Making Sense of Those

Little Lines – Advanced

ECG Interpretation

Cara Solodky-Hardy, ND,

ANP-BC, AACC
MD24 House Call
Cardiology

Image Sources
• My patients

• www.ecglibrary.com

• The Alan E. Lindsay Ecg Learning Center

http://medlib.med.utah.edu/kw/ecg/intro.html

• The EKG of the week from NCEMI http://www.ncemi.org

• Normal EKG
– Axis determination

• Blocks
– Bundle branch blocks
– Nodal blocks

• Dysrhythmias

• Patterns of Infarction

• EKG CASES

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 Normal Electrical Pathway

SA node

AV node

SA
Bundle of His

Bundle Branches

AV

NORMAL EKG

• P wave: atrial activity

• Q wave: first downward
deflection from
isoelectric line (t-p)
• R wave: first upward
deflection from
isoelectric line
• S wave: second
downward deflection

Basic Anatomy & Physiology

• Muscular pump.
• Left side is the larger and thicker. It does
more work, pumps oxygenated blood into
the aorta & throughout body.
• Right side of the heart, thinner, as it only
has to send a short distance into the lungs
via the pulmonary arteries.
• Each side of heart consists of two
chambers, an atrium and a ventricle. The
ventricles are the larger pumping chambers
that have thicker wall size that expel blood
from the heart with each beat
(contraction/systole.)

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 NORMAL EKG

qRs: small downward deflection, large

upward deflection, and small downward
deflection

rS: small upward deflection, and large

downward deflection

Qr: large downward deflection, and small

upward deflection

Rs: large upward deflection, and small

downward deflection

AXIS: NORMAL EKG - positive polarity(tall R) in inferior and

lateral leads with increasing positive polarity (r-wave
progression) across the precordium V1-6

I AVR V1 V4

II V2 V5
AVL

V6
V3

III AVF

In a “normal” patient the only leads that should have

negative polarity are AVR and V1-2
---To determine axis: Look at leads I and AVF

I AVR V1 V4

II V2 V5
AVL

V6
V3

III AVF

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 LAD - negative polarity (rS) in AVF

RAD: negative polarity(rS) in lead I

Severe RAD, negative polarity(rS) in 1& AVF

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Quick & Easy AXIS DETERMINATION
 Left axis deviation - negative QRS in lead AVF
I

AVF
I
AVF

 Right axis deviation - negative QRS in lead I

I

I
AVF AVF

 Severe Right axis deviation negative QRS in BOTH lead I

and AVF I

I AVF

AVF

Why do we care about axis determination

in the clinical practice?
Differential Diagnosis
LAD : LBBB, LAFB, Mechanical shift due to ascites or
elevated diaphragm, left atrial hypertrophy

RAD : RBBB, LPFB, right ventricular hypertrophy,

dextrocardia, Pulmonary Embolism

Both RAD and LAD can be caused by COPD,

Hyperkalemia, MI, WPW

LAD
Note negative
polarity in
AVF

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 RAD
Note negative
polarity (rS) in
I

Severe RAD
Note negative
polarity (rS) in
I & AVF

BUNDLE BRANCH BLOCKS

 Unifascicular
 Right BBB  Trifascicular
 Left Hemiblocks  Bifasicular PLUS AV
– Left anterior OR nodal block
– Left posterior
 Bifascicular
 Left BBB (implies both
hemiblocks present)
 Right BBB PLUS
– Left anterior
– Left posterior

Right Bundle Branch Block

 QRS > 0.12 sec

 Predominantly
positive rSR’ in
 V 1-2
 Wide slurred S in
lead I

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 LEFT BUNDLE BRANCH BLOCK
Left bundle branch block
(Both fascicles are
blocked)
 QRS > 0.12 sec
 Deep S in V 1-3
 Tall R and RsR’ in lateral
leads: I, AVL, & V 5-6

Left bundle divides into anterior and posterior branches

 Left anterior fascicular

block
• Left axis deviation:
negative polarity (rS) of
AVF
• rS waves in Inferior leads
• Small Q in I (qR)

Left posterior fascicular block

Right axis deviation

• RAD = negative
polarity (rS) of
Lead I
• SmallQ in
III (qR)

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 BIFASCICULAR BLOCKS

Right bundle branch

block associated
with Left anterior
fascicular block

• rS in AVF
• qR in I

BIFASCICULAR BLOCKS
Right bundle branch
block associated RBBB
with Left posterior RAD – rS I
fascicular block -- plus qR III
uncommon

SA BLOCK
• Sinus pause : 1 - 2 second pause
• sinus beat resumes
• Sinus arrest : > 2 seconds
• junctional escape beat intervenes at 40-55 bpm
• ventricular escape beat at 20 -40 bpm

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 AV-BLOCKS
• 1st degree - PR > 0.2 sec

AV-BLOCKS
• 2nd degree
– Mobitz I (Wenckebach) PR increases until a QRS is blocked

dropped

• 2nd degree
AV-BLOCKS
– Mobitz II - blocked QRS (2:1, 3:1, 4:1)
 PR interval is fixed and usually normal, then p-waves with
dropped beats

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 AV-BLOCKS
• 3rd degree - disassociation of PP and RR, the PP
intervals and RR intervals are constant.

PP RR

PEARLS
 Differential diagnosis for slow irregularly irregular rhythm
 Second Degree heart block : wenckebach
 Third Degree heart block

 If you see Left Axis Deviation, think about LAFB

 If you see Right Axis Deviation, think about LPFB

TYPES OF DYSRHYTHMIAS
• Re-entry (SVT, WPW)
• Two parallel pathways with different rates and refractory
periods
• Something alters the refractory period and the alternative
pathway becomes dominant
• This causes a unidirectional conduction block, and a circuitous
conduction pathway forms.

PAC

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 TYPES OF DYSRHYTHMIAS
• Enhanced or Triggered (PACs, PVCs, Afib,
MFAT)
• Conduction cells act as Pacemaker cells
• Conduction cells can be enhanced and become dominant in
the setting of ischemia, sepsis, electrolyte imbalance or
toxins.
• Some dysrhythmias start with enhanced or triggered
activity, but follow a circuitous pathway seen in re-
entry. (Atrial flutter, Vtach)

A 60 yo with COPD c/o palpitations & SOB. The EKG shows:

a. Atrial Fibrillation
b. Premature Atrial Complexes
c. Multi-Focal Atrial Tachycardia
d. Paroxismal Atrial Tachycardia with block

MULTIFOCAL ATRIAL TACHYCARDIA (MFAT)

 P waves of at least 3 different shapes
 No dominant atrial pacemaker
 Rate greater than 100 bpm
 Varying PR, RR, and PP intervals
 Enhanced or triggered automaticity

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 MFAT - CLINICAL SIGNIFICANCE

 Hypoxia  Treat the underlying

 COPD disease process causing the
triggered automaticity
 Methylxanthene
toxicity  OXYGENATION and
PERFUSION
 CHF or sepsis
 Magnesium Sulfate
 Calcium channel blocker
for rate control prn

MULTIFOCAL ATRIAL TACHYCARDIA (MFAT)

 P waves of at least 3 different shapes
 No dominant atrial pacemaker
 Rate greater than 100 bpm
 Varying PR, RR, and PP intervals

A 56 year old presents with palpitations. EKG shows:

a. Atrial fibrillation
b. Atrial flutter
c. Left anterior fasicular block
d. RBBB

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 B. ATRIAL FLUTTER : Rapid, regular flutter (F) waves at 250-350
per minute (ventricular conduction 1:2, ie ~150bpm)
 Sawtooth pattern of F waves in leads 2, 3 and AVF
 Little evidence of atrial activity in lead 1
 AV conduction variable, QRS typically normal width
 Enhanced automaticity leading to circuitous conduction/reentry

ATRIAL FLUTTER -
TREATMENT
 Atrial flutter is the most
electrosensitive of all
dysrhythmias therefore
cardioversion is the
treatment of choice for
conversion to sinus rhythm.
 Drug of choice for rate
control is Calcium channel
blockers.
 Drug of choice for diagnostic
purposes is Adenosine (as
long as QRS is narrow

Atrial flutter with 2:1 conduction is often

confused with SVT

But, look for the sawtooth flutter waves in the inferior leads.

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 Same patient after adenosine,
showing prominent flutter waves.

A 46 year old presents with palpitations. EKG shows:

a. Atrial fibrillation
b. Atrial flutter
c. Left anterior fasicular block
d. RBBB

EKG shows: a. Atrial fibrillation

– Prominent fibrillatory waves in V 1-3 & AVF
– Irregular ventricular response, greater than 100 / min
– Ventricular rate less than 100 implies AV block
– Triggered/enhanced automaticity

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 ATRIAL FIBRILLATION - treatment
• Cardiovert if unstable
• Ca Channel Blocker- Drug of
choice for rate control
• Beta blocker
• Digitalis
• ASA alone for afib < 48h
• ASA & Anti-coagulate all
others, if unknown or >48h

» the longer the patient has been in afib, the less likely you will be able to convert to NSR

Ashman’s phenomenon – short runs of wide complex tachycardia

during rapid atrial fibrillation.

The refractory period is rate-related, and when erratic changes in rate

occur, an impulse conducted during the refractory period will have an
aberrant (RBBB) pattern.

The most common dysrhythmia associated

with digitalis toxicity is:

A. Paroxysmal atrial tachycardia with AV nodal block

B. Premature ventricular contractions
C. Second degree AV nodal blocks
D. Ventricular tachycardia
E. Junctional tachycardia

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 DIGITALIS TOXICITY -
DYSRHYTHMIAS
• Most common : b. PVCs
• Most pathognomonic : PAT w/block
• Others
– AV nodal blocks
– sinus bradycardia, pause, SA block
– junctional escape beats or tachycardia
– Ectopic SVT, V-tach, V-fib

Paroxysmal atrial tachycardia with block is pathognomonic for

digitalis toxicity.
Note the p waves at a rate > 100 & blocked QRS complexes.
(Don’t mistake for aflutter with variable conduction or 3rd degree block)

Note the blocked

Impulses!!

A 23 yo male with c/o palpitations, EKG shows:

a. Atrial fibrillation
b. MFAT
c. SVT
d. PAT with block

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His EKG shows c. SVT or AV nodal reentry tachycardia with a
rapid, regular rate, absent p waves & narrow QRS complexes

AV nodal Re-entry tachycardia/SVT

•Two parallel pathways with different
rates and refractory periods
•Something alters the refractory
period and the alternative pathway
becomes dominant
•This causes a unidirectional
conduction block, and a circuitous SA
conduction pathway forms.

AV

AV nodal Re-entry tachycardia/SVT

• The circuitous impulse is
typically transmitted anterograde
(forward) over the relatively
slow AV nodal fibers, limiting
the rate to 200bpm.
SA

•WHAT’S THE BIG

DEAL???

• Treat by blocking the AV node AV

and allowing the normal
pacemaker to resume.
• Adenosine
• Ca channel blocker
• Beta blocker

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 SVT with Aberrancy (rate-related block)
SVT with aberrancy is a
supraventricular
tachycardia with a wide-
complex QRS due to a rate-
related bundle branch
block. SA

AV

SVT with Aberrancy (rate-related block)

• SVT with aberrancy is treated by
blocking the AV node and allowing
the normal pacemaker to resume
• Adenosine
• Ca ch blocker
• Beta blocker
• It is very difficult to differentiate
from Vtach SA
• if unsure, treat as stable
Vtach
• amiodarone
• procainamide
AV

• 44yo with complaint of palpitations and shortness of breath, ekg shows:

a. SVT with aberrancy
b. Ashman’s phenomenon
c. WPW
d. V-tach

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C. The EKG is WPW w/ retrograde conduction causing wide QRS.

• Because the etiology of a wide complex tachydysrhythmia is often

unknown in the ER, treat with amiodarone, procainamide, lidocaine
or cardioversion. (avoid procainamide in TCA OD or prolonged qt toursades)

Pre-Excitation Syndromes-
WPW & LGL
• Accessory pathway connects atria to the ventricles,
bypassing the AV node
• Wolff-Parkinson-White: short PR (< 0.12 s), Delta
wave (slurred upstroke QRS), slight wide QRS
>0.10s, and frequently a psuedoinfarction pattern
in the inferior leads and RBBB pattern.
• Lown-Ganong-Levine: short PR (< 0.12 s), NO
Delta wave, normal QRS & episodes of
tachydysrhythmias
WPW LGL

Delta waves, short pr interval, wide QRS

The underlying ECG in WPW is a fusion of the accessory pathway

(delta wave) and normal pathway of the QRS. During tachy-
dysrhythmias, the electrical impulse follows only the accessory
pathway in a circuitous fashion.

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 Underlying ECG
Fusion of accessory &
normal pathways

Accessory pathway with

circuitous impulses
traveling retrograde
(wide QRS)

Accessory Pathways-WPW

If narrow QRS d/t

forward conduction,
treat as SVT
(Adenosine)
SA

AV

Wide QRS b/c retrograde conduction –10%

Accessory Pathways-WPW
Wide QRS if
retrograde conduction

Adenosine, Ca channel blockers, B blockers and digitalis

block the forward conduction, not the retrograde SA
conduction. In a wide complex WPW (retrograde
impulses) most AV nodal blockers stop only anterograde
conduction and can allow the rate of retrograde conduction
to speed up and deteriorate into Vfib! This is seen in wide
complex WPW with Afib or Aflutter.
AV
Amiodarone and procainamide affect the
forward and retrograde pathways as well as
the ventricles and are safe in wide-complex
tachydysrhythmias.

(Caveat: Procainamide and Amiodarone not to be used in

Toursades)

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 Evaluation of Re-entry Tachycardias
- QRS Width
• Wide or Narrow
– If the QRS is narrow, it MUST have atrial origin and conduct
through the AV node in a forward manner.

– If the QRS is wide, more than 0.12 seconds, consider :

• Bypass tract (WPW) with retrograde conduction
• SVT with aberrancy (rate-related bundle branch block)
• Junctional origin
• Ventricular origin

Re-entry Tachycardias -
Treatment Modalities
• Based on hemodynamic stability & QRS width
– Unstable : synchronized cardioversion
– Stable :
• Narrow complex – vagal maneuvers, adenosine,
calcium channel blockers or beta blockers
• Wide complex – Amiodarone, Lidocaine or
Procainamide to treat both anterograde and
retrograde impulses and ventricular
dysrhythmias

Beware: it is very difficulty to tell the difference between the wide-

complex tachy-dysrhythmias. It is safer to treat as presumed V-tach.

PEARLS
 Wide complex QRS tachydysrhythmias of unknown
etiology – use amiodorone, procainamide, lidocaine
 Differential diagnosis for rapid, irregularly irregular
rhythm
 MFAT
 Atrial Fib
 Atrial flutter with variable conduction

 SVT at 150 or 300, consider Atrial flutter

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 DYSRHYTHMIAS OF

VENTRICULAR ORIGIN
 Idioventricular rhythms
 Ventricular Tachycardia
 Ventricular Fibrillation
 Torsades de pointes

VENTRICULAR
DYSRHYTHMIAS - Etiology
 V Tach, V Fib & Idioventricular rhythms
– typically caused by an ischemic focus which
allows a rapid reentry dysrhythmia
 Torsades de pointes - caused by a prolonged
QT interval
 Brugada syndrome – sodium ion channel-
apathy

IDIOVENTRICULAR
RHYTHMS
• Mechanism : re-entry with unidirectional block due to myocardial
ischemia
• QRS width > 0.12 sec and rate 40 - 140
• T waves typically have opposite polarity to QRS
• Treatment :
 Controversial, tends to be self-limited
 Supportive care & close observation

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 VENTRICULAR
TACHYCARDIA
• Mechanism : re-entry with unidirectional block due to
myocardial ischemia (Monomorphic)
• QRS width > 0.12 sec and rate > 140 bpm
• T waves have opposite polarity to QRS
• Treatment :
 Stable : Amiodarone, Procainamide, Sotolol, Lidocaine, Mag
 Unstable : Unsynchronized defibrillation plus meds

VENTRICULAR
FIBRILLATION
 Chaotic ventricular depolarization with loss of
organized QRS complexes
 Life-threatening
 Immediate loss of consciousness
 Loss of blood pressure & death
 Treatment : immediate unsynchronized
defibrillation at 200, 300, then 360 joules (if
Biphasic use ½ dose or 150j)

Brugada Syndrome: ST elevation V1-3 with RBBB-like

pattern which predisposes to ventricular dysrhythmias.
• 30% mortality within 3 years.
Brugada P & Brugada J. J Am Coll Cardiol 1992;20:1391-6

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 Brugada Syndrome: Look for ST elevation V1-3
• part of the syncope or palpitation work-up
• immediate cardiology referral for ICD placement

CARDIOVERSION PEARLS
 Atrial flutter is the most electro-responsive dysrhythmia
 10-50 joules ~ treatment of choice
 SVT and STABLE ventricular tachycardia often respond to
50 joules
 Atrial and Ventricular FIBRILLATION require 100 joules
or more
 Biphasic defibrillators use half the joules or 150j

TORSADES DE POINTES
 V-tach due to prolonged QT interval, in which the QRS axis
alternates between positive and negative (Polymorphic)
 Often self-limited, but may deteriorate into ventricular
fibrillation
 Treatment of Choice : Magnesium
 Overdrive pacing & Isoproterenol can be used to speed the heart and
decrease QT interval
 Avoid procainamide and amiodarone, as can worsen QT prolongation
 If refractory, defibrillate

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 QUESTION ~ All of the following
cause Torsades de pointes, except:

A. Hypomagnesemia
B. Tricyclic antidepressant overdose
C. Procainamide
D. Hyperkalemia
E. Quinidine

CAUSES OF PROLONGED
QT INTERVAL
 Hypo -Mg, -Ca, -K,
 Type Ia antidysrhythmics - quinidine,
procainamide
 Tricyclic antidepressant overdose
 drug reactions-EES, antihistamines,
antifungals
 d is incorrect, hyperkalemia does not cause
prolonged QT

Prolonged qt interval

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 Shortened qt: hypercalcemia

Peaked T waves ( > 1/3 QRS)

Prolonged PR interval
Hyperkalemia Widening of QRS

Sine Wave

U waves in Hypokalemia

Potassium 3.5mEq/L Potassium 2mEq/L

Potassium 3mEq/L
Potassium 1mEq/L

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Osborne J wave in hypothermia: notching at
end of a slurred downstroke of QRS

Tricyclic Antidepressant Overdose

• tall r in AVR
• slurring of the terminal portion of
the rS in AVR

Patterns of Infarction
• The LAD supplies the septal V1-2 and anterior leads V2-4
• The RCA supplies the Inferior leads: II, III & AVF
• The Circumflex supplies the high and low Lateral leads: V5-6
and I &AVL

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Inferior Wall MI – ST segment
elevation in II, III & aVF

Anterior Wall MI – ST segment elevation

in V2-4

Septal MI – ST segment elevation V1-2

Lateral Wall MI
– ST segment elevation in V5-6
and/or I & aVL

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 Posterior Wall MI
- Tall R in V1 & ST segment
depression in V1-2

Pericarditis –
diffuse ST segment elevation & PR depression,
with PR elevation in AVR

EKG PEARLS
 When you see a “normal” looking EKG on a test, start
looking for:
 Hyperkalemia :Peaked T waves
 Hypokalemia : U waves
 Hypomagnesimia : Prolonged QT
 Hypercalcemia: Shortened QT
 WPW : short PR, slurring of upstroke qrs
 Hypothermia : Osborne J waves (notched downstroke QRS; reversed
delta waves)
 TCA overdose : stach, widening QRS, slurring of the terminal
rS in aVR
 Axis deviation & Hemiblocks : LAFB, LPFB

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 EKG PEARLS
 Usefulness of aVR & V1
 Tall R wave in V1
 RBBB
 WPW
 Posterior wall MI
 Severe RV strain: PE, pneumothorax, severe COPD
 aVR is normally flipped/negative polarity
 slurring terminal rS in TCA OD
 PR elevation in pericarditis
 Diffuse ST elevation: think pericarditis

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