG interpreter is deciding what is normal vs
abnormal. Our purpose in devising Figure 09.12-1 is to facilitate remembering when the finding
of even a large Q wave or deep T wave inversion may be normal.
5 of the leads on a standard 12-lead ECG (= leads III-aVR-aVL-aVF-V1) may normally
display even moderate-to-large Q waves and/or T wave inversion in healthy adults who do
not have heart disease.
Thinking of a reverse Z ( la Zorro) may help to recall which leads these are (Figure
09.12-1).

Figure 09.12-1: Reverse Z memory aid for recalling the 5 leads that may occasionally display
even large Q waves and/or T inversion as an isolated finding in otherwise healthy adults who do
not have heart disease (See text).
KEY Points: When are Q Waves/T Inversion a Normal Finding?
Traditionally the finding of a deep and wide Q wave is thought to be a marker of myocardial
infarction. Other pathologic reasons for Q waves exist including cardiomyopathy
(scarring/fibrosis); conduction defects and WPW. The purpose of this Section is to highlight
instances when Q waves (and associated T wave inversion) may be a normal finding.
Normal septal q waves are common. As reviewed in discussion of bundle branch block
(Section 05.7) Septal q waves are small and narrow. They arise because the first part of the
ventricles to normally depolarize is the left side of the septum. As a result left-sided leads
see the initial depolarization vector as moving away from the left as the septum depolarizes from
left-to-right. This accounts for the normal small q wave that may commonly be seen in one or
more of the lateral leads (= leads I-aVL-V4-V5-V6) in asymptomatic individuals without heart
disease. The reason we do not include normal septal q waves in Figure 09.12-1 is because their
small and narrow dimensions makes it obvious that such q waves are unlikely to be pathologic.
Lead aVR is normally all negative (negative P wave, QRS and T wave as seen in Figure
09.12-1). Global negativity for lead aVR is logical given the remote right-sided location of this
unipolar lead (the depolarization vector continually moves away from right-sided lead aVR
under normal circumstances).
Lead V1 in adults typically shows a QS or rS complex and T wave inversion (Figure 09.121). A QS complex may normally still be seen in lead V2 without this necessarily meaning there
has been prior septal infarction (Section 09.10). However, by lead V3 at least some r wave
should be seen under normal circumstances. Regarding T wave appearance in lead V1 the T
should normally be upright by lead V2 in adults. Persistent T wave inversion in anterior leads
should prompt consideration of ischemia. NOTE: The situation is different in children for
whom anterior T wave inversion up to lead V3 (or even V4) may reflect a normal juvenile T
wave pattern (Section 01.4).
Leads III, aVL, aVF (as in Figure 09.12-1) may all normally show T wave inversion and/or
an isolated Q wave that is not the result of ischemia or infarction provided that these findings
are not also seen in neighboring leads (See Section 09.13).

09.13 FIGURE 09.13-1: Inferior Infarction/Ischemia?

To illustrate the concept of normal isolated Q waves/T inversion Consider the 6 limb lead
sequence shown in Figure 09.13-1. Which leads manifest Q waves? Which lead(s) show T wave
inversion of ST-T wave flattening?
Is prior or recent ischemia/infarction likely in Figure 09.13-1?

Figure 09.13-1: There is an isolated Q wave and T wave inversion in lead III. There are also small
q waves in leads I and aVL. How should this be interpreted? (See text).
Answer to Figure 09.13-1: The critical piece of information missing from the questions posed about
the 6 limb leads shown in Figure 09.13-1 is the history. Everything seen might not necessarily be
abnormal IF the patient was asymptomatic. On the other hand IF this patient had a history of
potentially worrisome chest discomfort, the findings in lead III would clearly be of concern. We
emphasize the following:
A Q wave is seen in lead III of Figure 09.13-1. Technically this is a QS complex, since
there is no R wave. Although this Q wave is not particularly deep (it is only 2mm) given lack
of any R wave, this Q wave (QS complex) portends the same clinical implications as would a
larger or wider Q wave. That said Q waves are not seen in the other 2 inferior leads (leads
II,aVF).
Figure 09.12-1 tells us that the finding of an isolated Q wave in lead III is not necessarily
abnormal (and is not necessarily indicative of prior infarction).
There is fairly deep symmetric T wave inversion in lead III (especially in view of the small
amplitude for the QRS complex in this lead). IF this patient had new-onset chest discomfort
We would clearly be concerned about acute ischemia. That said there is no more than
nonspecific ST-T wave flattening in lead aVF and no real ST-T wave abnormality in the other
inferior lead (= lead II) . Figure 09.12-1 tells us that the finding of an isolated Q wave
and/or T wave inversion in lead III (as well as the nonspecific ST-T wave flattening seen in
lead aVF) is not necessarily ischemic IF there is no ST-T wave abnormality in lead II.
NOTE: The T wave vector often follows fairly close behind the QRS vector. As a result
isolated T wave inversion in leads III, aVL or aVF is less likely to be ischemic IF the QRS
complex is predominantly negative in the lead that manifests T wave inversion. This is the case

for lead III in Figure 09.13-1.

Bottom Line: We would note the following on our interpretation: Q wave with T inversion in
lead III; nonspecific ST-T wave flattening in aVF; Suggest clinical correlation . All bets
would be off IF this patient had new-onset chest discomfort since absence of abnormality in
lead II does not completely exclude the possibility of acute ischemia/infarction. But IF the
patient was asymptomatic (especially if a prior tracing was available and showed similar
findings) We would strongly suspect that the ECG appearance in lead III was not indicative
of ischemia/infarction.
Take-Home Point: Most of the time when Q waves/T inversion reflects ischemia or
infarction neighboring leads (in this case lead II as well as leads III,aVF) will show
similar changes.

What about the Q Waves in Leads I and aVL?

Small narrow q waves are seen in leads I and aVL in Figure 09.13-1. This is a descriptive finding
that we add to our interpretation at the time we assess for Q-R-S-T changes.
These q waves in leads I and aVL of Fig. 09.13-1 are almost certainly normal septal q waves
given their small size and occurrence in association with no ST-T wave abnormalities in these
high lateral leads (Section 09.12).

09.14 ST Elevation: Shape/What is the Baseline?

09.15 ST Elevation or Depression: What is the Baseline?

Determining ST-T wave changes is essential to ECG interpretation. We favor use of the PR segment
baseline as the reference point for judging ST segment deviations (elevation or depression). The PR
segment is the connecting line that extends from the end of the P wave until the beginning of the
QRS complex (Panel A in Figure 09.15-1). With this reference point in mind We define the
following:
ST Elevation (Panel B) IF the ST segment arises from above the PR segment baseline.
ST Depression (Panel C) IF the ST segment arises from below the PR segment baseline.

Figure 09.15-1: Use of the PR segment baseline (Panel A) to determine if there is ST elevation
(B) or ST depression (C). Alternatively either the T-P segment or some combination of PR and
TP segments may be used as the baseline (See text). Panel D shows the J-point notching that is
characteristic of early repolarization (Section 09.20).
Clinical Notes: Given the importance of the ST segment baseline in determining ST-T wave
deviations (elevation or depression) it is important to appreciate the following caveat:
The PR segment baseline will be more difficult to see when the heart rate is faster. This is
because the PR interval shortens with tachycardia. This makes it more challenging to determine
a true baseline for the PR segment when the rate is fast. Other situations in which assessing
the PR segment may be problematic include: i) when there is artifact; ii) if there is baseline
wander; and iii) when there is PR depression (as may occur with acute pericarditis; atrial
infarction; and in some normal variants). Knowing what to use as the baseline for ST segment
deviations is sometimes no easy task.
An Alternative Baseline: Some clinicians favor using the TP segment as the baseline for judging
ST segment deviations (Panel A in Fig. 09.15-1). We feel this is appropriate and a matter of personal

preference.
KEY Point: Far more important than whether one selects the TP vs PR segment as the baseline
is to overview the entire tracing to assess for baseline wander that may affect whatever
baseline is selected.
When conditions are ideal (ie, no baseline wander; no PR depression; all complexes in a lead
look identical) it is easy to pick out the baseline (and it probably doesnt matter whether
you chose the TP or PR as your reference point).
Clinical Reality: Much of the time the optimal situation of no baseline wander and perfect
consistency from one-beat-to-the-next is simply not attainable. In such cases We suggest
surveying all 12 leads with goal to perceive a Gestalt (ie, to get the best possible feel as
to what seems to be the isoelectric baseline for the case at hand). Well reinforce this concept
through numerous clinical examples over remaining Sections in this ePub.

09.16 J-Point ST Elevation: Recognizing the J-Point

The J Point joins. It joins the two Ss (ie, the end of the QRS with the beginning of the ST
segment as shown in Panel D of Figure 09.15-1). A distinct J point is not always seen (since the
QRS and the ST segment often imperceptibly blend into one another).
When it is seen the J point is often slightly elevated (with respect to the PR segment
baseline). This is often a normal finding as will be discussed in detail in the sections on
Early Repolarization (Sections 09.20-through-09.23).
NOTE: The J point may be notched especially when seen in association with benign
repolarization variants (Panel A vs Panel B in Figure 09.16-1).
In contrast it is uncommon for acute MI to show J-point notching (although you may
occasionally see notching with acute pericarditis).

Figure 09.16-1: Comparison of a normal ST-T wave which shows no ST segment elevation (Panel
A) vs the typical J-point appearance (red arrow) of patients with normal repolarization variants
(Panel B). As will be discussed under Early Repolarization (Sections 09.20, 09.21) normal

variants often manifest J-point notching and slight ST elevation. Note imperceptible blending of the
normal ST segment and T wave in Panel A as distinguished from the J-point notch in Panel B that
marks the end of the QRS complex and beginning of the ST segment (See text).
09.17 SHAPE of ST Elevation: More Important than Amount!
A KEY principle to appreciate is that the shape of ST elevation is more important than the amount
of elevation (Figure 09.17-1). For example acute MI may occasionally occur with no more than
minimal ST elevation. There are other times when ST elevation may be much more marked, yet
not be due to an acute cardiac event. Bottom Line: Appreciation of ST segment shape in context
with the clinical situation is essential for accurate interpretation.
ST elevation with an upward concavity (ie, "smiley" configuration) is usually benign
especially when seen in an otherwise healthy, asymptomatic individual (and especially when
seen with notching of the J point in one or more leads). This ECG picture represents the
benign normal variant pattern known as early repolarization (Figure 09.17-1).
In contrast ST segment elevation with coving or a downward convexity (= "frowny"
configuration) is much more likely to be due to acute injury (from ischemia/infarction).

Figure 09.17-1: Shape of ST elevation is more important than amount. Upward concavity
(smiley-shape) ST elevation is more likely to reflect the benign normal variant of early
repolarization (especially if seen with J-point notching). In contrast coved (= convex down or
frowny-shape) ST elevation is more likely to indicate ischemia/infarction (See text).
09.18 HISTORY: Importance of Clinical Correlation
History is ever important in assessing the clinical significance of ST elevation. Although ST elevation
with upward concavity (= "smiley" configuration) and J point notching will most often reflect a
normal repolarization variant this is only true IF the patient is asymptomatic.
In contrast An identical smiley-shape ST pattern obtained from a patient with new-onset
chest discomfort must be assumed acute until proven otherwise. IF ever in doubt Admit the
patient to the hospital! Look for old tracings to compare. Repeat the ECG within a short period
of time. Dont move on to your next assignment until you are comfortable that an acute ischemic
process is not evolving.

NOTE: There is an uncommon form of repolarization variant that manifests an ST segment

coving (frowny) morphology. The clue that this otherwise worrisome pattern is likely to be
benign lies in the History: The patient is usually a young, healthy athlete (often AfricanAmerican) who is asymptomatic (See Figure 09.24-1 in Section 09.24). Having a prior
tracing for comparison may be invaluable. Without a prior tracing it might be impossible to
distinguish this pattern from acute MI if the patient presented to the ED with chest discomfort.
Bottom Line: The History is ever important!

09.19 FIGURE 09.19-1: Early Repolarization or Acute MI?

To solidify the concepts covered thus far We present the 12-lead ECG shown in Figure 09.19-1.
There is definite ST segment elevation in a number of leads. How would you interpret this ECG in the
context given for each of the 3 following clinical settings?
Scenario #1: IF the patient was an asymptomatic young adult?
Scenario #2: IF the patient was a young-to-middle-aged adult with recent URI and pleuritic
chest pain?
Scenario #3: IF the patient was an older adult with severe new-onset chest pain?
NOTE: The Descriptive Analysis for ECG findings on this 12-lead tracing does not change. Only the
Clinical Impression changes depending on which of the above 3 clinical settings is operative.

Figure 09.19-1: Sinus rhythm with ST elevation in a number of leads. What is the likely cause of ST
elevation? (See text).
Descriptive ANALYSIS: The rhythm in Figure 09.19-1 is sinus at ~60/minute. The PR, QRS, and
QT intervals are normal. We estimate the axis at +60 degrees. The sum of the S wave in lead V2 ( ~3
large boxes = 15 mm) plus the R wave in V5 or V6 (~5 large boxes = 25 mm) clearly exceeds 35.
This amplitude amount satisfies voltage criteria for LVH provided the patient is at least 35 years
old (Section 08.1).
QRST Changes A Q wave and T wave inversion is seen in lead III which as isolated
findings may be normal (Section 09.12). There are small septal q waves in V5,V6. Transition is

normal (the R wave becomes taller than the S wave is deep between lead V2-to-V4).
The most remarkable finding is ST elevation in multiple leads. ST segments manifest an
upward concavity (ie, smiley configuration). As seen in the blow-up of leads V5,V6 (Figure
09.19-2) there is notching of the J-point (arrow in lead V5). The combination of upward
concavity ST elevation in association with J-point notching looks very much like the
smiley-shape ST segment appearance of early repolarization previously seen in schematic
Figure 09.17-1.
Remarkably absent from the ECG in Figure 09.19-1 is reciprocal ST depression that would
be expected if infarction was acutely evolving.

Figure 09.19-2: Blow-up of leads V5,V6 from Figure 09.19-1. The upward concavity (smileyshape) ST segment in association with J-point notching (arrow) is characteristic of ERP (Early
Repolarization Pattern). Diffuseness of this ST elevation on the 12-lead (Fig. 09.19-1) lack of
significant Q waves and absence of reciprocal ST depression all support ERP as the diagnosis.
Clinical IMPRESSION: The most important point to emphasize about this ECG is that our
interpretation of Figure 09.19-3 will vary tremendously depending on history and the clinical
setting. Descriptive Analysis stays the same. However, what we would do clinically will be very
different:
Scenario #1: IF the patient is an asymptomatic 25-year old adult:
Voltage criteria for LVH would not be satisfied in Figure 09.19-3 (since the patient is less than
35 years old).
We would interpret the ST elevation seen in multiple leads of this tracing as most consistent
with ERP (Early Repolarization Pattern) since this young, asymptomatic adult manifests
benign-appearing concave up ST elevation with: i) J-point point notching in at least several of
the leads with ST elevation; ii) Lack of significant Q waves; and iii) An absence of reciprocal
ST depression.

Figure 09.19-3: We reproduce Figure 09.19-1. The likely significance of the diffuse ST elevation
seen depends on the clinical setting (See text).
Scenario #2: IF the patient whose ECG is shown in Figure 09.19-3 was a young-to-middle-aged
adult with history of recent URI (Upper Respiratory Infection) and pleuritic chest pain:
We would actively consider the possibility of acute pericarditis because: i) ST elevation is
seen in multiple leads (I,II,III,aVF; V2-through-V6) ; ii) Infarction Q waves are not seen; and
iii) Reciprocal ST depression is absent (ECG findings of acute pericarditis are discussed in
detail in Section 12.2).
Scenario #3: IF the patient was older with severe new-onset chest pain:
Voltage criteria for LVH now would be satisfied.
We would definitely contemplate the possibility of acute STEMI (ST Elevation Myocardial
Infarction) since there is unmistakable ST elevation in this patient presenting with newonset chest pain.
2-Things-To-Do to assist in evaluation would be: i) Repeat the ECG in a little while (to see
if there are any evolutionary changes ) ; and ii) Look for a prior ECG so that you can
determine IF the patient has early repolarization as a baseline finding.
We emphasize that several ECG features in Figure 09.19-3 are against this being an acute
STEMI. These include: i) How diffuse the ST elevation is; ii) upward concavity shape with Jpoint notching; iii) the q waves seen are small and narrow; and iv) general lack of reciprocal ST
depression. That said the onus of proof is on us and, there is a Q wave with T inversion
in lead III the ST segment takeoff in lead V3 is straighter than is usually seen with early
repolarization and patients with baseline ERP can develop superimposed acute infarction (so
the patient might have had a component of early repolarization prior to developing their
acute infarction).
BOTTOM Line: We need to know the clinical setting in order to be able to interpret the ECG in
Figure 09.19-3. Descriptive analysis will stay the same regardless of the history but clinical
interpretation will be vastly different depending on what the history is.

Beyond-the-Core: Did you notice the S1-Q3-T3 pattern in Figure 09.19-3? It turns out that this ECG
was obtained from a healthy, asymptomatic young adult and that the ST elevation was entirely due to
early repolarization.
As emphasized in Section 08.36 the isolated finding of an S1-Q3-T3 pattern in an otherwise
healthy individual may be normal. An S1-Q3-T3 is only helpful in the diagnosis of acute PE
(Pulmonary Embolus) IF the history is right and there are other suggestive ECG findings.

09.20 What is EARLY REPOLARIZATION?

Having discussed the elements required for determining whether there is ST elevation with
emphasis on the importance of assessing ST segment shape plus the clinical history we now
explore further the entity known as ERP (Early Repolarization Pattern).
The term ERP relates to a common ECG finding characterized by J-point abnormalities and
associated ST-T wave changes. These features are shown in Figure 09.20-1:
Typically there is J-point ST elevation with upward concavity (Panel A).
There may be frank notching defined as an upward deflection near the end of the R wave
downslope (Panel B).
Alternatively there may be slurring (without notching) of the terminal portion of R wave
downslope as it transitions into the ST segment (Panel C). Note that there is no more than
minimal ST elevation in association with such slurring in Panel C.

Figure 09.20-1: ECG features of early repolarization. There is concave up ST elevation (smileyshape) in at least several leads often with either J-point notching and/or terminal R wave slurring
in one or more of the leads that manifest ST elevation (See text).
09.21 Early Repolarization: Variations in the Definition
First described in the 1940s there are variations in how even the experts define ERP. Many
imply that the entity is defined by J-point ST elevation of characteristic shape. Others include J-point
abnormalities (notching, slurring) even when there is no more than minimal associated ST
segment elevation.
Typically there is at least 1-2 mm of upward concavity (smiley-shape) ST segment
elevation with prominent upright T waves in at least 2 contiguous leads.
Some include anterior lead ST elevation within their definition of ERP. Others maintain that
some degree (1-2mm) of anterior ST elevation (in V2-to-V4) is so common as to be a normal

finding (and not indicative of ERP).

The presence of 1-2mm upward concavity ST elevation in either inferior (II,III,aVF) or
lateral (I,aVL; V4,V5,V6) lead areas is much less common than anterior ST elevation and
clearly satisfies criteria for ERP.
More than one lead area may be involved with ERP. Occasionally there may even be global
ST elevation (in inferior, lateral, and anterior leads) which may understandably be difficult
to distinguish from acute pericarditis.
ECG changes of ERP may be dynamic. They may come or go with change in body position
(from supine to standing) with activity (they commonly disappear during exercise testing)
and ERP may change over time (especially if the patient becomes deconditioned or during
illness) . CAVEAT: Such ST-T wave changes do not necessarily indicate ischemia or acute
infarction!
Other Patterns of repolarization variants exist. These include anterior T wave peaking
(Figure 09.23-1) and ST segment coving (Fig 09.24-1).

09.22 ERP: Is Early Repolarization Benign?

In years past the incidental finding of upward concavity ST elevation in an otherwise healthy and
asymptomatic young-to-middle-aged adult was thought to be benign. As a result the name of this
entity evolved to the term, BER = Benign Early Repolarization. While fully agreeing on the
overall favorable prognosis for the overwhelming majority of patients with this type of ST elevation
We feel ERP (Early Repolarization Pattern) is a far better term than BER because:
The incidental ECG finding of early repolarization in young-to-middle-aged asymptomatic
adults is not necessarily benign. Tikkanen et al (NEJM 361:2529, 2009) have shown a 1.3fold increased risk of cardiac death with 1mm early repolarization ST elevation (and up to a
3-fold increased risk IF >2mm ST elevation). What to do with these results?
The Facts about ERP are the following:
Early repolarization is common. It is seen in at least 2-5% of the general population. Cardiac
arrest is rare in these patients. Most patients with incidental ERP on ECG have a benign
prognosis.
IF the patient is otherwise healthy and asymptomatic We choose not to be concerned by the
incidental finding of early repolarization on a baseline tracing.
There is general consensus that the isolated finding of anterior ST elevation conveys no
increase in cardiovascular risk. This form of ERP is benign.
Final answers are not yet in for inferior or lateral ERP. Consider further evaluation IF: i)
there is a positive family history of sudden death at early age; ii) the patient had unexplained
syncope/presyncope; and/or iii) there are other symptoms, arrhythmias or concerns.

09.23 FIGURE 09.23-1: Acute MI or Repolarization Variant?

Illustration of how best to interpret ECG findings suggestive of ERP is best accomplished by clinical
example. Consider the ECG shown in Figure 09.23-1 which was obtained from a 50-year old man
with atypical chest discomfort.
Is this ECG likely to reflect ERP or acute anterior MI?
How confident are you of your answer?
Are you comfortable enough to send this patient home IF he presented to an ED (Emergency
Department) with this tracing?
Would you send the patient home IF he presented to the office with this ECG and the same
history of atypical chest discomfort?

Figure 09.23-1: ECG obtained from a 50-year old man with atypical chest discomfort. Is the ST
elevation seen in leads V1,V2 likely to represent an early acute anterior STEMI? How confident are
you of your answer? (See text).
Answer to Figure 09.23-1: Descriptive analysis of this ECG reveals the rhythm to be sinus
arrhythmia. Intervals and the axis are normal. There is voltage for LVH ( deepest S wave in V1,V2 +
tallest R wave in V5,V6 35).
QRST Changes There are small q waves in the inferior and lateral precordial leads. R wave
progression is normal (ie, transition occurs between leads V3-to-V4) . T waves are peaked.
There is some J-point ST elevation (with upward concavity = smiley configuration) in
multiple leads and there is shallow symmetric T wave inversion in lead aVL (red arrow).
IMPRESSION Accurate clinical interpretation of this tracing depends on the history. Without any
history We would not know clinically how to proceed.
IF concerned that the history of atypical chest discomfort in this 50-year old man sounded
like angina (especially if his symptoms were of new-onset) the patient should be admitted to
the hospital! There is precordial lead ST elevation. We would: i) Look for a prior tracing for
comparison (to see if there was change from his baseline ECG) ; and ii) Repeat the ECG in

short order to see if there is acute evolution.

That said We strongly suspect ERP as the cause of ST elevation in Figure 09.23-1 because:
i) ST elevation manifests an upward concavity = smiley configuration; and ii) The lack of
reciprocal ST depression. Although there is shallow T wave inversion in lead aVL this is
probably a normal finding given predominant negativity of the QRS complex in this lead and
lack of associated T inversion in other lateral leads (Section 09.12).
Beyond-the-Core: Several additional ECG features in Figure 09.23-1 are present that favor
ERP (rather than acute infarction). These include the following: i) that precordial lead QRS
amplitude is increased (increased R wave amplitude in V1-through-V4 is less likely when
there is anterior infarction) ; ii) that the R wave is already fairly tall by V2,V3 (delayed
transition is commonly seen with anterior infarction); and iii) that the QT is definitely not long
(acute ischemia/infarction commonly results in at least some lengthening of the QT interval ).
That said the clinical history a repeat ECG and availability of prior ECGs for
comparison will ultimately dictate the course.
NOTE: Where the patient presents for evaluation does have a role in determining the likelihood
of being admitted to the hospital. Given identical clinical features and a similar ECG the
likelihood of being admitted to the hospital appears to be more IF the patient is seen in an ED
(Emergency Department). This is because: i) Emergency care providers are less likely to know
the patient and the previous medical history (and also less likely to have a prior ECG available
for comparison) ; and ii) There appears to be a tendency toward self-selection, whereby
patients with more acute cardiac disorders somehow know to go to the ED rather than the office.
That said the onus remains on us to assume the worst scenario (ie, ACS = Acute Coronary
Syndrome) until we can be comfortable that it is safe to send the patient home. BOTTOM Line:
The clinical history is needed in order to know what to do for a patient presenting with the ECG
shown in Figure 09.23-1. While a diagnosis of ERP without need for admission would be
reasonable IF the history was not of concern a very different conclusion would be reached IF
symptoms sounded acute.
T Wave Peaking: The final point to make from the ECG in Figure 09.23-1 is that repolarization
variants that occur in otherwise healthy adults may take on a number of different forms. These
include: i) Upward concavity (smiley-shape) ST elevation (Sections 09.20 and 09.21); ii) T wave
peaking (Figure 09.23-1); and iii) Other patterns (See Section 09.24).
The ECG finding of peaked T waves should prompt consideration of 3 entities. These include:
i) Hyperkalemia; ii) Ischemia; and iii) A normal repolarization variant. Morphologic
appearance, clinical correlation and comparison with prior tracings may be needed to
distinguish between these possibilities.
Against hyperkalemia in Figure 09.23-1 is that T waves are not pointed; the ascending and
descending limbs of the T waves are not symmetric; and the base of the T waves is not narrow
(Section 11.3). Patients with hyperkalemia almost always have either a predisposing medical
illness (severe renal disease; acidosis; dehydration; multi-organ failure ) or are taking
potassium-retaining medications.
Posterior ischemia may manifest as anterior T wave peaking. That said, ischemia is highly

unlikely IF T wave peaking is diffuse and the patient is a younger adult who is not having
chest pain (as occurs in this case).
T wave peaking (as seen in Figure 09.23-1) is a descriptive finding. We presume it is due to
a benign repolarization variant only after we are comfortable that it is not due to hyperkalemia
or ischemia.

09.24 FIGURE 09.24-1: Acute MI or Repolarization Variant?

Consider the ECG shown in Figure 09.24-1. No history is given.
Is this ECG likely to reflect ACS (Acute Coronary Syndrome) with possible recent infarction?
Can you think of a clinical scenario whereby the ECG shown in Figure 09.24-1 might be a
normal variant?
Extra Credit: Is there LVH?

Figure 09.24-1: No clinical history is given. Has there been recent infarction (or ongoing acute
ischemia)? Does this patient have LVH? What information is needed to answer these questions? ( See
text).
Answer to Figure 09.24-1: Descriptive analysis of this ECG reveals the rhythm to be sinus
arrhythmia. Intervals are normal. There is marked LAD (Left Axis Deviation) that satisfies criteria
for LAHB (Le f t Anterior HemiBlock) as the net QRS deflection in lead II is predominantly
negative (Section 07.13).
Chamber Enlargement Did you notice there is half standardization? The standardization
mark is seen at the very beginning of the tracing and is only 1 large box (5mm) tall (red
rectangle in lead II of Figure 09.24-2). This means that amplitude of the P wave and QRST
complex has been reduced in half in order to fit on the ECG recording paper (Section 08.5).
Therefore S wave depth in lead V2 is not 12 mm, but 24 mm and R wave amplitude in
lead V5 is not 10 mm, but 20 mm! Therefore voltage criteria for LVH will be satisfied IF
the patient is 35 years old.

Figure 09.24-2: The ECG shown in Figure 09.24-1 is reproduced highlighting that there is half
standardization (red rectangle in lead II; open arrows at the very beginning of leads I and III ). As
a result voltage for LVH is present IF this patient is 35 years old. Are you concerned about the
ST-T waves in the inferior leads and especially in leads V3-through-V6 (red arrows)?
Assessment of QRST Changes: No Q waves are present in Figure 09.24-2 as small-but-real
initial r waves are seen in each of the inferior leads. Transition occurs early due to a surprisingly tall
R wave in lead V2. That said the most concerning finding on this ECG is ST coving with slight
ST elevation and T wave inversion in multiple leads (red arrows in precordial leads).

IF this patient was older with a history of new chest pain this ECG would look like an acute
evolving MI. It turned out that the patient in this case was a young adult athlete with no heart
disease who had this ECG done as part of a pre-participation sports exam. Thus, the ST-T wave
changes seen are most likely to represent an unusual repolarization variant. In view of this
benign clinical setting there is no evidence for acute ischemia. Bottom Line: Be aware that
there are a number of different repolarization variants that may be seen on the ECG of normal
subjects. History is everything!
Beyond-the-Core: If we were evaluating this asymptomatic young adult athlete in the office as
part of a pre-participation exam We would recommend an Echo to rule out hypertrophic
cardiomyopathy given early transition with prominent septal forces (ie, disproportionately tall
R waves in leads V2,V3). If physical examination and the Echo were normal there would be
no reason not to allow full participation.

09.25 ST Segment Depression

As discussed in Section 09.15 We favor use of the PR segment baseline as the reference point for
judging ST segment deviations (elevation or depression). The PR segment is the connecting line
that extends from the end of the P wave until the beginning of the QRS complex (Panel A in
Figure 09.25-1). Using the PR baseline as our reference point We define the following:
ST Elevation (Panel B) IF the ST segment arises above the PR baseline.
ST Depression (Panel C) IF the ST segment arises below the PR baseline.

Figure 09.25-1: Use of the PR segment baseline (Panel A) to determine if there is ST elevation
(B) or ST depression (C). Alternatively either the T-P segment or some combination of PR and
TP segments may be used as the baseline (See text).
Clinical Caveats: The PR segment baseline is more difficult to see when the heart rate is faster.
This is because the PR interval shortens with tachycardia. This makes it more challenging to
determine a true baseline for the PR segment when the rate is fast.
Other situations in which assessing the PR segment may be problematic include presence of
artifact and baseline wander. Knowing what to use as the baseline for ST segment deviations is
sometimes no easy task.
NOTE: Instead of the PR segment some clinicians favor the TP segment as the baseline to
use for judging ST segment deviations (Panel A in Figure 09.25-1) . Either approach is
acceptable and, when conditions are ideal (ie, no artifact; no baseline wander; all
complexes in a lead look identical) determining the baseline is easy (and it doesnt really
matter whether you select the TP, PR, or some combination of the two as your reference
point).

09.26 LIST #4: Causes of ST Depression

There are over 50 causes of ST segment depression on ECG. Many of these causes are cardiac-

related but there are also many non-cardiac causes. Among the many non-cardiac causes are
hyperventilation; temperature extremes (excessive heat or cold exposure); anxiety or emotional
stress; anemia; tachycardia; sleep deprivation; pulmonary disease; electrolyte abnormalities; central
nervous system disorders; certain medications; and severe medical illness (among others).
BOTTOM Line: Rather than commit to memory an exhaustive list of conditions predisposing to ST
segment depression it suffices to appreciate the variety of entities that may produce changes on
ECG. Remember: Many of these conditions are non-cardiac.
We simplify recall of those clinical entities predisposing to ST depression that we feel are most
important to remember with our LIST #4 in Figure 09.26-1.
In general causes of T wave abnormalities (including T wave flattening or frank T wave
inversion) are similar to potential causes of ST segment depression.

Figure 09.26-1: Common Causes of ST Depression = LIST #4. A similar list may produce T wave
changes. More than a single cause may be operative in a given patient.
09.27 ST-T Wave Appearance: A Hint to the Cause
Although all 6 of the possibilities noted in List #4 should be considered each time you encounter STT wave abnormalities the specific cause(s) operative may be suggested by appearance of the STT wave on ECG (Figure 09.27-1):

Figure 09.27-1: ST-T wave appearance may suggest the cause(s) operative in a given patient (See
text).
Shape of the ST-T wave may suggest which of the 6 entities in List #4 is likely to be operative in
a given patient (Figure 09.27-1):
Ischemia is suggested by symmetric T inversion (red arrow in Panel B) especially when
seen in two or more leads of a given lead group (ie, in leads II, III and aVF or in both leads
I and aVL).
In contrast "Strain" from LVH (Panel A) is suggested by asymmetric ST depression

occurring in one (or more) of the lateral leads (less often in the inferior leads). Note the initial
slow sagging of the ST segment with strain (black arrow) with more rapid return to the
baseline (Section 08.9). Strain is more likely to be the cause of ST depression when voltage
for LVH is present although occasionally, there may be ST-T wave changes suggestive of
strain without accompanying voltage (Section 08.10).
"RV strain" is suggested IF the picture in Panel A of Fig. 09.27-1 is seen in right-sided
leads (II,III,aVF or V1,V2,V3) in a patient with RVH (Sections 08.28 and 08.29).
Use of Digoxin may affect ST-T waves in one of 3 ways: i) there may be scooped ST
depression in multiple leads (that simulates an inverted ice cream cone, as in Panel D of
Figure 09.27-1) ; or ii) Digoxin effect may produce a "strain"-like pattern (identical to
Panel A); or iii) Despite use of Digoxin ST-T waves may be unaffected. It is of interest that
the serum Digoxin level does not correlate well with ST-T wave appearance in a patient taking
this drug. Thus, a patient may manifest classic scoopies (scooped ST depression with a short
QT interval in multiple leads) yet be on no more than a low dose of the drug. In contrast,
another patient may have toxic serum levels of Digoxin yet manifest no ST-T wave
abnormalities at all. Bottom Line: ST-T wave appearance does not predict which patients have
Digoxin toxicity.
Panel C is the remaining pattern of ST-T wave change in Figure 09.27-1. We label this
pattern as, NS ST-T Abns. (= Non-Specific ST-T wave Abnormalities) since such ST
flattening and/or slight depression does not suggest any specific cause. Instead any of the
more than 50 potential causes of ST-T wave abnormalities may be contributing to the
appearance of this pattern. Bottom Line: The ST-T wave is not normal but the change that
we see is non-specific in that we dont know the cause.

09.28 FIGURE 09.28-1: What is the Cause(s) of ST Depression?

It is easiest to illustrate the concepts covered in Sections 09.26 and 09.27 by a clinical case. Interpret
the ECG shown in Figure 09.28-1 obtained from a woman on multiple medications. She has chest
pain and heart failure. Note the marked amount of ST depression in multiple leads which is
especially well seen in the blow-up inserts from leads V5,V6 (red arrows).
In view of this clinical history What are likely causes of this marked amount of ST
depression?
HINT: Feel free to refer back to LIST #4 in formulating your answer (Figure 09.26-1).

Figure 09.28-1: ECG obtained from a woman with chest pain and heart failure. She is taking multiple
medications. What are likely causes of the marked ST depression seen in multiple leads? (Feel free
to refer back to List #4 in Figure 09.26-1 when formulating your answer).
Answer to Figure 09.28-1: The rhythm is an almost regular SVT (narrow complex tachycardia) at
~180/minute. Given the rate and the lack of any definite P waves we presume PSVT for the rhythm
diagnosis (List #2 in Section 02.52). The axis is normal; there is voltage for LVH.
The most remarkable finding on this 12-lead ECG is marked and diffuse ST depression. ST
segments are depressed at least 3mm below the J-point baseline in multiple leads (seen
especially well in the blow-up inserts of leads V5,V6 red arrows in Fig. 09.28-1).
Recognition of the ECG finding of ST depression should prompt consideration of the clinical
entities noted in List #4 (in Figure 09.26-1).
The clinical History allows us to hone in on the likely causes of ST depression. In this case
any (probably several) of the entities in List #4 may be operative, since this patient has chest
pain (possible ischemia) she has heart failure and LVH ( LV strain is probably present )
she is on lots of drugs (possibly digoxin; probably diuretics predisposing to low
K+/Mg++) and she is tachycardic (SVT rhythm at ~180/minute).
Take-Home Point: The ECG in Figure 09.28-1 provides an excellent example of how best to
utilize List #4. We interpret the 12-lead tracing in the usual systematic fashion. Recognition of
diffuse ST depression should set off the light bulb to recall the entities on List #4. Clinical
correlation with the history given allows us to predict a likely contribution from each of the entities
on the list.
09.29 Recognizing Subtle ST Changes: ST Segment Straightening
Consensus among expert electrocardiographers is lacking regarding the definition of a normal ECG.
Much of this relates to semantics since minor ST-T wave abnormalities generally provide no more
than a nonspecific suggestion to potential etiologies. That said We feel it is important to hone in
on recognizing even minimal abnormalities, if for no other reason than to let those reading our
interpretation be aware that we saw the abnormality in question but did not think it clinically
important for the case at hand.

The above said there are times when even minimal ST-T wave changes may have clinical
relevance. In addition routine attention to recognizing subtle ST-T wave changes will go a
long way toward improving ones ECG interpretation ability.
For example What is the difference between the ST segment shown in Panel A vs Panel B in
Figure 09.29-1? Is the admittedly subtle difference in ST-T wave appearance between these two
complexes likely to be of clinical significance? If so How?

Figure 09.29-1: Compare the ST segment in Panel A with Panel B. What is the difference? Is this
likely to be clinically significant? (See text).
Answer to Figure 09.29-1: The ST-T wave in Panel A is normal. Note the smooth contour at the
point of transition between the end of the S wave and the beginning of the ST segment. Note an
equally smooth contour at the end of the ST segment and the point where the ascending limb of the T
wave begins.
In contrast Note the sharp angle in Panel B at the point where the straight (flat) ST segment
ends and the ascending limb of the T wave begins (red arrow). While admittedly splitting
hairs the ST-T wave in Panel B is not normal. Instead there is nonspecific ST segment
straightening (ie, loss of that smooth transition between end of the ST segment and the
beginning of the T wave ascending limb).
We emphasize that nonspecific ST segment straightening is a descriptive finding. It is
nonspecific. It may mean nothing especially if only seen in a single lead. In any case it is
not an acute change. On the other hand ST segment straightening as occurs in Panel B may at
times be a nonspecific indicator of underlying coronary disease especially when this finding
is seen in more than one lead. Clinical correlation is everything.

09.30 FIGURE 09.30-1: Are the ST Segments Normal?

Interpret the ECG shown in Figure 09.30-1 obtained from an adult with a recent history of atypical
chest discomfort.
Would you classify the ECG shown in Figure 09.30-1 as a normal tracing?
If not Why not?

Figure 09.30-1: ECG obtained from an adult with atypical chest discomfort. Would you interpret this
ECG as a normal tracing?
Answer to Figure 09.30-1: The rhythm is sinus bradycardia and arrhythmia (heart rate ~60/minute,
or a bit below this). The PR, QRS and QT intervals are all normal as is the axis (which is about
+30 degrees). There is no chamber enlargement.
Q-R-S-T Changes: A small and narrow q wave is seen in lead aVL. Transition is slightly
delayed (the R wave becomes taller than the S wave is deep between V4-to-V5). The most
remarkable finding on this ECG is ST segment flattening with slight ST depression in
multiple leads.
The amount of actual ST segment depression on this tracing is minimal (no more than 1mm in
the inferior leads) yet there is no denying that ST depression is present (See blow-up inserts
in the inferior leads in Figure 09.30-2).
There is no ST depression at all in leads I and V2-through-V6 (Figure 09.30-2). That said
ST-T waves are not normal in these leads. Instead there is subtle-but-real ST segment
straightening that resembles the picture in Panel B of Figure 09.29-1.
BOTTOM Line: The ECG in Figure 09.30-2 is not normal. Instead there is diffuse nonspecific
ST flattening and slight ST depression. These changes are subtle but real . Clinical correlation is
essential for knowing how to interpret this ECG finding. This patient may have coronary disease
possibly even severe coronary disease. On the other hand these changes are not acute and they
could be due in part or in combination to any of the other potential causes of ST depression (drug
effect, electrolyte disorder, hyperventilation, acutely ill patient, etc. ). We simply cannot tell on the
basis of this single ECG.

Figure 09.30-2: Reproduction of the ECG in Figure 09.30-1, with blow-up inserts illustrating subtle
ST-T wave abnormalities. Note that there is ST depression (of ~1mm) in the inferior leads. There is
also ST segment flattening (straightening) but no depression in leads I and V2-through-V6 (red
arrows in blow-up inserts in V5,V6). Although T wave amplitude in lead aVL is reduced note that
gradual transition from ST segment-to-T-wave is preserved in this lead ( blue arrow) compared to
clear straightening of the ST segment in leads V5,V6 (red arrows). This is not a normal ECG (See
text).

09.31 Clinical Uses of Lead aVR

In years past We virtually ignored lead aVR. No longer! This once forgotten right-sided lead is
now appreciated for a series of Pearls that it may provide in the diagnosis of a number of special but
important situations. These include identification (or at least suggestion) of the following:
LMCA (Left Main Coronary Artery) disease or occlusion (Section 09.40).
Proximal LAD (Left Anterior Descending) occlusion (Section 09.40).
Severe Coronary Artery Disease (Section 09.40).
Lead Misplacement/Dextrocardia (Section 09.32).
Acute Pulmonary Embolus (Section 09.33).
Acute Pericarditis (Section 09.34).
Atrial Infarction (Section 09.35).
Confirmation of Ventricular Tachycardia (Section 09.37).
Diagnosis of some SVT Rhythms (Section 09.36).
TCA (TriCyclic Antedepressant) Overdose (Section 09.38).
Takotsubo Syndrome (Section 09.39).
Our goal in this last part of Section 09 is to illustrate how use of lead aVR may serve as a
valuable adjunct to ECG interpretation. Some of the tracings shown here have already been
encountered. Others will be encountered again when addressing future topics (such as acute
pericarditis). The common theme is that by actively incorporating assessment of lead aVR
into your systematic approach, diagnostic accuracy will improve for a surprising number of clinical
conditions!
NOTE: Much of what follows represents advanced concepts that less experienced interpreters
need not necessarily concern themselves with unless looking to learn more. We emphasize that
lead aVR is not essential for the basics of ECG interpretation. That said awareness of the
insight that using lead aVR may provide will help advance your ECG interpretation ability to the
next level.

09.32 Lead aVR: Recognizing Lead Misplacement/Dextrocardia

We devoted Section 03 to discussion of lead derivation and recognition of potential technical errors
in lead placement. The remote, right-sided location of augmented lead aVR (looking down at the
heart from perspective of the right shoulder) provides a unique viewpoint that allows rapid
recognition when something is amiss (Figure 09.32-1).
The ECG waveform in lead aVR is derived from the difference in electrical potential between
that recorded from the RA (right arm) electrode minus the potential recorded from a central

reference point.
As shown in Figure 09.32-1 the remote right-sided and superior location of lead aVR
typically records a complex that manifests global negativity (of the P wave, QRS and T wave).
While other conditions exist that may produce a complex with significant R wave positivity in
lead aVR (ie, RVH, COPD, conduction defects, etc.) the possibility of technical error
should at least be contemplated when the QRS in lead aVR is predominantly positive.

Figure 09.32-1: Hexaxial lead system (reproduced from Figure 03.4-1). The remote superior and
right-sided perspective of lead aVR (looking down at the heart from the right shoulder)
typically results in an ECG appearance of global negativity (negative P wave, QRS and T wave) in
lead aVR, since predominant electrical activity is seen as moving away from this remote lead.
NOTE: Exceptions exist (the P wave and T wave in aVR are not always negative) but in general,
the finding of a predominantly positive narrow QRS complex in lead aVR should prompt one to
contemplate RVH, COPD or some technical error/dextrocardia.
Consider the ECG in Figure 09.32-2:
What is unusual about lead aVR?
What is unusual about lead I?
Why does this tracing not represent dextrocardia?

Figure 09.32-2: What are the unusual findings in leads I and aVR of this tracing (ECG reproduced
from Figure 03.16-1). Why does this tracing not represent dextrocardia? (See text).
Answer to Figure 09.32-2: Two findings should immediately capture your eye in assessing this 12lead tracing: i) There is global negativity in lead I (the P wave, QRS and T wave are all negative);
and ii) Lead aVR does not look as we normally expect it to look.
Given the left-sided location of lead I there should virtually never normally be global
negativity (of P wave, QRS, T wave) in this lead. Think dextrocardia or limb lead reversal!
Support that something is amiss is forthcoming from assessment of lead aVR. Note that both the
P wave and T wave are positive in aVR. In addition there is an initial positive r wave
deflection, instead of the QS or Qr complex that is most commonly seen in this lead.
Whatever might be wrong in Figure 09.32-2 is not a result of dextrocardia. We say this because
R wave progression is normal with transition (where the R wave becomes taller than the S
wave is deep) occurring between lead V3-to-V4, which is normal. R wave progression should
be reversed IF the heart was situated in the right side of the thorax.
The possibility of limb lead reversal is easily settled by repeat ECG after verifying lead position
(Figure 09.32-3). With limb leads now correctly placed Note the following:
Lead I in Fig. 09.32-3 now manifests a positive P wave, QRS complex and T wave, as it
normally does.
Lead aVR now shows global negativity (of P wave, QRS and T wave) as it most commonly
does when lead placement is normal.
R wave progression is unchanged compared to Figure 09.32-2. Since the technical error only
involved reversal of 2 limb leads (mixing up of the right and left arm electrodes) there was
no alteration of precordial lead R wave progression.

Figure 09.32-3: The ECG initially recorded in Figure 09.32-2 has been repeated after verifying
correct limb lead placement. Note that the R wave in lead I is now positive and global negativity
has been restored to lead aVR but that R wave progression is unchanged. This confirms limb lead
reversal as the cause of the unusual ECG findings that were seen in Figure 09.32-2 (See text).

BOTTOM Line: Technical errors will definitely be seen from time to time. Dextrocardia is rare
but important to recognize when it does occur. Full Review of this subject is covered in Section
03. Suffice it to say here that attention to lead aVR is an easy way to facilitate recognizing many
of the common technical mishaps (Figure 09.32-4).

Figure 09.32-4: Limb lead appearance in Panel A should immediately suggest something is amiss.
This is because: i) there is global negativity in lead I, which is virtually never seen under normal
circumstances; ii) Lead aVR shows global positivity (which is also virtually never seen normally);
and iii) the P wave is not upright in lead II (which means either a non-sinus rhythm; dextrocardia,
or lead reversal). IF the precordial lead sequence for the limb leads in Panel A looked like Panel B
(which shows normal R wave progression) We would suspect left and right arm limb lead
reversal. But IF the precordial lead sequence looked like Panel C the reverse R wave progression
in C would strongly suggest dextrocardia (See Section 03.11 for more details).
09.33 Lead aVR: in Acute Pulmonary Embolus
Interpret the ECG shown in Figure 09.33-1 obtained from a patient who presented with syncope,
shock and acute hypoxemia.
What clinical condition is suggested by this history and the combination of ECG findings seen in
Figure 09.33-1?
Does this clinical diagnosis account for the ST elevation seen in lead aVR?

Figure 09.33-1: ECG obtained from a patient who presented with syncope, shock and acute
hypoxemia (reproduced from Figure 08.32-1). What clinical diagnosis would account for all of the
ECG findings seen in this tracing (including ST elevation in lead aVR)?

Answer to Figure 09.33-1: As discussed in detail in Sections 08.34 through 08.38 the history and
combination of ECG findings in Figure 09.33-1 should strongly suggest the diagnosis of submassive
acute PE (Pulmonary Embolism). ECG findings supportive of this diagnosis include:
Sinus tachycardia.
RBBB (Right Bundle Branch Block).
Diffuse ST-T wave abnormalities consistent with RV strain.
S1Q3T3 pattern (Section 08.36).
ST elevation that is essentially limited to lead aVR and lead V1.
We emphasize that one can not rule out the possibility of acute anterior MI from the ECG shown
in Figure 09.33-1. That said virtually all facets of the history and this ECG can be explained by
one unifying diagnosis = a hemodynamically significant large acute PE.
Anterior (as well as inferior) ST-T wave abnormalities as seen in Figure 09.33-1 are consistent
with RV strain.
Very few conditions produce ST elevation that is most marked in lead aVR but minimal to
nonexistent elsewhere, with possible exception of right-sided lead V1. One of these conditions
i s acute PE, as a result of acute right heart strain (as seen in this case). This patient was
found to have a large saddle embolus.

09.34 Lead aVR: in Acute Pericarditis

Acute pericarditis is discussed in detail in Section 12. The hallmark of the ECG diagnosis of acute
pericarditis is generalized ST elevation that occurs in a clinical setting consistent with this
diagnosis. Reciprocal ST depression and large Q waves are absent. ST elevation typically manifests
an upward concavity (smiley-shape) in most leads with possible exception of right-sided leads
(leads aVR, V1 and sometimes lead III) that may show T wave inversion.
In addition to generalized ST elevation PR segment depression in at least several leads
(below the TP baseline) is another helpful clue in support of the ECG diagnosis of acute
pericarditis. PR depression is well seen in Figure 09.34-1 (red arrows).
The value of using lead aVR when contemplating a diagnosis of acute pericarditis is that this
lead often manifests PR segment elevation (blue arrow in Figure 09.34-1). As will be
emphasized in Section 12 PR segment depression is far from definitive for confirming acute
pericarditis. Nevertheless, recognition of PR depression in several leads in association with
P R elevation in lead aVR together with: i) generalized concave-up ST elevation in the
absence of reciprocal ST depression; and ii) a clinical setting consistent with acute pericarditis
go a long way toward increasing our comfort level in the likelihood of this diagnosis.

Figure 09.34-1: ECG obtained from a 35-year old man with atypical chest pain. The ECG diagnosis
o f acute pericarditis is suggested by: i) generalized concave-up ST elevation; ii) absence of
reciprocal ST depression; iii) absence of large Q waves; iv) PR depression in a number of leads (red
arrows); and v) PR elevation in lead aVR (blue arrow). Acute pericarditis is discussed in detail in
Section 12.
09.35 Lead aVR: in Atrial Infarction
Atrial infarction is rare. ECG findings are subtle and often overlooked. As a result most cases of
atrial infarction are only diagnosed post-mortem on autopsy study. Realistically Speaking being
able to diagnose acute atrial infarction is unlikely to alter management. As a result one is probably
none the worse IF you ignore routinely looking for signs of atrial infarction (as many clinicians seem
to do). That said recognition of ac ut e atrial infarction may explain abrupt onset of
supraventricular arrhythmias that are prone to occur in association with acute MI. We therefore
include this subject as an advanced topic. Consider the possibility of acute atrial infarction in the
following clinical setting(s) and in the presence of the following ECG signs:
There is an ongoing acute STEMI (ST Elevation Myocardial Infarction) that appears to be
large (as suggested by significant ST elevation and marked reciprocal ST depression).
Proximal occlusion of a major coronary artery is suggested by the ECG or acute catheterization
picture (the SA nodal artery is supplied by the Right Coronary Artery in ~60% of cases
with the circumflex accounting for most of the rest, though anatomic variations are possible ).
By far, acute inferior MI is the most common location for acute MI associated with atrial
infarction. Whether this is the result of more likely origin for the SA nodal artery from the RCA
or due to the much higher oxygen content of left atrial blood is uncertain. There is often
associated ECG evidence of acute posterior and R V (Right Ventricular) involvement
supporting the likelihood of proximal RCA occlusion (Figure 09.35-1).
There is abrupt onset of AFib or other atrial tachyarrhythmia in association with acute STEMI.
Less commonly there may be PR interval prolongation, sinus pauses or sinus arrest. Abrupt loss
of the atrial kick in a patient with a large acute MI may result in sudden cardiac decompensation
(from acute heart failure).
In addition to acute STEMI (usually from inferior MI) there are acute PTa deviations
(elevation or depression of the T wave component of the preceding P wave, during which time
atrial repolarization takes place = PTa wave ). These PTa segment deviations may vary in
lead location, depending on which atrium and what part of the atria is infarcting (left or right

atrium; atrial free wall or appendage). The ECG picture in schematic Figure 09.35-1 is
typical for the changes one might expect with acute right atrial infarction.

Figure 09.35-1: Schematic ECG illustrating expected findings from acute right atrial infarction. Note:
i) underlying acute infero-postero MI; ii) PTa segment depression in the inferior leads (red arrows )
and perhaps also in V2; and iii) PTa elevation in lead aVR and lead V1 (green arrows). Beyondthe-Core: Proximal RCA occlusion is suggested in this schematic tracing by the finding of more ST
elevation in lead III than lead II and by marked ST depression in lead aVL. Acute RV involvement is
suggested by the relatively flat ST segment in lead V1 in the face of marked ST depression in V2.
Right-sided leads could confirm acute RV involvement.
Now look at the ECG in Figure 09.35-2 obtained from a patient with chest pain. There is obvious
acute inferior STEMI which is most probably from acute RCA occlusion (marked ST elevation in
lead III > II; marked ST depression in lead aVL). ST depression in leads V1 and V2 suggest
associated posterior involvement.
Do you also see ECG signs suggestive of acute atrial infarction in Figure 09.35-2? Wouldnt it
be easy to overlook this?

Figure 09.35-2: Acute infero-postero STEMI. In addition there is ECG evidence of acute atrial
infarction. This is suggested by PTa depression in leads II,III,aVF and V5,V6 (red arrows ) plus

PTa elevation in lead aVR (blue arrow).

Bottom Line: Atrial infarction is rare. Even when present, this diagnosis is rarely made by ECG
while the patient is still alive as ECG signs are often extremely subtle (Figure 09.35-2).
Nevertheless attention to the clinical setting and recognition of PTa segment deviations ( PR
segment elevation or depression) may suggest the diagnosis and explain certain potential
complications of acute myocardial infarction. This is an advanced topic that clearly extends
beyond-the-core.
Beyond-the-Core: Note that both acute pericarditis (Figure 09.34-1) and atrial infarction
(Figure 09.35-2) are examples of relatively uncommon clinical conditions that may result in
PR depression in several leads with PR elevation in lead aVR. Clinical circumstances and the
overall ECG picture allow easy distinction between these 2 conditions.
Reference: Shakir DK, Arafa SOE: Right Atrial Infarction, Atrial Arrhythmia and Inferior MI
from a Missed Triad: Case Report & Review of the Literature. Can J Cardiol 23:995-997, 2007.
09.36 Lead aVR: in Supraventricular Arrhythmias
Among the most helpful uses of lead aVR is in the interpretation of cardiac arrhythmias. Lead aVR
may be beneficial in 2 principal ways: i) in detecting subtle atrial activity in certain
supraventricular tachyarrhythmias (Section 09.36) ; and ii) in making a definitive diagnosis of VT
(Section 09.37).
In general the best lead to look at for assessment of atrial activity is lead II. This is because
IF the P wave is upright and conducting in lead II (ie, the PR interval is constant) then there
i s sinus rhythm. In addition P wave amplitude is often greatest in lead II, which makes P
waves easy to see under normal circumstances.
The next-best lead to look at for assessment of atrial activity is lead V1. This is because this
right-sided lead conveniently provides an anatomically close electrical perspective of normal
atrial activity as the atria are depolarized.
Clinically atrial activity is not always clearly evident in leads II and V1. This is especially
true for certain regular SVT (SupraVentricular Tachycardia) rhythms in which the rapid
rate results in a shortening of the R-R interval. This may provide a cover (the preceding T
wave) within which atrial activity may be hiding. The unique electrical vantage point of lead
aVR may occasionally help to overcome this problem by providing a clue to underlying atrial
activity that may not be as readily evident in other leads (Figure 09.36-1).

Figure 09.36-1: 12-lead ECG demonstrating a regular SVT rhythm at ~150/minute without normal
atrial activity (ie, no upright P wave in lead II) . Question: Is there evidence of atrial activity in
other leads? (See text).
Answer to Figure 09.36-1: The rhythm is a regular SVT at ~150/minute but without normal
atrial activity (since lead II does not show an upright P wave). The principal differential diagnosis
consists of 3 entities: i) Sinus tachycardia; ii) PSVT; and iii) Atrial flutter. As discussed in Section
02.19 looking at additional leads in the hope of identifying atrial activity may be insightful.
PEARL: Use of calipers facilitates the process. Setting ones calipers at precisely half the R-R
interval allows you to walk out atrial activity in several leads (Figure 09.36-2). This
confirms the diagnosis of AFlutter with 2:1 AV conduction ( atrial rate = 300/minute;
ventricular rate = 150/minute).
Note how helpful looking at lead aVR is in Figure 09.36-2 for increasing our level of
comfort that 2:1 AV conduction is truly present. Clear demonstration of 2:1 AV conduction in
multiple leads (red and blue arrows ) may obviate diagnostic need for performing a vagal
maneuver.

Figure 09.36-2: Arrows have been added to Figure 09.36-1 to facilitate recognition of atrial activity.
Note that 2 evenly-spaced negative deflections are present for each QRS complex in lead II (red
arrows). Regular flutter waves are also well seen in lead aVR, as well as in selected other leads
(blue arrows).

Retrograde Atrial Activity: Another way in which additional leads may facilitate diagnosis of
regular SVT rhythms is in identifying retrograde atrial activity. Our 2 favorite leads to look
for retrograde P waves in are lead aVR and lead V1 (Figure 09.36-3).
As emphasized in Section 02.29 and Section 02.30 PSVT is a reentry tachycardia that
usually involves at least some portion of the AV node. Confirmation that reentry is the
mechanism of a regular SVT rhythm when normal P waves are absent is forthcoming from
identifying retrograde atrial activity during the tachycardia.
Retrograde P waves during PSVT are often subtle, if evident at all. They may be nothing more
than a tiny notch seen in the terminal portion of the QRS in one or more of the inferior leads
(red arrows in Figure 09.36-3).
Support that such notching is real and a reflection of retrograde atrial activity is forthcoming
from identifying retrograde P waves in other leads. While retrograde P waves are negative
when seen in lead II or other inferior leads they are generally positive when seen in lead V1
and/or lead aVR (blue arrows in Figure 09.36-3).

Figure 09.36-3: Regular SVT rhythm without normal P waves at a rate of ~180/minute (reproduced
from Figure 02.30-1). Retrograde atrial activity is suggested by subtle negative notching in the
terminal part of the QRS in each of the inferior leads (red arrows which are best seen in the lead
II blow-up in the center of the tracing). Support that such notching is real and reflects retrograde P
waves from a reentry mechanism is forthcoming from the pseudo-r-prime (positive terminal
notching) that is seen in the QRS complex in both leads aVR and V1 (blue arrows). This confirms
reentry and the diagnosis of PSVT as the mechanism of the arrhythmia (See text).
09.37 Lead aVR: for Definitive Diagnosis of VT
In Sections 02.47 through 02.51 We emphasized the importance of always assuming a regular
WCT (Wide-Complex Tachycardia) rhythm was VT (Ventricular Tachycardia) until proven
otherwise. This is because: i) VT is by far (>80-90% of the time) the most common cause of a
regular WCT rhythm when sinus P waves are not evident; and ii) VT is the most serious cause of a
regular WCT. That said Wouldnt it be nice to be able to increase our diagnostic certainty that a
regular WCT was VT beyond this 80-90% likelihood probability?

Consider the regular WCT rhythm shown in Figure 09.37-1 obtained from an adult with a
history of heart disease. How certain are you that the rhythm is VT?

Figure 09.37-1: Regular WCT rhythm obtained from a patient with heart disease. How certain are
you that the rhythm is VT? (See text).
Answer to Figure 09.37-1: The rhythm is a regular WCT at ~180/minute. There is no sign of atrial
activity. VT should be assumed until proven otherwise (LIST #1 from Figure 02.47-1).
I n Section 02.50 We emphasized how use of 3 Simple Rules can increase diagnostic
likelihood beyond the 90% probability level predicted by the presence of any regular WCT
rhythm in an adult with heart disease. Applying these 3 Simple Rules from Section 02.50 to the
rhythm in Figure 09.37-1 Note that there is: i) extreme axis deviation (entirely negative QRS
in lead aVF) ; ii) amorphous = ugly and very wide QRS morphology (the QRS is well over
0.16 second in duration) ; and iii) an almost entirely negative QRS complex in lead V6. We
estimate that these ECG findings during tachycardia increase VT likelihood to ~98%.
The additional finding of an entirely upright (monophasic) QRS complex in lead aVR during
this WCT rhythm increases diagnostic certainty of VT to virtually 100%! This is because the
only way a monophasic (entirely positive) QRS complex can be seen in lead aVR during WCT
is IF the electrical impulse originates from a site in the ventricular apex. Nothing else other
than VT does this (Figure 09.37-2).
In contrast we learn nothing about the etiology of a WCT rhythm IF lead aVR is either
initially negative or manifests anything but a large monophasic R wave (2nd and 3rd
examples in Figure 09.37-2).

Figure 09.37-2: The finding of a large monophasic R wave in lead aVR during a WCT rhythm is
diagnostic of VT with virtual 100% accuracy. In contrast anything but a large monophasic R
wave (2nd and 3rd examples in this figure) is of no diagnostic utility in differentiation (See text).
BOTTOM Line: The criterion of a monophasic upright R wave in lead aVR is admittedly
insensitive. As a result this finding will only be seen in a minority of WCT rhythms. Nevertheless,
we mention it as a special use of lead aVR in the diagnosis of cardiac arrhythmias because in
those few cases when a monophasic R wave is seen in lead aVR (Figure 09.37-3) the diagnosis of
VT is virtually assured.
As should be obvious diagnosis of VT is overwhelmingly likely in Figure 09.37-3, even
without use of lead aVR. That said once lead aVR appearance is noted, there is no longer the
slightest doubt that the rhythm is VT (which allows us to focus full effort on treatment).
Reference: Sasaki K: A New Simple Algorithm for Diagnosing Wide QRS Complex Tachycardia:
Comparison with Brugada, Vereckei and aVR Algorithms. Circulation 120:S671, 2009.

Figure 09.37-3: We reproduce Figure 09.37-1 with a blow-up insert of lead aVR. The presence of
a monophasic R wave in lead aVR makes diagnosis of VT a virtual certainty (See text).
09.38 Lead aVR: in TCA Overdose
Severe TCA (TriCy c l i c Antidepressant) Overdose may produce characteristic ECG
manifestations that are in part defined by lead aVR. Although far less commonly encountered than in
the past severe TCA poisoning is still occasionally seen. It is well to remember that overdose of

other medications (ie, quinidine; procainamide; flecainide) may produce a similar ECG picture of
sodium-channel blockade. The principal adverse effects of severe TCA overdose include: i)
Neurotoxicity (seizures; delirium) ; and ii) Cardiovascular toxicity (life-threatening ventricular
tachydysrhythmias; myocardial depression; hypotension; preterminal bradycardia ). The ECG
picture may be unique (Figure 09.38-1) and is recognized by the following:
Sinus Tachycardia is almost always seen with severe TCA ingestion until very late in the
course (ultimately there may be preterminal bradycardia).
QRS prolongation to at least 0.10 second. Rather than the QT it is QRS prolongation that
best predicts severity of the overdose. Potentially lethal ventricular arrhythmias are more likely
once QRS duration exceeds 0.16 second. Of interest QRS prolongation especially affects the
terminal portion of the QRS, such that the initial part of the QRS is often not overly abnormal.
RAD (Right Axis Deviation) which manifests as: i) a wide terminal S wave in lead I; and ii)
a prominent R (>3mm tall) in lead aVR, that is often taller than the S wave is deep in this
lead.
Predisposition to potentially lethal VT (Ventricular Tachycardia).
Other ECG findings that may be seen in severe TCA overdose include: i) QT prolongation; ii)
PR interval prolongation; iii) RBBB; iv) a transient Brugada pattern in anterior precordial leads.
Clinical NOTE: Given that ECG signs of severe TCA toxicity include: i) marked QRS widening
and ii) PR as well as QT prolongation it may at times be difficult (if not impossible) to distinguish
between: i) sinus tachycardia with a wide QRS and 1st-degree AV block ( with P waves hidden
within tall T waves made prominent by QT prolongation); vs ii) VT.
Fortunately clinical distinction between these 2 forms of wide-complex tachycardia (VT vs
sinus tach) is not essential for appropriate initial management because: i) Sodium Bicarbonate
is recommended as the drug of choice regardless of whether the wide rhythm is sinus
tachycardia or VT; and ii) antiarrhythmic drugs such as procainamide, amiodarone, sotalol or
flecainide are all contraindicated for treatment of VT with TCA overdose (because these agents
may all aggravate myocardial depression, hypotension, and conduction defects).
Bottom Line: Clinical context (ie, that the patient overdosed on a TCA) prior ECGs on the
patient and serial tracings may sometimes be needed in order to become comfortable
distinguishing between sinus tachycardia with severe TCA poisoning vs VT (Figure 09.38-1).

Figure 09.38-1: ECG obtained from a young adult who presented to the ED after TCA overdose.
Characteristic ECG signs of severe TCA toxicity are present. These include: i) Tachycardia; ii)
Marked QRS widening (to at least 0.16 second) with QRS widening primarily affecting the
terminal portion of the QRS complex; iii) RAD as manifest by a wide terminal S wave in lead I as
well as by a very tall R component in lead aVR (well over 3mm in amplitude) ; and iv) RBBB.
NOTE: We are not certain IF the rhythm in Figure 09.38-1 represents VT (marked QRS widening;
marked right axis; absence of normal atrial activity in lead II; predominant S wave in lead V6)
or a supraventricular tachycardia with marked QRS widening from severe TCA toxicity (it looks as
if P waves may be present in lead V2). In the context of severe TCA toxicity, it probably does not
matter since initial management entails Sodium Bicarbonate and avoidance of antiarrhythmic
drugs regardless of the etiology of the rhythm (See text).
Acknowledgement: My appreciation to Andrew Bowman for allowing me to publish (with slight
modification) the ECG in Figure 09.38-1.
References:
i) Thanacoody HKR, Thomas SHL: Tricyclic Antidepressant Poisoning. Toxicol Rev 24:205-214,
2005.
ii) Life-In-The-Fast-Lane: http://lifeinthefastlane.com/ecg-library/basics/tca-overdose/ 09.39 Lead aVR: in Takotsubo Syndrome
We discuss the syndrome of Takotsubo Cardiomyopathy with acute apical ballooning (and
resultant acute heart failure ) in Sections 10.62, 10.63. Many ECG findings are possible with
Takotsubo Cardiomyopathy. ECG changes are often out-of-proportion to the clinical picture. Among
the many ECG findings that may be seen are ST segment elevation in lead aVR.
See Section 10.61 for more on Takotsubo Cardiomyopathy.

09.40 Lead aVR: Severe CAD/Left Main Disease

We have found use of lead aVR to be extremely helpful in assessing certain more severe forms of
CAD (Coronary Artery Disease) especially with involvement of multiple vessels and/or with left
main disease. The illustrative examples that follow hopefully convey this key concept. NOTE: Use of
lead aVR in this manner is an advanced topic.
The remote superior and right-sided electrical viewpoint of lead aVR (looking down at the

heart from the right shoulder) provides a unique vantage point that assesses the basal part
of the interventricular septum. Ischemia of the septum (as may occur with severe left main
disease) produces a vector that points superiorly resulting in S T elevation in lead aVR.
There will often be associated ST elevation in lead aVL and ST depression in the inferior
leads).
Similar ECG findings may often be seen with acute proximal LAD (Left Anterior Descending)
occlusion, in which there is involvement of the 1st septal artery branch.
In contrast to proximal LAD occlusion more distal LAD occlusion generally does not
involve the same area of the septum. As a result ST elevation in lead aVR is not seen. Instead
ST elevation is most marked in anterior leads (V2,V3,V4).
Assessment of the clinical significance of ST elevation in lead aVR is complicated by the fact
that this lead provides reciprocal (mirror-image) information to one or more lateral leads.
Specifically ST depression in leads II, aVL, V5,V6 may result in some ST elevation in aVR
independent of septal involvement.
PEARL: Distinction between left-main disease vs proximal LAD occlusion may be suggested on
ECG by the relative amount of ST elevation seen in lead aVR compared to lead V1.
Think Left-Main disease when ST elevation in lead aVR > V1.
Think proximal LAD disease/occlusion when ST elevation in lead V1 > aVR.
NOTE: Distinction should be made between acute LMCA (Left Main Coronary Artery) occlusion
vs LMCA disease.
Most patients with acute LMCA occlusion do not survive. As a result this entity is not often
seen and unlikely to be appreciated clinically. Rapid deterioration with patient demise due to
cardiogenic shock is the usual result unless acute LMCA occlusion can be immediately
recognized and immediately acted on.
In those rare circumstances when acute LMCA occlusion is captured on ECG rather than
diffuse ST depression there should be diffuse precordial ST elevation in association with ST
elevation in lead aVR.
Consider the ECG shown in Figure 09.40-1 obtained from an older adult with a history of chest
discomfort over time.
What is the principal abnormality on this ECG? (HINT: Look at the white arrows).
Clinically Is CAD (Coronary Artery Disease) likely? If so Can you comment on the likely
severity of such CAD?

Figure 09.40-1: ECG obtained from an older adult with chest pain over time. Diffuse ST depression
is seen (white arrows). In addition, there is ST elevation in leads aVR and V1 (red arrows ). This
pattern suggests severe CAD (See text).
Answer to Figure 09.40-1: An important pattern to recognize on ECG is the finding of diffuse ST
depression (usually in 7-8 leads) in association with ST elevation in lead aVR. These findings are
seen in Figure 9.40-1:
Especially when seen in an older adult there is a high correlation with this ECG pattern and
severe CAD (usually 3-vessel or proximal LAD/left main disease).
It is difficult to distinguish between severe 3-vessel disease vs a proximal LAD or left main
lesion on the basis of this ECG alone.
Additional findings of potential concern in Figure 09.40-1 are: i) that there is also some ST
elevation in lead V1 and ii) that incomplete RBBB is present (rSr in V1; tiny-but-present S
waves in leads I,V6).
Beyond-the-Core: The ST elevation that is seen in lead V1 appears to be minimal and is less in
amount than the ST elevation seen in lead aVR. As a result the possibility of left-main disease
should at least be considered. In contrast left-main disease would be far less likely IF ST
elevation in lead V1 was greater than in lead aVR.
BOTTOM Line: Be aware of the ECG pattern shown in Figure 09.40-1 in which ST
flattening with at least some depression is seen in multiple leads in association with ST
elevation in lead aVR. Especially when seen in an older adult with symptoms consistent with
angina severe CAD is likely.
Now consider the ECG shown in Figure 09.40-2 obtained from an acutely ill patient with severe
new-onset chest pain. Having just emphasized how clinically rare it is to encounter a patient with
acute LMCA occlusion We feel this may be one exception. We note the following findings:
There is sinus tachycardia and QRS widening due to acute bifascicular block (RBBB/LAHB).
Although admittedly difficult to see the low amplitude upright P wave in lead II it looks like
there may also be 1st degree AV block.
There is marked diffuse ST elevation (in leads I,aVL; V1-through-V6; and in lead aVR).
There is marked reciprocal ST depression in inferior leads.
Small q waves have already formed in leads aVL; V1,V2,V3.
ST elevation is fairly marked (at least 2-3mm) in both lead aVR and in lead V1 (red arrows ).
While we cannot be sure if ST elevation is more in aVR or in V1 this patients acute

presentation in conjunction with new bifascicular block (plus possible 1st degree AV block )
and the dramatic ST-T wave changes seen here ( with marked ST elevation in lead aVR)
support high likelihood of acute proximal occlusion (of either the LMCA or proximal LAD).

Figure 09.40-2: ECG from an acutely ill patient with new-onset chest pain. New bifascicular block
in context with dramatic ST-T wave changes seen here ( including ST elevation in lead aVR and in
lead V1 red arrows) suggest acute proximal occlusion of either the LAD or LCMA (See text).
We conclude Section 09.40 with the ECG shown in Figure 09.40-3 obtained from a woman with
chest pain and heart failure. We previously encountered this ECG in Section 09.28 at which time
we focused attention on the diffuse ST segment depression that is seen (red arrows).
NOTE: In addition to diffuse ST depression there is also significant ST elevation in lead
aVR of Figure 09.40-3. Is this patient likely to have severe CAD because there is diffuse ST
depression with ST elevation in lead aVR?

Figure 09.40-3: ECG obtained from a woman with chest pain and heart failure (reproduced from
Figure 09.28-1). Note diffuse ST depression with ST elevation in lead aVR. Is this patient likely to
have severe CAD? (See text).

Answer to Figure 09.40-3: As discussed in Section 09.28 the rhythm is PSVT at a rate of
~180/minute. Although diffuse ST depression is present in association with ST elevation in lead aVR
this does not necessarily indicate significant coronary artery disease because there is marked
tachycardia. Instead each of the entities in LIST #4 (Section 09.26) should be considered as
possibly contributing to the ST depression that is seen. The list of common causes of ST depression
includes: i) Ischemia; ii) Strain; iii) Digitalis effect; iv) Low serum K+/Mg++; v) Rate-related
changes (from tachycardia); and/or vi) Any combination of causes i) through v).
We advise against even contemplating the possibility of severe CAD until after resolution of the
tachycardia. Then repeat the ECG.

10.0 Acute MI / Ischemia

10.1 The Patient with Chest Pain: WHY Do an ECG?

One of the KEY reasons for obtaining an ECG is to help evaluate the patient with new-onset CP
(Chest Pain). By doing so we hope to determine: i) IF there are any acute ECG changes? and ii) Is
there evidence of prior MI (Myocardial Infarction)? Specifically We want to know:
Is there ongoing ACS (Ac u t e Coronary Syndrome)? This is determined by history
troponins and by assessment of acute and serial ECG changes.
If there is ACS What area(s) of the heart are involved? How extensive is the area of
involvement?
What is the cardiac rhythm? (Any arrhythmias?).
Are there conduction defects? (BBB? AV block?).
KEY: Is patient a candidate for acute intervention?

10.2 What is a Silent MI?

As many as 1/3 of all infarcts are "silent" MIs which means that these infarcts are not associated
with chest pain. Approximately half of this group (ie, ~1/6 of all MI patients) have other
symptoms (but not chest pain). These non-chest-pain-equivalent symptoms may include: i) acute
dyspnea (shortness of breath) ; ii) GI symptoms; iii) vague myalgias or flu-like syndrome; or iv)
mental status change (especially confusion). The other half of this group (~1/6 of all MI patients)
have no symptoms at all.
Although silent MI is more common in the elderly this entity may occur in any age group
(regardless of whether or not the patient has diabetes or other medical issue that might
impair sensation).
By far the most common of the non-chest-pain equivalent symptoms is shortness of breath!
For this reason We advise obtaining an ECG on virtually any adult of a certain age who
presents with unexplained new-onset dyspnea. A silent MI may have precipitated pulmonary
symptoms/heart failure.
Awareness of the surprising prevalence of silent MI in the general population should
prompt you to inquire about a possible event (ie, infarction) whenever the patient presents
w i th unexplained symptoms that might be attributable to an undetected recent infarction.
Examples include: i) Recent new edema/heart failure but without a history of chest pain; and ii)
New fatigue and/or confusion in an older patient without plausible explanation. Have a low
threshold to obtain an ECG on such patients even though they are not having chest pain.
Comparison with a prior ECG may be invaluable for determining IF abnormalities seen on a
current ECG are new or old. IF old records are not readily available Use fax or cell phone

transmission to expedite the process.

Bottom Line: The entity of silent MI is much more common than is generally appreciated.
Not all silent MIs are truly silent. Instead other symptoms (especially shortness of
breath but also confusion, malaise, etc.) are commonly associated with this entity.
Maintaining a high index of suspicion is essential in order not to overlook previous MIs that
may have been subtle and without the usual symptom of cardiac-sounding chest pain.
Comparison of the patients current ECG with a prior ECG may be invaluable and indicate that
a patient you thought had no prior history of heart disease has actually had an MI at some time in
the past.

10.3 The ECG in Acute MI: What are the Changes?

Recent years have seen increased emphasis on use of the ECG for evaluation of ACS. We look for
acute ECG changes (Figure 10.3-1). The goal is to determine ASAP from wherever the patient is
first seen as to whether acute intervention is likely to be beneficial:
The KEY is to recognize acute STEMI (ST Elevation Myocardial Infarction) at the earliest
opportunity because this is the group of patients most likely to benefit from acute reperfusion
(angioplasty/stenting) of the occluded vessel.
Once acute STEMI is identified the process of notifying cardiology and/or activating the
cath lab is set into motion. This will ideally be accomplished within minutes of obtaining and
interpreting the patients initial ECG.
Most patients with NSTEMI (Non-ST Elevation MI) do not need acute intervention. The
reason for expediting assessment of the initial ECG is to find those who do.
Realize that what begins as a non-ST-elevation picture might evolve into an acute STEMI.
This is the reason for having a low threshold for repeating the ECG (sometimes more than
once) when evaluating a patient with new-onset ongoing chest pain. NOTE: Acute ECG
changes may evolve in as little as 20-30 minutes.
ECG Indicators of Acute MI are shown in Figure 10.3-1:

Figure 10.3-1: ECG Indicators of Acute MI: 1) ST segment elevation; 2) T wave inversion; 3) Q
wave development; and 4) Reciprocal ST depression in other lead areas.
10.4 ECG Indicators: 1) ST Segment Elevation
The hallmark of acute coronary artery occlusion i s ST segment elevation. This ST elevation is
typically seen in the leads that overly the area of acute infarction (Panel 1 in Figure 10.3-1). In
general the greater the amount of ST elevation and the more leads showing ST elevation the
larger the size of the acute MI (and the more the potential for benefit from acute reperfusion).
CAVEAT #1: Not all ST elevation is the result of acute MI. Other Reasons for ST elevation
that may not be due to acute STEMI include: i) Early repolarization (Section 09.19) ; ii)
Ventricular aneurysm (suspected when ST elevation persists for months after a previous large
infarction); iii) Acute pericarditis (Section 12.0); and iv) Other conditions (patients with LVH;
LBBB; IVCD; cardiomyopathy may at times manifest long-term ST elevation in certain leads
not due to acute stemi).
CAVEAT #2: STEMI equivalent patterns exist. The most notable example of this is acute
posterior MI that manifests anterior ST depression instead of elevation (Section 10.33);
Clinical implications of a stemi-equivalent are identical to those of frank STEMI.

10.5 ECG Indicators of Acute MI: 2) T Wave Inversion

Coronary ischemia is suggested by the ECG finding of symmetric T wave inversion (as seen in
Panel 2 in Figure 10.5-1). In general, the deeper the T wave inversion and the more leads involved
the more extensive the area of involvement is likely to be.

Figure 10.5-1: ECG Indicators of Acute MI (reproduced from Figure 10.3-1). In the paragraphs
below, we highlight assessment of symmetric T wave inversion (Panel 2).
While emphasizing pattern recognition of symmetric T wave inversion as seen in Panel 2 of Figure
10.5-1 it is well to recall several caveats:
CAVEAT #1: In addition to ischemia there are other reasons for T wave inversion. These

include: i) LVH or RVH with strain (Section 08.9 and Section 08.28) ; ii) Acute pulmonary
embolus (Section 08.37) ; iii) Juvenile T wave variant (Section 08.31) ; iv) Other conditions
(medications; electrolyte disorders; BBB; cardiomyopathy; longstanding coronary artery
disease; and various non-cardiac conditions may all manifest shallow or deep T wave
inversion not due to an acute ischemic process); plus v) A normal variant pattern (Isolated
symmetric T inversion may sometimes be seen as a normal variant in leads III, aVF, aVL,
aVR, and/or V1 Section 09.12).
CAVEAT #2: One can not tell IF even deep symmetric T inversion is new or old from looking
at a single ECG. Comparison with a prior tracing is needed. The interpreter simply describes
what is seen.
CAVEAT #3: Even when symmetric T wave inversion is indicative of acute ischemia in a
patient with new-onset chest pain this does not necessarily mean that an acute MI is evolving.
A tincture of time serial ECGs troponins and clinical follow-up are all needed to
determine IF symmetric T inversion present on initial ECG will evolve into a Q-wave or nonQ-wave infarction.
Consider the two 6-lead sequences shown in Figure 10.5-2. In both Panel A and Panel B there is
symmetric T wave inversion in lead III.
Which of these 2 sets of limb leads is more likely to represent ischemia?

Figure 10.5-2: Ischemic T wave inversion. Panel A shows fairly deep, symmetric T wave
inversion in lead III. T inversion in the other inferior leads (leads II and aVF) is not quite as deep
but it is present. We therefore interpret the picture in Panel A as highly suggestive of inferior
ischemia. In contrast Panel B (which we have reproduced from Figure 09.13-1) is much less
suggestive of ischemia because: i) T inversion is minimal (if present at all) in lead aVF and absent
in lead II; plus ii) the QRS complex is predominantly negative in lead III. This could be normal
since the T wave vector often follows close behind the QRS vector (Section 09.13). Clinical
correlation will be important to further assess these assumptions (See text).
Answer to Figure 10.5-2: The picture of ST segment coving and symmetric T wave inversion in lead
III is of potential concern for both Panel A and Panel B. That said we are clearly more concerned

with Panel A.
ST elevation or depression is always of more concern when similar findings are found in
neighboring leads. Whereas T inversion/ST depression is seen in each of the inferior leads in
Panel A (II,III,aVF) T inversion is isolated to lead III in Panel B (with no more than
nonspecific ST flattening in lead aVF).
Lead III is one of the leads that may normally manifest even moderate-to-large T wave
inversion, without this being due to ischemia (Section 09.12). That this is the case in Panel B
is made more likely by the associated finding of a predominantly negative QRS complex in the
lead showing T wave inversion.
NOTE: We can not exclude the possibility of acute ischemia (or even ongoing infarction) from
the limb lead sequence shown in Panel B. Clinical correlation and comparison with prior ECGs
is needed to do so. But our suspicion of ischemia/infarction is clearly less for Panel B than it is
for the limb lead sequence in Panel A.

10.6 ECG Indicators of Acute MI: 3) Q Waves

Development of Q waves has long been thought of as the marker that myocardial infarction has
taken place (Panel 3 in Figure 10.6-1). In general, the deeper and wider a Q wave is and the more
leads in a given lead area that manifest Q waves the more likely it is that this ECG sign indicates
ongoing or prior infarction. That said there are important caveats to be aware of:
CAVEAT #1: Not all patients with acute MI develop Q waves. Instead, there are non-Q-wave
infarctions in which acute MI is documented by history, evolutionary ECG changes and
positive cardiac markers (troponins).
Among patients who do develop Q waves with infarction transmural (full-thickness)
involvement is not necessarily needed for a Q wave to form.
CAVEAT #2: When Q waves do develop they do not necessarily last. Instead Q waves
may decrease in size with time. They may even disappear. As a result the term, significant
Q wave is problematic. Even a small Q wave may be significant in that it could be the only
ECG sign remaining from a prior infarction.
CAVEAT #3: There are other reasons for Q waves apart from serving as a marker of
infarction. These include: i) Scarring, fibrosis, cardiomyopathy; ii) Lead placement errors
(Section 09.8) ; iii) Other conditions (patients with LVH; RVH/COPD; LBBB; LAHB; IVCD;
chest wall deformity may all manifest poor R wave progression with resultant precordial Q
waves as listed in Figure 09.7-1); plus iv) Normal Variant (Be this in the form of normal
small septal q waves or even moderate-to-large isolated Q waves in leads III, aVF, aVL, aVR,
and/or V1). Recognizing when Q waves are likely to reflect a normal finding was discussed in
Section 09.12.

Figure 10.6-1: ECG Indicators of Acute MI (reproduced from Figure 10.3-1). In the paragraphs
below, we highlight development of Q waves (Panel 3).
10.7 Q Waves: Why Do they Form?
The theory for genesis of Q waves is simple (Figure 10.7-1):
After depolarization of the ventricular septum activation of ventricular myocardium begins.
If one thinks of the LV ( Left Ventricle) as a cylindrical structure the initial milliseconds of
the activation process are directed outward everywhere as the electrical impulse begins on its
path from inner endocardium (Endo) to the outer epicardial (Epi) layer of the heart (Panel A
in Figure 10.7-1).

Figure 10.7-1: Genesis of Q waves. Schematic cross-sectional view of the heart. Initial electrical
activity normally cancels out as electrical activity is opposing everywhere (Panel A). The reason
a Q wave forms over the area of infarction is that null electrical activity from myocardial necrosis is
no longer opposed (Panel B). With posterior infarction (shown in Panel C) a tall R wave is
seen in anterior leads because of loss of posterior forces (See text).
Looking Closer at Figure 10.7-1: An important concept to emphasize is that the overwhelming
majority of electrical forces involved in activation of the heart cancel each other out. The ECG
waveforms we see on an electrocardiogram represent the less than 10% of electrical forces are not
directly opposing each other. This concept is well illustrated in Panel A of schematic Figure 10.7-1

 in which virtually all electrical forces during the initial milliseconds of ventricular depolarization
cancel each other out (Note arrows in Panel A oppose each other in all directions resulting in a
null vector for the very first instant during ventricular activation).
Panel B schematically depicts what occurs during the initial milliseconds of ventricular
activation in the presence of anterior infarction (black area in Panel B). The reason a Q wave
develops over anterior leads is that outward-directed posterior forces are now unopposed
because of the null vector over the anterior area of infarction.
Panel C depicts what occurs with posterior infarction (to be discussed in detail in Sections
10.33-through-10.37). In this case the null electrical vector (black area) lies posteriorly
over the area of infarction. The result is unopposed forces that move anteriorly. This generates a
tall R wave in anterior leads.

10.8 ECG Terminology: Distinction between Q, q and QS waves?

You will often be asked to verbally describe the ECG findings noted on a given tracing. This
becomes especially relevant when evaluating patients for acute or prior infarction. It is therefore
important to clarify semantics of the ECG Terminology that is most commonly used for description
(Figure 10.8-1):
If a negative deflection precedes the QRS complex it is termed a Q wave.
The first upward deflection of the QRS complex is termed an R wave. If this is followed by a
second upward deflection (as occurs in lead V1 with RBBB) it is called an R (R prime).
The downward deflection that follows the R wave is termed an S wave. (NOTE: An S wave is
only said to be present IF the negative deflection after the R wave descends below the
baseline).
KEY Point: Given the importance of Q waves as a marker of infarction the initial
direction of the QRS complex should be closely scrutinized to determine IF it is up (an r wave)
or down (a q wave).

Figure 10.8-1: QRS Nomenclature. Although tiny the initial QRS deflection in Panel A is
upward. This deflection is therefore an r wave. In Panel B the initial QRS deflection is
downward. It is therefore a q wave. A lower case designation is used since this q wave in Panel B is
less than 3mm in depth. In Panel C there is a QRs complex (a wide and deep Q wave but a small

and narrow terminal s wave). Since there is no R wave at all in Panel D we describe the
complex seen as a QS complex (See text).
Large vs Small-Case Designation Large deflections are denoted by capital letters. In contrast
smaller deflections (that do not exceed 3 mm = 3 little boxes) are denoted by lower-case letters.
Thus, we designate the QRS complex in Panel A of Figure 10.8-1 as an rS complex (tiny initial r
wave; deep S wave). NOTE: The importance of recognizing that the initial deflection in Panel A is
upright is that without this tiny initial positive deflection, there would be a Q wave.
Panel B is a qR complex. The initial negative deflection is small and narrow (a q wave).
This is followed by a tall upright (R wave) deflection.
Panel C is a QRs complex. The initial deflection is not only deep, but also quite wide. We
call it a large Q wave. The tiny negative deflection following the tall R wave in Panel C is a
small terminal s wave.
Panel D is designated a QS complex. Because there is no positive deflection (R wave) in
Panel D we are unable to distinguish between a Q wave, an S wave, or some combination of
the two. QS complexes are commonly seen in the anterior leads. They may or may not serve as
a marker of infarction (Section 09.10).

10.9 Summary: When are Q Waves Normal?

We summarize below K E Y points brought out in Sections 10.6, 10.7, 10.8 regarding ECG
assessment for the presence and significance of Q waves:
The bigger and wider a Q wave is the more likely it is that infarction has at some time
occurred. This is especially true IF there is more than one Q wave in a given lead area. That
said some leads may normally manifest even large Q waves that are not necessarily
indicative of infarction. These leads are III aVR aVL aVF and V1 (See Figure 10.9-1
previously discussed in Section 09.12).
NOTE: Infarction Q waves may get smaller (and even disappear) with time. As a result
small size of a Q wave does not necessarily mean that no infarction has occurred.
Small septal q waves may normally be seen in one or more of the lateral leads (leads
I,aVL; V4,V5,V6). These septal q waves should not be confused with infarction q waves.
Clinical correlation and comparison with prior tracings is essential for optimal assessment of
the meaning of Q waves. For example Seeing small and narrow q waves limited to lateral
leads in an otherwise healthy patient without acute ST-T wave changes strongly suggests that
these q waves are benign.

Figure 10.9-1: Reverse Z memory aid (reproduced from Figure 09.12-1) for recalling the 5
leads that may display even large Q waves and/or T inversion as an isolated finding in otherwise
healthy adults who do not have heart disease (See text and Section 09.12 for more details).
10.10 ECG Indicators of Acute MI: 4) ST Segment Depression
We emphasized in Section 10.4, that with acute coronary occlusion the ECG leads that overly the
area of infarction manifest acute ST elevation. The opposite (mirror-image) picture is seen on ECG
in opposing walls of the heart (Figure 10.10-1):

Figure 10.10-1: ECG Indicators of Acute MI (reproduced from Figure 10.3-1). With acute STEMI
(ST Elevation Myocardial Infarction) ST elevation is seen in leads that overly the area of acute
infarction. The mirror-image picture (= reciprocal ST depression) is seen in opposing walls of the
heart (Panel 4).
KEY Clinical Points: Given the many potential causes of ST elevation other than acute STEMI
(Section 10.4) the ECG finding of reciprocal ST depression often provides an invaluable clue
that ECG changes are acute.
Reciprocal ST depression is not found in either early repolarization or acute pericarditis. The
persistent ST elevation of ventricular aneurysm is also rarely accompanied by more than
minimal ST depression.
The strongest ECG evidence that ST elevation is truly acute is finding a virtual mirrorimage picture of reciprocal ST depression. This concept is well illustrated in Figure 10.10-2
in which one can readily appreciate how the shape of the inferior ST depression in Panel A

would take on the shape of the ST elevation in leads I,aVL IF the tracing was to be flipped
over (Panel B in Fig. 10.10-2).

Figure 10.10-2: There is marked ST elevation in leads I and aVL. Note mirror-image (reciprocal)
ST depression in each of the inferior leads (leads II,III,aVF). That is, the depressed ST-T wave
seen in lead III from Panel A would look virtually identical to the elevated ST-T wave shape in
lead aVL IF in your minds eye you flipped over lead III (Panel B). With practice you can readily
recognize this mirror-image picture that is characteristic of acute reciprocal ST depression (See
text).

Regarding Reciprocal ST Depression: The question arises as to which lead areas may manifest
reciprocal ST depression with acute STEMI? Given the cylindrical configuration of the left ventricle
any other wall of the heart not showing ST elevation of acute STEMI may manifest reciprocal
ST depression. That is, with acute inferior MI reciprocal changes may be seen in anterior, lateral
and/or posterior walls.

As was the case for ST elevation (Section 10.4) the greater the amount of reciprocal ST
depression and the more leads showing ST depression the larger the size the acute MI is
likely to be (and the more the potential for benefit from acute reperfusion).
CAVEAT: There are many potential causes of ST depresssion (Section 09.26). It will not
always be easy to distinguish between ST depression due to primary ischemia or some other
cause of ST depression (LV strain; drug effect; electrolyte disturbance ) vs reciprocal
changes in a patient with acute infarction. That said clinical correlation with assessment of
the overall 12-lead ECG will usually indicate the clinical course to follow.

10.11 Acute MI: The Sequence of ECG Changes

Textbooks describe a sequence of evolutionary changes that occur during the course of acute
infarction. For those patients who read the textbook prior to having their acute MI schematic
Figure 10.11-1 shows the typical evolution sequence to expect during the course of an acute STEMI
(ST Elevation Myocardial Infarction):

Figure 10.11-1: The typical sequence of ECG changes to expect during the course of acute STEMI
(See text).
Regarding the typical sequence of ECG changes during acute MI:
Panels A and B (in Figure 10.11-1) are both normal complexes. We include Panel A to
remind that small and narrow septal q waves may be a normal finding in one or more lateral
leads (I,aVL,V4,V5,V6 Section 10.9). In contrast, the Q waves of acute MI tend to be bigger
and wider and infarction Q waves often increase in size during the course of acute MI.
Special NOTE: On occasion small septal q waves may also be seen in one or more inferior
leads (II,III,aVF) as a normal finding. This is especially true if the frontal plane axis is
relatively vertical (ie, close to 90 degrees).
Panel C (in Fig. 10.11-1) shows the "hyperacute" stage, which is the earliest change
during acute MI evolution. This stage may be subtle because there may be no more than
minimal ST elevation. Hyperacute T waves are recognized by being broader and peaked
almost as if the T wave is "trying" to lift up the ST segment. Awareness of hyperacute changes
is important because it allows recognition of acute STEMI-in-progress at a time when acute
intervention/reperfusion may provide optimal benefit. The hyperacute stage is usually shortlived and it may resolve within as little as 1-2 hours.
Panel D Conventional ST elevation follows (with ST coving = "frowny" shape) and
developing Q waves.
Panels E and F Q waves become bigger; ST segment elevation peaks and T wave inversion
begins. T waves evolve as the ST segment returns to baseline (shown in Panel F) . NOTE: As

opposed to the situation with acute pericarditis (Section 12) the ST segment is often still a
bit elevated with acute MI at the time that T wave inversion begins (Panel F). In contrast, with
acute Pericarditis the ST segment is no longer elevated in the later stage when there is T
wave inversion.
Panel G ST-T wave abnormalities resolve ( or nearly resolve) but Q waves persist and
serve as a marker that infarction has taken place.

10.12 Variation in the Sequence of Acute MI Changes

T he A-thru-G sequence from Figure 10.11-1 represents expected ECG findings for "typical"
evolution of acute MI. That said Many patients do not read the textbook! Variations on the
general theme depicted in Figure 10.11-1 are common. Consider the following:
Q waves do not always develop (Caveat #1 in Section 10.6). There may be non-Q-wave
infarction.
When infarction Q waves do form they may become smaller or even disappear over time.
ST depression or T wave inversion alone may at times be the only ECG change that is seen. The
appearance of these changes does not always follow the sequence shown in Figure 10.11-1.
Acute MI may develop in an area of the heart that is electrically silent. For example ECG
changes may not always be seen (or may be minimal) when there is high lateral or apical
infarction. Special leads may be needed to visualize acute RV infarction (Section 10.31).
There may be BBB (Bundle Branch Block) or IVCD that was either present before or
developed as a result of the acute MI. BBB may mask the ECG signs of acute or chronic
infarction (Sections 05.24 through 05.29).
There may be acute posterior MI that produces a STEMI-equivalent pattern that
manifests anterior ST depression rather than elevation (Section 10.33).

10.13 KEY Points: ECG Changes of Acute MI

Despite the above cited potential variations in ECG presentation of acute evolving MI awareness
of the typical sequence shown in Figure 10.11-1 will go a long way toward optimally rapid
recognition.
Focus on ASAP recognition of ST elevation (or stemi-equivalent) patterns since these are
the patients who are most likely to benefit from acute reperfusion (angioplasty/stenting) of the
occluded vessel. Even if positive troponins later confirm that infarction did occur acute
intervention is of limited (if any) benefit for pain-controlled, stable patients with non-STEMI
(Section 10.3 ).
Because ECG changes will not always be seen with acute MI and troponins may initially be
negative History becomes a KEY determinant for whether or not to admit a patient with chest
pain to the hospital. As a general rule, IF at all in doubt Admit the patient.
Have a low threshold to Repeat the ECG especially if the patient has ongoing chest pain or
if you are uncertain about whether the initial ECG represents an acute event. An acute evolving

infarction may show changes in as little as 20-40 minutes!

Acute ECG changes may be subtle (as in the hyperacute stage = Panel C in Figure 10.11-1).
Look especially for reciprocal ST depression in lead areas not showing ST elevation to
determine IF ECG findings are likely to be acute.
Use the concept of "patterns of leads". That is, if uncertain about whether a Q wave or T wave
inversion in lead III or aVF is clinically significant look at the other inferior lead (which is
lead II). ECG changes in the inferior leads are much more likely to reflect ischemia/infarction
IF present in each lead of the grouping (ie, in II, III and aVF). Similarly chest lead
abnormalities are more likely to reflect ischemia/infarction IF present in more than a single lead.
Use Prior Tracings to compare. Go lead-by-lead. Look not only at ST-T waves, but also at the
QRS in each lead (since axis change and/or lead placement errors may both affect ST-T wave
appearance).
NOTE: A change in QRS axis from baseline to current tracing may alter ST-T wave
appearance (as well as resulting in Q wave appearance or disappearance). Similarly a
change in the area of transition from baseline to current tracing may alter QRST appearance in
precordial leads without this indicating that there has been interval change.
PEARL: When the ECG was done Was the bed flat? If not Note the angle of the bed
when the ECG was recorded. Many patients are too sick to lie flat (Q waves and ST-T changes
may be produced by even small amounts of bed incline, especially in the inferior leads).

10.14 Assessing Acute ECG Changes

Apply the concepts discussed in this section for assessing acute ECG changes to the tracing in
Figure 10.14-1 obtained from a patient with new-onset chest pain.
Is there evidence of acute infarction? If so Is this an acute STEMI?
Are there reciprocal changes?

Figure 10.14-1: ECG from a patient with new-onset chest pain. Is there evidence of an acute
STEMI? (See text).
Answer to Figure 10.14-1: The rhythm is sinus. All intervals and the axis are normal. No chamber

enlargement.
Q-R-S-T Changes: There are large inferior Q waves (in leads II,III,aVF) and small q
waves in V5,V6. Transition occurs normally (between V3-to-V4) but there is subtle loss of R
wave from V2-to-V3.
There is hyperacute ST segment elevation in leads III and aVF. By the concept of patterns of
leads (ie, simultaneously looking at all leads in a given lead group) there is probably also
some ST elevation in lead II with reciprocal changes (ST depression/T wave inversion) in the
anterolateral leads.
Clinical Impression: Sinus rhythm. Acute inferior MI (as diagnosed by the presence of Q waves;
ST elevation; reciprocal ST depression ). There is also probable acute posterior MI (positive
mirror test in V2,V3 See Section 10.33).
The above-noted changes in Figure 10.14-1 qualify as an acute inferior STEMI as there is
ST elevation associated with acute ECG changes in this patient with new-onset chest pain. That
said it is difficult to date this infarction, because inferior Q waves are already well
established (they are especially wide and deep in lead III). Whether this is the result of prior
inferior MI with superimposed new acute MI vs recent inferior MI with acute extension
vs rapid evolution of a single ongoing event is uncertain. BOTTOM Line: Clinical implications
are similar regardless of whether the ECG in Figure 10.14-1 represents old-plus-new M I vs
single new MI since the combination of new-onset chest pain plus acute ECG changes (ST
elevation; hyperacute T waves; reciprocal ST depression ) means that the patient may benefit
from acute reperfusion.
The phenomenon of Hyperacute T waves is well illustrated in Figure 10.14-1 by T wave
appearance in lead III (and to a lesser extent in lead aVF). Note that the T wave in these leads
looks disproportionately tall and wide given the presence of ST elevation.
Reciprocal ST depression is also well seen in Figure 10.14-1 in multiple leads. In
particular Note the mirror-image appearance of the ST-T wave in lead III compared to
lead aVL.
K E Y Point: The presence of both hyperacute T waves and reciprocal ST depression in
multiple leads combine to strongly suggest that despite surprisingly deep and wide inferior Q
waves the ECG picture in Figure 10.14-1 is likely to be acute.

10.15 FIGURE 10.15-1: Use of Serial ECGs in Acute STEMI

The ECG in Figure 10.15-1 was obtained from a patient with new-onset chest pain and obvious acute
STEMI. Follow-up ECGs on this patient are shown in Figure 10.15-2 (obtained a short while later)
and finally in Figure 10.15-3 (obtained post-cath/reperfusion).
Is there evolution of the MI on these serial ECGs?
Was acute reperfusion successful (Figure 10.15-3)?

Figure 10.15-1: This is ECG #1 (blue border) from this patient with new-onset chest pain. There
is sinus bradycardia with marked precordial ST elevation. Q waves have not yet formed in the
anterior leads on this initial ECG #1. Note the hyperacute appearance of ST-T waves in leads
V2,V3,V4. Surprisingly reciprocal changes are minimal (no more than slight ST-T wave
flattening/depression in the inferior leads). Despite this there can be little doubt that this ECG
#1 represents a large acute STEMI in evolution.
What is the Culprit Artery?: We suspect acute proximal LAD occlusion as the culprit artery
for the acute STEMI seen in Figure 10.15-1. As will be discussed in Section 10.25 proximal LAD
(Left Anterior Descending) occlusion is suggested by the ECG finding of diffuse precordial ST
elevation that is especially marked in leads V2-to-V4.
Beyond-the-Core: Another finding in favor of acute proximal LAD occlusion is that ST
elevation is more marked in lead V1 than in lead aVR. In contrast ST elevation tends to be
more marked in aVR compared to V1 when there is left main disease.
KEY Clinical Point: This patient is an ideal candidate for acute reperfusion because there is
marked ST elevation in Figure 10.15-1, but no anterior Q waves have yet formed. Activate the
cath lab ASAP!
Two follow-up ECGs to Figure 10.15-1 are shown below. For clarity We use a different color
border for each tracing:
Figure 10.15-1 ECG #1 (blue border) = the initial ECG obtained at presentation.
Figure 10.15-2 ECG #2 (red border) = obtained a short while after ECG #1.
Figure 10.15-3 ECG #3 (green border) = obtained after acute cath and angioplasty/stenting
of the acutely occluded LAD.
As you evaluate these serial ECGs Keep in mind the following Questions:
Is there ECG evidence of evolution on these serial ECGs?
Was acute reperfusion successful (Figure 10.15-3)?

Figure 10.15-2: This is ECG #2 (red border) obtained a short while after ECG #1 from this
patient with acute STEMI. Note that since ECG #1 there has been interim development of RBBB
(an rSr complex is now seen in V1 with wide terminal S waves in leads I,V6). The appearance of
lead V2 is concerning as the large new Q wave and now T wave inversion in this lead suggest
ongoing evolution is in progress (comparable to Panel F in Figure 10.11-1).

Figure 10.15-3: This is ECG #3 (green border) obtained after acute catheterization and
angioplasty/stenting of the acutely occluded LAD. The good news is that this post-cath ECG #3
is encouraging! Note that the QRS complex has narrowed and RBBB is no longer present. The Q
wave seen earlier in lead V2 of ECG #2 has resolved and ST-T waves have essentially returned
to baseline. R wave progression is essentially normal (with transition between V3-to-V4). It appears
that acute reperfusion has salvaged significant myocardium!
BOTTOM Line: Use of serial ECGs may be extremely valuable in following the course of acute MI.
Lead-to-lead comparison of QRS morphology and ST-T wave changes facilitates determining which
changes are new as well as providing insight to the likely benefit obtained from acute intervention.

10.16 The Coronary Circulation

The most common cause of acute MI is sudden total occlusion of a major coronary artery. The area
of the heart affected will depend on distribution to the area from the coronary circulation. In these
next few sections We briefly review normal coronary anatomy with the goal of assisting in rapid
identification of the culprit artery.
Prompt recognition of acute coronary occlusion with rapid initiation of reperfusion therapy is
essential for optimal outcome. For this evaluation of the initial ECG is invaluable.
Appreciation of normal coronary anatomy and common variants facilitates the process.
NOTE: Basic core material review of the coronary circulation is presented in Section 10.17.
For those wanting additional material More advanced aspects of the coronary circulation
that extends Beyond-the-Core is covered in Sections 10.18 through Section 10.21.

10.17 Overview of Normal Coronary Anatomy & Variants

In Figure 10.17-1 We present a schematic overview of normal coronary anatomy (Panel A). Two
of the most important anatomic variants are shown in Panels B and C:
The two major vessels supplying the heart are the right and left coronary arteries. These most
commonly arise from the right and left aortic sinuses, respectively (Panel A).
In most patients (80-90%) the RCA (Right Coronary Artery) is a dominant vessel that
supplies the RV ( Right Ventricle) and then continues as the PDA (Posterior Descending
Artery) along the undersurface of the heart (unlabeled dotted vessel arising from the RCA in
Panel A) to supply the inferior and posterior walls of the LV ( Left Ventricle). Not shown the
AV nodal artery is most often supplied from the RCA.
As suggested in Panel A of Figure 10.17-1 the LMain (Le f t Main Coronary Artery) is
typically a short vessel (10mm) that then bifurcates into the LAD (Left Anterior Descending
Artery) and the LCx (Left Circumflex Coronary Artery).
Normally t h e LAD runs along the anterior epicardial surface of the heart in the
interventricular groove on its path toward the cardiac apex. The LAD generally supplies: i) the
anterior wall of the heart (via its diagonal branches) ; ii) the cardiac apex; and iii) a major
portion of the conduction system (via septal perforators that run vertically down through the
septum).
The LCx (Circumflex) Artery wraps around the lateral free wall of the LV ( Left Ventricle).
In most patients (ie, when the RCA is dominant) the LCx becomes relatively small after
giving rise to one or more obtuse marginal branches that supply the lateral free wall (dotted
vessels arising from the LCx in Panel A).

Figure 10.17-1: Overview of normal coronary anatomy. Panel A the most common situation (8090%), in which the RCA is a dominant vessel that supplies the RV as well as the posterior and
inferior walls of the LV. The LAD normally supplies the anterior wall of the heart (via diagonal
branches); part of the cardiac apex; and a major portion of the conduction system (via septal
perforators that run vertically down through the septum) . Panel B represents a left-dominant
circulation, in which the LCx (rather than the RCA) supplies the posterior and inferior walls of the
left ventricle. Panel C represents an L A D wrap-around variant, in which the LAD also
supplies part of the inferior wall as well as the anterior wall (See text).
Common Variants in Normal Coronary Anatomy: Figure 10.17-1 is purely schematic. Realize that
numerous variations exist on the most common picture of normal coronary anatomy that is shown in
Panel A. These depend on anatomic differences and extent of disease (development of collaterals)
plus any revascularization that may have occurred.
Anatomic appearance also depends greatly on projection angle for the basic views that are
shown (ie, septal perforator branches appear longer when viewed from a less superior angle).
Our discussion is limited to generalities.
Panel B (in Figure 10.17-1) represents a left-dominant circulation. This anatomic variant
is seen in ~15% of patients. In such cases the RCA is a smaller vessel than depicted in Panel
A. To compensate the LCx is typically larger and gives rise to the PDA (large unlabeled
dotted vessel arising from the LCx in Panel B). In a left-dominant circulation the inferior
and/or posterior wall of the LV is supplied by the LCx.
Clinically the existence of a left-dominant circulation in ~15% of patients explains why
inferior and posterior MIs will not always be due to acute RCA occlusion. Similarly, since the
AV nodal artery may be supplied by the LCx in a left-dominant circulation AV block may
also occasionally occur with LCx (rather than RCA) occlusion.
Panel C (in Figure 10.17-1) represents a wrap-around LAD variant circulation.
Occasionally the LAD (Left Anterior Descending Artery) is larger and longer, to the point
of extending beyond the cardiac apex and wrapping around to supply the undersurface of

the heart (dotted vessel extending underneath the apex from the LAD in Panel C). In extreme
cases a wraparound LAD may even serve the function of the PDA.
Clinically Awareness of the possibility of a wrap-around LAD circulation as an anatomic
variant may explain the occasional ECG pattern of simultaneous ST elevation in inferior and
anterior lead areas. Not surprisingly infarction the patient with a wraparound LAD variant
may be quite large. Beyond-the-Core: Another reason for the occasional occurrence of
simultaneous inferior and anterior ST elevation may be Takotsubo Cardiomyopathy ( See
Section 10.61).

10.18 The RCA: Taking a Closer Look

In Figure 10.18-1 We now take a closer look at normal (expected) coronary anatomy of the RCA
(Right-Coronary Artery). We emphasize that this closer look at coronary anatomy constitutes
advanced material for those wanting to know more. It is Beyond-the-Core for a basic ECG
curriculum.
As discussed in Section 10.17 the RCA arises from the right anterior aortic sinus (Figure
10.18-1). The usual path of the RCA is along the right atrioventricular (AV) groove on its way to
the crux (= the point on the diaphragmatic surface where the anterior AV groove
posterior AV groove and inferior interventricular groove all meet).
The 1st branch of the RCA is usually the conus artery which supplies the right ventricular
outflow tract (not shown on Figure 10.18-1).
The 2nd branch is usually the SAN (SA Nodal artery). Of note the RCA supplies the SAN in
~60% of patients. In the remaining ~40% the SAN arises either from the LCA or from both
the RCA and LCA. Beyond-the-Core: Awareness of the fact that the SAN is most often supplied
by the RCA explains why atrial infarction is most often seen in the setting of acute proximal
RCA occlusion (in association with acute infero-postero and right ventricular stemi See
Section 09.35).
The midportion of the RCA gives off one or more AM (Acute Marginal) branches that supply
the anterior wall of the RV ( Right Ventricle). On occasion AM branches may provide
collateral circulation to the anterior wall when the LAD is occluded.

Figure 10.18-1: Normal coronary anatomy of the RCA (Right Coronary Artery) and its major
branches. Panel A anterior view. Panel B RAO (Right-Anterior Oblique) view (See text).
Abbreviations: SAN (SA Nodal Artery) ; AM (Acute Marginal branches from the RCA) ; AVN (AV
Nodal Artery); PDA (Posterior Descending Artery).
Additional Notes on Figure 10.18-1: In most patients (80-90%) the RCA is a dominant vessel
that continues after giving off one or more AM branches as the PDA (Posterior Descending Artery)
along the undersurface of the heart. The PDA supplies the posterior and inferior walls of the LV
(Left Ventricle).
The PDA also gives rise to a number of small inferior septal branches that travel upward to
supply the lower septum, and which connect with septal branches traveling downward from the
LAD (not shown on Fig. 10.18-1).
On occasion the PDA may also give rise to exceptionally large PLA (Postero-Lateral
Artery) branches that extend laterally to supply parts of the LV free ( lateral) wall. Beyond-theCore: Awareness of the variant in which there may be large PLA branches arising from the PDA
(not shown on Fig. 10.18-1) explains why you may occasionally see acute infero-posterolateral stemi (with ST elevation in V5,V6) from acute RCA rather than LCx occlusion (See
Section 10.40.5).
The AVN (AV Nodal Artery) is a branch of the RCA in about 2/3 of patients (Panel A in Figure
10.18-1). In the remainder of patients the AVN arises from the LCA (Left Coronary Artery).
Clinically the reason AV Wenckebach ( Mobitz Type I 2nd-degree AV block ) is most
commonly seen with acute inferior MI is that that the AVN usually arises from the RCA.
Beyond-the-Core: Mobitz I 2nd-degree AV block may occasionally be seen with acute LCx
occlusion in patients with a left-dominant circulation (in which case the AVN is generally
supplied by the dominant circumflex vessel).
Summary: Acute occlusion of the RCA typically results in acute inferior infarction.
Awareness of the most common anatomic RCA patterns provides insight to possible associated
RV and posterior involvement as well as to potential SA nodal and AV nodal conduction

abnormalities.

10.19 The LEFT Coronary Artery: Taking a Closer Look

I n Figure 10.19-1 We take a closer look at normal ( expected) coronary anatomy of the LCA
(Left-Coronary Artery).
As discussed in Section 10.17 the LCA arises from the left aortic sinus (Figure 10.19-1).
This vessel begins as the LMain (Left Main Coronary Artery), which is typically a short vessel
(10mm) that then bifurcates into the LAD (Left Anterior Descending Artery) and the LCx (Left
Circumflex Coronary Artery).
Clinically It is important to emphasize that acute occlusion of the LMain usually results in
rapid demise of the patient (since this generally leads to infarction of the entire left
ventricle). These patients typically die before reaching the hospital (See Section 09.40).
Major Branches of the LAD: The LAD (Left-Anterior-Descending) Artery runs along the anterior
epicardial surface of the heart in the interventricular groove on its path toward the cardiac apex. The
LAD generally supplies the anterior wall of the heart, the cardiac apex and a major portion of the
conduction system.
The major branches of the LAD are i) the Septal perforator vessels; and ii) Diagonal branches.
Septal branch anatomy is highly variable. We show 2 septal branches in Figure 10.19-1 (S-1;
S-2) but instead there may be only one septal branch or many septal branches, depending on
individual anatomy. The 1st septal branch is typically the largest; its takeoff is generally just
after the takeoff of the 1st diagonal branch.
The interventricular septum is the most densely vascularized area of the heart. This is as it
should be given the integral role of the septum in providing blood supply to the hearts
conduction system. Septal perforators normally run a vertical path downward following their
takeoff from the proximal LAD.
Downward penetrating septal branches from the LAD typically connect with upward penetrating
septal branches from the PDA branch of the RCA. In this way there is usually a network of
collaterals from both LCA and RCA systems in the event of disease in one system. How
adequately collaterals from one system compensate for disease in the other is subject to
individual variation (as well as to how rapidly occlusive disease develops).
Clinical Note: Very proximal LAD lesions have been known as widow-makers. Especially
if proximal to the 1st septal perforator (and the 1st diagonal branch) these lesions are virtual
left-main-equivalents because of the extent of injury and conduction system damage they
cause.
Diagonal branch anatomy is also highly variable. We show 2 diagonal branches in Figure
10.19-1 (D-1; D-2) but there may be 1, 2, or 3 diagonal branches supplying the anterolateral
wall of the heart. Occasionally there is no diagonal branch per se, but rather a discrete
ramus intermedius arising from between the LAD and LCx to supply the anterolateral surface

(not shown on Fig. 10.19-1). Typically it is the 1st diagonal branch that is the largest.
Clinical Note Considerable variation in number and course of diagonal branch anatomy (and the
angulated path that these vessels follow) may require multiple views on cath to determine if
occlusion is present.

Figure 10.19-1: Normal coronary anatomy of the left coronary artery and its major branches. The
LCA (Left Coronary Artery) begins as a short LMain (Left Main Coronary Artery) branch which
then bifurcates into the LAD (Le f t Anterior Descending Artery) and the LCx (Le f t Circumflex
Artery) . Panel A anterior view. Panel B RAO (Right-Anterior Oblique) view (See text).
Abbreviations: S-1,S-2 (Septal Perforator branches) ; D-1,D-2 (Diagonal branches) ; M-1,M-2
(Obtuse Marginal branches from the LCx).
Major Branches of the LCx: The LCx (Left Circumflex) Artery is the other main branch of the
LCA (Figure 10.19-1). In most (80-90%) patients the LCx is limited in its course and primarily
supplies the lateral free wall of the LV.
After arising from the LMain the LCx wraps around the lateral wall of the heart, and then
typically runs in the left posterior atrioventricular groove in its path to the infero-posterointerventricular groove.
The main branches of the LCx are the Obtuse Marginals. We show 2 marginal branches in
Figure 10.19-1 (M-1; M-2) but the usual number may vary from 1-to-3. In most patients
the LCx becomes relatively small after giving rise to its marginal branches.
The marginals supply the lateral free wall of the LV (Think marginal = lateral free
wall).
Clinical Note Despite assessment of the lateral wall by no less than 5 of the 12 leads (I,aVL;
V4,V5,V6) the high-lateral wall may not be well visualized. This part of the LV is typically
supplied by the 1st Diagonal branch of the LAD (and not by the LCx).
Beyond-the-Core: The lateral leads that most consistently assess the part of the heart supplied

by the LCx are leads V5,V6. Therefore ST elevation in V5,V6 most often suggests acute
LCx occlusion. Exceptions Some patients may have either large PLA (Postero-Lateral
Artery) branches that arise from the RCA or they may have an unusual pattern of collateral
circulation. Otherwise acute ST elevation in V5,V6 = acute LCx occlusion.
PEARL: ST elevation in lead aVL may provide an invaluable clue to the location of the acutely
occluded coronary artery. According to a study by Birnbaum et al (Am Heart J 131:38, 1996):
Suspect acute LAD occlusion proximal to the 1st Diagonal if in addition to ST elevation in
aVL there is also ST elevation in leads V2-through-V5. This is the most common situation
when there is ST elevation in lead aVL.
Suspect 1st Diagonal branch occlusion if in addition to ST elevation in aVL there is ST
elevation in lead V2 (but not in V3,V4,V5).
Suspect occlusion of the 1st Obtuse Marginal branch of the LCx if in addition to ST elevation
in aVL there is ST depression in lead V2.
NOTE: Anterior ST elevation without ST elevation in aVL suggests LAD occlusion after
takeoff of the 1st Diagonal (= D-1 in Figure 10.19-1).

10.20 LEFT-Dominant Circulation: Taking a Closer Look

Approximately 15% of patients have a left-dominant circulation. In such cases the RCA is a
smaller vessel, terminating before it reaches the crux. To compensate the LCx is larger and gives
rise to the PDA (Figure 10.20-1).
Clinically Awareness of the left-dominant anatomic variant accounts for the occurrence of
most infero-postero-lateral infarction patterns.
Beyond-the-Core: As noted in Section 10.18-1 patients with a left-dominant circulation and
acute LCx occlusion may manifest Mobitz I 2nd-degree AV block ( because the AV Nodal artery
is usually supplied by the LCx when this vessel is dominant).

Figure 10.20-1: Schematic depiction of a left-dominant circulation (10-20% of patients). The RCA
is a smaller vessel. To compensate the LCx (Left Circumflex Coronary Artery) is much larger
and longer (Compare to Figure 10.18-1) . Panel A anterior view. Panel B RAO
(Right-Anterior Oblique) view (See text). Abbreviations: LAD (Left Anterior Descending Artery);
SAN (SA Nodal Artery) ; AM (Acute Marginal branches from the RCA) ; AVN (AV Nodal Artery);
PDA (Posterior Descending Artery) ; S-1,S-2 (Septal Perforator branches) ; D-1,D-2 (Diagonal
branches); M-1,M-2 (Obtuse Marginal branches from the LCx).
10.21 LAD Wrap-Around: Taking a Closer Look
In Section 10.18 We discussed and illustrated the usual distribution of the LAD (Left Anterior
Descending Artery). Normally, the LAD supplies the anterior wall of the heart and the cardiac apex.
Nevertheless, like other major coronary vessels the LAD is also subject to individual variation in
its size, course, and the areas of the heart that it vascularizes.
In some patients the LAD may terminate prior to attaining the apex. In such cases the apex
will be supplied by a larger and longer-than-usual PDA arising from either a very dominant
RCA or from a dominant LCx vessel (Figure 10.20-1).
Occasionally the LAD will be a larger and longer vessel, to the point of extending beyond the
cardiac apex and wrapping around to supply the undersurface of the heart (Figure 10.21-1).
At times this extension of the LAD may even serve the function of the PDA. This variant is
known as an LAD wrap-around.
Clinical Note Awareness of the possibility of acute LAD occlusion in a patient with this
anatomic variant (ie, an acute wraparound LAD lesion) explains the ECG pattern of
simultaneous ST elevation in inferior and anterior lead areas. Obviously, such infarctions
are extensive.
Beyond-the-Core: It is often difficult to assess acute apical infarction by ECG since this
area of the heart may not be optimally viewed by the standard 12 leads. At other times
notation of simultaneous ST elevation in inferior and anterior leads may suggest acute apical
involvement. Appreciation of the potential for LAD anatomic variation provides insight to the

various ECG patterns that may be seen. NOTE: Other reasons that may account for simultaneous
inferior and anterior ST elevation include: i) proximal RCA occlusion; and ii) Takotsubo
Cardiomyopathy (Section 10.61).

Figure 10.21-1: Schematic depiction of a wrap around LAD as an anatomic variant. The RCA is
a smaller vessel. To compensate LAD (Left Anterior Descending Artery) will wrap around
the apex to supply the inferior LV wall ( Compare to Figure 10.19-1) . Panel A anterior view.
Panel B RAO (Right-Anterior Oblique) view (See text). Abbreviations: SAN (SA Nodal Artery);
AM (Acute Marginal branches from the RCA); AVN (AV Nodal Artery); S-1,S-2 (Septal Perforator
branches); D-1,D-2 (Diagonal branches); M-1,M-2 (Obtuse Marginal branches from the LCx).

10.22 Identifying the Culprit Artery

Assessment of initial (and serial) ECGs during the early course of ACS (Ac u t e Coronary
Syndromes) may not only suggest the presence of acute (or impending) occlusion but also
indicate: i) the probable culprit vessel that is acutely occluded; ii) the location (and extent) of
evolving injury; iii) associated arrhythmias and conduction disturbances; and iv) the likelihood that
acute reperfusion will benefit the patient. The importance of promptly assessing the initial ECG in
a patient with new-onset chest pain has never been greater.
KEY Point: The amount of benefit that a patient is likely to derive from acute reperfusion of
the culprit (= infarct-related) artery is relative and depends on both size and acuity of the
infarct. The more ST deviation seen (ie, marked ST elevation and reciprocal depression
occurring in many leads) without yet forming large Q waves the more the potential for
benefit.
In these next few sections We review the expected ECG picture for acute occlusion of each of
the major coronary vessels. These include:
Acute RCA (Right Coronary Artery) occlusion Section 10.23.
Acute LMain (Left Main Coronary Artery) occlusion Section 10.24.
Acute LAD (Left Anterior Descending Artery) occlusion Section 10.25.
Acute LCx (Left Circumflex Artery) occlusion Section 10.28.
Suggestion: Feel free to refer back to review of the Coronary Circulation (in Sections 10.16
through 10.21) as you contemplate the expected ECG picture for each of the above entities.
10.23 Acute RCA Occlusion
As we discussed in Section 10.17 the RCA (Right Coronary Artery) serves as a dominant vessel
i n ~85% of patients with a normal coronary circulation. This anatomic picture is schematically
illustrated in Panel A of Figure 10.23-1 in which the RCA can be seen to supply the RV ( Right
Ventricle) before transitioning to the PDA (Posterior Descending Artery). The PDA then continues
along the undersurface of the heart as it supplies the posterior and inferior walls of the left ventricle
(unlabeled dotted vessel arising from the RCA in Panel A). Thus, the RCA (and its branches)
will normally supply the right ventricle and inferior plus posterior walls of the left ventricle.
In contrast to this picture of a right-dominant circulation in Panel A the remaining ~15% of
patients have a left-dominant circulation. In this case it is the LCx (Left Circumflex Artery)
rather than the RCA that supplies the posterior and inferior walls of the left ventricle (Panel B).

Figure 10.23-1: Comparison of a right-dominant circulation (Panel A) which is the most common
situation (~85% of patients) vs a left-dominant circulation (Panel B) in which the LCx (rather
than the RCA) supplies the posterior and inferior walls of the left ventricle (reproduced from Figure
10.17-1).
ECG findings arising from acute RCA occlusion will vary depending on: i) Whether the patient has
a dominant right or left circulation; ii) The relative site of occlusion within the RCA (ie, proximal or
more distal occlusion) ; iii) Any prior infarctions that may have occurred; and iv) The status of the
collateral circulation. For simplicity We describe expected ECG findings assuming no prior
infarctions and no alteration in collateral circulation.
In the 80-90% of patients with a right-dominant circulation (Panel A in Figure 10.23-1) the
most typical manifestation of acute RCA occlusion is ST elevation in all 3 inferior leads
(II,III,aVF) = acute inferior MI.
Acute RV (Ri ght Ventricular) MI is likely to be seen when there is proximal RCA
occlusion (Section 10.18). More distal RCA occlusion may spare much of the right ventricle.
PEARL: Proximal RCA occlusion is suggested when ST elevation in lead III is more than in
lead II (especially if there is marked ST depression in lead aVL). This picture is seen in
Figure 10.23-2. In contrast a left-dominant LCx occlusion is suspected when there is
inferior MI with less ST elevation in lead III and less ST depression in lead aVL (especially if
there is significant ST elevation in leads V5,V6).
Posterior MI is commonly seen with RCA occlusion (because the RCA most often supplies
both inferior and posterior walls of the LV). Posterior MI may also be seen with LCx occlusion
IF there is a left-dominant circulation (Section 10.17). In either case there will usually be
ECG evidence of inferior MI when there is posterior MI. NOTE: The converse is not
necessarily true in that there may be acute inferior MI without associated posterior MI.
Beyond-the-Core: Rarely isolated posterior MI may occur (if the occluded artery is at the
level of the PDA). Bottom Line: We look for associated acute posterior MI when we see ECG
evidence of acute inferior MI.

Figure 10.23-2: Acute infero-postero MI from acute proximal RCA occlusion. Note ST elevation
in lead III > II with marked reciprocal ST depression in lead aVL. Posterior involvement is
suggested by the ST depression in lead V2 (positive mirror test). There may also be acute RV
involvement (See text).
Additional Points regarding Acute RCA Occlusion: Keeping in mind the areas of the heart most
commonly supplied by the RCA facilitates recognizing acute occlusion of this vessel (Figure 10.232):
Lead III is more rightward (at +120 degrees) than lead II (at +60 degrees). As a result
acute occlusion of the RCA generally produces more ST elevation in lead III than in lead II
(Fig. 10.23-2).
The electrical perspective of lead aVL is virtually opposite that of lead III. As a result the
shape of the reciprocal ST depression in Lead aVL often looks like the mirror-image of the
ST elevation in lead III. ST-T wave changes in aVL are typically marked when there is
proximal RCA occlusion and are generally more prominent than in lead I.
Posterior MI is suggested in Figure 10.23-2 because of the positive Mirror Test for lead
V2 (ie, flipping lead V2 over would result in a Q wave with slight-but-real hyperacute ST
elevation in this lead). We discuss the Mirror Test in more detail beginning in Section
10.33.
NOTE: Associated posterior MI may be seen when acute inferior MI results from either RCA
occlusion or a left-dominant LCx occlusion. However, associated acute RV (Right
Ventricular) MI localizes the culprit artery to the RCA because the right ventricle is not
supplied by the LCx (Left Circumflex Artery). We discuss use of right-sided leads and the ECG
diagnosis of acute RV MI in Sections 10.31 and 10.32.
Beyond-the-Core: We suspect that there may also be associated acute RV MI in Figure 10.23-2
because the ST-T wave in lead V1 is relatively flat. Normally, with acute posterior MI
there is similar-appearing ST-T wave depression in each of the anterior leads (V1,V2,V3). In
contrast, when there is also acute RV MI right-sided ST elevation in lead V1 cancels out
some of the ST depression that would have been seen from the posterior infarction. Bottom
Line: Suspect associated acute RV MI with acute infero-postero MI from proximal RCA
occlusion IF you see ST segment coving with slight ST elevation in lead V1. The finding of a
flat (instead of depressed) ST segment in lead V1 (as is seen in Figure 10.23-2) suggests that
there may be some canceling out of V1 ST depression by acute RV ST elevation. IF important to

know right-sided leads would help answer this question (Section 10.31).
Clinical Note It is well to remember that 2nd-degree AV Block, Mobitz Type I (Section
02.72) is most often seen in association with acute RCA occlusion (since the RCA usually
supplies the AV nodal artery). That said Mobitz I may occasionally be seen with acute LCx
occlusion of a left-dominant circulation (in which case the AV nodal artery will usually be
supplied by the LCx).

10.24 Acute LMain Occlusion

As emphasized in Section 09.40 Most patients with acute LMain (Left Main Coronary Artery)
occlusion do not survive. As a result this entity is not often seen and unlikely to be appreciated
clinically. Rapid deterioration with patient demise due to cardiogenic shock is the usual result unless
acute LMain occlusion can be immediately recognized and immediately acted on.
In those rare instances when acute LMain occlusion is captured on ECG rather than the
picture of diffuse ST depression that is characteristic of severe LMain disease (Section 09.40)
there should be diffuse precordial ST elevation in association with ST elevation in lead
aVR (Figure 10.24-1).
PEARL: Distinction between acute LMain vs proximal LAD occlusion may be suggested on ECG by
the relative amount of ST elevation seen in lead aVR compared to lead V1.
Think LMain occlusion when ST elevation in lead aVR > V1.
Think proximal LAD occlusion when ST elevation in lead V1 > aVR.

Figure 10.24-1: ECG from an acutely decompensating patient with new-onset chest pain (reproduced
from Figure 09.40-2). New bifascicular block (LAHB/RBBB) in context with dramatic ST-T wave
changes seen here (including ST elevation in lead aVR and in lead V1) suggest acute occlusion
of either the proximal LAD or the LMain coronary artery. Given that ST elevation in lead aVR is at
least as much as in lead V1 (red arrows) We suspect acute LMain occlusion (See text).

Remember Most patients with acute LMain occlusion die before they reach the hospital. It will
therefore be rare indeed that you have occasion to evaluate the ECG of such patients. In such rare
instances the clinical presentation will usually be obvious: an acutely ill patient with cardiac
decompensation from impending cardiogenic shock.
T he ECG in Figure 10.24-1 highlights what to look for: i) Conduction defects (such as
RBBB/LAHB that is seen here); ii) Marked ST elevation in precordial leads (and often also in
lead aVL) ; iii) Marked reciprocal ST depression in other lead areas; and iv) ST elevation in
lead aVR that is at least as much (if not more) than the ST elevation in lead V1.

10.25 Acute LAD Occlusion

As discussed in Section 10.17 the LMain (Left Main Coronary Artery) is typically a short vessel
(10mm) that then bifurcates into the LAD (Left Anterior Descending Artery) and the LCx (Left
Circumflex Coronary Artery). This anatomic picture is schematically illustrated in Panel A of
Figure 10.25-1 in which the LAD can be seen to run along the anterior epicardial surface of the
heart on its path toward the cardiac apex.
The LAD generally supplies: i) the anterior wall of the heart (via its diagonal branches); ii) the
cardiac apex; and iii) a major portion of the conduction system (via septal perforators that run
vertically down through the septum).

Figure 10.25-1: Comparison of normal LAD circulation (Panel A) vs LAD circulation with a
wrap-around variant (Panel B). In this latter situation the RCA is a smaller vessel. To
compensate the LAD (Left Anterior Descending Artery) will wrap around the apex to supply
the inferior as well as anterior wall of the heart (reproduced from Figure 10.17-1).
ECG findings arising from acute LAD occlusion may vary depending on: i) The relative site of
occlusion within the LAD (ie, proximal to septal perforators and the 1st diagonal or more distal
occlusion); ii) Any prior infarctions that may have occurred; iii) Presence of any anatomic variants
(such as a wrap-around LAD circulation) ; and iv) The status of the collateral circulation. For
simplicity We describe expected ECG findings in this Section 10.25 assuming no prior

infarctions; no alteration in collateral circulation; and no anatomic variants.

I n Section 10.26 We put forth a reminder that not all that elevates ST segments in the
anterior leads is anterior infarction.
In Section 10.27 We discuss the ECG picture of acute LAD occlusion when there is an LAD
wrap-around variant (Panel B).
Acute LAD occlusion leads to acute anterior MI. This may be extensive and also involve the
lateral wall.
The most typical ECG manifestation of acute LAD occlusion is ST elevation in anterior leads
(usually in 2 leads between V1-to-V4).
PEARL: ST elevation in lead aVL may provide an invaluable clue to the location of the acutely
occluded coronary artery. According to a study by Birnbaum et al (Am Heart J 131:38, 1996):
Suspect acute LAD occlusion proximal to the 1st Diagonal IF in addition to ST elevation in
aVL there is also ST elevation in leads V2-through-V5. This is the most common situation
when there is ST elevation in lead aVL.
Suspect 1st Diagonal branch occlusion IF in addition to ST elevation in aVL there is ST
elevation in lead V2 (but not in V3,V4,V5).
Suspect LCx occlusion (especially of the 1st obtuse marginal branch) IF there is ST
elevation in aVL but not in lead V2 (and not in other anterior leads).
NOTE: Anterior ST elevation without ST elevation in lead aVL suggests more distal LAD
occlusion after takeoff of the 1st Diagonal.
PEARL: In addition to recognizing ST elevation in lead aVL with marked anterior ST elevation
there are 2 additional ways to identify patients at high risk of impending proximal LAD
occlusion. These are: i) Recognition of Wellens Syndrome (Section 10.54); and ii) Recognition
of DeWinter T Waves (Section 10.57).
Apply these concepts to the ECG shown in Figure 10.25-2 obtained from a patient with new-onset
chest pain. There is obvious evidence of a large acute anterior STEMI (marked anterior ST
elevation).
Is the ECG in Figure 10.25-2 likely to indicate acute LMain occlusion or is the culprit
artery more likely to be the LAD?
If you suspect acute LAD occlusion Is the occlusion more likely to be proximal or distal
LAD in location?

Figure 10.25-2: ECG obtained from a patient with new-onset chest pain. An obvious acute anterior
STEMI is present. What is the likely culprit artery? Is the lesion likely to be proximal or distal?
(See text).
Answer to Figure 10.25-2: The rhythm is sinus. The most remarkable finding on this ECG is the
marked ST elevation in leads V1-through-V5. There is also ST elevation in lead aVL. Subtle ST
depression is present in the inferior leads as a reciprocal change.
This ECG and the clinical picture is not suggestive of acute LMain occlusion because: i) Acute
LMain occlusion is rare. Most patients die before reaching the hospital; and ii) ST elevation is
marked in lead V1 and absent in lead aVR. This strongly suggests occlusion of the LAD and not
the LMain (Section 10.24).
We strongly suspect acute proximal LAD occlusion for the ECG picture shown in Figure
10.25-2. This is because: i) Anterior ST elevation is extensive and marked in amount; ii) There
i s significant ST elevation in lead aVL; and iii) ST elevation is significant in lead V1 and
absent in lead aVR.
Additional Clinical Notes Regarding Proximal LAD Occlusion: As noted earlier the major
branches of the LAD are: i) the septal perforators; and ii) one or more diagonal branches.
Patients with acute proximal LAD occlusion (that occurs before takeoff of the 1st septal
perforator) are at high risk of conduction system damage (Mobitz II 2nd-degree AV block;
anterior or posterior hemiblock; BBB).
Beyond-the-Core: In addition to the ECG signs of ST elevation in lead aVL and ST elevation in
lead V1 > aVR the finding of new RBBB (especially if a QR pattern is seen in lead V1
instead of an rSR pattern) makes it extremely likely that there is significant septal damage.
NOTE: In many ways a very proximal LAD lesion is almost a left-main equivalent, in
that extent of myocardial damage is large and risk of conduction system involvement is high.
Acute proximal LAD occlusion has been known as a widow-maker lesion because of the
understandably high mortality associated with this event. This explains the urgency of
recognizing the uncommon but foreboding ECG signs of Wellens syndrome (Section 10.54)

and DeWinter T waves (Section 10.57).

10.26 Anterior ST Elevation: Not Always an Anterior MI

In the interest of clinical relevance We feel it important to issue a reminder that the ECG finding
of anterior ST elevation is not always due to acute anterior STEMI. Other Causes of anterior ST
elevation that may need to be considered include: i) Early repolarization (discussed in detail in
Section 09.19 and Section 09.23); ii) Pericarditis iii) LVH (See below in Figure 10.26-1); iv) LBBB;
v) Takotsubo; and vi) LV aneurysm.
Clinical correlation and comparison with prior tracings may sometimes be needed to
distinguish such patterns from acute injury.

Figure 10.26-1: ECG obtained from a patient with longstanding hypertension illustrating ST
elevation not due to acute MI (reproduced from Figure 08.9-2) . IF this patient were to be having
chest pain at the time this ECG was recorded it might be easy to misinterpret the several
millimeters of ST elevation in leads V2,V3 as indicative of a new event. That said it is far more
likely that the anterior ST elevation seen in the blow-up insert is an infarct mimic and merely
reflects the reciprocal of the LV strain pattern seen in lead V6 because: i) the dramatic increase in
QRS amplitude and typical strain ST-T wave morphology in lead V6 shouts out that the patient
has LVH and not an MI; ii) ST elevation is essentially limited to 2 leads; and iii) the shape of ST
elevation in leads V2,V3 is concave up and the mirror-image reciprocal of ST-T wave depression in
V6 (vs ST coving that would be more characteristic of acute injury). That said it may sometimes
be difficult to distinguish between simple LVH vs LVH with superimposed acute ST elevation.
10.27 Acute Occlusion of an LAD Wrap-Around
In Sections 10.17 and 10.25 We discussed normal coronary anatomy of the LAD (Left Anterior
Descending Artery). This anatomic picture is schematically illustrated again in Panel A of Figure
10.27-1 in which the LAD is seen passing along the anterior epicardial surface of the heart on its
path toward the cardiac apex.

The LAD typically supplies: i) the anterior wall of the heart (via its diagonal branches); ii) the
cardiac apex; and iii) a major portion of the conduction system (via septal perforators that run
vertically down through the septum).
Approximately 5-10% of normal subjects have an anatomic wrap-around LAD variant
circulation (Panel B). In such cases the LAD is a larger and longer vessel, to the point of
extending beyond the cardiac apex and wrapping around to supply the undersurface of the
heart (dotted vessel extending underneath the apex from the LAD in Panel B of Figure 10.271). In patients with this anatomic variant the LAD provides the principal blood supply to both
anterior and inferior walls of the heart.

Figure 10.27-1: Comparison of normal LAD circulation (Panel A) vs LAD circulation with a
wrap-around variant (Panel B). In this latter situation (which is seen in ~5-10% of normal
subjects) the RCA is a smaller vessel. To compensate the LAD (Left Anterior Descending
Artery) will wrap around the apex to supply the inferior as well as anterior wall of the heart
(reproduced from Figure 10.25-1).
An ECG picture that has at times been confusing is simultaneous presence of acute ST elevation in
both anterior and inferior leads. This is because one normally associates acute inferior ST elevation
with RCA occlusion whereas acute anterior ST elevation is associated with LAD occlusion. A
study by Sadanandan et al (Am Heart J 146:653-661, 2003) provides insight to anatomic explanation
of this unexpected ECG finding. We integrate findings from the Sandanandan study while emphasizing
the following clinical points:
Approximately 15% of patients with acute anterior ST elevation also manifest inferior ST
elevation.
Surprisingly about half of these patients with acute anterior and inferior ST elevation are
found on cath to have proximal RCA rather than LAD occlusion as the culprit artery.
Presumably this is a result of RCA marginal branches extending over to supply part of the
anterior wall or some other collateralization pattern (Section 10.18).
ECG Clues suggesting the culprit artery is the proximal RCA rather than a wrap-around
LAD are: i) ST elevation in lead III > lead II; ii) ST elevation in lead V1 > lead V3 (as one
would expect if there was acute RV involvement); and iii) Lack of progression of ST elevation

as one moves from lead V1-to-V4 (with LAD occlusion ST elevation tends to become more by
leads V3,V4).
In contrast a wrap-around LAD should be suspected as the culprit artery IF: i) ST
elevation in lead II > lead III; ii) There is only minimal ST elevation in lead V1; and iii) There
i s progressive and persistent ST elevation as one moves from lead V1 toward leads V3,V4
(Figure 10.27-2).
Surprisingly patients with anterior STEMI from acute occlusion of a wrap-around LAD
d o not necessarily have large infarctions. This is because the site of acute occlusion is not
necessarily proximal, but may instead be in the mid- or distal-LAD.
Beyond-the-Core: Another entity to consider for the presence of acute simultaneous inferior and
anterior ST elevation is Takotsubo Cardiomyopathy which may produce an ECG picture
similar to that shown in schematic Figure 10.27-2. Cardiac catheterization is sometimes needed
to make this diagnosis (See Section 10.61).

Figure 10.27-2: Schematic ECG with both inferior and anterior ST elevation in a patient with newonset chest pain. The culprit artery could be either a proximal RCA or wraparound LAD lesion.
That said 3 clues that the culprit artery is a wraparound LAD in this case are: i) ST
elevation in lead III is less than in lead II; ii) ST elevation in V1 is minimal; and iii) ST elevation
progresses and persists as one moves from V1 toward V3,V4 (See text).
10.28 Acute LCx (Left Circumflex) Occlusion
As emphasized in Section 10.23 in most subjects (~85% of the population) the RCA (Right
Coronary Artery) is a dominant vessel. As such the RCA normally supplies the RV ( Right
Ventricle) on its way as it transitions to the PDA (Posterior Descending Artery). The PDA then
continues along the undersurface of the heart as it supplies the posterior and inferior walls of the left
ventricle (unlabeled dotted vessel arising from the RCA in Panel A of Figure 10.28-1).
The LCx (Circumflex) Artery wraps around the lateral free wall of the LV ( Left Ventricle).
In most patients (ie, when the RCA is dominant) the LCx becomes a relatively small vessel
after giving rise to one or more obtuse marginal branches that supply the lateral free wall
(dotted vessels arising from the LCx in Panel A).

In contrast to the situation in Panel A (in which the RCA is dominant) between 10-20% of
patients have a left-dominant circulation (Panel B). In this case the RCA is a smaller
vessel. To compensate the LCx (Left Circumflex Artery) is larger and gives rise to the PDA
(large unlabeled dotted vessel arising from the LCx in Panel B). In a left-dominant
circulation the inferior and/or posterior wall of the LV is supplied by the LCx (Panel B).

Figure 10.28-1: Comparison of a right-dominant circulation (Panel A) which is the most common
situation (~85% of patients) vs a left-dominant circulation (Panel B) in which the LCx (rather
than the RCA) supplies the posterior and inferior walls of the left ventricle (reproduced from Figure
10.23-1).
ECG findings arising from acute LCx occlusion will vary depending on: i) Whether the patient has a
dominant right or left circulation; ii) The relative site of occlusion within the LCx (ie, proximal or
more distal occlusion) ; iii) Any prior infarctions that may have occurred; and iv) The status of the
collateral circulation. For simplicity We describe expected ECG findings assuming no prior
infarctions and no alteration in collateral circulation.
Acute occlusion of the Circumflex (LCx) artery leads to lateral MI. This is manifest on ECG
by ST elevation in one or more of the lateral leads.
Despite assessment of the LV lateral wall by no less than 5 of the 12 leads (I,aVL; V4,V5,V6)
the high-lateral wall may not be well visualized. This part of the LV is typically supplied by
the 1st Diagonal branch of the LAD (and not by the LCx). Thus Lead aVL really provides
more information about the site of LAD occlusion (proximal or distal to the 1st Diagonal
branch) than it does about the LCx (Section 10.25).
The other high-lateral lead is Lead I. In general lead I provides little independent
information regarding the site of acute occlusion. It may be best to think of lead I as providing a
similar electrical viewpoint as lead aVL, albeit ECG changes in lead I are usually less
prominent than in aVL.
The lateral leads that most consistently assess the part of the heart supplied by the LCx are leads
V5,V6. Therefore ST elevation in leads V5,V6 most often suggests acute LCx occlusion.
Neighboring lead V4 may manifest similar findings as V5,V6 but by itself is of little help in
localizing the site of acute occlusion.

NOTE: Exceptions exist in which ST elevation in leads V5,V6 may not necessarily indicate
LCx occlusion. This may occasionally occur in patients with large PLA (Postero-Lateral
Artery) branches that arise from the PDA branch of the RCA and supply the lateral wall or in
patients with an unusual pattern of collateral circulation. Otherwise acute ST elevation in
leads V5,V6 = acute LCx occlusion.
Clinical Synthesis IF there is ST elevation in high-lateral leads (ie, lead I and/or lead aVL)
but there is no ST elevation in any of the lateral precordial leads (V4,V5,V6) the site of acute
occlusion is probably in the LAD. This premise will be supported by the presence of ST elevation in
one or more of the anterior leads (Section 10.25).
IF on the other hand, there is ST elevation in lead I and/or aVL and ST elevation in lateral
precordial leads (V4,V5,V6) but not in any anterior leads then acute LCx occlusion is the
likely culprit artery.
Beyond-the-Core: Recently MRI correlations with cardiac anatomy, coronary artery
distribution, and ECG findings suggest that traditional ECG terminology is not as accurate as
previously thought (Bayes de Luna et al: Circulation 114:1755, 2006). Therefore acute ECG
changes isolated to the high-lateral leads (= leads I,aVL) appear to more accurately
reflect acute infarction in the mid-anterior wall rather than in the lateral wall of the heart.
These MRI correlations are consistent with the Clinical Synthesis we propose above.
ECG findings differ with acute LCx occlusion in a left-dominant system. As emphasized in Panel
B of Figure 10.28-1 the LCx is a larger vessel in the 10-20% of patients with a left-dominant
circulation, in which case the LCx supplies the inferior and posterior walls of the LV as well as the
lateral wall.
Suspect Circumflex dominance IF i) you see infero-postero-lateral MI; and ii) there is
significant ST elevation in leads V5,V6.
Consider the situation in Figure 10.28-2 obtained from a patient with new-onset chest pain.
Interpret this ECG. Localize the area(s) of acute infarction.
Which coronary artery is likely to be acutely occluded?

Figure 10.28-2: Acute infero-postero-lateral MI. This distribution on ECG suggests a left-dominant
circulation with acute LCx occlusion. Findings against RCA involvement are: i) Less ST elevation
in lead III than lead II; ii) minimal ST depression in aVL; and iii) ST elevation in V5,V6 (See text).
Answer to Figure 10.28-2: The rhythm is sinus. Intervals and axis are normal. No chamber
enlargement. Regarding Q-R-S-T Changes:
Small q waves are seen in leads II,III,aVF; and V5,V6.
Transition is normal (occurs between lead V2-to-V3) albeit the R wave is a bit taller-thanexpected in leads V2,V3.
There is subtle-but-real ST elevation in each of the inferior leads (II,III,aVF) with
suggestion of hyperacute T waves (especially in lead II). A similar pattern of slight J-point ST
elevation is seen in leads V5,V6 with suggestion of hyperacute T waves in these leads.
There is marked ST depression in leads V1-thru-V4.
Impression: Sinus rhythm with acute infero-postero-lateral STEMI (ST Elevation Myocardial
Infarction). The cath lab should be activated. We suspect acute LCx (Le f t Circumflex Artery)
occlusion in a left-dominant system.
Although q waves in the infero-lateral leads are small and narrow these are the very same
leads that manifest ST elevation with hyperacute T waves. While these might possibly be
normal septal q waves it is far more likely that they reflect ongoing acute infarction. In any
case We should know the answer shortly ( if the q waves become larger as the infarct
evolves or if they resolve after reperfusion).
The ECG picture in leads V1,V2,V3 strongly suggests associated acute posterior infarction.
We say this despite the reality that none of the standard 12 leads directly visualize the posterior
wall of the LV ( Left Ventricle). As will be discussed in Section 10.35 t o diagnose acute
posterior MI, one either has to: i) Obtain additional leads that directly visualize the posterior
wall (= leads V7,V8,V9); or ii) Perform a mirror test (turning the tracing over and holding
it up to the light which provides a mirror-image view of the anterior leads Figure
10.28-3).

Figure 10.28-3: Diagnosis of acute posterior MI is made from Figure 10.28-2 by applying the
mirror test (ie, turning the tracing over and holding it up to the light). Doing so (TOP tracing)
shows the anterior ST depression and relatively tall R waves in V2,V3 of the LOWER tracing
become Q waves and ST elevation when the tracing is flipped over (See within the red rectangle of
the TOP tracing).

Figure 10.28-2: Localizing the Culprit Artery Given the presence of acute inferior infarction
without anterior ST elevation in Figure 10.28-2 the culprit artery is almost certainly either the
RCA (Right Coronary Artery) or the LCx (Left Circumflex Coronary Artery).

As discussed in Section 10.23 acute proximal RCA occlusion would be suggested by: i) ST
elevation in lead III > lead II; ii) marked reciprocal ST depression in lead aVL that is more than
the ST depression in lead I; and iii) ECG evidence of acute RV MI (the LCx does not supply the
right ventricle). While on occasion acute RCA occlusion may produce ST elevation in leads
V5,V6 (ie, if there is a large posterolateral branch arising from the PDA branch of the RCA )
ST elevation in lead V6 should not be more than in lead III.
In Figure 10.28.2 (reproduced in the LOWER tracing of Fig. 10.28-3) We strongly suspect
the culprit artery is the LCx in a left-dominant system because: i) ST elevation in lead III
is less than in lead II; ii) There is no ST elevation in lead aVL; iii) There is no hint of acute RV
involvement (ST depression is prominent in V1 whereas wed expect either a flat or coved
ST segment with slight elevation in V1 if there was associated RV involvement); and iv) There
is ST elevation in V5,V6 and this ST elevation in lead V6 is clearly more than it is in lead III.

10.29 Acute Right Ventricular Infarction

10.30 Acute RV MI: Hemodynamics

A substantial proportion of patients with acute inferior MI also manifest RV involvement. This is
especially true when there is proximal RCA occlusion as suggested by the ECG signs of: i) ST
elevation in lead III > lead II; and ii) marked ST depression in lead aVL that is more than in lead I
(Section 10.23).
The importance of recognizing RV involvement with inferior MI relates to its different
hemodynamics (nitroglyercin not advised because it may excessively lower BP; volumedependent hypotension that often responds well to IV fluid infusion; frequent need for
extremely close ICU monitoring).
Many patients with acute inferior MI from RCA occlusion have at least some degree of RV
involvement. This should not be unexpected given normal distribution of the RCA that
typically supplies both the RV as well as the inferior wall of the LV. That said, even when there
is some RV involvement LV involvement often predominates. The KEY is to identify those
patients at high risk of decompensation from altered hemodynamics. Clinically this may be
suggested by: i) ECG evidence of a large acute RV MI (Section 10.32); ii) The combination of
inferior MI with borderline or low BP especially if signs of left-sided heart failure (ie,
rales) are absent; and iii) A hypotensive response to nitroglycerin especially in patients with
acute inferior MI.
Clinical NOTE: Some emergency systems eliminate all use of NTG (nitroglycerin) in any
patient with acute inferior MI. While realizing the rationale for this practice (possibility of
associated RV involvement with risk of inducing hypotension) global elimination of NTG
for all patients with inferior MI is not necessarily needed or advisable. BOTTOM Line: We
suggest the following: i) Do not use NTG in acute MI patients when BP is low (or relatively
low) especially when hypovolemia is suspected; ii) Be especially cautious in patients
suspected of having significant RV involvement; iii) Careful titration of IV NTG may be
indicated in selected patients with adequate BP. In contrast use of sublingual NTG in such
patients may be ill-advised because of inability to take a sublingual dose back; and iv) You
should follow the standard-of-care protocols put forth at your institution.

10.31 Acute RV MI: Use of Right-Sided Leads

Definitive ECG diagnosis of acute RV (Right Ventricular) MI is made by use of right-sided ECG
leads. A right-sided ECG is performed using similar anatomic placement of precordial leads
except that chest leads are positioned on the right side of the chest (Figure 10.31-1).
Right-sided ECG leads are labeled V1R,V2R,V3R,V4R,V5R,V6R.

When obtaining leads V1R and V2R one simply reverses the anatomic lead position of
normal leads V1 and V2. That is normally placed lead V1 will be the equivalent of rightsided lead V2 (V2R). Similarly normally placed lead V2 will be the equivalent of rightsided lead V1 (V1R). This explains why normally-placed lead V1 is really a right-sided lead
(Section 10.32).

Figure 10.31-1: Anatomic landmarks for normal (left-sided) precordial lead placement (Panel A
which was previously discussed in Section 03.6). To obtain right-sided precordial leads (Panel B)
similar anatomic landmarks are used, but leads are placed on the right side of the chest (See text).
10.32 Acute RV MI: Making the Diagnosis by ECG
As stated ECG diagnosis of acute RV (Right Ventricular) MI is made by use of right-sided ECG
leads. The following findings should be looked for:
ECG evidence of associated proximal RCA occlusion (ie, acute inferior MI with ST
elevation in lead III > II and marked ST depression in lead aVL).
Progressively increasing ST elevation as one moves across right-sided leads. Right-sided ST
elevation is often maximal in lead V4R.
ST segment coving or straightening (especially if there is slight ST elevation) in lead V1 in
association with acute infero-postero MI (Figure 10.32-1).

Figure 10.32-1: Schematic ECG showing acute infero-postero MI. Proximal RCA occlusion is
suggested by ST elevation in lead III > lead II with marked reciprocal ST depression in lead aVL that

is more than in lead I. Acute RV MI is suggested by ST coving in lead V1 and confirmed by

obtaining right-sided leads (Note ST elevation in V2R through V4R).
KEY Point: Use of Lead V1 in Figure 10.32-1: Although right-sided leads V2R,V3R,V4R confirm
the diagnosis of acute RV MI in Figure 10.32-1 these extra leads are not essential for making the
diagnosis:
As illustrated in Figure 10.31-1 lead V1 is really a right-sided lead. Anatomic landmarks for
placement of lead V1 are the same as they are for placement of lead V2R.
T h e schematic ECG in Fig. 10.32-1 shows ac ut e infero-postero MI. Acute posterior
involvement is suggested by the shape of ST depression in leads V2,V3 (= positive mirror
test as will be discussed in Section 10.35). When there is simply posterior infarction
lead V1 will manifest a similar shape of ST depression as is seen in leads V2,V3. However, IF
there is also acute RV MI then the ST depression that should have been seen in lead V1 (as
a result of the posterior MI) will be cancelled out by the ST elevation in lead V1 from the
acute RV MI. BOTTOM Line: The fact that the ST segment in lead V1 of schematic Figure
10.32-1 is coved (if not slightly elevated instead of being depressed) strongly suggests that
in addition to acute infero-postero MI, there is also acute RV MI. This is different than the
situation with acute anterior MI in which case not only lead V1, but also other anterior leads
will manifest ST elevation (V2,V3,V4).
Clinical Notes: Beyond-the-Core: Opinions vary as to the need for additional leads to make the
diagnosis of acute RV MI. Depending on the ECG recording system used and experience of the
person recording the 12-lead tracing a certain amount of additional time will be required to obtain
more than the standard 12 leads. This time may be minimal (seconds) or it may take a precious
minute or more. You will not know how long it takes to get right-sided lead(s) unless and until you
actually time yourself under real-life circumstances.
Our Bias: We prefer to start with 12 leads. Much (most) of the time 12 leads are all that
will be needed in order to determine what you need to know to optimally manage the patient.
That said We fully acknowledge that there are times when additional leads may be extremely
helpful.
Clearly, a balance must be struck between urgency of the situation How Long it will take to
obtain additional leads and whether this time is really worth what youll actually learn from
getting more leads. For example IF there is obvious acute proximal RCA occlusion on initial
ECG obtained by EMS providers in a prehospital setting there is little to learn that will
change management by spending extra time prior to transport in recording right-sided leads (ie,
the cath lab will need to be activated regardless).
In a more stable setting when there is time to obtain additional leads the most sensitive ECG
indicator of acute RV MI is the presence of 1mm ST elevation in lead V4R. This finding may
be transient so right-sided leads should be obtained as early as feasible when looking for
RV MI.

Consider the situation in Figure 10.32-2 obtained from a patient with new-onset chest pain. Note
that right-sided leads = V3R and V4R have been obtained (and are seen instead of leads V3,V4 on
this 12-lead tracing).
Localize the area(s) of acute infarction.
What is the location of acute coronary occlusion?

Figure 10.32-2: Acute infero-postero MI. In addition ST coving with slight elevation in lead V1
(blue blow-up insert) suggests acute RV MI. This is supported by the presence of marked ST
elevation in right-sided leads V3R and V4R (red blow-up inserts). Posterior MI is diagnosed by the
positive mirror test in lead V2 (See text).

Answer to Figure 10.32-2: The rhythm is sinus bradycardia. There is marked ST elevation in each of
the inferior leads. ST elevation in lead III > lead II suggesting acute proximal RCA occlusion.
This is supported by the finding of marked ST depression in lead aVL that is more than in lead I.

Acute posterior MI is suggested by the shape of ST depression in lead V2 (positive

mirror test).
Acute RV MI is suggested by ST segment coving (with a hint of ST elevation) in lead V1 in the
presence of ST depression in lead V2.
Use of right-sided leads V3R and V4R confirms the diagnosis of acute RV MI. Note how
marked ST elevation is in leads V3R and V4R. Given the presence of sinus bradycardia
marked inferior ST elevation with equally marked reciprocal ST depression and large
associated acute RV MI this patient is likely to manifest volume-dependent hemodynamics,
and will clearly require intensive care monitoring.

10.33 Posterior MI: Use of the Mirror Test

One area of the heart that is not well visualized by any of the 12-leads of a standard ECG is the
posterior wall of the left ventricle. This clinical reality makes it challenging to recognize new or old
posterior infarction.
Use of the Mirror Test facilitates recognizing ECG changes of acute posterior MI from the
standard 12-lead tracing (Figure 10.33-1).

Figure 10.33-1: The Mirror Test. None of the standard 12 leads of an ECG directly visualize the
posterior wall of the left ventricle. As a result indirect visualization of the opposite (= anterior)
wall may be used to provide insight regarding acute posterior changes that may be ongoing. Anterior
leads V1,V2,V3 (within the red rectangle) are used in the mirror test (See text).
10.34 BEYOND-the-Core: Is there Truly a Posterior Wall?
Recently MRI correlations with cardiac anatomy, coronary artery distribution, and ECG findings
suggest that traditional ECG terminology is not as accurate as previously thought (Bayes de Luna et
al: Circulation 114:1755, 2006 ). Thus, the anatomic relationship of the posterior wall is in
reality not as directly posterior as depicted in Figure 10.33-1. Instead what traditionally has been
thought of as posterior wall involvement is more accurately referred to as involvement of part of
the lateral LV wall.
A new, more anatomically accurate terminology has been proposed. This would change

reference to the posterior LV wall to the lateral wall instead.

MY BIAS: Realizing the potential tremendous benefit MRI correlations may provide toward
more accurate anatomic localization traditional ECG terminology appears entrenched at
the current time. Rather than confusing the issue with a novel ECG terminology that is not yet in
general use We favor continued use of the term posterior infarction (with continued
distinction between lateral vs posterior walls of the heart). We devote Sections 10.33 through
10.37 to recognition of posterior wall MI according to the traditional terminology that we use
throughout this ePub. We realize that at some point in the future this terminology may change.

10.35 FIGURE 10.35-1: Applying the Mirror Test

We illustrate application of the Mirror Test in schematic Figure 10.35-1. The test is based on the
principle that anterior leads provide a mirror image of electrical activity occurring over the
posterior wall of the LV. We emphasize the following points:
Most patients with acute posterior MI also manifest ECG evidence of acute inferior MI.
This is seen in the lower tracing (Panel B) of Figure 10.35-1 in which there are small q
waves and ST segment elevation in each of the inferior leads (II,III,aVF). In support of the
diagnosis of acute inferior infarction is reciprocal ST depression in leads I and aVL.
One looks for a tall R wave in lead V1 (or at least taller-than-expected R waves in V2, V3)
plus a peculiar shape of anterior ST depression. This is well seen in leads V1,V2,V3 within
the red rectangle in Panel B.
Flipping the tracing over and holding it up to the light (ie, performing the mirror test) reveals
that what was ST depression and a disproportionately tall R wave in anterior leads (in Panel
B) becomes a Q wave with worrisome ST elevation = a positive mirror test (Panel A).
This strongly suggests that in addition to acute inferior MI there is also ongoing acute
posterior MI.

Figure 10.35-1: Positive mirror test as seen when the upright initial ECG in Panel B is flipped
over (Panel A) and held up to the light. NOTE: The more ST depression you see in anterior leads
V1,V2,V3 (Panel B) the more extensive the infero-postero MI is likely to be!
NOTE: The mirror test is nothing more than a visual aid that we have conceived to facilitate
recognition of posterior infarction (Grauer K, circa 1983). We have already seen application of this
visual aid to facilitate recognition of the peculiar shape of anterior ST depression in the example of
acute infero-postero-lateral MI that was presented in Figure 10.28-3 which we reproduce below
in Figure 10.35-2.

Figure 10.35-2: Illustration of a positive mirror test in this patient with acute infero-lateralpostero MI due to acute occlusion of a dominant LCx (reproduced from Figure 10.28-3). The
original upright ECG is shown in the lower tracing (Panel B). Note ST elevation in leads II,III,aVF
and in leads V5,V6 consistent with acute infero-lateral MI. Diagnosis of associated acute
posterior MI is made by applying the mirror test (ie, turning the tracing in Panel B over, and
holding it up to the light). Doing so (as shown for leads V1,V2,V3 within the red rectangle in Panel
A) reveals how the anterior ST depression and relatively tall R waves in leads V2,V3 of Panel B
become Q waves and ST elevation when the tracing is flipped over.
10.36 FIGURE 10.36-1: Anatomic Landmarks for Posterior Leads
An alternative approach to using the mirror test is the use of posterior leads to diagnose or
confirm diagnosis of posterior MI. These may be obtained separately incorporated into a 15-lead
ECG (which typically adds leads V4R, V8, and V9 to the standard 12 leads) or substituted for
one or more lateral precordial leads on a standard ECG.
Posterior leads most commonly include leads V7, V8, and/or V9. These leads are obtained by
continuing laterally along the same horizontal level as lead V6 in the posterior axillary line (=
lead V7) at the tip of the left scapula in the back (= lead V8) and in the left paraspinal
area in between the scapula and posterior spine (= lead V9).
Anatomic landmarks for posterior leads are shown in Figure 10.36-1. We then conclude this
segment on posterior infarction by illustrating how posterior leads are used to confirm acute
posterior MI in Section 10.37.

Figure 10.36-1: Anatomic landmarks for posterior leads. The Lead V7 electrode is placed in the
posterior axillary line at the same horizontal level as lead V6. Lead V8 is placed in the back at
the tip of the left scapula (at the same horizontal level as lead V6). Lead V9 is placed in the back
in the left paraspinal area in between the scapula and posterior spine (at the same horizontal level as
lead V6).

10.37 FIGURE 10.37-1: Isolated Posterior Infarction

As emphasized in Section 10.35 most patients with acute posterior MI also manifest ECG
evidence of acute inferior MI. This is because the RCA commonly supplies both the inferior and
posterior walls of the left ventricle. Acute occlusion of the RCA therefore commonly results in acute
infero-postero MI.
Even when there is acute occlusion of a dominant LCx artery (as in Panel B of Figure 10.35-2)
acute inferior and posterior infarction almost always occur together.
On occasion, however posterior MI may be isolated. This may occur IF the acute occlusion
is at the level of the PDA (Posterior Descending Artery). Because the PDA may arise from
either the RCA or the LCx (if there is a left-dominant circulation as described in Section
10.28) it may not be possible by ECG to identify the culprit artery on those relatively rare
occasions when there is isolated posterior MI.
Consider the ECG shown in Panel A of Figure 10.37-1 in which there is ECG evidence of
isolated acute posterior MI. Note the absence of any indication of acute inferior MI (no inferior ST
elevation and no more than minimal if any ST depression in leads I and aVL).
Acute changes in Panel A of Figure 10.37-1 are subtle. Nevertheless the R wave in leads
V2,V3 of Panel A are disproportionately tall ( especially in view of no more than a tiny r wave
in lead V1) and there is significant ST depression that is most marked in leads V2,V3,V4.
Acute posterior MI is strongly suggested by a positive mirror test (Panel C compared to
upright leads V1,V2,V3 in Panel B).
Acute posterior MI is confirmed by Q waves with ST elevation in posterior leads V7 and V9
(leads outlined in red in Panel D).

Figure 10.37-1: An example of isolated posterior MI. Diagnosis of acute posterior MI is suggested
i n Panel A by anterior ST depression (most marked in V2,V3,V4) and disproportionately tall R
waves in V2,V3. A positive mirror test in Panel C (compared to upright leads V1,V2,V3 in Panel
B) supports this diagnosis. Use of posterior leads V7 and V9 showing Q waves and ST elevation
confirms the diagnosis of posterior MI (Panel D).

10.38 Acute MI: PRACTICE Tracings

We consolidate principles covered thus far in discussion of the ECG diagnosis of Acute
MI/Ischemia with a series of Practice Tracings.
We begin with a full 12-lead tracing (Section 10.39).
There follows a series of 12 schematic ECGs (Section 10.40).
For each tracing Identify ECG findings suggestive of ischemia/infarction. IF relevant Try
to identify the culprit artery in each case.
HINT: Feel free to refer back to previous segments on:
ECG Changes of Acute Infarction (Sections 10.1 through 10.10).
Sequence of ECG Changes (Sections 10.11 through 10.15).
The Coronary Circulation (Sections 10.16 through 10.21).
Identifying the Culprit Artery (Sections 10.22 through 10.28).
Acute RV MI (Sections 10.29 through 10.32).
Posterior MI/Mirror Test (Sections 10 through 10.37).

10.39 FIGURE 10.39-1: What is the Culprit Artery?

Interpret the ECG in Figure 10.39-1 obtained from a patient with new-onset chest pain.
Can you localize the site(s) of acute infarction?
What is the culprit artery likely to be?

Figure 10.39-1: Sinus rhythm with PACs. Can you localize the site(s) of acute infarction? What is the
culprit artery likely to be? (See text).

Answer to Figure 10.39-1: Although at first glance, the rhythm irregularity apparent for the first few
beats looks like atrial fibrillation (AFib) the rhythm then becomes more regular (right after the
first lead switch to leads aVR,aVL,aVF). From this point on sinus P waves with a constant PR
interval precede QRS complexes in most leads. Thus, the rhythm is sinus with PACs. The QRS is of
normal duration, and the QT interval is not prolonged. The axis is normal (about +60 degrees). There
is no chamber enlargement. The most remarkable findings relate to QRST changes:
Q-R-S-T Changes: There are Q waves in the inferior leads (II,III,aVF) and small q waves
are also seen in lateral precordial leads V5,V6. R wave progression reveals transition to be
normal (between V2-to-V3) albeit R wave amplitude in lead V3 appears to be somewhat
taller-than-expected for this lead. The most striking findings relate to ST-T wave changes.
There is ST elevation in each of the inferior leads. ST elevation is clearly most marked in lead
III.
There is reciprocal ST depression in leads I and aVL. This ST depression is more prominent
in lead aVL.
There is also subtle-but-real J-point ST depression in leads V2,V3,V4. Finally there is
prominent T wave peaking in lead V3, and perhaps to a lesser extent in lead V4.
In view of the history of new-onset chest pain the ECG in Figure 10.39-1 is virtually diagnostic of
acute infero-postero STEMI.
As to the culprit artery We strongly suspect acute RCA occlusion because: i) there is acute
inferior MI with ST elevation in lead III > lead II; ii) there is significant reciprocal ST
depression in lead aVL that is at least as marked as in lead I; and iii) there is no ST elevation in
lateral precordial leads V5,V6 as there generally is when the culprit vessel is a dominant
LCx (Section 10.28).
Support that QRS morphology and the ST-T wave changes seen in the anterior leads of Figure
10.39-1 is suggestive of acute posterior involvement is forthcoming from a positive
mirror test (seen in Panel B of Figure 10.39-2).

Figure 10.39-2: Leads V1,V2,V3 from the ECG in Figure 10.39-1 are reproduced in Panel A. There
is a positive mirror test in Panel B in that the relatively tall R wave, depressed ST segment and
markedly peaked T wave in lead V3 of Panel A becomes a deep Q, elevated ST and deeply
inverted T wave when the tracing is flipped over in Panel B.

Additional Points on Localizing the Culprit Artery: We expand on our rationale for strongly
suspecting the RCA as the culprit artery for the ECG in Figure 10.39-1. Practically speaking the
majority of acute infero-postero STEMIs will be the result of RCA (rather than LCx) occlusion, as
~85% of patients have a right-dominant circulation (Section 10.17). Recognizing that the amount of
ST elevation in lead III is clearly more than in lead II strongly favors RCA occlusion (especially
when there is significant reciprocal ST depression in lead aVL).

We next look to see IF there is ST elevation in leads V5,V6? IF there is then the culprit
artery could be either the RCA or a dominant-left Circumflex (LCx) artery (since large
postero-lateral artery branches may occasionally arise off the PDA from an RCA occlusion
as described in Section 10.18 and as illustrated in Figure 10.28-3).
BUT IF there is acute infero-postero-lateral STEMI but no ST elevation in leads V5,V6 (as
is the case in Figure 10.39-1) it becomes highly likely that the culprit artery is the RCA
(since one expects ST elevation in V5,V6 with left-dominant LCx occlusion).

Beyond-the-Core: A final reason to support our suspicion of acute RCA occlusion for the ECG in
Figure 10.39-1 is the ST-T wave appearance in lead V1, which shows a flat ST segment (rather
than ST segment depression).

In the presence of simple acute infero-postero MI lead V1 typically manifests a similarshape ST segment as leads V2,V3. Thus, there should usually be some ST depression in lead V1
albeit less than is usually seen in other anterior leads.
IF instead of being depressed the ST-T wave in lead V1 is flat or coved (or elevated) then
associated acute RV (Ri ght Ventricular) involvement is likely. This is because the ST
elevation from acute RV MI that we would expect to see in right-sided lead V1 is in part
cancelled out by ST depression from the posterior infarction (Section 10.32).
IF there is a need to confirm acute RV involvement then obtaining right-sided leads (Section
10.31) should tell us for certain.
Identification of acute RV involvement localizes the culprit artery to the RCA because the
LCx does not supply the right ventricle.

10.40 Schematic PRACTICE Tracings: Acute MI/Ischemia

As PRACTICE We consolidate Review of the principles for identifying the probable culprit
artery with acute STEMI in the following 12 schematic tracings (Sections 10.40.1 through
10.40.12).
For each of these schematic ECGs the rhythm is sinus and the patient presents with chest
pain. Assess each tracing for evidence of acute infarction? IF present Can you identify the
probable culprit artery?
NOTE: To keep you honest We include several schematic tracings that are not suggestive of
acute STEMI. Can you recognize what may be going on in these cases?
HINT for the Tracings in Section 10.40: Feel free to refer back to previous segments on:
ECG Changes of Acute Infarction (Sections 10.1 through 10.10).
Sequence of ECG Changes (Sections 10.11 through 10.15).
The Coronary Circulation (Sections 10.16 through 10.21).
Identifying the Culprit Artery (Sections 10.22 through 10.28).
Acute RV MI (Sections 10.29 through 10.32).
Posterior MI/Mirror Test (Sections 10 through 10.37).

10.40.1 FIGURE 10.40-1: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-1: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).

ANSWER to Figure 10.40-1: There is marked ST elevation in both of the high lateral leads
(I,aVL). In addition leads I and aVL also manifest a small q wave and beginning T wave
inversion. Other acute findings on this tracing include:

Leads V5,V6 manifest a small q wave and ST elevation.

Inferior leads (II,III,aVF) manifest marked reciprocal ST depression.
There is also subtle-but-real reciprocal ST depression in leads V2,V3. Note the red arrow in
Figure 10.40-1 which defines the J-point (junction between the end of the S wave and the
beginning of the ST segment). The slope changes at the J-point with the ST segment seen to
be significantly below the PR baseline.
Impression: Extensive acute lateral STEMI involving high lateral leads I,aVL and lateral
precordial leads V5,V6.
Probable Culprit Artery: Acute occlusion of the LCx (Section 10.28).

Additional Comments on Figure 10.40-1: As emphasized in Section 10.28 the lateral leads that
most consistently assess the part of the heart supplied by the LCx are leads V5,V6. It will be rare
indeed that youll encounter the combination of lateral lead findings shown in Figure 10.40-1, with
near tombstone-type ST elevation in leads I and aVL. Thus, this schematic tracing is admittedly
theoretical. Nevertheless, as a practice exercise lack of inferior and anterior ST elevation suggest
the LCx as the culprit artery.

Finally Note the small and narrow q waves in lateral leads I, aVL, V5 and V6 of Figure
10.40-1. Because these q waves are small and narrow the question arises as to whether they
might represent normal septal q waves instead of infarction q waves? Small septal q waves
may normally be seen in healthy subjects in one or more of the lateral leads. That said
associated dramatic ST-T wave changes in this tracing strongly suggest they are infarction q
waves. Subsequent tracings should clarify the issue as we would expect these Q waves to
deepen and widen as the infarct evolves.

10.40.2 FIGURE 10.40-2: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-2: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-2: There is ST elevation in both high lateral leads (ie, in lead I and
lead aVL). The only other lead showing ST elevation on this tracing is lead V2. This is indeed an
unusual picture. Other acute findings include:
Reciprocal ST depression in the inferior leads (II,III,aVF) and in leads V3,V4.
Impression: Acute high lateral STEMI, with in addition ST elevation that is localized to
lead V2.
Probable Culprit Artery: Acute occlusion of the 1st Diagonal branch of the LAD
(Section 10.25).
Additional Comments on Figure 10.40-2: The ECG picture shown in this schematic tracing is an
uncommon but important pattern to aware of. It emphasizes the utility of ST elevation in lead aVL
for localizing the probable culprit artery. We repeat below the PEARL we presented in Section
10.25 on acute LAD occlusion:
PEARL: ST elevation in lead aVL may provide an invaluable clue to the location of the acutely
occluded coronary artery. According to a study by Birnbaum et al (Am Heart J 131:38, 1996):
Suspect acute LAD occlusion proximal to the 1st Diagonal IF in addition to ST elevation in
aVL there is also ST elevation in leads V2-through-V5. This is the most common situation
when there is ST elevation in lead aVL.

Suspect 1st Diagonal branch occlusion IF in addition to ST elevation in aVL there is ST

elevation in lead V2 (but not in V3,V4,V5).
Suspect LCx occlusion (especially of the 1st obtuse marginal branch) IF there is ST
elevation in aVL but not in lead V2 (and not in other anterior leads).
NOTE: Anterior ST elevation without ST elevation in lead aVL suggests more distal LAD
occlusion after takeoff of the 1st Diagonal.

Beyond-the-Core: We are aware of several cases in which awareness of the pattern shown in Figure
10.40-2 was of great assistance to the consulting cardiologist in identifying the site of acute coronary
occlusion. A totally occluded 1st or 2nd LAD Diagonal branch may not always be readily apparent
(since no dye enters an occluded vessel). Recognizing the specific localizing value of ST elevation
in lead aVL and in lead V2 but not in any other anterior leads helped the cardiologist to know
exactly where to look on acute cardiac cath for the site of occlusion.

10.40.3 FIGURE 10.40-3: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-3: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-3: There is ST segment coving (frowny shape appearance) with ST
elevation in the precordial leads. This is most marked in leads V2,V3,V4. Other acute findings on
this tracing include:
Preservation of the initial r wave in leads V1,V2,V3. This implies that the septum is still intact.
That said there is loss of r wave between lead V1-to-V2 (in that r wave amplitude decreases
slightly from V1-to-V2). Normally, the R wave will be taller-than-seen in Figure 10.40-3 by
lead V3.
Several other leads manifest ST elevation. These include lead I, lead aVL and lead aVR.
There is reciprocal ST depression in the inferior leads (II,III,aVF).
Small and narrow q waves are seen in leads aVL,V5,V6.
Impression: Acute extensive antero-lateral STEMI.
Probable Culprit Artery: Acute occlusion of the proximal LAD (Section 10.25). As
opposed to the case presented in Figure 10.40-2 ST elevation in lead aVL is accompanied by
diffuse precordial ST elevation. ST elevation is also present in lead aVR but it is not
markedly more than in lead V1. This localizes the likely site of acute occlusion to the proximal
LAD.
Additional Comments on Figure 10.40-3: Note that the amount of ST elevation in lead V5 is not
nearly as much as it is in neighboring leads V4 and V6. This highlights the concept of patterns of
leads.

Rather than looking at each of the 12 leads on a standard ECG as a separate entity the
experienced ECG eye simultaneously assesses acute changes in specific lead areas. Thus,
each of the inferior leads (II,III,aVF) are best looked at together. In Figure 10.40-3 leads
II,III,aVF all show similar ST depression.
Despite the relatively minimal amount of ST elevation in lead V5 of Figure 10.40-3 definite
and marked ST elevation in neighboring leads (V4 and V6) tell us that significant ST elevation
is truly present in all precordial leads!

10.40.4 FIGURE 10.40-4: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-4: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-4: There are both q waves and ST elevation in the inferior and lateral
precordial leads (V5,V6). Other acute findings on this tracing include:
ST depression in leads I,aVL and in leads V1 through V4.
There is a positive mirror test in the anterior precordial leads (Section 10.33).
Impression: Acute infero-postero-lateral STEMI.
Probable Culprit Artery: Acute occlusion of a dominant LCx (Section 10.28). This
schematic tracing closely resembles the ECG picture previously seen in Figure 10.28-3. ECG
findings on this tracing that strongly suggest the culprit artery is a dominant LCx (rather
than the RCA) include: i) ST elevation in lead III is not more than in lead II; ii) ST depression in
lead aVL is not more than in lead I; iii) There is significant ST elevation in leads V5,V6 that
appears to be more than the amount of ST elevation in lead III; and iv) There is no suggestion of
acute RV involvement (ie, the ST segment in lead V1 is depressed and similar in shape to the
ST depression seen in leads V2,V3).
Additional Comments on Figure 10.40-4: Note the presence of small and narrow q waves in both
inferior and lateral precordial leads. The question arises as to whether these are likely to represent
normal septal q waves vs infarction q waves?
Small septal q waves may normally be seen in one or more of the lateral leads. While possible
for small and narrow q waves to also be septal when seen in the inferior leads this is less

likely (especially when the patient does not have a vertical axis). Given the overall ECG
picture in Figure 10.40-4 We strongly suspect that the infero-lateral q waves seen on this
tracing are infarction q waves that will probably become larger as the infarct evolves.

10.40.5 FIGURE 10.40-5: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-5: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-5: There is ST elevation in the inferior and lateral precordial leads
(V5,V6). Other acute findings on this tracing include:
Small q waves in the inferior leads.
ST depression in leads I,aVL and in leads V1 through V4.
There is a positive mirror test in the anterior precordial leads (Section 10.33).
Impression: Acute infero-postero-lateral STEMI.
Probable Culprit Artery: Acute occlusion of the proximal RCA (Section 10.23). ECG
findings on this tracing that strongly suggest the culprit artery is the proximal RCA (rather
than a dominant LCx) include: i) ST elevation in lead III that is clearly more than in lead II; ii)
Marked ST depression in lead aVL that is more than in lead I; iii) No more than minimal ST
elevation in leads V5,V6 that is less in amount than the ST elevation seen in lead III; and iv)
Suggestion of acute RV involvement by the upright T wave and level ST segment in right-sided
lead V1. One usually expects to see ST depression in lead V1 (similar to ST depression in
leads V2,V3) when there is simple posterior MI without associated RV involvement ( Section
10.32).
Additional Comments on Figure 10.40-5: The ECG picture in this schematic tracing illustrates an
instance in which there may be ST elevation in leads V5,V6 that is not the result of acute LCx
occlusion.

On occasion the PDA may give rise to large PLA (Postero-Lateral Artery) branches that
extend laterally to supply parts of the LV free ( lateral) wall. This may account for ST elevation
in leads V5,V6 in a patient with acute RCA occlusion (Section 10.18). As noted above there
are no less than 4 reasons why we strongly suspect that the culprit artery in this case is the
RCA (and not the LCx).

10.40.6 FIGURE 10.40-6: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-6: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-6: The most remarkable findings on this schematic tracing are seen in
leads V2 through V4. Other than small, narrow (septal) q waves in leads V5,V6 the rest of the
tracing is unremarkable. We highlight the following:
Although small r waves are present in each of the anterior leads. Thus, there are no
infarction q waves.
The ST segment appears to be coved and slightly elevated in leads V2,V3. It is coved but
without ST elevation in lead V4.
There is a peculiar very steep downslope to the initial portion of the T wave in leads V2,V3.
Impression: This schematic tracing suggests Wellens Syndrome. As will be discussed in
more detail in Section 10.54 this ECG pattern is highly suggestive of a critical stenosis in
t h e proximal LAD. The patient should be immediately referred for timely cardiac
catheterization.
Additional Comments on Figure 10.40-6: Recognition of Wellens Syndrome is a clinical
diagnosis. There should be a history of at least some symptoms consistent with coronary disease.
These symptoms may be fairly acute or they could be ongoing for a period of time. The ECG
pattern of ST-T wave changes seen in Figure 10.40-6 may be intermittent (due to slight changes in
the degree of LAD obstruction) or it may become persistent.
A key component to Wellens syndrome is that infarction has not yet occurred. Thus, although

there is some ST elevation in Figure 10.40-6 it is minimal in amount and no Q waves have
yet formed. This is important because the GOAL is to recognize Wellens Syndrome before
acute infarction (= occlusion of the LAD) occurs.

10.40.7 FIGURE 10.40-7: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-7: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-7: The remarkable finding on this schematic tracing is seen in the
anterior leads which show fairly deep and symmetric T wave inversion in leads V2 through
V4. There are no Q waves and R wave progression is normal (transition occurs between lead
V3-to-V4). There may be slight ST elevation in lead aVR but there are no other findings of note.
Impression: Symmetric T wave inversion in leads V2 through V4. This is consistent with
anterior ischemia. Strongly suggest clinical correlation!
KEY Points: Clinical correlation is needed for meaningful interpretation of this schematic ECG. We
simply can not tell from this single tracing IF the ECG finding of symmetric T wave inversion is new
or old. More history and comparison with prior and serial tracings is needed.
The findings in Figure 10.40-7 could reflect recent completed infarction. Alternatively
these findings could reflect ongoing evolution of a non-Q-wave MI. Serial troponins may be
needed to tell the difference.
The symmetric T wave inversion seen here could reflect ischemia of uncertain duration. IF due
to coronary disease this could reflect significant narrowing of the LAD.
Alternatively T inversion could be due to some other cause (including a noncardiac
etiology). For example anterior T wave inversion may sometimes be an ECG indicator of
acute pulmonary embolus (Section 08.37). BOTTOM Line: Clinical correlation is needed for
meaningful clinical interpretation of this tracing.

10.40.8 FIGURE 10.40-8: How to Date an Infarct?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-8: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-8: There are many important findings on this schematic tracing. These
include:
In the inferior leads there are large (and wide) Q waves in leads II,III,aVF. These are
associated with flat ST segments.
In the anterior leads there are QS complexes in leads V1 through V4. No R wave at all is
seen until lead V5. ST segments in the anterior leads are coved, slightly elevated and
associated with T wave inversion.
Impression: There clearly is evidence that infarction has taken place. The challenge is to
attempt dating the one or more events that may have occurred (See below). That said our
interpretation of this schematic tracing would be as follows: i) O ld inferior MI; and ii)
Anterior MI of uncertain age, possibly acute. We would once again emphasize in our
interpretation that, Clinical correlation is needed.
KEY Concept: How to Date an Infarct? When assessing a symptomatic patient for the possibility
of acute ischemia or infarction ECG terminology frequently refers to the presence or absence of
acute changes. Given the importance of prompt revascularization for acute coronary occlusion
the GOAL is to identify high-risk patients with greatest potential for benefit. That said Our ability
to date an infarct is limited. Practically speaking the best we can do is to classify ECG signs of
infarction as likely to be: i) Acute; ii) Old; or iii) Infarction of Uncertain Age.

Examples of acute ECG findings are obvious in Figures 10.40-1 through 10.40-5. None of
these tracings should pose any difficulty for recognizing the presence of acute MI.
T he addition of History to the ECG picture may provide invaluable assistance for
determining onset of the event. This is especially true when chest pain is severe and begins
abruptly.
In contrast determining the likely age of an infarct becomes problematic when history for an
event is indistinct (minimal or only intermittent chest pain or no chest pain at all) and
when ECG signs are less definite. This is the case for assessing the anterior leads in Figure
10.40-8. The very deep QS complexes in leads V1 through V4 clearly suggest that anterior MI
has occurred at some point in the past. Q waves of this depth (QS complexes) generally require a
certain amount of time to develop. That said ST segments in leads V2 through V4 of Figure
10.40-8 are coved, slightly elevated and associated with T wave inversion. Whether this picture
is due to recent anterior MI new anterior MI (superimposed on old infarction) or
persistent ST elevation from ventricular aneurysm will require clinical correlation (and
comparison with prior tracings) to sort out.

10.40.9 FIGURE 10.40-9: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-9: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-9: The ECG finding we wish to highlight on this schematic tracing is
subtle: there is slight ST elevation in leads V2,V3 and in leads V5,V6. Given smoothness of the Jpoint in leads V2,V3 it is difficult to be certain how much ST elevation is actually present. It does
not appear to be much.
The shape of ST elevation in leads V2,V3 is concave up (smiley configuration). It also
manifests an upward concavity in leads V5,V6.
There is J-point notching of the initial part of the ST segment in lead V6.
Small and narrow q waves are seen in lateral precordial leads V5,V6. These look to be normal
septal q waves.
Impression: Slight ST elevation in leads V2,V3 and V5,V6 with an upward concavity. Jpoint notching in lead V6. Small lateral q waves and no reciprocal ST depression. The overall
pattern is most suggestive of Early Repolarization (Section 09.19). Strongly suggest clinical
correlation!
Additional Comments on Figure 10.40-9: Clinical correlation is essential
interpretation of this tracing:

for meaningful

IF the patient in question was an otherwise healthy young adult and the history of chest pain
w a s not suggestive of acute coronary disease then we would strongly favor Early
Repolarization as our clinical interpretation. The only q waves present are small the shape

of ST segment elevation looks benign (concave-up) there is J-point notching and there are
no reciprocal changes. (Sections 09.17 through 09.21).
On the other hand We would be less comfortable calling the ECG pattern in Figure 10.40-9
benign IF the patient was older, had risk factors and presented with new-onset severe chest
pain.
BOTTOM Line: Sometimes Ya just gotta be there in order to make a clinical
determination of how best to proceed. Availability of a prior tracing for comparison may prove
invaluable for assuring that ST elevation is not new. On occasion a tincture of time
(including serial tracings/troponins and a period of time to observe the clinical course) may
be needed.

10.40.10 FIGURE 10.40-10: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-10: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-10: The schematic tracing shown here is similar in some regards to that
from Figure 10.40-9 in that there once again is ST elevation in anterior precordial leads. That
said there are some very important differences between the 2 tracings:
ST elevation is present not only in leads V2,V3 but also in lead V1.
The shape of ST segments in these leads is coved (frowny configuration). While possible
that coved ST elevation could be a benign repolarization variant (See Section 09.24) it is far
more likely to indicate an acute coronary process (Section 09.17).
There is subtle-but-real ST segment flattening and slight depression in each of the inferior leads
(II,III,aVF). Given the findings seen in leads V1,V2,V3 this qualifies as reciprocal ST
depression.
Small q waves with slight ST elevation is seen in leads V5,V6. There is J-point notching in lead
V6. It is difficult to tell from this single tracing if this is a benign finding or something of
possible concern.
Impression: We are suspicious of acute anterior STEMI. Lateral precordial ST elevation
may or may not be part of this process.
Probable Culprit Artery: Acute occlusion of the LAD though not necessarily in its
proximal portion (Section 10.25).

10.40.11 FIGURE 10.40-11: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-11: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-11: There are a number of findings of concern on this schematic tracing.
These include:
In the inferior leads small Q waves with definite ST elevation.
In the anterior leads ST segment coving with definite ST elevation in leads V1 through V4.
Small q waves are seen in leads V5,V6 but there is no ST elevation in these leads.
There is reciprocal ST depression in leads I and aVL.
There appears to be no ST elevation in lead aVR.
Impression: The ECG picture clearly looks like acute ongoing infarction. In a patient with
chest pain we interpret these changes as suggestive of acute inferior and anterior STEMI.
The question arises as to whether there is a single anatomic lesion that might give rise to these
ECG changes that are seemingly occurring in 2 different lead areas?
Probable Culprit Artery: The left ventricular apex is often a difficult anatomic area to
visualize on ECG. Changes may be subtle or they may manifest in inferior and/or anterior
leads. As emphasized in Section 10.27 approximately 5-10% of normal subjects have an
anatomic wrap-around LAD as a coronary artery variant circulation. In such cases the
LAD is a larger and longer vessel, to the point of extending beyond the cardiac apex and
wrapping around to supply the undersurface (inferior wall) of the heart. Thus, we suspect
acute occlusion of a wrap-around LAD as the culprit artery in this case (Section 10.27).
As will be discussed in Section 10.61 Takotsubo Cardiomyopathy is another potential
cause of acute ST elevation in both inferior and anterior lead areas.

10.40.12 FIGURE 10.40-12: Ischemia/Infarction?

The rhythm in this schematic tracing is sinus and the QRS complex is narrow. The patient is having
chest pain.
Is there ECG evidence of acute infarction?
If so What is the culprit artery likely to be?

Figure 10.40-12: Schematic ECG from a patient with chest pain. Is there acute infarction? If so
what is the culprit artery likely to be? (See text).
ANSWER to Figure 10.40-12: The ECG picture in this schematic tracing is clearly of concern.
There is marked diffuse ST depression in virtually all leads except for ST elevation in lead aVR.
Impression: The ECG pattern of diffuse ST depression in multiple leads (usually in at least
7 leads) with ST elevation in lead aVR is highly suggestive of 3-vessel or proximal
LAD/left-main disease. This is especially true when this pattern is seen in an older adult who
presents with chest discomfort (Section 09.40).
To emphasize key points regarding the recognition of this ECG pattern We repeat below the
PEARL and NOTE previously presented in Section 09.40:
PEARL: Distinction between left-main disease vs proximal LAD occlusion may be suggested on
ECG by the relative amount of ST elevation seen in lead aVR compared to lead V1.
Think Left-Main disease when ST elevation in lead aVR > V1.
Think proximal LAD disease/occlusion when ST elevation in lead V1 > aVR. In Figure
10.40-12, given marked ST elevation in lead aVR in the absence of any ST elevation in lead V1
one has to be concerned about significant left-main coronary artery narrowing.
NOTE: Distinction should be made between acute LMCA (Left Main Coronary Artery) occlusion
vs LMCA disease.

Most patients with acute LMCA occlusion do not survive. As a result this entity is not often
seen and unlikely to be appreciated clinically. Rapid deterioration with patient demise due to
cardiogenic shock is the usual result unless acute LMCA occlusion can be immediately
recognized and immediately acted on.
In those rare circumstances when acute LMCA occlusion is captured on ECG rather than
diffuse ST depression there should be diffuse precordial ST elevation in association with
significant ST elevation in lead aVR. Thus, the ECG picture in Figure 10.40-12 should not be
misinterpreted as consistent with LMCA occlusion. Instead it suggests that there may be
significant LMCA narrowing.

10.41 LIST #5: Ant. ST Depression with Acute Inf. MI

As discussed at the very beginning of this ECG-2014-ePub (in Section 00.7) We have developed
6 Essential Lists to remember for optimal ECG and arrhythmia interpretation. The purpose of a
List is that it readily recalls the most common/important entities to remember for the particular
entity.
We have already covered the first 4 of these Lists.
For convenience We consolidate all 6 Lists in Section 00.7 (Make a bookmark and/or
Search for 00.7 to locate these 6 lists).
We present below in Section 10.42 our LIST #5.
The 6th (and last) of our 6 Lists follows in Section 10.47.

10.42 LIST #5: Causes of Anterior ST Depression

We have already reviewed a series of tracings showing inferior infarction. In the setting of acute
inferior MI ST depression is commonly seen in two or more anterior leads (leads V1,V2 and/or
V3). This concept is illustrated in the schematic ECG shown below in Figure 10.42-1:

Figure 10.42-1: Schematic ECG from a patient with acute inferior MI. Note the presence of
anterior ST depression (in leads V1,V2,V3) the common causes of which make up our LIST #5
(See text).
LIST #5: The purpose of our 5th List is to facilitate recall of the 3 principal causes of anterior ST
depression that commonly occur in the setting of acute inferior MI. Each of these 3 causes should be
actively considered when confronted with an ECG such as that shown in schematic Figure 10.42-1.
CAUSE #1 reciprocal ST depression (that may occur in response to the acute inferior

infarction).
CAUSE #2 anterior ischemia. Acute inferior MI is usually due to acute RCA occlusion.
Anterior ischemia might be seen if at the same time there was symptomatic narrowing of the
LAD.
CAUSE #3 posterior MI.
The above 3 Causes make up our LIST #5. Keep in mind that more than one of these causes may be
operative in any given patient (Figure 10.42-2):

Figure 10.42-2: The Common Causes of Anterior ST Depression in the setting of Acute Inferior MI
= LIST #5. More than one cause may be operative in any given patient (See text).
KEY Points about LIST #5: In any given patient it may not be possible to distinguish which
causes in List #5 are operative. That said this does not matter clinically.
Regardless of the cause(s) significant anterior ST depression on ECG in association with
acute inferior MI means a larger infarct (and therefore more potential benefit from acute
intervention).
Acute Posterior MI will very often present when there is anterior ST depression in the
setting of acute inferior MI. This is because the RCA most commonly supplies both the inferior
and posterior wall of the LV ( Section 10.17). Even when the culprit artery is a dominant LCx
instead of the RCA acute inferior and posterior infarction will commonly be seen together
(Section 10.17). Use of the mirror test facilitates recognition of acute posterior MI (Figure
10.42-3).

Figure 10.42-3: Application of the mirror test to Figure 10.42-1 (which we reproduce in Panel
A). Flipping the tracing in Panel A over and holding it up to the light to perform the mirror test
(Panel B) supports the premise that acute posterior MI may be one of the causes of anterior ST
depression that was seen in Panel A (See text).
10.43 FIGURE 10.43-1: Ant. ST Depression with Acute Inf. MI
Practice applying List #5 by interpreting the ECG shown in Figure 10.43-1 obtained from a patient
with new-onset chest pain.
Is this patient having an acute STEMI? If so What is the likely culprit artery?
Note the marked ST depression in anterior leads V1,V2,V3 (red arrows in Figure 10.43-1).
What is the likely cause(s) of this ST depression?
HINT: Feel free to refer back to LIST #5 in Figure 10.42-2 in formulating your answer.

Figure 10.43-1: ECG from a patient with new-onset chest pain. What is the likely cause of the
marked anterior ST depression? HINT: Feel free to refer back to List #5 (in Figure 10.42-2) in
formulating your answer.
Answer to Figure 10.43-1: The rhythm is sinus. This patient with new-onset chest pain is in process
of evolving a large acute infero-postero STEMI. Relevant findings include the following:
Dramatic ST elevation (with hyperacute ST segments) in each of the inferior leads. ST
elevation in lead III is more than in lead II suggesting the RCA is the culprit artery
(Section 10.23).

There is reciprocal ST depression in numerous other leads. This ST depression is especially

marked in lead aVL supporting the premise that there is acute RCA occlusion. ST depression
is also seen in leads I; V1,V2,V3; and to a lesser degree in leads V4,V5,V6.
Beyond-the-Core: Note that there is marked RAD (Right Axis Deviation) as determined by
the predominantly negative QRS complex in lead I. Given the extensive acute infarction seen
here this may reflect new isolated LPHB (Le f t Posterior HemiBl ock discussed in
Section 07.25).
What is the Cause of Anterior ST Depression? The purpose of List #5 is to remind us of the 3
principal causes to consider when confronted with acute inferior MI and associated ST depression in
the anterior leads (red arrows in Figure 10.43-1). These 3 Causes are: i) reciprocal ST depression;
ii) anterior ischemia from concomitant LAD narrowing; and iii) posterior MI.
I n Figure 10.43-1 We suspect at least 2 ( if not all 3) of these causes are operative. ST
depression is present in multiple leads in addition to leads V1,V2,V3. This suggests that at least
a component of the anterior ST depression reflects reciprocal changes.
Given the extensive size of the acute MI in Figure 10.43-1 there may well be associated
anterior ischemia. This is especially true in view of the marked RAD (probable LPHB) as
the LAD more often provides blood supply to this hemifascicle.
Finally there almost certainly is associated acute posterior MI, which so often accompanies
acute inferior MI (especially when size of the infarct appears to be large ). Note taller-thanexpected R wave amplitude in lead V2 of Figure 10.43-1 with the peculiar shape of ST
depression in V2,V3 that characterizes acute posterior MI. The mirror test is definitely
positive (Figure 10.43-2).

Figure 10.43-2: Note anterior ST depression (red arrows) in this patient with acute inferior MI
(ECG in Panel A reproduced from Figure 10.43-1). Application of the mirror test in Panel B
which is positive and supports the premise that acute posterior MI is one of the causes of anterior ST
depression that was seen in Panel A.

10.44 LIST #6: Tall R Wave in Lead V1

As discussed at the very beginning of this ECG-2014-ePub (in Section 00.7) We have developed
6 Essential Lists to remember for optimal ECG and arrhythmia interpretation. The purpose of a
List is that it readily recalls the most common/important entities to remember for the particular
entity.
We have already covered the first 5 of these Lists.
For convenience We consolidate all 6 Lists in Section 00.7 (Make a bookmark and/or
Search for 00.7 to locate these 6 lists).
We present below in Section 10.47 our last list = LIST #6.

10.45 Normal Appearance of the QRS in Lead V1

As emphasized in Sections 05 and 09 the QRS complex in lead V1 will be predominantly
negative under normal circumstances. This is because this right-sided lead (V1) normally sees
electrical activity as moving away from V1 (or toward the large left ventricle ). This concept is
illustrated in schematic Figure 10.45-1.
The finding of predominant positive activity in lead V1 (an R wave that equals or exceeds the S
wave in this right-sided lead) is not normal. This is the premise on which our List #6 is
based (Section 10.46).

Figure 10.45-1: Transverse (cross-sectional) view of the heart illustrating precordial lead
appearance in leads V1-through-V6 (reproduced from Figure 09.3-1). Transition occurs in the above
Figure between lead V2-to-V4. Note that the QRS complex in lead V1 is predominantly negative

under normal circumstances (red box). Septal depolarization normally moves left-to-right (small
black arrow). The major component of ventricular activation moves to the left and posteriorly (large
red arrow) which reflects the relative size and anatomic position of the left ventricle. This
explains why lead V1 normally sees predominant electrical activity as moving away from this rightsided lead.
10.46 The Purpose of List #6
It is easy to overlook the finding of a tall (or relatively tall) R wave in lead V1. It is equally easy to
overlook the finding of early transition in which the R wave in precordial leads V2 or V3
becomes disproportionately tall much sooner than expected.
The KEY to not overlooking the ECG findings of a tall R wave in lead V1 or early transition
is to routinely apply a systematic approach to your ECG interpretation. This is our purpose for
including the R component (looking for R Wave progression) when assessing for
Q-R-S-T Changes (Section 00.6.6).
The purpose of our LIST #6 is to facilitate recall of the principal causes of a
disproportionately tall R wave in lead V1 (Section 10.47). Awareness of these causes is
especially important because computerized ECG interpretations typically fail to pick up a
taller-than-expected R wave in leads V1,V2,V3.

10.47 LIST #6: Causes of a Tall R Wave in Lead V1

In LIST #6 We note 6 important causes of a tall R wave in lead V1. The best way not to overlook
any of these causes is to work through each of the entities on this list (Figure 10.47-1) whenever
you recognize that the R wave in lead V1 is taller than you expect.

Figure 10.47-1: The Common Causes of a Tall R Wave in Lead V1 = LIST #6. Normal variant is a
diagnosis of exclusion (See text).
Looking Closer at LIST #6: The way to narrow down which of the entities on List #6 is likely to be
operative is to look for associated findings.
WPW Look for the QRS to be wide with delta waves and a short PR interval (discussed in
detail in Section 05.37).
RBBB Look for the QRS complex to be wide with an rSR ( or equivalent) in lead V1 and
wide terminal S waves in leads I,V6 (Section 05.4).
RVH Look for ECG criteria of RVH including right or indeterminate axis; RAA (Right Atrial
Abnormality); tall R wave in V1; RV strain; persistent precordial S waves (Section 08.23).
Posterior MI Look for ECG evidence of associated inferior infarction and for a positive
mirror test (Section 10.33).
Cardiomyopathy increased septal forces from HCM (Hypertrophic CardioMyopathy) may
manifest as a disproportionately tall R wave in lead V1 (discussed in more detail in Section
10.49). On occasion other forms of cardiomyopathy (such as that associated with muscular
dystrophy) may also result in a tall R wave in V1 (Section 10.65).
Normal Variant to be considered only after the above 5 causes have been ruled out. Thus,
the diagnosis of normal variant as the reason for a disproportionately tall R wave in lead V1
is a diagnosis of exclusion!

10.48 PRACTICE Tracings: The Cause of the Tall R in V1?

As PRACTICE in clinical application of List #6 We present the following 5 schematic tracings

and the real tracing in Figure 10.50-1:

For each tracing the rhythm is sinus and a tall R wave is seen in lead V1. Can you identify
the likely cause of the tall R wave in lead V1 for each case? HINT: Feel free to refer back to
LIST #6 (in Figure 10.47-1) when formulating your answer.

Figure 10.48-1: The rhythm is sinus. The QRS is wide. Why the tall R wave in lead V1?
Answer to Figure 10.48-1 The QRS is wide. A tall R wave with an RSR ( taller right rabbit ear)
pattern is seen in lead V1. There are wide terminal S waves in leads I,V6. The cause of the tall R in
V1 = RBBB (Section 05.4).

Figure 10.48-2: The rhythm is sinus. The QRS is wide. Why the tall R wave in lead V1?
Answer to Figure 10.48-2: The rhythm is sinus. The QRS is wide. The PR interval is short and there
is initial slurring of the QRS upslope in the form of a delta wave in multiple leads. The cause of the
tall R in V1 = WPW (Section 05.37).
Note how this schematic example of WPW simulates RBBB in V1 and simulates LBBB in
leads I,V6. Remember delta waves will not always be seen in all leads.

Figure 10.48-3: The rhythm is sinus. The QRS is narrow. Why the tall R wave in lead V1?
Answer to Figure 10.48-3: The rhythm is sinus and the QRS complex is narrow. The cause of the tall
R in V1 = RVH (Section 08.23). Note the following features in support of this diagnosis:
RAD (Right Axis Deviation) as determined by the markedly negative QRS complex in lead I.
RAA (Right Atrial Abnormality) as determined by tall, peaked and pointed P waves in leads
II,III,aVF.
RV strain in lead V1 as suggested by ST-T wave depression in V1 that occurs in
association with the tall R wave in this lead.
Persistent precordial S waves as suggested by the deep S wave that is still present in lead
V6.
KEY Point: Remember to think of RVH as the detective diagnosis that is generally made by a
combination of ECG findings that occur in the right clinical setting (Section 08.24).
Practically speaking By the time one sees as many ECG indicators of RVH in an adult as are
present in schematic Figure 10.48-3 the patient has either: i) end-stage pulmonary disease;
and/or ii) pulmonary hypertension.
NOTE: The finding of a relatively tall R wave in lead V1 is much more common in children
where it is not necessarily abnormal during the first few years of life (Section 08.31).

Figure 10.48-4: The rhythm is sinus. The QRS is narrow. Why the tall R wave in lead V1?
Answer to Figure 10.48-4: The rhythm is sinus. The QRS complex is narrow. There are small
inferior Q waves and marked ST elevation consistent with acute inferior MI. ST depression is seen
in leads I and in anterior leads V1,V2,V3. There is a positive mirror test (See below in Figure
10.48-5).
Impression: We suspect the tall R in V1 is due to acute posterior MI. That said the other 2
causes of anterior ST depression in LIST #5 may also be contributing (Figure 10.42-2). As
emphasized in LIST #5 ST depression in leads V1,V2,V3 that occurs in association with
acute inferior MI may be due to: i) posterior MI; ii) reciprocal ST depression (in response to
the acute inferior infarction); and/or iii) anterior ischemia.

Figure 10.48-5: Application of the mirror test to the schematic tracing shown in Figure 10.48-4.
The postive mirror test supports acute posterior MI as at least one of the causes of the tall R
wave in lead V1 of Figure 10.48-4.
Finally Consider the schematic tracing shown in Figure 10.48-6. The patient was an
asymptomatic and otherwise healthy young adult. The ECG was obtained for screening purposes.

Figure 10.48-6: The rhythm is sinus. The QRS is narrow. The patient is an asymptomatic and
otherwise healthy young adult. The ECG was obtained for screening purposes. Why the tall R wave in
lead V1?
Answer to Figure 10.48-6: The rhythm is sinus. The QRS complex is narrow. We diagnose normal
variant as the likely reason for the moderately tall R wave (R=S) in lead V1 by the process of
elimination. That is the other causes in List #6 must first be ruled out. We do this as follows:
Since the QRS complex is narrow the cause for the relatively tall R wave in lead V1 is not
RBBB and not WPW.
This is not posterior MI because: i) the patient is an asymptomatic and healthy young adult; ii)
there is no ECG evidence of inferior MI; and iii) the mirror test is not positive.
This is not RVH because: i) the axis is normal; ii) there is no RAA; iii) there is no RV
strain; and iv) there is no persistent S wave in lead V6.
Admittedly We can not rule out HCM (Hypertrophic CardioMyopathy) without an
Echocardiogram. This does not necessarily mean that one needs to obtain an Echo on all patients
with an ECG such as seen in schematic Tracing 10.48-6. Clinical judgement is needed. IF this
patient was an athlete competing in high intensity sports and/or had a heart murmur or positive
family history of early sudden death then an Echo is clearly indicated. It is not necessarily
needed without any of these factors.

10.49 Hypertrophic Cardiomyopathy: How to Recognize on ECG?

Be aware of the 5th cause in List #6 of a Tall R in Lead V1 which is HCM (Hypertrophic
CardioMyopathy). Although not overly common HCM is an important potential cause of sudden
death (especially in young athletes) . Echo is diagnostic! On the other hand ECG findings are
highly variable. These may include a moderately tall R wave in lead V1 as shown in Figure 10.48-6
and which indicates prominent septal forces. It might also include deep septal Q waves; LVH by
voltage; IVCD/ LBBB or no ECG changes at all. The reason for emphasizing awareness of HCM
is the risk of sudden death that HCM poses among previously healthy young adults. While cost
concerns prohibit mass screening by Echo of all young adults Echo is indicated when there is a
history of syncope during exercise; with a positive family history for early sudden death; when a noninnocent murmur is heard or when a pre-participation ECG reveals abnormal findings that may

be consistent with the diagnosis.

10.50 FIGURE 10.50-1: WHY the Tall R in V1?
We conclude this segment on recognizing the cause of a disproportionately tall R wave in lead V1
with the ECG shown in Figure 10.50-1. The patient is a middle-aged adult. No other clinical
information is available. What is the cause of the tall R wave in lead V1?

Figure 10.50-1: ECG obtained from a middle-aged adult. No other clinical history is available. Why
the tall R wave in lead V1?
Answer to Figure 10.50-1: The QRS complex looks to be slightly wide. The rhythm appears to be
sinus as suggested by the presence of an upright P wave in lead II. The PR interval in lead II looks
normal. The QT is not prolonged. The most remarkable finding on this tracing is the very tall R
wave in lead V1. This is clearly not expected and should prompt consideration of the 6 entities in
LIST #6 as a possible explanation. We suspect that the answer will probably also explain: i) the
marked left axis (and/or QS complex in inferior leads); and ii) ST flattening and shallow T inversion
seen in multiple leads. As we work through the entities on List #6 We note the following:
This is not a normal variant tracing. Other than the tall R wave in lead V1 there is really
nothing to suggest RVH ( no right axis; no RAA; no RV strain in lead V1). And although it
almost looks as if there are inferior Q waves this is not the usual picture of inferior
infarction, and the mirror test is not suggestive of posterior infarction.
Finally the patient does not have RBBB. There is no rSR in lead V1 and no S wave is
seen in lead I. The QRS complex is also not as wide as is generally seen with bundle branch
block.
The patient has WPW! It is important to appreciate that the QRS complex is not always overly
wide with WPW. This is because there may occasionally be simultaneous conduction down
both normal and accessory pathway which will result in only partial pre-excitation (Section
05.38). It is because of awareness of LIST #6 that one looks extra hard for delta waves
whenever the finding of a tall R wave in V1 is seen. Close inspection reveals such delta waves
are seen (red and blue arrows in Figure 10.50-2).

Figure 10.50-2: Arrows highlight delta waves that were subtly present in the ECG shown in Figure
10.50-1. The QRS complex with WPW will not always be overly wide as there may only be
partial pre-excitation (if impulses are simultaneously conducted down normal and accessory
pathway). Although the PR interval looks to be normal in lead II of this tracing it appears to be
short in leads V4,V5,V6 (red arrows in these leads ). Delta waves are present. They are negative in
the inferior leads (blue arrows) and positive in other leads in which they are seen (red arrows ).
No delta wave is evident in leads aVR, aVL or V2.

10.51 Giant T Wave Syndrome

We have already discussed on a number of occasions ECG recognition and clinical implications of T
wave inversion. When T waves are symmetrically inverted (as they are in Figure 10.51-1) the
possibility of ischemia should be strongly considered.
Depending on the history other entities might also account for the symmetric T wave
inversion seen in Figure 10.51-1. For example, this could be due to acute pulmonary embolus
IF the patient experienced sudden shortness of breath (Section 08.37). It could even be a
normal variant (Juvenile T wave pattern) IF the patient in question was an otherwise
healthy and asymptomatic child (Section 08.31).

Figure 10.51-1: Schematic ECG illustrating symmetric T wave inversion in the anterior leads (red
arrows in leads V2,V3,V4). This ECG picture should suggest ischemia although depending on the
history, other causes might also be considered (See text).
10.52 When Inverted T Waves are GIANT in Size!
Although some T wave inversion is a common ECG finding the occurrence of truly huge T waves
that are inverted in multiple leads is much less often seen. We reserve the term, Giant T Wave
Syndrome for a select number of clinical entities that produce truly deep (>5mm amplitude) T
wave inversion. An example of this phenomenon is shown in Figure 10.52-1:

Figure 10.52-1: Sinus bradycardia with Giant T Wave Inversion that is present in multiple leads.
As suggested by the blow-up insert T waves exceed 10mm in size. A number of potential clinical
causes should be considered (See text).
Causes of Giant T Wave Inversion: Think of the following 6 entities when you see truly giant
inverted T waves in multiple leads:
Apical (Yamaguchi) Cardiomyopathy.
Severe CNS disorders (increased intracranial pressure).
Stokes-Adams attacks (especially when due to severe bradycardia/complete AV block).
Anterior ischemia/coronary artery disease.
Post-Tachycardia Syndrome.
Massive Pulmonary Embolism (acute right heart strain).
Taking a Closer Look at the Causes: We highlight the following clinical points regarding the 6
common causes of Giant T Waves:
Giant T waves were first described in association with Stokes-Adams attacks in which
patients presented with syncope from complete AV block/bradycardia.
The most bizarre ECG changes occur with severe CNS disorders (stroke, subarachnoid or
intracranial hemorrhage, seizure, coma, brain tumors, trauma). Often the QT interval will
be prolonged (sometimes markedly so) with CNS catastrophes. In addition to giant T waves
there may be marked ST elevation that mimics acute MI.
Apical (Yamaguchi) Cardiomyopathy is a special form of HCM (Hypertrophic
CardioMyopathy) in which the left ventricular apex is disproportionately involved. Giant T
waves are highly characteristic. Although Echo is the diagnostic procedure of choice for
detecting HCM (Section 10.49) localized apical thickening may occasionally be missed by
Echo (and only picked up by MRI scanning).
Deep, symmetric anterior T wave inversion may suggest coronary ischemia from LAD (Left
Anterior Descending) narrowing/occlusion (Section 10.40.7). Usually other clues in history
(chest pain) or the ECG will be present but on occasion, the diagnosis (and indication to

perform cardiac cath) will only be forthcoming from incidental recognition of giant T waves.
Post-Tachycardia Syndrome (as its name implies) follows an episode of sustained
tachycardia. This is a transient phenomenon after SVT or VT that does not indicate infarction.
Usually T waves are not overly deep.
Finally anterior T inversion may suggest acute RV strain and be a sign of acute
pulmonary embolism (Section 08.37). The history should suggest acute PE; there should be
other ECG signs (right axis; RAA; fast rate; tall R in V1).

10.53 FIGURE 10.53-1: Cause of the Giant T Waves?

Return to the ECG that was shown in Figure 10.52-1 (which we reproduce below in Figure 10.53-1).
IF told that the patient is an older adult who was found unresponsive Which causes of Giant T
Wave Inversion should be most strongly considered?

Figure 10.53-1: Sinus bradycardia with Giant T Wave Inversion that is present in multiple leads
(reproduced from Figure 10.52-1). The patient is an older adult who was found unresponsive. What
is the likely cause(s) of the giant inverted T waves? (See text).
Answer to Figure 10.53-1: The rhythm is sinus bradycardia. There is marked increase in QRS
amplitude with disproportionately tall R waves in leads V1,V2,V3. Regarding ST-T wave changes:
There is Giant T Wave Inversion with depth of these inverted T waves easily exceeding
5mm in multiple leads.
There is ST segment coving in several leads (V2,V3,V4) albeit no significant ST segment
elevation. There appears to be slight J-point ST depression in most of the leads that manifest T
wave inversion.
The QT interval appears to be no more than slightly prolonged. We measure the actual QT at
over 0.50 milliseconds (more than 2.5 large boxes in duration in lead V3) but given marked
bradycardia, the QTc is really not overly long.

IMPRESSION: All of the entities discussed in Section 10.52 should be considered as possible
contributing causes of the Giant T Wave Inversion seen in Figure 10.53-1:

This older adult has definite LVH (marked increase in QRS amplitude; ST-T wave
abnormalities consistent with strain and/or ischemia). Echo (and possibly MRI) would be
needed to determine IF the patient had Yamaguchi (Apical) Cardiomyopathy.
Deep symmetric T inversion should always suggest ischemia which may well be due to
significant narrowing of the LAD. This would be more likely IF there was a history of chest pain
prior to becoming unresponsive.
Given this patients unresponsive state the possibility of a CNS catastrophe (stroke;
bleed; trauma; post-seizure; metabolic disturbance) needs to be strongly considered. That said
the QT interval will typically be profoundly prolonged when the cause of giant T waves is a
CNS catastrophe, whereas the QTc in this case is no more than slightly prolonged.
We have no idea if this patients unresponsive state could have been preceded by an episode of
ventricular tachycardia or a Stokes-Adams attack resulting from profound bradycardia with AV
block.
Finally massive pulmonary embolism may sometimes present with an unresponsive state, and
could produce the giant T waves seen here.
BOTTOM Line: All 6 entities listed in Section 10.52 should to be considered as possible cause
of the Giant T Waves in Figure 10.53-1. Additional work-up will be needed to determine which
cause(s) is likely to be operative in this case.

10.54 Wellens Syndrome

There are a number of instances in ECG interpretation in which a particular ECG pattern
correlates strongly with a specific anatomic entity. Perhaps the most important clinical examples of
this phenomenon are: i) Wellens Syndrome; and ii) DeWinter T waves:
We address ECG recognition and clinical implications of Wellens Syndrome below in
Sections 10.55 and 10.56.
Recognition of DeWinter T waves is addressed in Section 10.57.

10.55 Wellens Syndrome: Clinical Implications & ECG Recognition

In a small but significant percentage of patients who present with ischemic heart disease the
initial ECG may be strongly suggestive of a nearly (but not totally) occlusive pattern. Prompt
recognition is essential in such cases and may prove invaluable as a myocardial sparing and
potential life-saving measure.
Consider the ECG shown in Figure 10.55-1 obtained from a patient with intermittent chest
discomfort. How would you interpret this ECG?
What intervention is needed?
What anatomic lesion is suggested?

Figure 10.55-1: Wellens Syndrome. This patient had intermittent chest pain. What intervention is
needed? What anatomic lesion is suggested?
Answer to Figure 10.55-1: First introduced by Wellens and his group in 1982 the ECG pattern
seen in Figure 10.55-1 has been found to be highly predictive (with ~90% accuracy) of critical
narrowing in the proximal LAD (Left-Anterior Descending).

Identification of this ECG pattern (known as Wellens Syndrome) is indication for prompt
cardiac catheterization with expectation that revascularization will likely be needed.
We highlight the following KEY Clinical and ECG Features of Wellens Syndrome:
There is a history of prior angina or chest discomfort.
There is little or no elevation of cardiac markers (troponins).
No pathologic precordial Q waves.
Slight (but not marked) ST elevation in precordial leads.
Progressive and symmetric T wave inversion that may be diffuse (especially in precordial
leads).
A characteristic abrupt takeoff (steep angle) to the deep T wave inversion that is seen in leads
V2,V3 and/or V4.
KEY Clinical Point: The importance of recognizing the above features of Wellens Syndrome is
that there is a very high incidence among these symptomatic patients who have not yet infarcted (no
more than minimal troponin elevation; no significant Q waves; minimal ST elevation) of going
on to develop extensive infarction IF they do not undergo prompt revascularization.
FIGURE 10.55-1: What Features are Seen in this Case? The ECG shown in Figure 10.55-1
strongly suggests Wellens Syndrome. We note the following findings:
There is a history of intermittent symptoms (chest pain).
There is slight (but not marked) ST elevation in anterior leads V2,V3,V4 (and perhaps also in
lead V1).
The ST segment in these leads is straightened (with a hint of downward coving in V3,V4).
Given this slight ST elevation in leads V2,V3 the downward slope of the T wave inversion
to follow in these leads is remarkably steep!
There is not yet sign of definite infarction (no Q wave in leads V2,V3,V4).
Clinical Course: This patient was found to have a >95% proximal LAD lesion. He was stented
with excellent result (Figure 10.55-2).

Figure 10.55-2: Cath films Before and After stenting the tight proximal LAD lesion from the
patient whose Wellens Syndrome ECG was shown in Figure 10.55-1. (Acknowledgement: My
appreciation to Jason Roediger for contributing this case, including the ECG and cath films).
10.56 FIGURE 10.56-1: What Wellens Syndrome is Not!
There are 2 ECG patterns that have been associated in the literature as representing Wellens
Syndrome. We favor use of only one of these patterns to define the syndrome (Figure 10.56-1):
Many clinicians interpret the pattern of symmetric anterior T wave inversion as one
expression of Wellens Syndrome (Panel A in Figure 10.56-1). We feel this is a mistake that
defeats the goal of recognizing this syndrome.
While anterior symmetric T inversion (as seen in Panel A of Figure 10.56-1) clearly does occur
in patients with ischemic heart disease seeing this pattern on ECG without slight ST elevation
and the steep T wave downslope in Panel B is simply not nearly as predictive of a proximal
critical LAD lesion. Instead patients who only manifest the symmetric T inversion of Panel
A might have: i) milder (non-critical) coronary disease, which could be in any part of the LAD
(not necessarily the proximal LAD); ii) any of the other causes of T wave inversion that were
listed in Section 10.52; or iii) no heart disease at all.

Figure 10.56-1: The ECG finding of symmetric anterior T wave inversion (as schematically shown
in Panel A) is not specific for a proximal LAD lesion. In contrast the pattern seen in Panel B
which shows slight ST elevation with a steep T wave downslope is highly specific for a critical
proximal LAD lesion. OUR Preference: While fully acknowledging that some patients who manifest
the T inversion pattern of Panel A will have coronary disease We favor reserving the term,
Wellens Syndrome for the ECG picture in Panel B, which in a symptomatic patient is much more
specific for a proximal critical LAD narrowing.

10.57 DeWinter T Waves

In follow-up to Wellens Syndrome ( Section 10.54) the 2nd ECG pattern we highlight as being
highly specific for the presence of a critical proximal LAD narrowing is the presence of
DeWinter T waves.
Recognition of DeWinter T waves is mandate
catheterization/acute reperfusion).

for immediate intervention (cardiac

10.58 ECG Recognition: What are DeWinter T Waves?

Awareness of the relatively uncommon but highly characteristic DeWinter T wave sign is essential
for not overlooking the approximate 2% of acute anterior MI patients who present with this ECG
manifestation (DeWinter,Wellens,Wilde: NEJM 359: 2071, 2008).
Rather than frank ST elevation that usually accompanies acute LAD occlusion there is instead
the unique DeWinter complex, with upsloping J-point ST depression blending into very tall
upright hyperacute T waves in usually several of the precordial leads (red arrows in leads
V2,V3 of Figure 10-58.1).

Figure 10.58-1: Schematic ECG from a hypothetical patient with new-onset chest pain. DeWinter T
waves are seen in several of the precordial leads (especially V2,V3 but also lead V4). Note
disproportionately tall upright (hyperacute) T waves that arise from the characteristic J-point ST
depression (red arrows in V2,V3). An encouraging sign that infarction has not yet taken place is
the presence of r waves with appropriate r wave progression in the anterior leads (transition is
slightly delayed but the r wave does get progressively taller as one moves from lead V1-to-V4 ).
Prompt catheterization and reperfusion is essential!

10.59 DeWinter T Waves: Clinical Characteristics

We emphasize the following key points about patients who present with chest pain and DeWinter T
waves on ECG:
Recognition of DeWinter T waves in patients with new-onset chest pain is highly
correlated with the finding of acute proximal LAD critical stenosis on cardiac catheterization.
Rather than evolution of tall, peaked (hyperacute) T waves into frank ST segment elevation
the DeWinter T wave pattern is often surprisingly static over the ensuing few hours.
None of the patients in the DeWinter series who manifested this ST-T wave pattern had acute
left main occlusion on catheterization (NEJM 359: 2071, 2008). Thus, the DeWinter T wave
complex appears highly specific for proximal LAD stenosis (and not for a left main lesion).
Despite prompt recognition and intervention a significant percentage of patients developed
positive cardiac markers for acute infarction. One ECG sign that infarction may have already
occurred is development of an anterior QS wave or loss of r wave amplitude (See Figure
10.60-1 below).

10.60 FIGURE 10.60-1: What is the Culprit Artery?

Consider the ECG shown in Figure 10.60-1 obtained from a patient who presented to the ED with
new-onset chest pain.
Should the cath lab be activated for acute STEMI?
IF so What do you suspect the culprit artery is likely to be?
How many ECG signs are present in Figure 10.60-1 to support your clinical impression?

Figure 10.60-1: ECG obtained from a patient with new-onset chest pain. Should the cath lab be
activated for acute STEMI? IF so What is the culprit artery likely to be? (See text).
Answer to Figure 10.60-1: The rhythm is sinus. All intervals and the axis are normal. There is no
chamber enlargement. There are however, a series of alarming findings that were recognized by the
emergency team. Cardiac catheterization was performed within 15 minutes after this patient walked
into the ED with successful reperfusion of a 100% proximal LAD occlusion. Clues to the need for
immediate catheterization and clues indicating localization of the culprit artery to the proximal
LAD including the following:

Hyperacute T waves in multiple leads. These are best seen in leads aVL; and in V2,V3,V4.
DeWinter T Waves Rather than frank ST elevation (as is usually seen with acute anterior
infarction) there is 1-to-3 mm of upsloping J-point ST depression in one or more
precordial leads that continue into tall, positive symmetric T waves (seen best in leads V3,V4
of Figure 10.60-1).
Loss of anterior R waves (with reduction in R wave amplitude between leads V1-to-V2).
Marked inferior reciprocal ST depression.
ST elevation in leads aVR and V1.
Incomplete RBBB (rSr in lead V1; narrow terminal S waves in leads I,V6).

ECG PEARLS: In addition to precordial DeWinter T waves and loss of r wave between V1-to-V2
there are a few more signs suggestive/consistent with an acute proximal LAD lesion. These
include: i) Significant ST elevation in leads aVR and V1 (with the amount of ST elevation in aVR
not more than the amount in lead V1); ii) Incomplete RBBB (that is presumably new); iii) Marked
inferior reciprocal ST depression; and iv) The presence of a hyperacute T wave with ST elevation
in lead aVL.
ACKNOWLEDGMENT: My appreciation to Andrew Bowman for allowing me to use the case and
ECG from the patient whose tracing is shown in Figure 10.60-1.

10.61 Takotsubo Cardiomyopathy

One of the most interesting new entities in clinical cardiology is Takotsubo Cardiomyopathy.
First described by Sato et al in 1990 as a reversible form of cardiac dysfunction the precise
mechanism of this intriguing clinical entity remains elusive. It is still all-too-commonly overlooked
as a potential etiology for what otherwise might constitute difficult-to-explain ECG and clinical
findings.
10.62 FIGURE 10.62-1: Acute STEMI or Something Else?
Consider the ECG shown in Figure 10.62-1 which was obtained from an older woman with severe
abdominal pain. No chest pain. Serial troponins were no more than minimally elevated. She
presented with heart failure.
How might you explain this clinical picture?
How can definitive diagnosis be made?

Figure 10.62-1: ECG obtained from an older woman with abdominal pain and evidence of heart
failure. No chest pain. How might you explain this clinical picture? (See text).
Answer to Figure 10.62-1: The rhythm is sinus at ~100/minute. The PR and QRS intervals appear to
be normal but the QT is prolonged (clearly more than half the R-R interval). The axis is normal
(+70 degrees). No chamber enlargement. An rSr complex is noted in lead V1.
Assessment of Q-R-S-T Changes is remarkable for the presence of inferior Q waves
normal transition (R wave becoming taller than the S wave between leads V3-to-V4) and ST
segment coving with marked ST elevation in the inferior leads. This is accompanied by deep
T wave inversion. Similar abnormal ST segment coving and elevation (albeit not as marked) is
also present in leads V4,V5. Deep, symmetric T wave inversion that begins in lead V3 is seen

in V4,V5. Reciprocal ST depression is seen in lead aVL, and to a lesser extent in V1,V2.
Impression: Despite the absence of chest pain the initial interpretation of this ECG was probable
acute STEMI (ST-Elevation Myocardial Infarction) in need of immediate cardiac catheterization for
possible reperfusion. After all there are Q waves, ST segment coving and elevation, deep T
wave inversion and reciprocal ST depression. Acute RCA occlusion vs an LAD wrap-around
lesion was suspected. However, cardiac catheterization revealed normal coronary arteries!
Instead of acute infarction the ventriculogram revealed the diagnostic picture of apical
ballooning with hypercontractility of the cardiac base that is characteristic of Takotsubo
Cardiomyopathy. The patient was treated supportively with recovery of left ventricular function
over the next few weeks.

10.63 Takotsubo CMP: Clinical Features

Takotsubo CMP (CardioMyoPathy) is an underappreciated cause of acute ECG abnormalities that
are often accompanied by a degree of new-onset heart failure:
First described in Japan in 1990 the entity derives its name from a specially designed
container used by Japanese fishermen to trap octopuses. The unusual round bottom and narrow
neck design of takotsubo resembles the diagnostic picture on cardiac catheterization obtained as
a result of ballooning of the cardiac apex with hypercontraction of the base (Figure 10.63-1).

Figure 10.63-1: Collection of actual takotsubo showing the round bottom and narrow neck that
resembles the diagnostic picture seen on the cardiac catheterization ventriculogram (shown here
during end-systole). Note characteristic ballooning of the apex and hypercontractility of the base
during cardiac cath (See text).

The precise mechanism for Takotsubo CMP remains elusive. While factors such as coronary spasm;
disturbance of the microcirculation; coronary artery anatomic variation; and neurogenic myocardial
stunning have all been implicated their role is uncertain. What has been shown is that
abnormal response to an increase in endogenous catecholamines is almost always involved.
Blood epinephrine and norepinephrine levels are unmistakably elevated (sometimes dramatically) in
patients with Takotsubo CMP.
In addition there is more-than-coincidental preceding occurrence of intense situational or
psychological stress in many patients. This may be in the form of severe emotional stress
(death of a loved one; break-up from significant other; overwhelming anxiety/depression )
pain and/or fear (from earthquake or other catastrophic event ). It is easy to understand the
rationale for other names that have been used for this syndrome (ie, Stress Cardiomyopathy
or Broken-Heart syndrome).
Although consensus is still lacking regarding specific criteria for defining Takotsubo CMP
there is general agreement that cardiac cath is diagnostic (ie, apical ballooning but no
culprit artery).
SUMMARY of the Clinical Picture: Takotsubo CMP is most typically seen in an older patient
(most often in a post-menopausal woman) who presents with chest pain or new heart failure.
Look for the following features:
Likelihood of preceding severe physical/emotional stress.
Markedly abnormal initial ECG often with diffuse ST elevation in inferior and anterolateral leads (apical or LAD wraparound distribution ). Associated T wave inversion and/or
Q waves (sometimes deep) may be seen. Acute extensive STEMI-in-evolution is frequently the
initial diagnosis (as was the case in Figure 10.62-1).
Usually no more than modest troponin elevation (troponins are often elevated but generally
not nearly as high as expected given how marked ECG changes are).
Transient LV dysfunction which may be severe initially (some patients present in
pulmonary edema/cardiogenic shock requiring intra-aortic balloon pump support ). LV
function usually resolves within a few weeks.
Possibility of potentially life-threatening arrhythmias during the acute phase (including
VT/Torsades de Pointes).
Absence of pheochromocytoma, myocarditis or other underlying cardiac pathology to explain
findings.
Generally favorable prognosis (often with full recovery within 1 month) but fatalities have
been reported (from LV free wall rupture; intractable pulmonary edema).
NOTE: Variations on the above theme do exist. The syndrome of Takotsubo CMP is not limited to
post-menopausal women the ECG does not always show marked abnormality and severe stress
does not uniformly precede presentation.
Anatomic areas other than the apex may also be affected. For example there may be an

inverted takotsubo form, in which the apex is spared but the base of the heart is hypokinetic.
The existence of such Takotsubo variants helps to explain the likely multifactorial etiology to
this interesting syndrome.
Final Clinical PEARL: Think of the possibility of Takotsubo CMP when confronted with a patient
who presents with a markedly abnormal ECG that doesnt quite fit the clinical picture.
ECG findings may be out of proportion to clinical findings. ECG changes may involve several
lead areas (especially inferior and anterior precordial leads which typically assess the
cardiac apex).
There may be an element of heart failure. Serum troponins may be positive.
The patient is usually an older adult (especially a post-menopausal woman).
There has usually been some form of severe preceding stress.

10.64 Muscular Dystrophy

Among non-ischemic etiologies for markedly abnormal ECGs in young individuals is the series
o f muscular dystrophies. The best known and most common of these is Duchenne Muscular
Dystrophy (DMD) but there are more than 20 different genetic forms of these rare muscular
dystrophy disorders. DMD occurs in ~1/3,000 boys (it is an X-linked disorder) with unfortunate
outcome of progressive muscle deterioration leading to death at an early age.
Among the many other forms of muscular dystrophy is Becker Muscular Dystrophy (BMD)
which is felt to be a less severe form than DMD. There are similarities among the different
forms of muscular dystrophy (re being genetic defects leading to progressive muscle
weakness/deterioration) though variations exist depending on muscle groups affected and
prognosis.
The defect in DMD is the absence of a critical muscle protein (ergo rather than dystrophy
it is really a myopathy).
Symptoms of DMD typically begin before age 5 (sometimes in infancy). The boy with DMD
will lag in development. He may be clumsy, unbalanced, weaker and easily prone to fatigue.
Pseudohypertrophy (enlargement of calf and deltoid muscles) occurs and may be an early
sign (due to replacement of injured muscle cells by fibrous or scar tissue).
Progressive muscle weakness develops beginning proximally (legs, pelvis) before spreading
to other areas.
Diagnosis of DMD (and other muscular dystrophies) is suspected by increased CK levels on
lab testing and confirmed by muscle biopsy and genetic testing.
DMD is uniformly fatal. The disorder is progressive and ultimately affects all voluntary
muscles. The heart and respiratory muscle groups are typically affected by the teens. Myocardial
deterioration (cardiomyopathy) and respiratory failure represent the major threat to life. There
is no cure (most boys die before age 25).
Prognosis in other forms of muscular dystrophy is not necessarily uniformly fatal as it is in
DMD. Cardiac involvement (and ECG changes) are common in many (but not all) of these
other forms. Females may be affected in some of the other forms.
BOTTOM Line: It is well to be aware of the group of muscular dystrophies as one of the causes
of a markedly abnormal ECG in a young adult (especially in males). Given the variation in
severity and presentation the diagnosis of a form of muscular dystrophy might not always be
known at the time an ECG is done.

10.65 Muscular Dystrophy: Common ECG Abnormalities

By young adulthood the ECG with DMD (and with many other forms of muscular dystrophy) will
usually be abnormal. Among the ECG abnormalities that are commonly seen include the following:
Abnormal Q waves not due to infarction. These are most often seen in lateral leads.

Sinus tachycardia (due to impaired cardiac function).

RBBB that often manifests a peculiar polyphasic rsr or rsrs in lead V1.
Tall anterior R waves that may manifest surprisingly high amplitude. This may result in
early transition or even as a Tall R in V1 (Section 10.47).
Other conduction defects may be seen including nonspecific IVCD with unusual QRS
morphology.
BOTTOM Line: The ECG of a patient with muscular dystrophy may be markedly abnormal. This
should be easy to understand given the genetic fault in muscle protein (with replacement of
myocardial tissue by fibrous and scar tissue ). This also explains the unusual array of ECG
abnormalities and conduction defects that may be seen.
10.66 FIGURE 10.66-1: Abnormal ECG in a Young Subject
Consider the ECG shown below in Figure 10.66-1 obtained from a 22-year old man in a
wheelchair because of longterm disability and weakness. No chest pain.
How would you interpret this ECG?
Can you think of a clinical entity that might account for this clinical scenario?

Figure 10.66-1: 12-lead ECG obtained from a 22-year old man in a wheelchair with longterm
disability. What medical diagnosis might explain this clinical scenario in association with this ECG?
Answer to Figure 10.66-1: The ECG shows sinus rhythm at ~70/minute. The PR interval is normal
but the QRS is prolonged to at least 0.12 second. QRS morphology in the 3 key leads (I,V1,V6) is
not consistent with either left or right bundle branch block. Therefore We would classify the
conduction defect as nonspecific IVCD (IntraVentricular Conduction Delay).
Continuing with the interpretation We note marked LAD (Le f t Ax i s Deviation) that is
consistent with LAHB (Left Anterior HemiBlock) in view of the predominantly negative QRS
complex in lead II.
QRS amplitude is markedly increased in lead aVL although reliability of the ECG diagnosis
of LVH is reduced in the presence of conduction defects.

Regarding Q-R-S-T Changes there are deep and wide Q waves in the high lateral leads
(I,aVL). In addition there is a small q wave in lead V2.
QRS morphology in lead V1 is peculiar as there is an rSrs complex . This is followed by
abrupt early transition that takes place between lead V1-to-V2. A disproportionately tall R
wave is noted in lead V2.
R wave amplitude drops off by lead V3 with persistent S waves seen throughout the
remaining precordial leads.
There is ST depression in lateral leads I and aVL, which may reflect LV strain from
suspected LVH. That said ST-T wave changes do not appear to be acute.
IMPRESSION: This ECG is clearly abnormal and highly unusual for a young adult. The diagnosis
of a form of muscular dystrophy would explain all of the abnormalities seen (Section 10.65).
ACKNOWLEDGMENT: My appreciation to Dr. Harsha Nagarajarao for allowing me to use the case
and ECG from the patient whose tracing is shown in Figure 10.66-1.

10.67 Hypothermia (Osborn Wave)

The Osborn Wave was first described in 1953 by JJ Osborn. The wave is commonly linked to
hypothermia but other entities (including CNS injury and ventricular fibrillation) may also be
associated with it. A number of other names have been attributed to this ECG finding (camel-hump
sign; hypothermic wave; prominent J wave).
T he Osborn Wave is a positive deflection that occurs just after the QRS and at the
beginning of the ST segment (Figure 10.67-1).
Osborn waves are often not seen until the temperature drops below -32 degrees Centigrade
(=89.6 degrees Fahrenheit).
Other commonly associated ECG features with Hypothermia include: i) Bradycardia (which
may be marked) ; ii) Atrial fibrillation; and iii) Artifact (from baseline undulations resulting
from associated shivering).

Figure 10.67-1: Osborn wave highlighted by the red arrow. The ST segment is flat. Note fine
undulations in the baseline that are commonly seen with hypothermia from associated shivering.
10.68 FIGURE 10.68-1: ECG Features of Hypothermia
Consider the ECG shown below in Figure 10.68-1 obtained from a homeless man who was
stuporous and intoxicated when found in an open wet field.
What would you guess this patients core temperature to be?

Figure 10.68-1: ECG obtained from a homeless man who was stuporous and intoxicated when found
in an open wet field. Prominent Osborn Waves are noted in multiple leads (blue arrows). Note fine
undulations in the baseline from associated shivering (large red arrow in lead II rhythm strip).

Answer to Figure 10.68-1: There is baseline artifact. We suspect the rhythm is sinus based on what
appear to be low amplitude P waves with a fixed PR interval in lead II (and overall regularity of the
rhythm) but it is difficult to be sure of atrial activity given the artifact. Frequent occurrence of
atrial fibrillation in hypothermic patients is another potential reason for baseline undulations (and
another reason rhythm determination may be challenging).

Osborn Waves are present. These are especially marked in leads V3,V4,V5 (blue arrows) in
which they attain at least 5 mm in amplitude! Osborn waves are also seen to a lesser degree in
leads V2 and V6. They may also be present (hiding in the terminal portion of the QRS
complex) in the inferior leads but the distinct notching of an Osborn wave is absent in these
leads.
Small inferior q waves are seen but ST-T wave changes do not appear to be acute.
T waves appear prominent and somewhat peaked in V3,V4,V5.

Clinical Correlation: The patients core temperature on arrival was 30 degrees Centigrade (86
degrees Fahrenheit). Serum K+=7.3 mEq/L; arterial pH=6.89. Tremor (producing baseline artifact
as seen here) is common in hypothermic patients. Of interest Osborn waves resolved as the patient
was warmed. Despite tropical location (Costa Rica) this case illustrates that hypothermia may
occur in warm weather places if predisposing circumstances are present (in this case alcohol
intoxication and poor choice of shelter).
ACKNOWLEDGMENT: My appreciation to Leonardo Chacon for allowing me to use the case and
ECG from the patient whose tracing is shown in Figure 10.68-1.

11.0 Electrolyte Disorders

With possible exception of hyperkalemia an electrolyte disorder will rarely be the primary
indication for obtaining an ECG. That said the ECG may be of definite assistance in assessing
some patients with certain types of electrolyte disorders, especially for explaining some of the ST-T
wave abnormalities that may be seen. Consider the following:
Potassium There is a surprisingly good correlation between serum K+ (potassium) levels
and the ECG when serum K+ is elevated. There are times when the ECG will be completed
before blood results are back strongly suggesting not only the diagnosis of hyperkalemia, but
i t s likely severity (and the need for immediate treatment even before serum value
confirmation). Unfortunately correlation between serum levels and ECG changes is poor
when serum K+ is normal or low (Section 11.7).
Magnesium is still all-too-often the forgotten cation. Hypomagnesemia is common when
serum K+ is low. Low serum Mg++ (magnesium) levels produce virtually identical ECG
changes as hypokalemia (Section 11.8). On the other hand Hypermagnesemia usually does
not produce ECG changes until serum Mg++ levels are markedly increased (usually >8-10
mEq/L) at which time there may be bradycardia, prolongation of PR/QRS/ QT intervals
and/or AV block. Clinical hypermagnesemia to this degree is distinctly uncommon in clinical
practice unless there is renal failure with Mg++ supplementation.
Calcium either in excess or deficiency, will not often produce recognizable effects on the
ECG. That said there are changes to look for: i) Hypocalcemia typically prolongs the QT
interval without affecting the subsequent ST segment; and ii) Hypercalcemia may shorten the
QT (Section 11.1).
Other Electrolyte Disorders (including abnormalities in serum Sodium and Phosphorus)
in our experience do not produce any specific (recognizable) ECG picture. That said, there will
often be more than a single electrolyte abnormality at a time so additive effects are possible.
In this segment We limit discussion and illustration of electrolyte-induced ECG Changes to the
following:
Calcium disorders Section 11.1.
Hyperkalemia Section 11.3.
Hypokalemia Section 11.7.
Hypomagnesemia Section 11.8.
Discussion of U waves Section 11.9.

11.1 CALCIUM: ECG Changes of Hyper- & HypoCalcemia

As noted above it will not be often that you will be able to look at an ECG and say, These ECG

changes are due to an excess or deficiency in serum Calcium. There are several reasons for this:
i) ECG changes of hypo- and hypercalcemia are both subtle and often do not occur until excess or
deficiency of this cation is marked; and ii) Calcium disorders are commonly associated with other
metabolic and/or clinical problems. That said it is still useful to be aware of the effect that
Calcium disorders may have on the ECG. Consider the following:
HypoCalcemia typically prolongs the QT interval. As a result a low serum Calcium
level is one of the causes in our LIST #3 for a long QT (Section 06.2). In theory the ST
segment is not affected by hypocalcemia, such that the T wave at the end of the long QT looks
normal. This effect is schematically illustrated in Figure 11.1-1 in which compared to the
situation when serum Calcium and the QT interval are both normal (Panel A) a seemingly
unaltered T wave is delayed in appearance by the long QT of hypocalcemia (Panel B).
Clinically the ECG picture seen in Panel B is typically not seen until serum calcium is
markedly decreased. Even then, it may be difficult to distinguish the ECG effect of low serum
calcium from that of other associated electrolyte disorders. Bottom Line: Dont expect to
recognize hypocalcemia on ECG.
Panel C Be aware that Hypocalcemia and Hyperkalemia may occur together in patients
with renal failure. Clinically this combined electrolyte disorder may occasionally be
suspected by the ECG finding of peaked (pointed) T waves with narrow base that occur at the
end of a long QT (Panel C in Figure 11.1-1).
HyperCalcemia may shorten the QT interval. That said Dont expect to see QT
shortening until serum Ca++ levels are markedly increased (usually to more than 12mg/dL).
Even then it will often be exceedingly difficult to distinguish between a QT interval that is
normal (Panel A in Figure 11.1-1) vs a QT that is short with early peaking of the T wave
(as is theoretically seen with hypercalcemia Panel D).

Figure 11.1-1: Schematic illustration of ECG changes with Calcium disorders. Panel A the ST-T
wave and the QT interval are both normal. Panel B Hypocalcemia, which may lengthen the QT
interval. The ST-T wave is otherwise unaffected. Panel C Hypocalcemia with Hyperkalemia, as
may occur with renal failure. The tall, peaked (pointed) T wave with narrow base of hyperkalemia
is delayed by the long QT of hypocalcemia. The preceding long ST segment is flat. Panel D
Hypercalcemia, which may shorten the QT (with reduced time until T wave peaking). Clinically
it is usually difficult to distinguish between a normal vs short QT interval (See text).
11.2 Figure 11.2-1: Acute STEMI or HyperCalcemia?
Consider the ECG shown below in Figure 11.2-1 obtained from a 60-year old man being treated
for advanced lung cancer. He presented to the ED (Emergency Department) with weakness and

palpitations, but no chest pain.

Should the cath lab be activated for acute STEMI?
If so what do you suspect the culprit artery is likely to be?
Is anything else likely to be going on in Figure 11.2-1 in view of this clinical history?
HINT #1: Be systematic in your interpretation (including assessment of all intervals).
HINT #2: Feel free to review Section 11.1 that was just covered before formulating your
answer.

Figure 11.2-1: ECG obtained from a 60-year-old man with lung cancer, weakness and palpitations
but no chest pain. Is this ECG diagnostic of an acute STEMI? Is anything else likely to be going on?
(HINT: Feel free to review Section 11.1 before formulating your answer).
Answer to Figure 11.2-1: The rhythm is sinus tachycardia. One PVC (Premature Ventricular
Contraction) is seen (the early wide-complex beat in simultaneously recorded leads V1,V2,V3).
The PR and QRS intervals are normal. The QT interval is difficult to assess given the tachycardia
and lack of distinct end point of T wave inversion. The axis is normal at +70 degrees. No chamber
enlargement.
Regarding Q-R-S-T Changes there are no definite q waves; transition is normal (occurring
between leads V2-to-V3). The most remarkable finding relates to ST-T wave changes.
There is coved ST elevation in each of the inferior leads (II,III,aVF) and in lateral
precordial leads (V4,V5,V6). In each of these leads, there appears to be T wave inversion
following descent of the ST segment.
There is reciprocal ST depression in leads aVL, V2, and to a lesser extent in lead V3. Lead V3
shows transition between the flat ST depression in lead V2 and the ST coving and T wave
inversion that begins in lead V4.
Initial Impression: The ECG in Figure 11.2-1 suggests acute STEMI (ST Elevation Myocardial
Infarction) in that there is coved ST elevation with T wave inversion and reciprocal ST
depression. That said there are 3 elements about the history given and the ECG in Figure 11.2-1
that should be cause for contemplation: i) There is no history of chest pain; ii) The patient has

advanced lung cancer; and iii) The shape of the ST segment elevation is a bit off for acute STEMI.
KEY Clinical Point: Despite valid concern about possible acute infero-postero-lateral STEMI
(either from a proximal right coronary vs dominant left circumflex occlusion ) the lack of chest
pain and lack of any defined onset of symptoms in the context of a patient with advanced cancer
should prompt additional data gathering prior to cath lab mobilization.
Initial serum troponins were negative.
The patient was taken to the cath lab. No acute lesion and no significant coronary disease was
found.
While in the cath lab additional lab values returned showing a markedly elevated serum
Calcium value = 17 mg/dL.
Comparison ECGs were ultimately found. These were clearly abnormal. While a similar degree
of ST elevation was not seen on prior tracings there was definite ST segment coving with T
wave inversion present on earlier tracings.
Clinical SYNTHESIS: This case is admittedly subtle and complex. It is clearly beyond-the-core for
the beginning interpreter. Nevertheless We feel it is an excellent teaching example for emphasizing
a number of clinical points that are of interest for providers of any level. These include the following
principles:
All ST segment elevation is not necessarily the result of acute coronary occlusion! In
addition to common other causes of ST elevation (ie, early repolarization variants; LVH;
acute pericarditis) chronic ST elevation may result from either ventricular aneurysm or
cardiomyopathy. This case serves to remind that Hypercalcemia is yet another potential
STEMI-mimic.
Textbooks describe QT interval shortening as the principal ECG manifestation of
hypercalcemia. That said recognition that the QT interval is short is not easy to detect
because: i) Usually marked hypercalcemia (levels >12.0 mg/dL) are needed before the QT
noticeably shortens; ii) it will often be difficult to distinguish clinically between a QT interval
that is within the normal range vs one that is too short; and iii) ECG manifestations of
hypercalcemia are superimposed on any baseline abnormalities that may be present.
We mentioned that the shape of the ST elevation in this case was a bit off for acute STEMI.
By this we mean that the coved ST segments seemingly peak a tad earlier than is usually seen.
That said the overall QT interval in this case is not shortened. If anything the overall QT
interval is lengthened by preexisting T wave inversion that was seen to be present on prior
comparison tracings.
BOTTOM Line It is virtually impossible to attain 100% accuracy in knowing when to activate the
cath lab based on assessment of a single initial ECG. Centers that boast an accuracy rate of 100% are
clearly missing a certain percentage of acute MI patients who would probably benefit from early
reperfusion.
Occasional false activation of the cath lab is inevitable and clearly understandable in this

case given the ECG picture of ST elevation with T wave inversion and reciprocal ST
depression. Hindsight is 100% in the retrospectoscope (Grauer circa 1980). That said
the lesson to be learned is that the ECG is not a perfect tool and the patient in this case gave
no history of chest pain, and no defined onset of symptoms. There are times when slight delay
before activating the cath lab is appropriate so that some additional evaluation can be
performed.
ACKNOWLEDGMENT: My appreciation to Jiann Ruey Ong for allowing me to use the case and
ECG from the patient whose tracing is shown in Figure 11.2-1.
11.3 HYPERKALEMIA: ECG Manifestations/Clinical Features
The ECG may prove invaluable in expediting recognition of clinically important hyperkalemia. This
is because with Hyperkalemia there is a surprisingly close correlation between serum K+ levels
and ECG findings. We highlight this relationship in schematic Figure 11.3-1:
Panel A the serum K+ level is normal (between ~3.5-5.0 mEq/L). The QRS is of normal
duration. The T wave is smooth.
Panel B shows peaking of the T wave, which is generally the earliest change of
hyperkalemia (K+ ~5.5-6.5 mEq/L). This may initially be subtle.
Panel C The T wave becomes taller and more peaked (K+ ~6.5-7.5 mEq/L). With
progressive hyperkalemia the T wave takes on an Eiffel Tower appearance. Not only is
the T wave tall and peaked but it manifests a narrow base (like the Eiffel Tower ). This is in
contrast to the T wave that is sometimes seen in healthy individuals as a Normal Variant
(lower right insert within Figure 11.3-1) in which the T wave is rounded, its sides are not
symmetric (slower ascent than descent) and the T wave has a broader base (Discussed
momentarily in Section 11.6).
Panel D P wave amplitude decreases; the PR interval lengthens and the QRS widens (K+
>8 mEq/L). Recognition of these ECG features signals potentially life-threatening
hyperkalemia.
Panel E P waves often disappear at serum K+ levels >8-9 mEq/L. Yet despite no longer
seeing P waves on the surface ECG the rhythm is still initiated by SA nodal impulses
(sinoventricular rhythm). The result may be a wide-QRS rhythm without P waves that is still
supraventricular (due to associated hyperkalemia See Section 11.4). Eventually (at serum
K+ levels >9-10 mEq/L) the QRS complex becomes sinusoid. Ventricular fibrillation and/or
asystole usually follow.

Figure 11.3-1: ECG Manifestations of Hyperkalemia. Starting from a normal T wave (Panel A)
the T wave becomes progressively taller and more peaked from Panel B (K+~5.5-6.5 mEq/L) to
Panel C (K+~6.5-7.5 mEq/L) as it takes on an Eiffel Tower appearance. Panel D P wave
amplitude decreases; the PR interval increases; the QRS widens (K+>8mEq/L) until the pre-lethal
stage in Panel E (K+>8-9 mEq/L) with sinoventricular rhythm (P wave no longer seen); marked
QRS widening; and ultimately a sinusoidal pattern prior to VFib or asystole. Note the difference in
shape between the T wave in Panel C vs the Normal Variant pattern (lower right insert
asymmetric T wave; rounder; with a wider base).
Clinical NOTE: At the bedside our first inclination when told of an elevated K+ level is to
validate the reading (and rule out hemolysis). We do this by repeating the blood test.
At times simply obtaining an ECG may be a faster way to determine IF there is cause for
concern. The absence of ECG signs shown in Figure 11.3-1 suggests that serum K+ is
probably not significantly elevated.
Increasing Incidence of HyperKalemia: Clinically the incidence of Hyperkalemia continues to
increase. This is at least in part because of the increasing number of patients on longterm dialysis.
More patients have diabetes than ever before (obesity epidemic in the general population).
These patients are living longer so more of them than ever before go on to eventually require
dialysis. As a result virtually all health care providers will encounter patients with
hyperkalemia at some frequency.
K E Y Clinical Point: With rare exceptions (ie, hyperkalemic periodic paralysis)
Hyperkalemia does not usually develop unless there are one or more predisposing factors.
These should be inquired about in the history. Potential predisposing factors may include: i) Use
of K+-retaining medications (ACE-inhibitors; angiotensin-receptor blockers; K+-sparing
diuretics) ; ii) Potassium supplementation; iii) Renal failure/dialysis; iv) Acidosis; v)
Dehydration; and vi) Severe trauma.

11.4 Figure 11.4-1: Ventricular Rhythm vs Hyperkalemia?

Consider the 2 rhythm strips shown below in Figure 11.4-1. Imagine each tracing was obtained from

a hemodynamically stable older adult.

Is the rhythm in Panel A ventricular escape?
Is the rhythm in Panel B a slow form of VT?
How would you proceed clinically in each case?
What clinical information would you want to know about each patient? (HINT: How might
these 2 rhythms relate to the content of Section 11.3?).

Figure 11.4-1: Ventricular rhythms vs hyperkalemia? (See text).

Answer to Figure 11.4-1: Although our initial impression for both arrhythmias in this Figure is that a
ventricular rhythm is present in each case this is not necessarily the correct answer. For example
IF told that each patient was hemodynamically stable and on longterm dialysis (or had a history
of chronic kidney disease) then a stat serum K+ value becomes essential for accurate diagnosis
and optimal management.
Rhythm A (in Figure 11.4-1) shows QRS widening a slow ventricular rate (~45/minute)
lack of P waves and suggestion of T wave peaking. In a patient on longterm dialysis
one has to consider hyperkalemia!
Rhythm B closely resembles AIVR (Accelerated IdioVentricular Rhythm) as was
discussed in Section 02.38. But IF this patient had renal failure Hyperkalemia would again
become a key consideration.
BOTTOM Line: IF it turned out that marked hyperkalemia was the reason for the wide rhythms in
Panel A and Panel B then rather than Pacing/Atropine the treatment of choice would be
Bicarb/Calcium.
History is ever important! Sometimes a stat K+ level is needed for accurate diagnosis. Given
the hemodynamically stable condition of each patient in Figure 11.4-1 there is time for lab
confirmation of the diagnosis.
Knowing that a hemodynamically stable patient with a wide-QRS rhythm without sinus P waves
has renal failure goes a long way toward suggesting that what we are seeing in Figure 11.4-1
is a rhythm in a patient with hyperkalemia (with changes in QRST morphology corresponding
to that seen in Panel D or Panel E from Figure 11.3-1). This is important since optimal

treatment of this patient depends on accurate diagnosis of the reason for QRS widening.

11.5 Figure 11.5-1: Ischemia vs Hyperkalemia?

Consider the ECG shown in Figure 11.5-1. Clinically What is likely to be going on? Is there ECG
evidence of ischemia?

Figure 11.5-1: Ischemia vs hyperkalemia? (See text).

Answer to Figure 11.5-1: Sinus rhythm at ~100/minute. The PR interval is normal; the QRS and QT
are borderline prolonged. Rightward axis. No chamber enlargement.
QRST Changes There is a Q wave in lead I and there are QS complexes in leads
aVL,V1,V2. Transition is slightly delayed (occurs between V4-to-V5). The most remarkable
finding is the very tall, peaked T waves with narrow base (Eiffel Tower effect) in at least
several precordial leads. This strongly suggests hyperkalemia perhaps with a serum K+ ~67.5 mEq/L (See Figure 11.3-1). In addition, T waves are inverted sharply in leads III and aVF
and there is some ST depression in infero-antero-lateral leads.
We would want to inquire from the history IF there were predisposing factors (such as renal
failure) to the severe hyperkalemia that we suspect from this tracing.
Clinical NOTES: The ECG is the net result of the hearts electrical activity. Therefore ECG
changes from new hyperkalemia will be superimposed on any preexisting ST-T wave abnormalities.
Well have to wait until hyperkalemia is corrected before knowing IF abnormal findings (right
axis; QS complexes; T wave peaking; ST depression and T inversion) are due to ischemia as
well as hyperkalemia.
In our experience We have seen a great variety of abnormal ECG findings disappear once
hyperkalemia is corrected. For unknown reasons marked right axis (as seen in Figure 11.5-1)
often resolves once serum K+ is again normal.
Note in Figure 11.5-1 that the negative peak of the inverted T waves in leads III,aVF is sharp
(pointed). Although positive peaked and pointed T waves are much more commonly associated
with hyperkalemia T wave peaking may occasionally be negative with this electrolyte

disorder. Well only know for sure after serum K+ is corrected and a repeat ECG is obtained.
BOTTOM Line: Be sure to repeat the ECG after hyperkalemia is corrected and correlate
tracings to the clinical situation (ie, chest pain with possible ischemia vs simple
hyperkalemia?).

11.6 Figure 11.6-1: Hyperkalemia vs Normal Variant?

Finally, consider the ECG in Figure 11.6-1 obtained from a healthy 30-year old man. How might
your interpretation change IF the patient was older on longterm dialysis?

Figure 11.6-1: Hyperkalemia vs Normal Variant? (See text).

Answer to Figure 11.6-1: Sinus arrhythmia. Normal intervals and axis. No hypertrophy (since the
patient is only 30 years old). T waves are peaked and there is slight J-point ST elevation with an
upward concavity (smiley configuration) in several precordial leads. IMPRESSION: Given that
the patient is a young, otherwise healthy adult this ECG almost certainly represents ERP (Early
Repolarization Pattern Section 09.02).
But IF the patient was older with chronic kidney disease then we would definitely check the
serum K+ value. Even though T waves here do not manifest the typical Eiffel Tower effect in
that they had a broad base with asymmetric ascent and descent of the T wave (Figure 11.6-2)
all bets would be off IF the patient had renal disease or other potential reason for hyperkalemia.
BOTTOM Line: Clinical correlation is key to optimal interpretation.

Figure 11.6-2: Comparison of ECG characteristics for the T wave of hyperkalemia (Panel C

reproduced from Figure 11.3-1) vs what is commonly seen as a normal variant in otherwise
healthy adults. Note that the T wave of Hyperkalemia (in Panel C) generally manifests a more
peaked (pointed) T wave with narrow base and symmetric ascent/descent of T wave. In contrast
the T wave in a normal repolarization variant tends to be rounder with wider base and asymmetric
ascent/descent of T wave. Exceptions exist so clinical correlation is essential (See text).
11.7 HYPOKALEMIA: ECG Manifestations/Clinical Features
In contrast to hyperkalemia the ECG is not a reliable tool for assessing hypokalemia. While true
that it is unlikely for the ECG to be normal IF clinically significant hypokalemia is present
ECG changes are often nonspecific they may be difficult-to-interpret and in our experience,
ECG changes are suboptimal in ability to correlate with degree of severity. We highlight the
following Clinical Caveats regarding ECG assessment of HypoKalemia:
Patients with hypokalemia do not always manifest ECG changes. In fact, the ECG of patients
with even moderate hypokalemia may at times be relatively normal (with little more than
nonspecific abnormalities).
In contrast Some patients who have normal serum K+ levels do manifest ECG changes that
seem to suggest they have hypokalemia.
BOTTOM Line: The ECG is simply not very accurate as a tool for assessing either the presence
or severity of hypokalemia. This is not to say that the ECG should not be monitored in patients
with hypokalemia. On the contrary ECG monitoring may be helpful in a number of ways.
These include: i) Detection of arrhythmias (PVCs are common with hypokalemia; risk of VT is
increased); ii) The QT (or QU) interval may be significantly prolonged with hypokalemia
with associated increased risk of Torsades de Pointes ( Section 06.3) ; and iii) Serial ECG
changes that are followed as hypokalemia is treated and serum K+ returns to normal may
provide insight to the likelihood of associated ischemia vs ECG abnormalities being
primarily a result of the electrolyte disorder. Clinical correlation is KEY.
FIGURE 11.7-1: What are the ECG Changes? Having conveyed potential clinical caveats of
depending on the ECG to assess hypokalemia We review in schematic Figure 11.7-1 those ECG
Changes that have been associated with low serum K+ values:
Panel A The ST-T wave is normal. This is the baseline tracing.
Panel B shows relative flattening of the T wave and ST segment. This is typically the
earliest change.
Panel C and Panel D In association with ST-T wave flattening ( and often with some degree
of ST depression) a U wave develops (Section 11.9). A "pseudo-P-pulmonale" pattern
(with P wave peaking in inferior leads) may sometimes be seen.
Panel E and Panel F ST depression becomes more noticeable and the U wave increases in
size (red arrow in Panel E) until ultimately the U wave overtakes the T wave. At this point,
distinguishing between the T wave and U wave may be almost impossible (ie, there is really
Q-U" rather than Q-T prolongation as in Panel F).

Figure 11.7-1: ECG Manifestations of Hypokalemia. Starting from a normal ST-T wave ( Panel A)
the earliest change is ST-T wave flattening ( Panel B). This may be followed by some degree of
ST depression and development of a U wave (in Panel C and Panel D). ST depression becomes
more noticeable and the U wave increases in size (red arrow in Panel E) until ultimately the U
wave overtakes the T wave. At this point, distinguishing between the T wave and U wave may no
longer be possible (Panel F). Despite this well described sequential evolution of ECG changes
many patients with hypokalemia fail to read the textbook (See text).
11.8 HYPOMAGNESEMIA: Clinical Features/ ECG Signs
In our introduction to this segment on electrolyte abnormalities We referred to magnesium as the
all-too-often forgotten cation. Serum Mg++ is still often excluded from routine chemistry profiles
in many institutions. As a result Hypomagnesemia often goes undetected unless the clinician is
aware of the need to specifically assess for this cation.
Hypomagnesemia is common in clinical practice. As is the case for potassium the vast
majority (>98%) of body magnesium resides within the intracellular compartment. As a result
serum levels (measuring a minority of body magnesium that resides within the extracellular
compartment) do not reliably reflect body (and intracardiac) magnesium stores. Thus, it is not
uncommon for a patient to have a serum Mg++ level that is still within the low-normal range (ie,
1.8 mg/dL) yet nevertheless having significant body depletion of this critical cation.
Therefore: Decidedly low serum levels of Mg++ are diagnostic for hypomagnesemia but
blood levels in the low-normal range still could reflect low body stores that may nevertheless
be clinically important.
Certain conditions predispose to Hypomagnesemia. These include: i) associated electrolyte
deficiency (hypokalemia; hyponatremia; hypocalcemia; hypophosphatemia); ii) Use of certain
medications (diuretics, digitalis) ; iii) Overuse of Alcohol; iv) Diabetes and other metabolic
disorders; v) renal disease; and vi) Certain cardiac conditions (low Mg++ is common with
acute MI; post-cardiac arrest; and in patients with various cardiac arrhythmias ) . KEY
Clinical Point: Consider hypomagnesemia (even if the blood level is within the low normal
range) in patients with any of the above potential predisposing conditions.
Hypomagnesemia may produce virtually identical ECG changes as may be seen with
hypokalemia (Figure 11.7-1). That is the ECG of a patient with low serum Mg++ may vary
from showing little more than minimal nonspecific changes to showing diffuse ST-T

flattening, ST depression, U waves, and moderate-to-marked QT (or QU) prolongation.

Clinically Hypomagnesemia often coexists with hypokalemia. The importance of not
overlooking coexistent hypomagnesemia is that hypokalemia may prove resistant to K+
replacement until serum Mg++ levels are restored to normal.

11.9 U Waves: Definition/Clinical Significance

The most commonly cited ECG sign of hypokalemia is the presence of U waves. A U wave is
recognized as the ECG deflection that occurs after the T wave but before the next P wave (red
arrow in Panel B of schematic Figure 11.9-1). Physiologically U waves are thought to represent
repolarization of Purkinje fibers. We highlight the following clinical points about ECG recognition
and the clinical significance of U waves:
U waves are not always present on an ECG tracing (Panel A in Figure 11.9-1). When seen
they are often evident only in certain leads (usually most easily recognized in leads II;
V2,V3,V4).
U waves are not specific for hypokalemia. They may also be seen with hypomagnesemia
LVH bradycardia or simply on normal tracings without other abnormality.
Like T waves U waves may become inverted as a sign of ischemia (Panel C). This is usually
quite subtle and difficult to see. To complicate recognition further there may be ST
depression with a biphasic terminal T wave (Panel D). As a result We Suggest the
following: IF not obvious on the patients ECG Do not worry about U waves!

Figure 11.9-1: Recognition of U Waves on ECG. Panel A A U wave will not always be seen on
ECG. When present, a U wave is recognized as the ECG deflection that occurs after the T wave
but before the next P wave (red arrow in Panel B). U waves are usually best seen in leads II;
V2,V3,V4 but they may be seen in any lead. They are not specific for hypokalemia (U waves may
also be seen with hypomagnesemia, LVH, bradycardia and sometimes as a normal variant in
healthy subjects) . Panel C U waves may be subtle in appearance and they may be inverted
(sometimes as a sign of ischemia) . Panel D It is not always easy to know if late baseline
deflections reflect U waves or not (See text).
11.10 Figure 11.10-1: Electrolyte Disturbance or Ischemia?
We conclude this segment on hypokalemia with the ECG shown below in Figure 11.10-1. This
tracing was obtained from a patient with a history of alcohol abuse and atypical chest pain. Obvious

ST-T wave abnormalities are present.

Given this clinical scenario Are the ECG abnormalities seen likely to reflect ischemia or
electrolyte disturbance? How can you tell?

Figure 11.10-1: ECG obtained from a patient with a history of alcohol abuse and atypical chest pain.
Are the ECG abnormalities seen likely to reflect ischemia or electrolyte disturbance? (See text).
Answer to Figure 11.10-1: There is sinus arrhythmia. PR and QRS intervals are normal but the
QT is prolonged (clearly more than half the R-R interval in lead II, as well as in other leads). The
axis is normal. No chamber enlargement.
The most remarkable finding is diffuse ST-T wave flattening/depression with symmetric T
inversion in leads V4,V5,V6. In addition U waves are seen in multiple leads (most obvious
in leads V2,V3 = blue arrows). The U wave in lead II (large red arrow ) seems to blend with
the T wave in this lead (similar to Panel F in Figure 11.7-1).
Clinical Impression: There are 2 principle abnormalities in Figure 11.10-1: i) A long QT interval;
and ii) Diffuse ST-T wave flattening, some ST depression, and symmetric T wave inversion. Clinical
correlation is needed for optimal determination of likely etiologies. Comparison with a prior ECG
(if available) would be extremely helpful in knowing whether the changes seen are likely to be
new or old.
The long QT interval should prompt consideration of our LIST #3 (Section 06.2). In brief
Consider: i) Drugs; ii) Lytes (especially low K+ and/or low Mg++ given this patients
history of alcohol abuse); and iii) CNS disturbance.
Diffuse ST-T wave abnormalities including ST flattening, ST depression and T wave inversion
should prompt consideration of our LIST #4 (Section 09.26). Among potentially relevant
entities to consider on this list in view of this patients history of alcohol abuse and chest pain
are: i) drug effect (if this patient was on digitalis or a diuretic) ; ii) electrolyte disturbance
(especially low K+ and/or low Mg++); and iii) ischemia.

BOTTOM Line: There is no way to be certain from this single ECG whether the abnormalities seen
i n Figure 11.10-1 represent ischemia electrolyte disturbance or some combination of these,
perhaps in association with other factors.

Clinical correlation including lab values, serial tracings and close follow-up of this patients
clinical course will be needed in order to know for certain. Even IF serum electrolyte values
initially come back low this would not exclude the possibility of ischemic T wave inversion
superimposed on electrolyte-induced ST-T wave abnormalities.
That said We strongly suspect hypokalemia (and probably also hypomagnesemia) are at
least in part responsible for the ECG abnormalities seen in Figure 11.10-1 because: i) the
history of alcohol abuse predisposes the patient to low K+/low Mg++ levels; and ii) the
presence of very prominent U waves in several leads plus marked QT prolongation are both
highly characteristic of these electrolyte disorders. Resolution of ECG abnormalities on serial
tracings as electrolyte disturbance is corrected would confirm a cause-and-effect relationship.

12.0 Acute Pericarditis

Pericarditis is an inflammation of the fibrous lining of the heart. The pericardium itself is a doublelayered membrane which covers the heart, as well as containing the roots of the great vessels. There
are 2 layers to the pericardial lining. These are: i) the inner visceral pericardium (which is attached
to the epicardium, or outer layer of the heart); and ii) the parietal pericardium (which is the outer
layer of the pericardial sac).
Normally there is a potential space between the visceral and parietal pericardial layers = the
pericardial cavity. Lubrication by a small amount of pericardial fluid allows normal free
movement of the heart within the pericardial sac.
Problems arise when because of inflammation (or other insult to the pericardial lining) the
amount of pericardial fluid increases. This results in pericardial effusion. In its extreme
there may be pericardial tamponade, with inability of the heart to contract within the pericardial
sac due to massive effusion and/or rigidity of the sac itself.
Clinical Points: The finding on Echo of a small pericardial effusion is usually a normal
phenomenon. Some fluid is needed for normal lubrication between visceral and parietal layers.
Echo is an excellent modality for detecting pericardial fluid and estimating the amount of fluid.
Anything more than a small effusion is not normal.
Echo is invaluable as a bedside diagnostic aid for detecting larger effusions and determining IF
pericardial tamponade is present.
Simple viral pericarditis (the most common kind of acute pericarditis) often does not
produce any abnormality on Echo because: i) The pericardium is a thin layer. Inflammation
generally produces no abnormality detectable on echo; and ii) Uncomplicated viral pericarditis
usually does not produce significant pericardial effusion. Therefore A normal Echo does
not rule out acute pericarditis. On the contrary a normal Echo is the most common finding
you will see.

12.1 Acute Pericarditis: How to Make the Diagnosis?

Pericarditis can be a challenging diagnosis to make. Recognition of acute pericarditis may be
facilitated by thinking of the diagnosis as a 3-part process. These 3 components consist of: i) History;
ii) Physical examination; and iii) ECG findings.
History: The 1st step in making the diagnosis of acute pericarditis rests with obtaining the history.
Information regarding the patients prior medical history recent health issues and the presence
and nature of symptoms are all relevant.
Potential Etiologies of acute pericarditis are many and extend beyond the scope of this ECG-

2014-ePub. The most common scenario is acute or recent viral illness occurring in a relatively
young adult. Almost any viral agent may be responsible. That said identification of the
specific causative agent (ie, by obtaining acute viral studies) is often not undertaken because
most cases of acute viral pericarditis (also known as idiopathic pericarditis) are
relatively benign, spontaneously resolve and do not recur. Knowing which virus is the culprit
agent does not alter treatment, is expensive, and does not affect the ultimate course in most
patients. Clinical NOTE: Given that up to 90% of all cases of acute pericarditis occurring in
out-patients are viral (idiopathic) and usually occurring in otherwise healthy adults KEY
Questions to ask relate to: i) Whether there is a history of preceding viral illness; ii) Prior
health status; and iii) Previous episodes (viral pericarditis may recur, though this is not
common).
KEY Point A different set of diagnostic considerations should be contemplated when
considering acute pericarditis in an older patient with underlying medical disorders. Among
the many possible other etiologies for pericarditis include: i) Non-viral infections
(tuberculosis, bacterial or fungal septicemia; immunocompromise ); ii) Uremia (pericarditis is
a common complication of end-stage renal disease) ; iii) Malignancy (metastasis to the
pericardium) ; iv) Collagen vascular disease (rheumatoid arthritis; lupus; scleroderma) ; v)
Post-radiation pericarditis; vi) Chest trauma; vii) Post-myocardial infarction pericarditis
(Dressler syndrome ); viii) Post-pericardiotomy syndrome; and ix) Still other causes. Clinical
NOTE: Pericarditis caused by any of the above entities is usually a different disease than
uncomplicated viral pericarditis that occurs in a previously healthy young adult. The course is
often far more severe, longer lasting, and much more likely to be associated with pericardial
effusion and/or tamponade. Awareness of the patients past medical history may be KEY to
suspecting the diagnosis for these other forms of non-viral pericarditis.
Symptoms: We limit discussion of symptoms to Chest Discomfort. Fever and dyspnea may also be
seen with acute pericarditis but these symptoms are nonspecific. The chest pain associated with
acute pericarditis may be moderate or severe. It is characterized by being: i) Pleuritic; and ii)
Positional in nature.
Pleuritic chest pain is often sharp in nature and increases with inspiration (a result of
associated pleural inflammation).
Positional chest pain is typically relieved by sitting up and exacerbated by lying supine
(lying supine stretches the inflamed pericardium whereas sitting up takes tension off the
inflamed pericardium).
Clinical NOTE #1: Although the nature and severity of chest pain associated with acute
pericarditis is highly variable eliciting a pleuritic and/or positional component can be very
helpful in suspecting the diagnosis, especially when the patient is a previously healthy young
adult.
Clinical NOTE #2: Given the common diagnostic dilemma of distinguishing between ERP
(Early Repolarization Pattern) vs Pericarditis (Section 12.9) it is helpful to remember that
acute viral pericarditis is very unlikely in the absence of symptoms. In contrast chest pain
is less uniformly present in some of the other non-viral etiologies of acute pericarditis.

Physical Examination: There are 2 Goals of physical exam: i) To try to make a definitive diagnosis
by hearing a pericardial friction rub; and ii) to r ul e out other causes of chest discomfort
(pulmonary problems; musculoskeletal pain; herpes zoster; etc.).
Characteristics of a pericardial friction rub are that it is a scratchy, superficial sound (like
walking on snow). There may be only one or several components to the rub. It may wax and
wane in loudness often becoming louder during inspiration. The rub is often transient, and
may be intermittent so it is worthwhile auscultating the patient on at least several occasions.
BOTTOM Line: IF a pericardial friction rub is heard then the diagnosis of acute pericarditis
is made! However not hearing a rub does not rule out pericarditis. Clinical Reality: Despite
a cited incidence in the literature of well over 50% of patients with acute pericarditis having a
rub at some point during their course the diagnosis of many (if not most) cases of acute
pericarditis is made in the absence of hearing a rub.
As noted above the history for acute pericarditis is often nonspecific (ie, recent nonspecific
viral infection) and the nature of chest pain may be variable. As a result other causes of
chest pain may be confused with the diagnosis. The other major purpose of physical
examination is therefore to rule out some of these other pulmonary or musculoskeletal causes
of chest pain.

12.2 ECG FINDINGS of Acute Pericarditis

In clinical practice the diagnosis of acute pericarditis is most often made on the basis of ECG
findings. ECG Changes are divided into 4 stages. The easiest way to remember these sequential
ECG findings is to conceptualize the 4 stages as follows (Figure 12.2-1):
Stage I Everything is UP. That is there is ST elevation in almost all leads (except
perhaps in the right-sided leads = leads III,aVR,V1).
Stage II Transition. There may be pseudonormalization in this stage that temporally
occurs between the diffuse ST elevation of Stage I and the diffuse T wave inversion to follow.
Stage III Everything is DOWN. That is there is diffuse T wave inversion in virtually all
leads.
Stage IV Normalization (as the ECG changes of acute pericarditis eventually resolve).

Figure 12.2-1: The 4 Sequential Stages of Pericarditis. Stage I (diffuse ST elevation) is the only
one of the 4 stages that is diagnostic of acute pericarditis. The amount of time spent in each stage is

variable. Pseudonormalization in Stage II explains why even relatively new-onset pericarditis

may sometimes manifest minimal ECG changes (or no ECG changes at all). The Stage III phase
(diffuse T wave inversion) is nonspecific and may be impossible to distinguish from ischemia.
Ultimately, ECG changes resolve (Stage IV) though this may take weeks or months. PEARL: To
remember the 4 stages Think everything UP (1st Stage) transition (2nd Stage) everything
DOWN (3rd Stage) Resolution (4th Stage).
KEY Points regarding Figure 12.2-1: The amount of time for evolution through the 4 ECG stages
of acute pericarditis is highly variable (it may take hours to days to weeks or more).
Practically speaking the only ECG stage that is diagnostic is Stage I. This means that IF
Stage I has already passed it will no longer be possible to diagnose pericarditis by ECG
(because the ECG may almost look normal in Stage II and in Stage III it shows diffuse T
wave inversion that may be indistinguishable from ischemia).
Awareness of the above expected sequence of changes explains why the ECG may look
relatively normal at an early stage in the process (ie, during transitional Stage II in which ST
segments return to baseline before going on to evolve into diffuse T wave inversion).
Clinical Notes: Additional lab tests (including Echo) will often be ordered on patients with
suspected pericarditis. That said it is rare that these other tests will be the test that makes the
diagnosis.
Echo is usually normal because the inflamed but nevertheless thin pericardial lining is not
picked up by simple Echo unless an associated significant pericardial effusion is present
(Section 12.0). Pericardial effusion is absent in many (if not most) cases of acute viral
pericarditis that occurs in otherwise healthy subjects without other underlying systemic disease.
The diagnosis of acute pericarditis can be easy IF a pericardial friction rub is heard. But IF
no rub is heard (as is often the case) then diagnosis must be presumptive (based on history
and ECG findings). Fortunately a presumptive approach is reasonable given the generally
benign and self-limiting course of most cases of acute viral (idiopathic) pericarditis that occur
in otherwise healthy individuals.

12.3 Stage I of Acute Pericarditis

Given that ECG diagnosis of acute pericarditis can really only be made in Stage I We focus on
recognizing ECG findings in this stage (Figure 12.3-1):
There will often be sinus tachycardia. While sinus tachycardia is a nonspecific finding that is
not essential for diagnosis of acute pericarditis the absence of at least a relatively rapid
heart rate is a factor against the diagnosis of acute pericarditis.
There is diffuse ST segment elevation (Stage I is the everything UP stage). This
generalized ST elevation is thought to reflect a diffuse subepicardial injury current. The only
leads that do not consistently show ST elevation are one or more of the right-sided leads (III,

aVR and V1) that view the heart from a more distant perspective (leads shaded in blue in Figure
12.3-1).
The shape of ST elevation with acute pericarditis is often quite similar to that seen with early
repolarization (concave up = smiley configuration, sometimes with J-point notching). It is
almost as if the ST segment itself is normal and has been lifted above the baseline.
With acute pericarditis the appearance of ST segments in leads I and II tends to look
similar. This differs from the usual situation with acute inferior MI in which lead III is much
more likely to resemble lead II.
There is no reciprocal ST depression! This is a key distinguishing feature of acute pericarditis
from acute MI.
Infarction Q waves are absent (No more than small q waves are seen).
PR segment depression is often noted in several leads (seen in Figure 12.3-1 in leads I,II and
V2,V3 but not in leads aVL,aVF; V4,V5,V6). PR depression is thought to reflect an atrial
injury current. As was the case with atrial infarction (Section 09.35) look to lead aVR for
reciprocal PR elevation (which is present in Figure 12.3-1).

Figure 12.3-1: ECG Findings in Stage I Acute Pericarditis. The most characteristic finding is
diffuse ST elevation in all but one or more of the right-sided leads (leads III,aVR,V1). ST
elevation is generally concave up (smiley-shape) although coved ST elevation is seen here in
leads V2,V3. As commonly occurs with early repolarization there may be J-point notching in one
or more leads (seen here in leads I,V6). Lead I often resembles lead II (rather than lead III, as
would occur with acute inferior MI). There is no reciprocal ST depression. Finally, PR depression
is often seen in at least several leads (here in leads I,II and V2,V3) with PR elevation in lead
aVR.
12.4 PR Depression: How Helpful a Sign is this?
Normally the PR segment is isoelectric with respect to the ST segment baseline (Panel A in
Figure 12.4-1). It is from this PR segment baseline that we generally judge ST segment deviations
(elevation or depression) assuming baseline wander is minimal and that the heart rate is not so
fast as to preclude identification of the PR segment (Section 09.15).
With generalized inflammation of the pericardial lining depression of the PR segment below
the ST baseline will often be seen in at least several leads. Recognition of PR depression
should be evident in Figure 12.4-1 by comparing the PR segment in Panel B (relative to its

dotted ST segment baseline) with the normal (isoelectric) PR segment seen in Panel A.

Figure 12.4-1: Comparison of a normal PR segment (Panel A) with PR depression seen in Panel
B, in which the PR segment descends below the ST baseline (See text).
Clinical CAVEATS: PR depression is often subtle. As a result this finding is subject to inter- and
intra-observer variability.
PR depression is not always seen with acute pericarditis.
PR depression may occasionally be seen in other conditions. These include: i) normal
repolarization variants; ii) patients with acute MI (and/or with atrial infarction) ; and iii) with
tachycardia (the PR shortens with tachycardia, which makes PR assessment more challenging
at faster heart rates).
BOTTOM Line: Be aware of the term PR depression as this will often come up in diagnostic
discussion about possible acute pericarditis. Definite identification of PR depression in several
leads is possible and is diagnostically useful (Figure 12.4-2). Support that the finding of PR
depression is real and meaningful may be derived by the finding of PR elevation in lead aVR. That
said Be aware that both false positive and false negative diagnosis of acute pericarditis is
frequently associated with the phenomenon of seeing PR depression.
Therefore It is probably best not to base your diagnosis of acute pericarditis on whether or
not you see PR depression.

Figure 12.4-2: Schematic tracing illustrating ECG findings of acute pericarditis (reproduced from
Figure 12.3-1). In addition to seeing diffuse ST elevation in the absence of reciprocal ST depression
PR depression is seen in several leads (red arrows). Support that this finding of PR depression is
real is forthcoming from the finding of PR elevation in lead aVR (blue arrow). While not enough
by itself to make the diagnosis of acute pericarditis PR depression (in association with PR
elevation in lead aVR) is clearly supportive of the diagnosis (See text).
12.5 What is Spodicks Sign?
An additional ECG diagnostic sign that is often mentioned with discussion of acute pericarditis is
Spodicks sign (named after Dr. David Spodick who is internationally known for his work on
pericarditis).
Spodicks Sign is a downsloping of the TP (or entire QRS-TP) segment that may be present
in a number of leads with acute pericarditis (downward slanting red dotted line in Figure 12.51). When seen in at least a few leads in association with a suggestive clinical history and other
typical ECG findings this sign further supports the diagnosis of acute pericarditis.

Figure 12.5-1: Spodicks sign defined as a downsloping of the TP (or entire QRS-TP) segment
(red dotted line). Clinical Caveat In our experience, determination of whether or not Spodicks
sign is present is often subjective and suboptimally reproducible. While we regularly look for this
sign when contemplating the diagnosis of acute pericarditis We caution against depending on
presence or absence of Spodicks sign as your sole criterion for diagnosing acute pericarditis (See
text).
12.6 Differential Diagnosis: Acute MI vs Early Repolarization?
Distinction between Stage 1 pericarditis and early repolarization or acute MI can usually be made
because:
Early Repolarization is most often seen in otherwise healthy young adults. ST elevation is
usually localized to one (at most two) areas of the heart vs more diffuse ST elevation with
pericarditis. Be aware that the shape of ST segment elevation may be similar with both
conditions (smiley configuration) and J-point notching may be seen in both conditions.
Acute MI is usually suggested by the history (older patient with risk factors; chest pain is
more constant and severe and chest pain is less likely to be pleuritic or positional). The
ECG may show Q waves and Q waves may increase in size as the infarct evolves. There

will usually be at least some reciprocal ST depression during the course of acute MI
whereas neither pericarditis nor early repolarization manifest reciprocal changes.
PEARL: A distinguishing feature between acute MI and pericarditis is that with acute MI, T wave
inversion will often be seen while the ST segment is still elevated (Figure 12.6-1). In contrast, with
acute pericarditis ST segments are first diffusely elevated (1st Stage) then ST segments return
to baseline (2nd Stage) and only then is there T wave inversion (3rd Stage). Thus, the picture in
schematic Figure 12.6-1 is strongly suggestive of acute MI rather than pericarditis because the T
wave is inverted while the ST segment is still elevated.
Final Point: As previously noted (in Section 12.3) ST segments in leads I and II tend to look
similar with acute pericarditis. This is in contrast to what is usually seen with acute inferior MI
in which case lead III is much more likely to resemble lead II in appearance.

Figure 12.6-1: With acute Pericarditis the T wave typically does not invert until after the ST
segment has returned to baseline (Section 12.2). In contrast, with acute MI (as seen here) the T
wave may invert while the ST segment is still elevated.
12.7 Acute Myocarditis/Endocarditis: ECG Changes?
The causes and symptoms of acute Myocarditis and Endocarditis are many and extend beyond the
scope of this ECG PB book. Our purpose in this brief subsection is merely to increase awareness of
the ECG abnormalities that may be seen. The ECG picture is not predictable with either
myocarditis or endocarditis. It may include:
Various forms of SA and AV nodal block ( from 1st degree up to 3rd degree AV block with
long pauses).
Conduction system defects (BBB, hemiblocks, IVCD).
Atrial and ventricular arrhythmias (including VT/VFib).
T h e gamut of ST-T wave abnormalities ( ST elevation/depression; T wave inversion;
nonspecific ST changes).

BOTTOM Line: ECG findings with myocarditis and endocarditis are highly variable and
nonspecific. Abnormalities may be minimal or marked. Awareness of this variability may help to
explain extreme abnormalities that may be seen when either myocarditis or endocarditis are
suspected.
12.8 FIGURE 12.8-1: Acute MI or Pericarditis?
Consider the ECG shown in Figure 12.8-1 obtained from a 35-year old man with atypical chest
pain.
Are the findings suggestive of acute MI or acute pericarditis?
How certain are you of your diagnosis?

Figure 12.8-1: Acute MI vs Acute Pericarditis.

Answer to Figure 12.8-1: The rhythm is sinus. All intervals and the axis are normal. No chamber
enlargement. Early transition (the R wave becomes taller than the S wave is deep by lead V2).
Otherwise the principal finding is diffuse ST elevation that is present in virtually all leads except
for leads I,aVR and aVL.
The amount and extent of ST elevation in Figure 12.8-1 is more than is usually expected with
early repolarization. ST elevation is concave up. There is J-point notching or slurring in a
number of leads.
PR depression is seen (red arrows ). In addition there is PR elevation in lead aVR (blue
arrow). Together with the presence of diffuse ST elevation this all favors acute pericarditis
as the diagnosis.
P.S.: We find it difficult to tell if Spodicks sign (Section 12.5) is present or not in leads II and
III of Figure 12.8-1. As previously noted We caution against dependence on this sign when
its presence is questionable because of subjectivity in its interpretation.
Finally The likelihood of acute MI is low. This is because: i) ST elevation is diffuse and
manifests an upward concavity with J-Point notching; and ii) There is no reciprocal ST
depression. In contrast the ST elevation of acute MI is typically coved; localized to one (or
at most 2) lead areas; not notched; and associated with reciprocal ST depression. The patients

relatively younger age and atypical symptoms in this case are also against acute MI. This
patient did have acute pericarditis.

12.9 FIGURE 12.9-1: Pericarditis or Early Repolarization?

We conclude this segment on acute pericarditis by revisiting the ECG shown in Figure 12.9-1
which we initially encountered in Section 09.19 when discussing early repolarization.
How would you interpret this tracing IF told that it was obtained from an otherwise healthy
young adult?
Would your interpretation change IF told that this young adult had a recent upper respiratory
infection and was complaining of pleuritic-type chest pain?
Despite ST elevation in several leads Why is the ECG shown in Figure 12.9-1 not suggestive
of an acute MI?

Figure 12.9-1: ECG obtained from a young adult (reproduced from Figure 09.19-1). Would your
interpretation of this tracing change IF the clinical scenario was recent URI with pleuritic chest
pain? vs sudden-onset of crushing chest pain in an older patient? vs a young adult who was
not having symptoms? (See text).
Answer to Figure 12.9-1: As emphasized in Section 09.19 our descriptive analysis for ECG
findings on this 12-lead tracing does not change regardless of the history. Only the relative
probabilities for our clinical impression will change depending on the clinical scenario.
Descriptive Analysis: There is sinus rhythm with normal intervals and axis. Voltage for LVH
would not be present if the patient was younger (less than 35 years of age). Transition is normal
(occurs between lead V3-to-V4).
A Q wave with T wave inversion is seen in lead III. Small, narrow q waves are seen in V5,V6.
Taken in isolation none of these findings are necessarily abnormal.
Instead the most remarkable finding on this ECG is ST elevation in multiple leads. This ST
elevation manifests an upward concavity (smiley-configuration) in most leads in which it is
seen although the ST segment is coved in lead V2, and the ST segment takeoff is straightened

in lead V3.
J-point notching is seen in several leads. This is most notable in leads V5,V6 but also
present in leads I,II,aVF and V4. The shape of this J-point notching is characteristic of early
repolarization.
Infarction Q waves are absent. That is the q waves in leads V5,V6 are small and narrow,
with the appearance of being normal septal q waves. The Q wave in lead III is deeper but as
an isolated finding, this is not necessarily abnormal (Section 09.12).
There is no reciprocal ST depression (isolated T wave inversion in lead III does not qualify in
this case as reciprocal ST depression).
We do not appreciate PR depression.
Lead II seems to resemble lead I more than lead III.
We can easily talk ourself into a positive Spodick sign for the sloping TP segment in leads
V4,V5,V6.
Putting Together ECG Findings in Figure 12.9-1: Our reason for presenting this ECG again
(reproduced from Figure 09.19-1) is to emphasize: i) How challenging it may sometimes be to
assess the ECG of a patient with chest pain and ST elevation; and ii) How important the clinical
scenario is in our interpretation.
IF this patient was an asymptomatic otherwise healthy young adult We would not hesitate
calling this Early Repolarization (concave up ST elevation in multiple leads; J-point
notching; no infarction q waves and no reciprocal ST depression).
On the other hand IF this young adult had pleuritic chest pain with a recent URI We
would have to be concerned about the possibility of acute pericarditis (diffuse ST elevation
and lack of reciprocal ST depression in the setting of a history consistent with acute
pericarditis). Although the slow heart rate and highly characteristic J-point notching seen here
might lead us to question this diagnosis in the absence of a prior tracing to document
longstanding early repolarization, it would be difficult to exclude acute pericarditis.
Finally IF this patient was older with new-onset chest discomfort All bets would be off
(especially in the absence of a prior ECG for comparison)! Although the ECG in Figure 12.9-1
does not show infarction Q waves, reciprocal ST depression, or ST coving more suggestive of
acute injury the onus of proof when the history is concerning falls on us to rule out the
possibility of early acute MI (rather than having to rule it in). At the least, we would start by
repeating the ECG in short order to see if any evolution occurs. Whether or not to admit this
patient (and/or to consider acute investigation) would depend on a series of factors as
discussed in detail in Section 10.
BOTTOM Line: An ECG such as that seen in Figure 12.9-1 could be consistent with acute
pericarditis or even early acute injury IF clinical features suggesting either diagnosis were
present. As relevant to Section 12 Assessing the patient with chest pain for the possibility of acute
pericarditis is often a challenging task that entails far more than simply looking at the patients ECG.
P.S. It turned out in this case that the ST segment elevation seen in multiple leads in Figure

12.9-1 was a normal repolarization variant (and not due to acute coronary syndrome or
pericarditis).
PEARL: Making this patient a miniaturized copy of his ECG that he can carry in his wallet
may be a prudent way to avoid unnecessary hospital admission in the event chest discomfort is
experienced in the future.

13.0 Computerized ECG Interpretations

A frequent question that arises is, How best to use (or not use) the computerized ECG
interpretation? Opinions vary. We feel the answer depends on the goals and experience level of
the interpreter.
Computerized ECG analysis systems are not infallible. Although they clearly have merit in
certain regards they are far from perfect at ECG interpretation. Our task is to appreciate the
positives of computer systems while being aware of their drawbacks.

13.1 Computerized Systems: Pros & Cons

At the current time virtually all modern ECG machines automatically provide a computerized
interpretation. This has benefits and drawbacks. Consider the following:
Computerized systems excel at computing values. This is because thats what computers do. As
a result computerized systems are extremely accurate in calculating: i) Rate; ii) Intervals
(PR/QRS/QT intervals); and iii) Axis.
Computerized systems are usually reliable in recognizing sinus rhythm mechanisms and
normal tracings.
For the Expert Interpreter the best feature of computerized systems is that they save time!
There is no longer need to calculate rate, intervals or axis since the computer instantly
provides legible and accurate print-out of these values. IF the computer says, Normal ECG
it may literally take no more than 2-3 seconds for an experienced interpreter to peruse the
tracing and sign the report (provided there is agreement with the computer interpretation).
For the Non-Expert Interpreter the major benefit of computerized systems is the backup
opinion the system provides. The computer may suggest findings not initially thought of by a less
experienced interpreter. This encourages more careful, targeted review of the tracing. It may
also be educational by the suggestions it makes. Finally confidence is boosted when
computer analysis agrees with the clinicians interpretation.
NOTE: The computer backup opinion may also help the expert-in-a-hurry by reducing the chance
that any ECG findings will be overlooked.
Interpretation of any one ECG by an expert provided with: i) a moment of time; and ii) the
clinical history will always be superior to interpretation by a machine. That said this is
not reality.
Reality in the real world is that the clinician assigned to interpret all tracings on a given
hospital or ambulatory service usually has limited time to interpret a large number of ECGs and

is often asked to do so without the benefit of clinical history. As a result it becomes easy for
even an expert interpreter to overlook certain findings on occasional tracings. Knowing how to
use the computerized interpretation as a backup opinion can be invaluable even for the most
experienced of interpreters! (Grauer, Nelson, Marriott et al: J Am Bd Fam Prac 1:17-24,
1989).
CAVEATS ( What the Computer May Miss): Computerized systems do not do nearly as well in
evaluation of abnormal tracings as they do in assessing ECGs with minimal abnormalities. The more
complex the abnormal ECG is the more difficult it becomes for a computerized system to render
an entirely accurate interpretation.
Computerized systems are far less accurate interpreting rhythms that do not have a sinus
mechanism.
They may miss subtle infarctions.
They tend to overinterpret the J-point ST elevation that is commonly seen with early
repolarization patterns. As a result computerized systems may be prone to mislabel these
normal variants as acute MI.
Computerized systems may miss pacemaker spikes/WPW/tall R in V1. They are unlikely to
appreciate certain clinical entities such as Wellens syndrome or DeWinter T waves.
Many hospitals do not utilize special computer programs for interpretation of ECGs obtained on
pediatric patients. Obvious problems with interpretation will arise IF a pediatric ECG is
interpreted by a computer program using adult criteria.
Finally computerized systems by definition lack the human Gestalt by an expert of the
overall tracing.

13.2 Suggested Approach: How to Use the Computer

The most important point to emphasize in this Section is that clinical use of the computerized
report by non-expert interpreters should be very different than use of this same report by the expert
who regularly interprets a large volume of tracings. Expertise of the interpreter therefore dictates
the approach we recommend (Grauer: Practical Guide to ECG Interpretation; Mosby, St. Louis;
pp 375-379, 1998).
For the Non-Expert Interpreter Do not initially read the computer report. Instead WRITE
OUT (or at least think out) your interpretation first. Only after independently making your own
interpretation should you look at the computerized report. At this point Check each of the
findings you note with each computer statement. Then delete, modify and/or add to the computer
interpretation as needed.
For the Expert Interpreter Review the computer report either before or after evaluation of
the ECG itself. Minimize time devoted to determination of heart rate, intervals and axis (since
the computer is very accurate for these parameters). Consider more careful evaluation IF the
rhythm is not sinus or IF the ECG is interpreted by the computer as abnormal. Overread each
computer statement. Place a check mark next to those that are accurate. Delete, modify or add to

incorrect statements.
KEY Point: The expert interpreter is not using the computerized report to learn. This is because
by definition the interpretation of an expert electrocardiographer is the gold standard. Since
computerized systems are programmed by experts the best they can realistically hope for is to put
out interpretations that equal the level of accuracy of the expert that programmed them.
The expert uses the computer: i) to save time; and ii) to prevent overlooking findings when
forced to read many ECGs in a limited period of time.
Less experienced interpreters do look to the computer to assist in accuracy. They are usually
called on to read no more than one ECG at any one time. Therefore the most important step
for the non-expert is to first COVER UP the computerized report. It is otherwise all too easy to
be biased by what the computer says. Used in this way comparing ones own interpretation
with what the computer says optimally incorporates potential benefit from any discrepancy in
interpretation that may exist.

13.3 FIGURE 13.3-1: Do You Agree with the Computer?

Perhaps the best way to illustrate potential pros and cons of computerized interpretations is by
clinical example. Consider the ECG shown in Figure 13.3-1 obtained from a 78 year old woman
with atypical chest pain.
The computerized interpretation was: Sinus rhythm; left axis (-10 degrees) but otherwise
normal ECG.
Do you agree with the computerized interpretation?
HINT: Be sure to interpret this ECG in its entirety by the systematic approach first before
you compare what the computer said with your interpretation.

Figure 13.3-1: ECG obtained from a 78 year old woman with atypical chest pain. The computerized
report interpreted this tracing as, left axis but otherwise normal. Do you agree with the
computerized report?

Answer to Figure 13.3-1: The rhythm is sinus. All intervals are normal. The axis is leftward
(predominantly negative QRS in lead aVF) but not negative enough to qualify as LAHB (since the
QRS in lead II is still upright). No chamber enlargement.
Regarding Q-R-S-T Changes There are QS complexes in leads V1,V2. An r wave develops
by lead V3 and transition occurs normally between lead V3-to-V4. Although there is no more
than minimal (at most) ST elevation T waves are dramatically peaked in anterior
precordial leads (especially in lead V2). There is shallow T inversion in lead III, and perhaps
some nonspecific ST-T wave flattening in lead aVF.

IMPRESSION: This example highlights the importance of overreading the computerized

interpretation after you have independently arrived at your own conclusion. This is not a normal
ECG. That statement should be crossed out on the computerized report. This is because the
computerized interpretation is a medical record and statements you disagree with should therefore
be crossed out.

Clinical correlation is needed to determine the meaning of the abnormal findings you identified.
Of Concern is the fact that i) this woman is of a certain age (78 years old so clearly old
enough to have coronary disease); and ii) she is having chest pain (even though it is
described as atypical in nature).
While not definitive the QS complexes in leads V1,V2 could reflect septal infarction of
uncertain age. This should at least be noted in your interpretation (it was ignored by the
computerized report).
There is marked T wave peaking especially in leads V2,V3. This is not normal (despite
also being ignored by the computerized report ). Possible explanations for this abnormal T
wave peaking include: i) Hyperkalemia (less likely because T wave peaking is not generalized
and the base of these T waves is not narrow but a serum K+ level should nevertheless be
checked to rule this out); ii) Ischemia (which when posterior in location sometimes manifests
as anterior T wave peaking); and iii) DeWinter T waves. Given the history of chest discomfort
we are most concerned with this 3rd possibility. While the J-point ST depression that is
usually seen with DeWinter T waves is missing in Figure 13.3-1 the ECG picture in this
tracing is otherwise perfectly compatible with this harbinger sign of possible impending
proximal LAD occlusion (Section 10.58).

BOTTOM Line: It might be easy to overlook the QS complexes in leads V1,V2 of this tracing IF you
allowed the computerized report to bias you prior to rendering your own independent interpretation.
Hopefully you did not overlook the obviously abnormal T wave peaking in anterior leads that
somehow escaped detection by the computer. Recognition of DeWinter T waves is indication for
immediate cath/acute reperfusion so this possibility mandates immediate attention. This would
have been missed had the computer report been accepted without overread. Computerized
interpretations can be extremely helpful to both expert and non-expert interpreters but knowing
HOW to use the computer report always assumes first priority.

14.0 Electrical Alternans

We conclude this ECG-2014-ePub with brief comment on the fascinating phenomenon of electrical
alternans. This relatively uncommon clinical entity is frequently misunderstood and often
overlooked when it does occur. Electrical alternans is a general term that encompasses a number of
different pathophysiologic mechanisms. Its occurrence is not limited to pericardial tamponade but
instead has been associated with an expanding array of clinical conditions.
Distinction should be made between electrical and mechanical alternans. The term alternans
itself merely indicates that there is phasic fluctuation in some cardiac signal from one beat
to the next within the cardiac cycle. This may be in the strength of the pulse (or the blood
pressure recorded) or it may be in one or more waveforms in the ECG recording.
NOTE: Discussion is limited in this Section 14 to ECG manifestations of alternans. Nevertheless
it may be helpful to first define other alternans phenomena that may sometimes be confused with the
various ECG manifestations (especially since these other forms of alternans phenomena may also
be seen with cardiac tamponade).
Pulsus alternans is a mechanical form of alternans. The rhythm is regular but cardiac
output varies from beat-to-beat. It is seen with severe systolic dysfunction. Pulsus alternans
should be distinguished from a bigeminal pulse in which a weaker beat follows the stronger
beat by a shorter time interval (as occurs when the alternating beat is a PVC, which
understandably generates less cardiac output).
Pulsus alternans should also be distinguished from pulsus paradoxus in which there is a
palpable decrease in pulse amplitude (or a measured drop of >10mm in blood pressure ) during
quiet inspiration. While pulsus alternans and paradoxus may both be seen with pericardial
tamponade they are different phenomena than the various types of electrical alternans.

14.1 Electrical Alternans: Definition/Features/Mechanisms

Electrical alternans is a beat-to-beat variation in any one or more parts of the ECG recording. It
may occur with every-other-beat or with some other recurring ratio (3:1; 4:1; etc.). Amplitude or
direction of the P wave, QRS complex, ST segment and/or T wave may all be affected (although P
wave alternans is rare). Alternating interval duration (of PR, QRS or QT intervals) may also be
seen.
Electrical alternans was first observed in the laboratory by Herring in 1909. It was reported
clinically by Sir Thomas Lewis a year later, who characterized the phenomena as occurring,
either when the heart muscle is normal but the heart rate is very fast or when there is
serious heart disease and the rate is normal. This 1910 description by Lewis serves well to
this day to remind us of the 2 principal clinical situations in which electrical alternans is most

often encountered: i) Supraventricular reentry tachycardias; and ii) Pericardial tamponade.

Mechanisms: There are 3 basic types of electrical alternans phenomena each relating to a
different pathophysiologic mechanism: i) Repolarization
alternans; ii) Conduction and
Refractoriness alternans; and iii) Alternans due to abnormal cardiac motion. A common cellular
mechanism may underlie each of these processes relating to abnormal calcium release or reuptake
within the sarcoplasmic reticulum.
Repolarization alternans entails beat-to-beat variation in the ST segment and/or T wave.
Alternation in ST segment appearance (or in the amount of ST elevation or depression) is
often linked to ischemia. In contrast T wave alternation is more often associated with changes
in heart rate or in QT duration (especially when the QT is prolonged). In patients with a long
QT T wave alternans may forebode impending Torsades de Pointes. Both ST segment and T
wave alternans have been known to precede malignant ventricular arrhythmias. Thus, this type of
electrical alternans may convey important adverse prognostic implications when seen in certain
situations. That said a variety of clinical conditions have been associated with
repolarization alternans, such that adverse prognostic implications do not always follow.
Among these clinical conditions are congenital long QT syndrome severe electrolyte
disturbance (hypocalcemia; hypokalemia; hypomagnesemia) alcoholic or hypertrophic
cardiomyopathy acute pulmonary embolus subarachnoid hemorrhage cardiac arrest and
the post-resuscitation period and various forms of ischemia (spontaneous or induced by
treadmill testing or other stimulus).
Conduction and Refractoriness alternans entails variance of impulse propagation along
some part of the conduction system. This may result from fluctuations in heart rate or in nervous
system activity or from pharmacologic treatment. ECG manifestations from this form of alternans
may include alternating appearance of the P wave , QRS complex or alternating difference in
P-R or R-R interval duration. In particular QRS alternans during narrow SVT rhythms has
been associated with reentry tachycardias. While identification of QRS alternans during a
regular SVT often indicates retrograde conduction over an AP ( Accessory Pathway) this
phenomenon has also been seen in patients with simple PSVT/AVNRT that exclusively limits its
reentry pathway to the AV Node. Therefore identification of QRS alternans during a regular
SVT does not prove the existence of an accessory pathway. Conduction and refractoriness
alternans may be seen with WPW-related as well as AV Nodal-dependent reentry tachycardias
atrial fibrillation acute pulmonary embolus myocardial contusion and severe LV
dysfunction.
Cardiac Motion alternans is the result of cardiac movement rather than electrical
alternation. The most important clinical entity associated with motion alternans is large
pericardial effusion though motion alternans has also been observed in some cases of
hypertrophic cardiomyopathy. It is important to appreciate that not all pericardial effusions
produce electrical alternans. Development of total electrical alternans (of P wave, QRS
complex and T wave) is likely to be a harbinger of impending tamponade. Unfortunately
the sensitivity of total electrical alternans is poor for predicting tamponade (ie, most patients
who develop tamponade do not manifest preceding electrical alternans). Therefore it may

be helpful if you see total electrical alternans in a patient with a large pericardial effusion but
failure to see this ECG sign in no way rules out the possibility that tamponade is occurring. Echo
studies in patients with documented cardiac tamponade confirm that electrical alternans is
synchronous with and a direct result of the pendulous movement of the heart within the enlarged,
fluid-filled pericardial sac of a patient with large pericardial effusion (See Section 14.4).

14.2 Electrical Alternans: KEY Clinical Points

In summary, electrical alternans is not common but it does occur. You will see it. You have
probably already seen it a number of times without even realizing it. Electrical alternans is a
fascinating but advanced concept. It is clearly beyond-the-core for many who are using this ECG2014-ePub but we choose to include it because of its uniqueness and the clinical insights that this
fascinating ECG sign may provide.
In our experience electrical alternans is most often seen in association with regular SVT
rhythms. Seeing it in this context suggests (but does not prove) the existence of an AP
(Accessory Pathway). Regardless of whether the mechanism of the regular SVT is AVNRT or
AVRT it is likely that reentry is involved. This conclusion may prove useful in contemplating
potential investigative and therapeutic interventions.
In a patient with pericarditis a large heart on chest X-ray or simply unexplained dyspnea
recognition of electrical alternans should suggest the possibility of a significant pericardial
effusion that may be associated with tamponade. That said electrical alternans is a
nonspecific ECG sign that may also indicate myocardial ischemia, LV dysfunction and/or
possibility of any of a number of other precipitating factors. BOTTOM Line: If you see
electrical alternans Look for an underlying clinical condition that may be responsible for this
ECG sign.
Development of electrical alternans per se conveys no adverse prognostic implications
beyond those associated with severity of the underlying disorder. Two exceptions to this
general rule are: i) In a patient with QT prolongation or severe ischemia recognition of
electrical alternans may portend deterioration to Torsades or VT/VFib; and ii) In a patient with
a large pericardial effusion development of total electrical alternans (of P wave, QRS
complex and T wave) suggests there may now be tamponade.

14.3 FIGURE 14.3-1: Alternans in an SVT Rhythm?

Consider the 3-lead rhythm strip shown in Figure 14.3-1 obtained from a patient in a regular SVT
rhythm.
Is electrical alternans present? If so What kind (ie, involving the P wave; QRS complex; ST
or T wave; or involving the PR or R-R interval?).
What are clinical implications for electrical alternans of this rhythm?

Figure 14.3-1: 3-lead rhythm strip obtained from a patient in a regular SVT rhythm. Is electrical
alternans present? If so What kind? (See text).
Answer to Figure 14.3-1: Although we describe the rhythm seen here as a regular SVT
(SupraVentricular Tachycardia) there appears to be slight-but-real phasic variation in the R-R
interval occurring every-other-beat (ergo, R-R alternans). In addition there is both QRS
alternans (red and blue double arrows in Figure 14.3-1) and T wave alternans (red and blue
circles). That is QRS morphology changes every-other-beat. This is subtle in lead V1 but more
noticeable in lead V2 where the initial R wave manifests an obvious difference in height from one
beat to the next. Similarly T wave morphology changes every-other beat, with this clearly more
noticeable in lead V2 which manifests extra peaking of every-other-T wave (red and blue circles in
lead V2).
Clinical implications of these forms of electrical alternans in a patient with SVT are that
reentry is almost certain to be involved in the mechanism. There may or may not be a concealed
accessory pathway.

14.4 FIGURE 14.4-1: Alternans in a Patient with Lung Cancer?

Consider the 12-lead ECG and accompanying rhythm strip in Figure 14.4-1 obtained from a
longtime smoker who presented with new-onset dyspnea. Pulmonary nodules suspicious of cancer
had been identified on this patients admission chest X-ray. In addition a large heart shadow was
seen.
Note the bigeminal pattern for the ECG in Figure 14.4-1. Is the rhythm ventricular bigeminy
(every-other-beat a PVC)?
Given the history What clinical entity should be considered?
What might this patients Echocardiogram show?

Figure 14.4-1: 12-lead ECG and lead V6 rhythm strip obtained from a patient with dyspnea and
suspected lung cancer. What is the likely cause of the bigeminal rhythm? (See text).
Answer to Figure 14.4-1: There is obvious QRS alternans with marked variation in QRS
amplitude from beat-to-beat. This is most dramatic in lead V3 in which there is a 180 degree
alternation in QRS direction from one beat to the next.
The rhythm is not atrial or ventricular bigeminy because P wave morphology is constant and
the P-P interval is perfectly regular throughout the tracing. The PR interval remains the same.
Therefore the rhythm is sinus and the change in QRS morphology must be solely the result of
electrical alternans.
ST-T wave morphology does not appreciably change from beat-to-beat in any of the 12 leads on
this tracing. Thus, alternans appears limited to a change in QRS morphology.
Clinical Note: Knowing this patients history supports our presumption of electrical alternans.
The patient is a longtime smoker suspected of having lung cancer. He now presents with acute
dyspnea and a large heart shadow on chest X-ray. In view of electrical alternans on ECG a
large pericardial effusion with possible tamponade should be suspected. An Echo should be
done in timely fashion (Figure 14.4-2).
Beyond-the-Core: Overall QRS amplitude appears reduced in Figure 14.4-1 especially for
every-other-QRS complex. The finding of low voltage in the context of the above history and
electrical alternans all support the likelihood of finding a significant pericardial effusion. An
Echo is the investigative procedure of choice (Figure 14.4-2).

Figure 14.4-2: Serial 4-chamber views from the Echo performed on the patient whose ECG was
shown in Figure 14.4-1. An extremely large pericardial effusion is seen (arrows). As a result a

swinging heart pendular motion is set up. This marked free-floating displacement of the heart
occurs in phasic fashion within the fluid-filled pericardial sac and accounts for the dramatic beatto-beat variability in QRS amplitude and direction that was seen in Figure 14.4-1.

ACKNOWLEDGMENT: My appreciation to Jenda Enis Stros for allowing me to use the ECG in
Figure 14.3-1 and to Jason Roediger for allowing me to use the case, ECG and Echo in Figures
14.4-1 and 14.4-2.