Sei sulla pagina 1di 131


Terminology and Basics

Ectopic Beats or Rhythms

• beats or rhythms that originate in places other than the SA node
• the ectopic focus may cause single beats or take over and pace
the heart, dictating its entire rhythm
• they may or may not be dangerous depending on how they affect
the cardiac output

Causes of Ectopic Beats or Rhythms

• hypoxic myocardium - chronic pulmonary disease, pulmonary embolus
• ischemic myocardium - acute MI, expanding MI, angina
• sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism
• drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,
imbalances of calcium and magnesium
• bradycardia - a slow HR predisposes one to arrhythmias
• enlargement of the atria or ventricles producing stretch in pacemaker cells
Terminology and Basics
Arrhythmia or Dysrhythmia?
• dysrhythmia accurate, but arrhythmia most widely

Supraventricular: origin is above the ventricle, i.e., SA, atrial

muscle, AV or HIS origin
Ventricular: origin is in ventricle
Arrhythmia is generally named for anatomical site or
chamber of origin

Automaticity: Spontaneous Phase 4 Depolarization (SA, AV,

Purkinje tissue)
• rate dependent on:
• Threshold potential
• slope of phase 4 depolarization
• resting membrane potential

Mechanisms of Arrhythmias
• Altered automaticity
• Normal, enhanced normal, abnormal
• Triggered activity
• Reentry
2. Triggered Activity
 Afterdepolarization reaches threshold
 Early: interrupt repolarization
 Congenital or acquired long QT syndrome: altered K+ and Na+
currents during phase 2 can produce dangerous V-tach
 Delayed: after completion of AP.
3. Reentry (circus movement, reciprocal or echo beat, reciprocating
 Anatomic: nodal tissue, Purkinje, BB, accessory path
 Example: WPW
 Functional
 Local differences in conduction velocity and membrane characteristics
 Anisotropic:
 circuit determined by difference in conduction velocity through length of
 Reflection
 Parallel pathways with depressed segments
3. Reentry (circus movement, reciprocal or echo beat, reciprocating
 Requires: available circuit, unidirectional block, and different
conduction speed in limbs of circuit
 Conditions that depress conduction velocity or shorten refractory period
promote functional block
 Exp: WPW reciprocating tachycardia, AV-nodal reentry, V-tach due to
bundle branch reentry, infarcted area.
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

Tissues with these type of circuits may exist:

• in microscopic size in the SA node, AV node, or any type of heart tissue
• in a “macroscopic” structure such as an accessory pathway in WPW
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Premature Beat Impulse
Repolarizing Tissue Conduction
(long refractory period) Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

1. An arrhythmia is triggered by a premature beat

2. The beat cannot gain entry into the fast conducting
pathway because of its long refractory period and
therefore travels down the slow conducting pathway
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

3. The wave of excitation from the premature beat

arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

4. On arriving at the top of the fast pathway it finds the

slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit
Re-entry Circuits as Ectopic Foci and Arrhythmia Generators

Atrio-Ventricular Nodal Re-entry

• supraventricular tachycardia
Atrial Re-entry Ventricular Re-entry
• atrial tachycardia • ventricular tachycardia
• atrial fibrillation
• atrial flutter

Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular tachycardia
Clinical Manifestations of Arrhythmias
• many go unnoticed and produce no symptoms
• palpitations – ranging from “noticing” or “being aware” of ones heart
beat to a sensation of the heart “beating out of the chest”

• if Q is affected (HR > 300) – lightheadedness and syncope, fainting

• drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,
imbalances of calcium and magnesium

• very rapid arrhythmias u myocardial oxygen demand r ischemia

and angina

• sudden death – especially in the case of an acute MI

• mechanism differentiation from ECG very difficult to impossible
Clinical Application
• No rhythms precisely regular
• Incidence: common (PVC, PAC), increase with age
• ECG differentiation may be impossible
• Monitor leads V1 or MCL1: L&R ventricular ectopy, RBBB &
LBBB, good P-waves
• Where to look for clues
• P-wave morphology
• PR interval
• QRS morphology
• QTc interval
• Matching atrial rate with ventricular
• Look for gaps in the rhythm
Clinical Application
• Eight basic rhythm disturbances
• early beats (extrasystole)
• unexpected pauses (nonconducted atrial extrasystole)
• bradycardia (sinus bradycardia)
• tachycardia (ventricular or atrial)
• bigeminal rhythm (ventricular or supraventricular extrasystolic)
• group beating (2nd degree heart block)
• total irregularity (atrial fibrillation)
• regular non-sinus rhythm at normal rate (accelerated AV rhythm)
Abnormal rhythm
It can be one of the two extreme forms –

 Tachyarrhythmia –a) supraventricular

b) Ventricular origin
 Bradyarrhythmia
Supraventricular Tachycardia-
AV node dependant tachycardias AV node Independent (atrial)
AVNRT Sinus tachycardia
Typical( ‘common’, slow –fast) Physiologic
Atypical( ‘uncommon’, Fast-slow) Inappropriate
Sinus node re-entry

AVRT Atrial Tachycardia

Concealed accessory pathway Unifocal
Wolf-Parkinson –White syndrome Multifocal

Junctional Atrial Flutter

Junctional ectopic tachycardia Atrial fibrillation
Mechanisms of SVT


Atrial Tachycardia AVNRT AVRT

Sinus Rhythm

• Originates in sinus node

• Innervated from right sided
sympathetic and
parasympathetic trunks
• Parasympathetic (i.e. vagal
tone) predominates
• Normal range is 60 to 100
bpm with gradual
changes in rate
• Sinus “p waves” are upright
(+) in lead II
Sinus rhythm
It is characterized by P waves of sinus origin,
constant and normal PR interval, and constant P
wave configuration in a lead with rate between
60-80 / minute and rhythm under the influence
of autonomic system
Sinus p wave

Rate of 78 bpm

Normal sinus rhythm

Sinus Arrhythmia
Phasic (respiratory) sinus arrhythmia is characterized
by an acceleration of the heart rate with inspiration and
slowing with expiration.
Electrocardiographic features
 1.A variation of at least 0.12 s between the longest and
shortest PP intervals, with normal and constant P-wave
 2.Maximum cycle length minus minimum cycle length
divided by minimum cycle length is > 10%
Fig 3

Sinus Tachycardia >100b/min

Normal sinus rhythm 1. Normal P waves
2. Normal or shortened PR
3. QRS and T vectors are normal
4. ST segments are normal
Sinus tachycardia
5. RR interval short <15mm
1500/100 = 15

Sinus bradycardia
Fig 3

Sinus Bradycardia <60b/min

1. P waves are present and all
Normal sinus rhythm are followed by a QRS
2. Normal and constant PR
3. QRS and T vectors are
Sinus tachycardia
4. ST segments are normal
5. RR interval long >25mm
1500/60 = 25
Sinus bradycardia
Premature atrial contraction (PAC)
1. Arises from an ectopic focus in the atria.
2. Will have an identifiable P wave but the shape of the
P wave may be altered
3. May have a normal QRS
4. May have a compensatory pause
The compensatory pause The QRS may be altered
is lacking because the SA if some of the ventricle is
node was reset. still in its refractory
The rhythm has been period.
Supraventricular Rhythms

Primarily concerned with SVT – supraventricular tachycardia

• Ectopic Atrial Tachycardia
•Atrial fibrillation and flutter
• Atrioventricular Nodal Reentry (AVNRT)
• SVT associated with the Wolff-Parkinson-White Syndrome
Atrial Tachycardia
 Ectopic atrial focus
 Reentrant, automatic or triggered
 150-250 bpm
 1:1 AV conduction
 Paroxysmal or “warm up”
 P wave morphology variable
Focal Atrial Tachycardia


SN * * *


20 yr woman with post-partum congestive heart failure

Specific Diagnostic Evaluation
Ectopic atrial focus
 Since the rhythm is initiated by enhanced
automaticity of a single focus, the first ectopic
and the subsequent P-wave morphology are
 The rate at onset varies and gradually accelerates
as the focus "warms up."
 AV nodal block may exist.
Specific Diagnostic Evaluation
 Vagal maneuvers do not terminate the rhythm,
although they may produce AV block and thus, reduce
heart rate
 The PR interval is related to the rate of tachycardia.
 The vector of the ectopic P wave is usually normal with
upright P waves in leads II, III, and aVF, although the P
wave appear slightly different from the normal P wave.
Atrial tachycardia
Multifocal Atrial Tachycardia
The rate is usually 100 to 150/min with at least
three P waves of at least three different
morphologies identified in a single lead. The
atrial rate is slightly irregular, and the PR interval
also varies.
Atrial fibrillation and
Atrial Fibrillation

• Over 2.2 million

Americans have atrial
• Prevalence in the
general population is 0.4%
• Prevalence increases
with age, rising to over 8%
in people 80 years or older
 AF is characterised by wavelets propagating in different directions
causing disorganized atrial depolarization without effective atrial

 Electrical activity of atrium can be detected in ECG as small irregular

baseline undulations of variable amplitude & morphology (f waves) at
rate of 350 to 600

 Ventricular response is irregularly irregular, & in untreated patients with

normal AV conduction, is usually between 100 to 160
Atrial fibrillation
1. Irregularly irregular
2. No P waves
Underlying causes of AF
 CVS  Tumors
 Rheumatic heart disease  WPW syndrome
 ASD  Systemic
 Cardiac surgery  Alcohol (holiday heart syndrome)
 Cardiomyopathy
 Hypertrophic
 Idiopathic  COPD
 Infiltrative  Defibrillation
 Hypertension  Effort
 CAD (Acute & chronic)  Electrocution
 Electrolyte abnormalities
 Non rheumatic mitral or tricuspid valve
disease  Fever
 Pericarditis  Hypothermia
 Tacycardia-bradycardia syndrome
Underlying causes of AF…

 Pneumonia  Congenital
 Pulmonary embolism  Multiple sclerosis
 Sudden emotion  Muscular dystrophy
 Thyrotoxicosis  Pheochromocytoma
 Trauma  Right atrial cold injections
 Rare  Swallowing
 Acute hypovolemia  Tyramine foods
Atrial Fibrillation
Mechanism is activation of
multiple wavelets within the
right and left atrium

Recent studies have shown

pulmonary vein foci trigger
some episodes
Atrial fibrillation

Atrial Fibrillation
Clinical Classification

 Paroxysmal

 Persistent

 Permanent
 Paroxysmal AF
 Short lasting < 1 hour
 Long lasting >1; < 48 hours
 AF interspersed with periods of sinus rhythm & usually terminates
 Persistent AF
 Occur between 2days - weeks
 Intervention is needed to restore the sinus rythum
 Chronic or permanent AF
 Persists for months to years
 No spontaneous conversion
 Interventions to restore sinus rythum are either ineffectual or not tried
Atrial Fibrillation

Atrial Fibrillation
1).Absence of P waves
2).P waves replaced by f waves.
3).f waves : irregular in size ,shape ,and spacing.
Rate between 350 and 600
4). Irregularly irregular ventricular rhythm, best seen in
Ⅱ,Ⅲ,Avf,V1 or V2.
Variable RR intervals

No clear p waves

Atrial Fibrillation
 Type – I --- Activation consisted of single, broad wavefronts
propagating without conduction delay & either only short arcs of
conduction block or small areas of slow conduction that did not disrupt
the main course of propagation

 Type – II --- Activation consisted of either the presence of 2 wavelets

or of single wave (with either considerable conduction block or slow
conduction or both)

 Type – III --- Activation was characterized by 3 or more wavelets

combined with areas of slow conduction & multiple arcs of conduction

 As the fibrillation changed from type I to III, AFs frequency &

irregularity increased, creating a higher incidence of continuous electrical
activity & reentry
of AF
Atrial Fibrillation with
Apparent regularity of RR interval

1. A Fib with CHB

 Degenerative AV block
 Dig Toxicity
 End stage Sick Sinus Syndrome

2. Afib at very fast heart rates

Atrial Flutter

“Typical isthmus dependent

atrial flutter” is due to a
macro reentrant circuit
around the tricuspid valve
• This rhythm can be
stopped by pacing and
cured with ablation
• Embolic risk may be less
than in fibrillation, but same
recommendations apply
Ventricular rate 150 bpm

“Saw tooth” p waves

Atrial Flutter
Reentry Circuit of Common
Atrial Flutter

Morady F. N Engl J of Med. 1999;340:534-544.

ECG Recognition counterclockwise
 Counterclockwise atrial flutter
Atrialrate: 240 - 340 bpm
Rhythm: Regular

Ventricular rate: Variable

 Dependent upon:
– AV node conduction properties
– Usually a 2:1, 4:1 fixed conduction ratio

Recognition: “Sawtooth” appearance on the

surface ECG
ECG Recognition counterclockwise
ECG Recognition – Clockwise
 Clockwise atrial flutter
Atrial rate: 240 - 340 bpm
Atrial rhythm: Regular

Ventricular rate: Variable

 Dependent upon:
– AV node conduction properties
– Usually a 2:1, 4:1 fixed conduction ratio

Recognition: “notched” upright pattern on the

inferior surface ECG
ECG Recognition – Clockwise flutter

ECG used with permission of Dr. Brian Olshansky.

Atrial Flutter
right atrial reentry
LA is passively
Atrial Flutter

Ablation in
Atrioventricular Nodal Reentrant Tachycardia
(AV Node Reentry or AVNRT)
• Most common cause
of paroxysmal SVT in
the young adult
• Occurs over a small
reentrant circuit located
near the AV node
• The circuit consists of
a fast and slow pathway
connected by a common
top and bottom pathway
Supraventricular Tachycardia Due to AV
Nodal Reentry(AVNRT)
This supraventricular tachycardia with a regular
ventricular rate varying between 160 to 260
beats per minute is due to AV nodal reentry.
Mechanism- Dual pathway
physiology in AV node
Specific Diagnostic Evaluation
Examination of a 12-lead electrocardiogram may reveal a
retrograde P wave buried in the QRS complex or immediately
following the QRS complex,
P waves may fall on terminal part of S wave in V1, so as to produce
pseudo R’ wave in V1
P waves may fall in terminal part of R waves in lead II, so as to
produce a pseudo S wave
The PAC initiating AV nodal tachycardia has a long PR interval as a
result of antegrade conduction down the slow-conducting
alpha pathway.
The rhythm may be initiated and terminated by a PAC or PVC.
Vagal maneuvers may slow and then abruptly terminate the rhythm
Adenosine conversion of AVNRT
to SR
Retrograde p waves

Rate of 145 bpm

RP = 60 msec

AV Node Reentry Tachycardia

(Short RP tachycardia)
Wolff-Parkinson-White Syndrome
• Relatively common
cause of paroxysmal
SVT in children and
young adults
• Due to an “extra”
muscular bridge that
connects the atrium and
ventricle and allows the
ventricle to be “excited”
before the signal passing
through the AV Node
Wolff-Parkinson-White Syndrome
 Preexcitation exists when, in relation to atrial
events, all or part of the ventricular muscle is
activated by an impulse over an accessory
(bypass) pathway sooner than the impulse
arriving by way of the normal AV system.
Specific Diagnostic Evaluation
12 lead ECG during SR
• Short PR interval (less than 0.12 s]
• Normal P-wave vector.
• QRS duration greater than 0.10 s. A 12-lead
electrocardiogram during atrial fibrillation or
atrial flutter may reveal delta waves.
QRS is wide
Rate = 62 bpm
(over 120 msec)

PR interval is short
(80 to 90 msec)

Wolf-Parkinson-White (WPW) Syndrome

(Right sided pathway)
PR interval is short Rate = 100 bpm
(80 to 90 msec)

QRS is wide
(over 120 msec)

Wolf-Parkinson-White (WPW) Syndrome

(Left sided pathway)
Types of accessory pathways
Based on site of origin and insertion
a.Atrioventricular( Kent fibres)
i. Right sided: anteroseptal , RV free
wall, posteroseptal
ii.Left sided: anteroseptal , LV free
wall, posteroseptal
b. Atriofsicular (Brechenmacher fibres)
c. Nodofacicular fibres( Mahaim)
Types of accessory pathways
II. Based on direction of conduction
Retrograde( concealed)
III. Based on conduction property
Slow, decremental
Fast, non decremental
IV. Based on numbers
Types of conduction over
accessory pathway
Types of conduction over
accessory pathway

Orthodromic conduction: A premature impulse (APC, VPC) conducts

antegradely through AV node, retrogradely through accessory pathway
Antidromic conduction: Impulse conducts antegradely over accessory pathway
and retrogradely over AV node
Wolff-Parkinson-White Syndrome Tachycardias
WPW: Initiation of SVT
Supraventricular tachycardia
• initiated by a closely coupled
premature atrial complex
• blocks in the accessory
• but conducts through the AV
• retrograde conduction via
accessory pathway
• inverted P wave produced by
retrograde conduction visible
in the inferior ECG leads
AV reentrant tachycardia
 often reveal a negative P wave in lead-I. The RP
interval is usually less than one-half the RR interval.
 The rhythm may be initiated and terminated by a PAC
or a PVC.
 Vagal maneuvers sometimes slow and abruptly
terminate the rhythm.
 QRS alternance can be seen in few cases
 Prolongation of tachycardia cycle length associated
with bundle branch block usually localizes the
accessory pathway to the side of bundle branch block
AVRT- note short RP interval, well seen P waves, an example
of orthodromic conduction
Atrial fibrillation with antegrade conduction
over accessory pathway
Wolf-Parkinson-White (WPW) Syndrome

Asymptomatic patient - no further evaluation or treatment is


• Some “high risk” occupations - such as airline pilots - may

require further evaluation even if they are

• Some physicians will advocate exercise treadmill testing or

the induction of atrial fibrillation to access the
patients risk of SCD even if the patient is
Wolf-Parkinson-White (WPW) Syndrome

Symptomatic patients - first step is correlating the patient’s

symptoms with SVT. This is especially true if the
patient complains of “palpitations”. If syncope or SCD
has occurred, however, most would proceed to EPS.

• After the presence of SVT has been established, most

cardiologists would recommend diagnostic
electrophysiology study (EPS) to characterize the
accessory pathway.

• Treatment can be best defined by EP study

Atrial fibrillation can coexist with WPW.
• If the patient with WPW can conduct rapidly down the
accessory pathway, it is possible that the patient could
have ventricular fibrillation and SCD by rapidly
conducting the atrial impulses down the pathway

• The administration of AV nodal blocking agents can

increase the risk of this rapid conduction

• If a patient with WPW demonstrates consecutive preexcited

(i.e. wide) QRS complexes during atrial fibrillation
that are less than 250 msec apart, they are at increased
risk for SCD.

Dr Dattatreya
Ventricular Tachyarrhythmias
1. Unifocal
2. Multi focal
3. Monomorphic
4. Poly morphic
B. Ventricular tachycardia
2. Sustained VT
3.Mnomorphic VT
4. Polymorphic VT

C. Ventricular flutter
D. Ventricular fibrillation
Ventricular Beats & Rhythms

QRS is wide and much different ("bizarre") looking

than the normal beats. This indicates that the beat
originated somewhere in the ventricles and
consequently, conduction through the ventricles did
Escape Beat
not take place through normal pathways. It is
therefore called a “ventricular” beat

there is no p wave, indicating that the beat

did not originate anywhere in the atria
actually a "retrograde p-wave may sometimes be
seen on the right hand side of beats that
originate in the ventricles, indicating that
depolarization has spread back up through the
atria from the ventricles
Ventricular Beats & Rhythms
Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles):
• A ventricular ectopic focus discharges causing an early beat
• Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre"
• QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant)
• In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion
• PVC’s are sometimes described by lay people as “skipped heart beats”, often normal variant

R on T

Multifocal Compensatory pause

PVC's after the occurance of a PVC
Ventricular Beats & Rhythms
Characteristics of PVC's
PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)
• T-waves for PVC’s are usually large and opposite in polarity to terminal QRS
• Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle
• Every other beat being a PVC (bigeminy) may indicate coronary artery disease
• Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s

The classic PVC – note the

compensatory pause Interpolated PVC – note the sinus
rhythm is undisturbed
Premature Ventricular Complex (PVC) - Summary
ECG Patterns
Rate: can occur at any rate and with any rhythm
Rhythm: normally irregular due to pause after PVC
P wave: normally none associated with PVC; may be
P-R: none evident
QRS: usually wide (>.11s) and bizarre with T
directed opposite QRS deflection;
BBB configuration; different from
flanking beats
Comment: usually followed by fully compensatory
pause; usually don't generate a
peripheral pulse
PVC Summary (cont)
• Post extrasystolic cycle may be less than compensatory when:
• retrograde conduction to atria disturbs SA
• Post extrasystolic cycle ends with escape beat
• interpolated PVC
• Mechanism
• Ectopic focus or reentry???
Morphology of PVC's
• left vs right PVC's - best recognized in V1
•'+' in V1 => LV origin; called RBBB pattern
• usually monophasic R or qR in V1
• rS or QS in V6
• left rabbit ear taller than right in V1; often opposite if
true RBBB
• ‘-” in V1 => RV origin, LBBB pattern
• importance
• LV more likely with HD
• LV more likely to precipitate V-tach in acute MI
Ventricular Beats & Rhythms
PVC's are Dangerous When:
• They are frequent (> 30% of complexes) or are increasing in frequency
• The come close to or on top of a preceding T-wave (R on T)
• Three or more PVC's in a row (run of V-tach)
• Any PVC in the setting of an acute MI
• PVC's come from different foci ("multifocal" or "multiformed")

These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:

• Ventricular Tachycardia The sooner defibrillation takes place,
• Ventricular Fibrillation the increased likelihood of survival

“R on T phenomenon”


Unconverted V-tach r V-fib

sinus beats V-tach
Ventricular Beats & Rhythms
Notes on V-tach:
• Causes of V-tach
• Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause)
• Typical V-tach patient
• MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm)
•V-tach complexes are likely to be similar and the rhythm regular
• Irregular V-Tach rhythms may be due to to:
• breakthrough of atrial conduction
• atria may “capture” the entire beat beat
• an atrial beat may “merge” with an ectopic ventricular beat (fusion beat)

Fusion beat - note p- Capture beat - note that

wave in front of PVC and the complex is narrow
the PVC is narrower than enough to suggest normal
the other PVC’s – this ventricular conduction.
indicates the beat is a This indicates that an
product of both the sinus atrial impulse has made it
node and an ectopic through and conduction
ventricular focus through the ventricles is
relatively normal.
Ventricular Tachycardia (VT)
Rate: 140-220 (200±50); at least 3 ectopic QRS in row
Rhythm: generally regular (may be slightly irregular)
P wave: no related P waves
P-R: none
QRS: normally wide and bizarre; ($ 0.14 sec favors
• Usually associated with MI or other organic HD; unusual in normals
• Often serious requiring quick treatment if sustained
• Mechanism? Reentry or rapid firing ectopic??
ECG diagnosis - clues to rule in VT
• Difficult to rule out SVT with aberrant ventricular conduction
• use more leads whenever possible - MCL1 or V1
• Unrelated P's (independent atrial activity) - rules out atria
• Presence of fusion beats suggests VT as contrasted to SVT
• LVT favored - monophasic pattern in R chest leads (V1 or MCL1)
with taller left 'rabbit ear‘
• Concordant positivity (all complexes positive) in V leads => favors
LV ectopy (rule out WPW)
concordant negativity = favors RV ectopy (rule out LBBB)
• QRS interval > .14 sec (prior tracing available to rule out BBB)
Sustained vs. Nonsustained
 Sustained VT
 Episodes last at least 30 seconds
 Commonly seen in adults with prior:
 Myocardial infarction
 Chronic coronary artery disease

 Dilated cardiomyopathy

 Non-sustained VT
 Episodes last at least 6 beats but < 30 seconds
Premature Ventricular
 Ectopic beat in the ventricle that can occur singly
or in clusters
 Caused by electrical irritability

 Factors influencing electrical irritability

 Ischemia
 Electrolyte imbalances

 Drug intoxication
 Ventricular Tachycardia
 Monomorphic
 Idiopathic VT
 Bundle branch reentry tachycardia

 Ventricular flutter

 Ventricular fibrillation

 Polymorphic
 Torsades de pointes (TdP)
Monomorphic VTs
Monomorphic VT
 Heart rate: 100 bpm or greater
 Rhythm: Regular
 Mechanism
 Reentry
 Abnormal automaticity
 Triggered activity

 Recognition
 Broad QRS
 Stable and uniform beat-to-beat appearance
ECG Recognition

ECG used with permission of Dr. Brian Olshansky.

Idiopathic Right
Ventricular Tachycardia
 Right ventricular idiopathic VT
 Focus originates within the right ventricular
outflow tract
 Ventricular function is usually normal

 Usually LBBB, inferior axis

 Treatment options:
 Pharmacologic therapy (beta blockers, verapamil)
 RF ablation
ECG Recognition

Kay NG. Am J Med 1996; 100: 344-356.

Bundle Branch Reentry
 Reentry circuit is confined to the left and right
bundle branches
 Usually LBBB, during sinus rhythm
 Presents with:
 Syncope
 Palpitations

 Sudden cardiac death

 Treatment: RF ablation of right bundle

VT Due to Bundle
Branch Reentry
Ventricular Flutter
 Heart rate: 300 bpm
 Rhythm: Regular and uniform
 Mechanism: Reentry
 Recognition:
 No isoelectric interval
 No visible T wave
 Degenerates to ventricular fibrillation

 Treatment: Cardioversion
Ventricular Fibrillation
 Heart rate: Chaotic, random and asynchronous
 Rhythm: Irregular
 Mechanism: Multiple wavelets of reentry
 Recognition:
 No discrete QRS complexes
 Treatment:
 Defibrillation
ECG Recognition

 P waves and QRS complexes not present

 Heart rhythm highly irregular
 Heart rate not defined
Polymorphic VT
Polymorphic VT
 Heart rate: Variable
 Rhythm: Irregular
 Mechanism:
 Reentry
 Triggered activity

 Recognition:
 Wide QRS with phasic variation
 Torsades de pointes
ECG Recognition

EGM used with permission of Texas Cardiac Arrhythmia, P.A.

Torsades de Pointes (TdP)
 Heart rate: 200 - 250 bpm
 Rhythm: Irregular
 Recognition:
 Long QT interval
 Wide QRS

 Continuously changing QRS morphology

 Events leading to TdP are:
 Hypokalemia
 Prolongation of the action potential duration

 Early afterdepolarizations

 Critically slow conduction that contributes to reentry

ECG Recognition

 QRS morphology continuously changes

 Complexes alternates from positive to
Possible Causes
 Drugs that lengthen the QT:
 Quinidine
 Procainamide

 Sotalol

 Ibutilide

 Physical
 Ischemia
 Electrolyte abnormalities
 Pharmacologic therapy:
 Potassium
 Magnesium

 Isoproterenol

 Possibly class Ib drugs (lidocaine) to decrease

refractoriness/shorten length of action potential
 Overdrive ventricular pacing
 Cardioversion
Wide ComplexTachycardias

 Ventricular Tachycardia
 SVT with aberrancy (functional bundle branch
 SVT with underlying bundle branch block
 SVT with pre-excitation
Additional Mimimics of Wide
Complex Tachycardias

 SVT with severe hyperkalemia

 SVT with use of antiarrhythmic agents
particularly 1C agents
 SVT with acute MI
Wide-Complex Tachycardia
 Majority are sinus tachycardia with bundle
branch block
 In higher risk population , previous MI,
Decreased Left ventricular dysfunction
 Predominantly Ventricular Tachycardia
Differentiating Ventricular Tachycardia from
SVT with Aberrancy

 Leads to correct initial therapy

 Avoids use of Verapamil which may precipitate
hemodynamic collapse with V.T.
 Cannot use rate or the presence or absence of
symptoms as discriminator !
 Use ECG criteria for diagnosis
 Use presence of risk factors for V.T. as
Differentiation of VT vs. SVT
with Aberrancy
 Clinical history – if the patient has had an MI in
the past?…it is VT until proven otherwise
 AV dissociation
 QRS morphology
 QRS axis
 Fusion beat
 Capture beat
A-V Dissociation, Fusion, and
Capture Beats in VT
V1 E F C


Fisch C. Electrocardiography of Arrhythmias. 1990;134.
ECG Distinction of VT from SVT with

Favors VT Favors SVT

with Aberrancy
Duration RBBB: QRS > 0.14 sec. < 0.14 sec.
LBBB: QRS > 0.16 sec. < 0.16 sec.

Axis QRS axis -90° to ±180° Normal

ECG Distinction of VT from SVT with
Favors VT Favors SVT
with Aberrancy
Morphology Precordial concordance

If LBBB: V1 duration > 30 ms

S wave > 70 ms
S wave notched or slurred
V6: qR or QR R wave

If RBBB: V1: monophasic R wave

If triphasic, R > R1 R < R1
V6: R < S
The Brugada Criteria
Table I.

Diagnosis Of Wide QRS Complex Tachycardia With A Regular Rhythm

Step 1. Is there absence of an RS complex in all precordial leads V1 – V6?

If yes, then the rhythm is VT.

 Sens 0.21 Spec 1.0

Step 2. Is the interval from the onset of the R wave to the nadir of the S
wave greater than 100 msec in any precordial leads?

If yes, then the rhythm is VT.

 Sens 0.66 Spec 0.98

Step 3. Is there AV dissociation?

If yes, then the rhythm is VT.

 Sens 0.82 Spec 0.98

Step 4. Are morphology criteria for VT present? See Table II.

If yes, then the rhythm is VT.

 Sens 0.99 Spec 0.97
Morphology Criteria for VT
Table II.

Morphology Criteria for VT

Right bundle type requires waveform from both V1 and V6.

V1 V6

Monophasic R wave QS or QR

QR or RS R/S <1

Left bundle type requires any of the below morphologies.

V1or V2 V6

R wave > 30 msec QR or QS

Notched downstroke
S wave.

Greater than 60msec

nadir S wave.

Adapted from Brugada et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex.
Circulation 1991; 83:1649-59.
Therapy for Ventricular
 Clinical condition of patient
 Unstable requires DC cardioversion
 Stable may be treated with Drugs or Cardioversion
 Presence or absence of Left ventricular Dysfunction
determines choice of pharmacologic therapy
 Amiodarone 150 mg I.V. over 10 minutes may be RX of
choice maximum 2.2 gm/24 hours class IIA recommendation