Basics of ECG

Dr Awadhesh Kr Sharma
MD, DM
Consultant Cardiology
Dr Awadhesh Kr Sharma
 Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his
graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college
jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher
Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in
DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief
minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many
national & international publications.He is also in editorial board of international journal- Journal of clinical
medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee
fellow of American college of cardiology. He is currently working in NABH Approved Gracian
Superspeciality Hospital Mohali as Consultant Cardiologist.
 The goal of this academic session is-
To have basic understanding of ECG waves &

intervals.
Interpretation of ECG

 Outline the criteria for the most common

electrocardiographic diagnoses in adults.

Describe critical aspects of the clinical application of

the ECG
 HISTORY
1842- Italian scientist Carlo Matteucci realizes that electricity
is associated with the heart beat.
1895 - William Einthoven , credited for the invention of ECG.

1906 - using the string electrometer ECG,William Einthoven

diagnoses some heart problems.
1924 - The noble prize for physiology or medicine is given to
William Einthoven for his work on ECG
 ELECTROCARDIOGRAM
The electrocardiogram (ECG) is a
representation of the electrical events of the
cardiac cycle.
Each event has a distinctive waveform, the
study of waveform can lead to greater insight
into a patient’s cardiac patho physiology.
 ECGs can identify
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)
Recent advances have extended the importance
of the ECG.
It is a vital test for determining -
1. The presence and severity of acute myocardial
ischemia/infarction.
2. Localizing sites of origin and pathways of tachyarrhythmias,
3. Assessing therapeutic options for patients with heart failure,
4. Identifying and evaluating patients with genetic diseases who
are prone to arrhythmias.
Fundamental Principles
Transmembrane ionic currents are generated by ion fluxes
across cell membranes and between adjacent cells.
These currents are synchronized by cardiac activation and
recovery sequences to generate a cardiac electrical field in
and around the heart that varies with time during the
cardiac cycle.
The currents reaching the skin are then detected by
electrodes placed in specific locations on the extremities
and torso that are configured to produce leads.
Fundamental Principles
Transmembrane ionic currents are ultimately responsible
for the potentials that are recorded as an ECG.
Electrophysiological currents are considered to be the
movement of positive charge.
An electrode senses positive potentials when an activation
front is moving toward it and negative potentials when the
activation front is moving away from it.
 Depolarization

Contraction of any muscle is associated with

electrical changes called depolarization.

These changes can be detected by electrodes

attached to the surface of the body.
Repolarization
Phase of recovery/relaxation.

The dipole moment at any one instant during recovery is

less than during activation.

Recovery, is a slow process, lasts 100 msec or longer and

occurs simultaneously over extensive portions of the fiber.

 Pacemakers of the Heart
SA Node - Dominant pacemaker with an intrinsic rate of 60 -
100 beats/minute.

AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60

beats/minute.

Ventricular cells - Back-up pacemaker with an intrinsic rate of

20 - 45 bpm.
The Normal Conduction System
MODERN ECG INSTRUMENT
 ECG Leads
Measure the difference in electrical potential
between two points
1. Bipolar Leads: Two different points on the body.

2. Unipolar Leads: One point on the body and a virtual

reference point with zero electrical potential, located in the
center of the heart .
 ECG Leads
The standard ECG has 12 leads:

3 Standard Limb Leads

3 Augmented Limb Leads
6 Precordial Leads
Recording of the ECG
Limb leads are I, II, II.
Each of the leads are bipolar; i.e., it requires two sensors on
the skin to make a lead.
If one connects a line between two sensors, one has a vector.
There will be a positive end at one electrode and negative at
the other.
The positioning for leads I, II, and III were first given by
Einthoven (Einthoven’s triangle).
Standard Limb Leads
Standard Limb Leads
Augmented Limb Leads
All Limb Leads
Standard Chest Lead Electrode Placement

The Right-Sided 12-Lead ECG The 15-Lead ECG

Precordial Leads
The ECG Paper
Horizontally
One small box - 0.04 s
One large box - 0.20 s
Vertically
One large box - 0.5 mV
Clinical Interpretation of the ECG

Accurate analysis of ECGs requires thoroughness and

care.
The patient's age, gender, and clinical status should
always be taken into account.
Many mistakes in ECG interpretation are errors of
omission. Therefore, a systematic approach is
essential.
NORMAL ECG
NORMAL ECG
The following 14 points should be analyzed carefully in every
ECG:
1. Standardization (calibration) and technical features (including lead
placement and artifacts)
2. Rhythm
3. Heart rate,
4. PR interval/AV conduction
5. QRS interval
6. QT/QTc interval
7. Mean QRS electrical axis
8. P waves
9. QRS voltages
10. Precordial R-wave progression
11. Abnormal Q waves
12. ST segments
13. T waves
14. U waves
Standardization
The first step while reading ECG is to look for wheather

standardization is properly done.

Look for the vertical mark and see that the mark exactly covers

two big squares(10 mm or 1mV) on the graph.

Standard calibration

 25 mm/s

 0.1 mV/mm
Standardization
RHYTHM
Evaluate the rhythm strip at the bottom of the 12-lead for
the following-
 Is the rhythm regular or irregular?
 Is there a P wave before every QRS complex?
 Are there any abnormal beats?
The Heart Rate

1. Rule of 300/1500(Regular
rhythm)
2. 10 Second Rule
 Rule of 300

Count the number of “big boxes” between two

QRS complexes, and divide this into 300.
(smaller boxes with 1500) for regular rhythms.
Rule of 300

(300 / 6) = 50 bpm
 Heart rate?

(300 / ~ 4) = ~ 75 bpm
Heart rate?

(300 / 1.5) = 200 bpm

 10 Second Rule

Count the number of beats present on the ECG during

1o seconds ie 50 big squares.
Multiply them by 6
For irregular rhythms.
 Heart rate?

33 x 6 = 198 bpm
Normal intervals
The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for the
atria to contract before the
ventricles contract)
Normal PR interval
0.12 to 0.20 s (3 - 5 small squares).
Short PR – Wolff-Parkinson-White.
Long PR – 1st Degree AV block
Long PR Interval
First degree Heart Block
Short PR Interval
WPW (Wolff-
Parkinson-White)
Syndrome
Accessory pathway
(Bundle of Kent)
allows early activation
of the ventricle (delta
wave and short PR
interval)
QRS INTERVAL(DURATION)
Normal QRS duration is 110-120 msec.
Intrinsic impairment of conduction in either the right or
the left bundle system (intra ventricular conduction
disturbances) leads to prolongation of the QRS interval.
With complete bundle branch blocks, the QRS interval
exceeds 120 ms in duration; with incomplete blocks, the
QRS interval is between 110 and 120 msec.
Bundle Branch Blocks
Bundle Branch Blocks
Conduction in the
Bundle Branches and
Purkinje fibers are seen
as the QRS complex on
the ECG.

Therefore, a conduction
block of the Bundle
Branches would be Right
reflected as a change in the BBB
QRS complex.
Bundle Branch Blocks
Right Bundle Branch Blocks

For RBBB the wide QRS complex assumes a

unique, virtually diagnostic shape in those leads
overlying the right ventricle (V1 and V2).

V1

“M shape”
RBBB
Left Bundle Branch Blocks

For LBBB the wide QRS complex assumes a

characteristic change in shape in those leads
opposite the left ventricle (right ventricular leads -
V1 and V2).

Broad,
Normal deep S
waves
LBBB
QT Interval
QT INTERVAL
It includes the total duration of ventricular activation and
recovery.
When the interval is to be measured from a single lead, the lead
in which the interval is the longest, most commonly lead Avl,
V2 or V3, and in which a prominent U wave is absent should be
used.
The normal range for the QT interval is rate-dependent
A commonly used formula was developed by Bazett in 1920.
The result is a corrected QT interval, or QTc, defined by the
following equation:
QTc=QT/ RR
QT INTERVAL
The upper normal limit be set at 450 or even 460
msec.
The Bazett formula remains significantly affected by
heart rate and that as many as 30% of normal ECGs
would be diagnosed as having a prolonged QT
interval when this formula is used.
One formula that has been shown to be relatively
insensitive to heart rate is-
QTc= QT +1.75(HR-60)
Prolonged QTc
During sleep
Hypocalcemia
Acute myocarditis
Acute Myocardial Injury
Drugs like quinidine, procainamide, tricyclic
antidepressants
Hypothermia
HOCM
Prolonged QTc
Advanced AV block or high degree AV block
Jervell-Lange –Neilson syndrome
Romano-ward syndrome
Shortened QT
Digitalis effect
Hypercalcemia
Hyperthermia
Vagal stimulation
 The QRS Axis

The QRS axis represents overall direction of the

heart’s electrical activity.
Abnormalities hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
 The QRS Axis

Normal QRS axis from -30° to

+90°.

-30° to -90° is referred to as a

left axis deviation (LAD)

+90° to +180° is referred to as a

right axis deviation (RAD)
The QRS Axis
 Determining the Axis

The Quadrant Approach

The Equiphasic Approach

 Determining the Axis

Predominantly Predominantly Equiphasic

Positive Negative
 The Quadrant Approach
1. QRS complex in leads I and aVF
2. Determine if they are predominantly positive or negative.
3. The combination should place the axis into one of the 4
quadrants below.
Quadrant Approach: Example 1

Negative in I, positive in aVF  RAD

Quadrant Approach: Example 2

Positive in I, negative in aVF 

LAD
 The Equiphasic Approach
1. Most equiphasic QRS complex.
2. Identified Lead lies 90° away from the lead
3. QRS in this second lead is positive or Negative
QRS Axis = -30 degrees
QRS Axis = +90 degrees
 Equiphasic Approach

Equiphasic in aVF  Predominantly positive in I  QRS axis ≈ 0°

The “PQRST”

P wave - Atrial
depolarization

 QRS - Ventricular
depolarization

 T wave - Ventricular
repolarization
 P wave
Always positive in lead I and II
Always negative in lead aVR
< 3 small squares ie 0.12sec in
duration
< 2.5 small squares(2.5mm) in
amplitude
Commonly biphasic in lead V1
Best seen in leads II
Atrial abnormality
 Right Atrial
Enlargement
Tall (> 2.5 mm), pointed P waves (P Pulmonale)
Right atrial enlargement

The P waves are tall, especially in leads II, III and

avF.
 Left Atrial Enlargement
Notched/bifid (‘M’ shaped) P wave (P ‘mitrale’)
in limb leads
Left atrial enlargement
 To diagnose LAE you can use the following criteria:
 II > 0.04 s between notched peaks, or
 V1 Neg. deflection > 0.04 s wide x 1 mm deep

Normal LAE
Left atrial enlargement

Notched

Negative deflection

The P waves in lead II are notched and in lead V1 they have

a deep and wide negative component.
QRS Complex

Q waves
Normal QRS

V1
V6
Normal QRS

Septal r wave

Septal q wave
QRS Complexes
Normal QRS patterns in the precordial leads follow an orderly
progression from right (V1) to left (V6).
In leads V1 and V2, left ventricular free wall activation
generates S waves following the initial r waves generated by
septal activation (an rS pattern).
As the exploring electrode moves laterally to the left, the R
wave becomes more dominant and the S wave becomes smaller
(or is totally lost).
In the leftmost leads (i.e., leads V5 and V6), the pattern also
includes the septal q wave to produce a qRs or qR pattern.
Normal R Wave Progression

Transition Zone?
Early & Delayed Transition
V1 V2 V3 V4 V5 V6

• Figure 4-7
QRS Complexes
Non-pathological Q waves may present in I, III, aVL,

V5, and V6
Pathological Q wave > 2mm deep and > 1mm wide or

> 25% amplitude of the subsequent R wave

QRS in LVH & RVH
Left Ventricular Hypertrophy
Sokolow & Lyon Criteria
S in V1+ R in V5 or V6 > 35 mm
An R wave of 11mm (1.1mV) or more in lead aVL
is another sign of LVH
Right ventricular hypertrophy
Right ventricular hypertrophy
 To diagnose RVH you can use the following criteria:
 Right axis deviation, and
 V1 R wave > 7mm tall
 ST Segment
ST Segment is flat (isoelectric)

Elevation or depression of ST segment by 1 mm or

more is significant.
“J” (Junction) point is the point between QRS and

ST segment
ST Segment
Variable Shapes Of ST Segment Elevations in AMI

Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th

ed: Mosby Elsevier; 2006.
 T wave
Normal T wave is asymmetrical, first half having a
gradual slope than the second.

Should be at least 1/8 but less than 2/3 of the

amplitude of the R.

T wave amplitude rarely exceeds 10 mm.

Abnormal T waves are symmetrical, tall, peaked,

biphasic or inverted.

T wave follows the direction of the QRS deflection.

 U wave
U wave related to afterdepolarizations which
follow repolarization
U waves are small, round, symmetrical and
positive in lead II, with amplitude < 2 mm
U wave direction is the same as T wave
More prominent at slow heart rates
 ECG
Acute
coronary
syndrome
 S – T Segment
I V1

Normal Elevated

V3

Depressed

7
 T wave morphology
AVR
I

Upright T Inverted T

8
Acute Coronary Syndrome
Definition: a constellation of symptoms related to
obstruction of coronary arteries with chest pain being the
most common symptom in addition to nausea, vomiting,
diaphoresis etc.

Chest pain concerned for ACS is often radiating to the left arm
or angle of the jaw, pressure-like in character, and associated
with nausea and sweating. Chest pain is often categorized into
typical and atypical angina.
Acute coronary syndrome
Based on ECG and cardiac enzymes, ACS is classified
into:
STEMI: ST elevation, elevated cardiac enzymes
NSTEMI: ST depression, T-wave inversion, elevated
cardiac enzymes
Unstable Angina: Non specific EKG changes, normal
cardiac enzymes
ECG
 First point of entry into ACS algorithm

 Abnormal or normal

 Neither 100% sensitive or 100% specific for AMI

 Single ECG for AMI – sensitivity of 60%, specificity 90%

 Represents single point in time –needs to be read in context

 Normal ECG does not exclude ACS – 1-6% proven to have AMI, 4%
unstable angina
GUIDELINES
 Initial 12 lead ECG – goal door to ECG time 10min, read by experienced
doctor (Class 1 B)
 If ECG not diagnostic/high suspicion of ACS – serial ECGs initially 15 -30
min intervals (Class 1 B)

 ECG adjuncts – leads V7 –V9, RV 4 (Class 2a B)

 Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs

(Class 2a B)
Evaluating for ST Segment Elevation
Locate the J-point

Identify/estimate where the isoelectric line is noted to be

Compare the level of the ST segment to the isoelectric line

Elevation (or depression) is significant if more than 1 mm

(one small box) is seen in 2 or more leads facing the same

anatomical area of the heart
 The J Point

J point – where the QRS complex and ST segment

meet
ST segment elevation - evaluated 0.04 seconds (one
small box) after J point
Coved shape
usually
indicates acute
injury.

Concave
shape is
usually benign
especially if
patient is
asymptomatic.
Evolution of AMI
A - pre-infarct (normal)
B - Tall T wave (first few minutes of
infarct)
C - Tall T wave and ST elevation
(injury)
D - Elevated ST (injury), inverted T
wave (ischemia), Q wave (tissue
death)
E - Inverted T wave (ischemia), Q wave
(tissue death)
F - Q wave (permanent marking)
Anatomic Groups
Anatomic Groups
Anatomic Groups
Anatomic Groups
Anatomic Groups
NSTEMI:
 ST depressions (0.5 mm at least) or T wave inversions ( 1.0
mm at least) without Q waves in 2 contiguous leads with
prominent R wave or R/S ratio >1.
 Isolated T wave inversions:
 can correlate with increased risk for MI
 may represent Wellen’s syndrome:
 critical LAD stenosis

 >2mm inversions in anterior precordial leads

Unstable Angina:
 May present with nonspecific or transient ST segment
depressions or elevations
MI- Few ECGs
Evolution of acute anterior myocardial infarction at
3 hours
Lateral MI

Reciprocal changes
IWMI
Metabolic Factors and Drug Effects

Hyperkalemia produces a sequence of changes , usually

beginning with -
Narrowing and peaking (tenting) of the T waves.
AV conduction disturbances
Diminution in P-wave amplitude
Widening of the QRS interval
Cardiac arrest with a slow sinusoidal type of mechanism
("sine-wave" pattern)
Asystole.
SEVERE HYPERKALEMIA
HYPERKALEMIA
HYPERKALEMIA
Metabolic Factors and Drug Effects
Hypokalemia prolongs ventricular repolarization, often with

prominent U waves.
Hypocalcemia typically prolongs the QT interval (ST portion).

 Hypercalcemia shortens it.

Digitalis glycosides also shorten the QT interval, often with a

characteristic "scooping" of the ST–T-wave complex (digitalis

effect).
HYPOKALEMIA
HYPERCALCEMIA
HYPOCALCEMIA
Classification
Sinus Bradycardia
Junctional Rhythm
Sino Atrial Block
Atrioventricular block
SA Block
Sinus impulses is blocked within the SA junction
Between SA node and surrounding myocardium
Occures irregularly and unpredictably
 Present :Young athletes, Digitalis, Hypokalemia,
Sick Sinus Syndrome
AV Block
First Degree AV Block
Second Degree AV Block
Third Degree AV Block
First Degree AV Block
Delay in the conduction through the conducting system
Prolong P-R interval
All P waves are followed by QRS
Associated with : Acute Rheumatic Carditis, Digitalis, Beta
Blocker, excessive vagal tone, ischemia, intrinsic disease in
the AV junction or bundle branch system.
Second Degree AV Block
Intermittent failure of AV conduction
Impulse blocked by AV node
Types:
Mobitz type 1 (Wenckebach Phenomenon)
Mobitz type 2
Mobitz type 1 (Wenckebach Phenomenon)

Mobitz type II
CHB evidenced by the AV dissociation
A junctional escape rhythm at 45 bpm.
The PP intervals vary because of ventriculophasic sinus arrhythmia;
Arrhythmia Formation
Arrhythmias can arise from problems in the:
 Sinus node
 Atrial cells
 AV junction
 Ventricular cells
• Rate? 30 bpm
• Regularity? regular
• P waves? normal
• PR interval? 0.12 s
• QRS duration? 0.10 s
Interpretation? Sinus Bradycardia
• Rate? 130 bpm
• Regularity? regular
• P waves? normal
• PR interval? 0.16 s
• QRS duration? 0.08 s
Interpretation? Sinus Tachycardia
Premature Atrial Contractions

Deviation from NSR

 These ectopic beats originate in the atria (but not in
the SA node), therefore the contour of the P wave, the
PR interval, and the timing are different than a
normally generated pulse from the SA node.
Supraventricular Arrhythmias
Atrial Fibrillation

Atrial Flutter

Paroxysmal Supraventricular
Tachycardia
• Rate? 70 bpm
• Regularity? regular
• P waves? flutter waves
• PR interval? none
• QRS duration? 0.06 s
Interpretation? Atrial Flutter
Atrial Fibrillation

Deviation from NSR

 No organized atrial depolarization, so no normal P waves
(impulses are not originating from the sinus node).
 Atrial activity is chaotic (resulting in an irregularly
irregular rate).
 Common, affects 2-4%, up to 5-10% if > 80 years old
PSVT

Deviation from NSR

 The heart rate suddenly speeds up, often triggered by a
PAC (not seen here) and the P waves are lost.
Ventricular Conduction

Normal Abnormal
Signal moves rapidly Signal moves slowly
through the ventricles through the ventricles
• Rate? 60 bpm
• Regularity? occasionally irreg.
• P waves? none for 7th QRS
• PR interval? 0.14 s
• QRS duration? 0.08 s (7th wide)
Interpretation? Sinus Rhythm with 1 PVC
Ventricular Arrhythmias

Ventricular Tachycardia

Ventricular Fibrillation
Ventricular Tachycardia

Deviation from NSR

 Impulse is originating in the ventricles (no P waves, wide
QRS).
Ventricular Fibrillation

Deviation from NSR

 Completely abnormal.
ECG in Valvular Heart Disease

Aortic Stenosis
 LV hypertrophy which is found in approximately 85% of patients with severe AS.
 T wave inversion and ST-segment depression in leads with upright QRS complexes
are common
 Left atrial enlargement in more than 80% of patients
 AF occurs in only 10% to 15% of AS patients.
 Atrioventricular and intraventricular block in 5% of patients
Aortic
Regurgitation
LV diastolic volume
overload, characterized by an
increase in initial forces
(prominent Q waves in leads
I, aVL, and V3 through V6)
and a relatively small wave
in lead V1.
Mitral Stenosis

Left atrial is found in 90% of patients with significant MS

and sinus rhythm.
AF is common with long-standing MS.
RV hypertrophy correlates with RV systolic pressure.
Mitral Regurgitation

Left atrial enlargement and AF

Electrocardiographic evidence of LV enlargement occurs
in about one third of patients with severe MR.
ECG Signs of Acute Pulmonary
Embolism
Sinus tachycardia:8-73%
P Pulmonale : 6-33%
Rightward axis shift : 3-66%
Inverted T-waves in right chest leads: 50%
S1Q3T3 pattern: 11-50% (S1-60%, Q3-53% ,T3-20%)
Clockwise rotation:10-56%
RBBB (complete/incomplete): 6-67%
AF or A flutter: 0-35%
No ECG changes: 20-24%

Am J Med 122:257,2009
Electrocardiogram from a 33-year-old man who presented with a left main
pulmonary artery embolism on chest CT scan. He was hemodynamically stable
and had normal right ventricular function on echocardiography. His troponin
and brain natriuretic peptide levels were normal. He was managed with
anticoagulation alone. On the initial electrocardiogram, he has a heart rate of
90/min, S1Q3T3, and incomplete right bundle branch block, with inverted or
flattened T waves in leads V1 through V4.
ACUTE PERICARDITIS
The electrocardiogram (ECG) is the most important
laboratory test for diagnosis of acute pericarditis
The classic finding is diffuse ST-segment elevation in all
leads except aVR and often V1.
The ST segment is usually coved upward
PR-segment depression is also common. PR depression
can occur without ST elevation and be the initial or sole
electrocardiographic manifestation of acute pericarditis.
The ECG reverts to normal during days or weeks.
ACUTE PERICARDITIS
CARDIAC TAMPONADE
PERICARDIAL EFFUSION-
Electrical alterans
CVA
Electrocardiographic
abnormalities are
observed in
approximately 70% of
patients with
subarachnoid hemorrhage.
ST-segment elevation
and depression, T wave
inversion, and pathologic
Q waves are observed
Peaked inverted T
waves and a prolonged
QT interval
Normal Variants
Numerous variations occur in subjects without heart disease.
T waves can be inverted in the right precordial leads in normal
persons-occurs in 1% to 3% of adults and is more common in
women(persistent juvenile pattern).
The ST segment can be significantly elevated in normal
persons, especially in the right and midprecordial leads.
The elevation begins from an elevated J point and is commonly
associated with notching of the downstroke of the QRS
complex.
This occurs in 2% to 5% of the population and is most
prevalent in young adults
Normal Variants
Persistent juvenile pattern Early repolarization pattern
Technical Errors and Artifacts
Artifacts that may interfere with interpretation can come
from movement of the patient or electrodes, electrical
disturbances related to current leakage and grounding
failure, and external sources such as electrical stimulators
or cauteries.
Misplacement of one or more electrodes is a common
cause for errors.
Significant misplacement of precordial electrodes.
 ECG RULES
If we follow Professor Chamberlains 10 rules they'll
give you an understanding of what is normal:-
 RULE 1

PR interval should be 120 to 200

milliseconds or 3 to 5 little squares
 RULE 2

The width of the QRS complex should not

exceed 110 ms, less than 3 little squares
 RULE 3

The QRS complex should be dominantly upright in

leads I and aVF
 RULE 4

QRS and T waves tend to have the same general

direction in the limb leads
 RULE 5

All waves are negative in lead

aVR
 RULE 6

The R wave must grow from V1 to at least V4

The S wave must grow from V1 to at least V3
and disappear in V6
 RULE 7

The ST segment should start isoelectric.

 RULE 8

The P waves should be upright in I, II, and V2 to V6

 RULE 9

There should be no Q wave or only a small q less than 0.04 seconds

& <25% of R wave in width in I, II, V2 to V6
 RULE 10

The T wave must be upright in I, II, V2 to V6

ECG
Axis?
Type of Bundle branch block?
Type of Bundle branch block?
LVH OR RVH?
Type of MI?