VENTRICULAR TACHYARRHYTHMIAS

Dr.Syed Tahir Shah

Consultant Cardiologist & Head of Cardiology Department,
Kuwait Teaching Hospital,
Assistant Professor, Peshawar Medical College ,
Peshawar
Ventricular Ectopic Beats
 AKA
 Ventricular Extrasystoles
 Ventricular Premature Beats
 Premature Ventricular Contraction
 Premature Ventricular Depolarization

 Definition
 A premature beat arising from an ectopic focus within the
ventricles.
Ventricular Ectopics
 Ectopic firing of a focus within the ventricles
bypasses the His-Purkinje system & depolarises the
ventricles directly.

 This disrupts the normal sequence of cardiac activation

 Leading to asynchronous activation of the two ventricles

 The consequent interventricular conduction

delay produces QRS complexes with prolonged
duration and abnormal morphology.
Electrocardiographic Features
 PVCs have the following features:
 Broad QRS complex (≥ 120 ms) with abnormal
morphology.
 Premature — i.e. occurs earlier than would be
expected for the next sinus impulse.
 Discordant ST segment and T wave changes.

 Usually followed by a full compensatory pause.

 Retrograde capture of the atria may or may not occur.

Discordance
 “Discordance” describes a pattern of repolarization
abnormality in which the ST segment and T wave are
directed opposite to the main vector of the QRS
complex:
 Typically seen with left bundle branch block, paced
rhythms, VT
 ST depression and T wave inversion in leads with a dominant
R wave.
 ST elevation with upright T waves in leads with a dominant S
wave.
Appropriate discordance
Contd
 Full compensatory pause
 The next normal beat arrives after an interval that is equal to
double the preceding R-R interval.
 Retrograde capture
 Describes the process whereby the ectopic impulse is conducted
retrogradely through the AV node, producing atrial
depolarisation.
 This is visible on the ECG as an inverted P wave (“retrograde P
wave”), usually occurring after the QRS complex.
 Frequent
 More than 5 PVCs per minute on the routine ECG, or

 More than 10-30 per hour during ambulatory monitoring.

Full Compensatory Pause
 Compensatory Pause

Usually a PVC is followed by a complete compensatory pause because the sinus node timing is not interrupted;
one sinus P wave isn't able to reach the ventricles because they are still refractory from the PVC; the following
sinus impulse occurs on time based on the sinus rate.
In contrast, PACs are usually followed by an incomplete pause because the PAC usually enters the sinus node
and resets its timing; this enables the following sinus P wave to appear earlier than expected.
Classification
PVCs may be either:

 Unifocal — Arising from a single ectopic focus; each

PVC is identical.

 Multifocal— Arising from two or more ectopic foci;

multiple QRS morphologies.
On basis of origin
 The origin of each PVC can be discerned from the
QRS morphology:

 PVCs arising from the right ventricle have a left bundle

branch block morphology (dominant S wave in V1).

 PVCs arising from the left ventricle have a right bundle

branch block morphology (dominant R wave in V1).
 Ventricular Ectopy Vs. Abberrancy

Monophasic R waves or R waves with a notch or slur on

the downstroke of the R waves suggests ventricular ectopy > 90% of the
time

rsR' or rSR' QRS morphologies suggests RBBB aberrancy >90% of the time!
PVCs vs aberrant conduction
 PVCs vs aberrant conduction

Use of QRS morphology in a right-sided lead (V1 or MCL-1) to distinguish

between PVCs vs aberrant conduction.
Only a typical RBBB pattern (rsR’ with descent of S wave below the
baseline and with terminal taller right rabbit ear) is predictive of aberration (A
or B). Any other pattern (C, D, E, F ) predicts ventricular ectopy.
 PVCs vs aberrant conduction

Monophasic R wave with a notch or slur on the upstroke of R wave: 50-50 possibility or
either!
qR morphology suggests ventricular ectopy unless a previous anteroseptal MI or unless the
patient's normal V1 QRS complex has a QS morphology (i.e., no initial r-wave)!
 PVCs vs Aberrant conduction

Rapid down stroke of the S wave with or without a preceding "thin" r wave suggests
LBBB aberrancy almost always!

"Fat" r wave (0.04s) or notch/slur on down stroke of S wave or > 0.06s delay from
QRS onset to nadir of S wave almost always suggests ventricular ectopy!
 PVCs vs Aberrant conduction

The timing of the premature wide QRS complex is also important because aberrantly
conducted QRS complexes only occur early in the cardiac cycle during the refractory
period of one of the conduction branches.

Therefore, late premature wide QRS complexes (after the T wave, for example) are
most often ventricular ectopic in origin.
Patterns
 PVCs often occur in repeating patterns:

 Bigeminy — every other beat is a PVC.

 Trigeminy — every third beat is a PVC.

 Quadrigeminy — every fourth beat is a PVC.

 Couplet — two consecutive PVCs.

 Triplet — three consecutive PVCs.

 Patterns

Bigeminy — every other beat is a PVC. Trigeminy — every third beat is a PVC.

Quadrigeminy — every fourth beat is a PVC. Couplet — two consecutive PVCs.

Triplet — three consecutive PVCs.

Clinical Significance
 PVCs are a normal electrophysiological phenomenon
 Not usually requiring investigation or treatment.
 Prevalence increase with age

 Patients are usually asymptomatic but frequent PVCs

may cause
 Palpitations
 A sense of the heart “skipping a beat” or

 Abnormally strong beats (due to the increased output of the

post-ectopic sinus beat).
Contd
 In patients with underlying predispositions (e.g.
ischaemic heart disease, WPW)
 A PVC may trigger the onset of a re-entrant
tachydysrhythmia — e.g. VT, AVNRT/AVRT.

 The significance of VEBs depends on the presence

or absence of underlying heart disease.
Ventricular ectopic beats in otherwise
healthy subjects
 Ectopic beats in patients with otherwise normal hearts are
more prominent at rest and disappear with exercise.
 Treatment is not necessary, unless the patient is highly
symptomatic, in which case
 β-blockers or, in some situations, catheter ablation can be used.
 VEBs are sometimes a manifestation of otherwise subclinical
heart disease, such as coronary artery disease or
cardiomyopathy.
 There is no evidence that anti-arrhythmic therapy improves
prognosis
 But the discovery of very frequent VEBs should prompt investigations,
such as an echocardiogram (looking for structural heart disease) and an
exercise stress test (to detect underlying ischaemic heart disease).
Ventricular ectopic beats associated
with heart disease
 VEBs in Acute MI
 Frequent VEBs often occur during acute MI but need no
treatment.
 Persistent, frequent (over 10/hr) VEBs in patients who have
survived the acute phase of MI indicate a poorer long-term
outcome.
 Other than β-blockers, anti-arrhythmic drugs do not
improve and may even worsen prognosis.
 VEBs in Heart Failure
 Are common in patients with heart failure of any cause,
including cardiomyopathy.
Contd
 While they are associated with an adverse prognosis,
this is not improved by anti-arrhythmic drugs.
 Effective treatment of the heart failure may suppress
the ectopic beats.
 VEBs with Digoxin
 Are also a feature of digoxin toxicity, and may occur
as ‘escape beats’ in patients with bradycardia.
 Treatment is that of the underlying condition.
Contd
 Frequent PVCs are usually benign
 Except in the context of an prolonged QTc, when they
may predispose to malignant ventricular arrhythmias
such as Torsades de Pointes by causing “R on T”
phenomenon.
Causes
 Frequent or symptomatic PVCs may be due to:
 Anxiety

 Sympathomimetics

 Beta-agonists

 Excesscaffeine
 Hypokalaemia

 Hypomagnesaemia

 Digoxin toxicity

 Myocardial ischemia
Multifocal PVCs

Sinus rhythm with PVCs of two different morphologies (arrows).

Note the appropriately discordant ST segments / T waves.
The pause surrounding the PVC is equal to double the preceding R-R interval (=
a full compensatory pause).
Ventricular Tachyarrhythmias
 Ventricular Tachycardia
 Ventricular Flutter
 Ventricular Fibrillation
Ventricular tachycardia
 Definition
 VentricularTachycardia (VT) is a broad complex
tachycardia originating in the ventricles.

 There are several different varieties of VT — the most

being Monomorphic VT.
Tachyarrhythmias

Tachyarrhythmias

Narrow Complex Wide Complex

Tachyarrhythmias Tachyarrhythmias
Wide Complex Tachycardia

Wide Complex
Tachycardia

Regular Irregular

Atrial
Ventricular SVT with Fibrillation
Tachycardia Aberrancy with
Preexcitation
(WPW)
Clinical Significance
 Ventricular tachycardia may impair cardiac output with consequent
 Hypotension

 Collapse

 Acute cardiac failure

 This is due to extreme heart rates and lack of coordinated atrial

contraction (loss of “atrial kick”).
 The presence of pre-existing poor ventricular function is strongly
associated with cardiovascular compromise.
 Decreased cardiac output may result in decreased myocardial
perfusion with degeneration to VF.
 Prompt recognition and initiation of treatment (e.g. electrical
cardioversion) is required in all cases of VT.
Classification of Ventricular Tachycardia

 Ventricular tachycardia can be classified based on:

 1. Morphology
 Monomorphic
 Polymorphic VT
 Torsades De Pointes (Polymorphic with QT prolongation)
 Right Ventricular Outflow Tract Tachycardia
 Fascicular Tachycardia
 Bidirectional VT
 Ventricular Flutter
2. Duration

 Sustained = Duration > 30 seconds or requiring

intervention due to hemodynamic compromise.
 Non-sustained = Three or more consecutive
ventricular complexes terminating spontaneously in
< 30 seconds.
3. Clinical Presentation
 Haemodynamically stable

 Haemodynamically unstable — e.g

 Hypotension

 Chestpain
 Cardiac failure

 Decreased conscious level

Clinical Features Suggestive of VT
 Age > 35 (positive predictive value of 85%)
 Structural heart disease
 Ischaemic heart disease
 Previous MI
 Congestive heart failure
 Cardiomyopathy
 Family history of sudden cardiac death
 Suggesting conditions such as
 HOCM, congenital long QT syndrome, Brugada syndrome or
arrhythmogenic right ventricular dysplasia that are associated
with episodes of VT
Electrocardiographic Features of Ventricular Tachycardia

 Ventricular tachycardia can be difficult to

differentiate from other causes of broad complex
tachycardia.
 The following characteristics aid in the identification
of VT.
 Features common to any broad complex
tachycardia
 Rapid heart rate (> 100 bpm)
 Broad QRS complexes (> 120 ms)
Contd
 Capture beats
 Occur when the sinoatrial node transiently ‘captures’ the
ventricles, in the midst of AV dissociation, to produce a QRS
complex of normal duration.
 Fusion beats
 Occur when a sinus and ventricular beat coincide to produce
a hybrid complex of intermediate morphology.
 Positive or negative concordance throughout the chest
leads,
 i.e. leads V1-6 show entirely positive (R) or entirely
negative (QS) complexes, with no RS complexes seen.
Contd
 Brugada’s sign
 The distance from the onset of the QRS complex to the nadir
of the S-wave is > 100ms
 Josephson’s sign
 Notching near the nadir of the S-wave
 RSR’ complexes with a taller “left rabbit ear”
 This is the most specific finding in favour of VT
 This is in contrast to RBBB, where the right rabbit ear is taller
Contd
 Absence of typical RBBB or LBBB morphology
 Extreme axis deviation (“northwest axis”)
 QRS is positive in aVR and negative in I + aVF
 AV dissociation
 P and QRS complexes at different rates
Features more in keeping with ventricular tachycardia

 History of MI
 AV dissociation (pathognomonic)
 Capture/fusion beats (pathognomonic;
 Extreme left axis deviation
 Very broad QRS complexes (> 140 ms)
 No response to carotid sinus massage or IV
adenosine
Contd
 Idioventricular rhythm (‘slow’ VT)
 Patientsrecovering from MI sometimes have periods of
idioventricular rhythm (‘slow’ VT) at a rate only slightly
above the preceding sinus rate and below 120/min.
 These episodes often reflect reperfusion of the
infarct territory and may be a good sign.
 Usually self-limiting & asymptomatic, and do not
require treatment.
Contd
 Other forms of sustained VT will require treatment,
often as an emergency.
 VT occasionally occurs in patients with otherwise
healthy hearts (‘normal heart VT’), usually because
of abnormal automaticity in the right ventricular
outflow tract or one of the fascicles of the left
bundle branch.
 The prognosis is good and catheter ablation can
be curative.
AV Dissociation

AV dissociation: P waves (arrowed) appear at a different rate to the QRS

complexes
Capture beat & Fusion beat
Capture beat: the sinus node “captures” the ventricles producing
a narrow-complex beat

Fusion beats: the first of the narrower complexes is a fusion

beat (the next two are capture beats).
POSITIVE concordance in the precordial leads
NEGATIVE concordance in the precordial leads
Brugada’s sign (red callipers) and Josephson’s sign (blue
arrow)
Monomorphic VT

 Regular rhythm.
 Originates from a single focus within the ventricles.
 Produces uniform QRS complexes within each lead
— each QRS is identical (except for fusion/capture
beats).
Causes of Monomorphic VT

 Ischaemic Heart Disease

 Dilated cardiomyopathy
 Hypertrophic cardiomyopathy
 Chaga’s Disease
Monomorphic VT

Classic monomorphic VT with uniform QRS complexes.

Indeterminate axis.
Very broad QRS (~200 ms).
Notching near the nadir of the S wave in lead III = Josephson’s sign.
Monomorphic VT

Very broad QRS complexes (~ 200 ms) with uniform morphology.

Fusion and capture beats are seen in the rhythm strip.
Brugada’s sign is present: the time from the onset of the QRS complex to
nadir of S wave is > 100 ms (best seen in V6).
NB. The rhythm strip is recorded after the other 12 leads rather than
simultaneously.
Monomorphic VT

Extreme axis deviation / northwest axis is present

-150 degree; QRS positive in aVR, negative in I + aVF
There is a RBBB-like pattern in V1 with a taller left rabbit ear – this is very
specific for VT.
An rS complex in V6 (small R wave, big S wave) – this pattern is also very
specific for VT.
Differential Diagnosis of Wide-Complex Tachycardia

 Several arrhythmias can present as a wide-complex

tachycardia (QRS > 120 ms) including:
 Ventricular Tachycardia
 SVT with aberrant conduction due to bundle branch block

 SVT with aberrant conduction due to the Wolff-Parkinson-

White syndrome
 Pace-maker mediated tachycardia

 Metabolic derangements e.g. hyperkalaemia

 Poisoning with sodium-channel blocking agents (e.g. tricyclic

antidepressants)
Remember

 If in doubt, treat as VT!

Management
 Prompt action to restore sinus rhythm is required and should
usually be followed by prophylactic therapy.
 Hemodynamically Unstable:
 Synchronized DC cardioversion is the treatment of choice if
systolic BP is less than 90 mmHg.
 Hemodynamically Stable:
 If the arrhythmia is well tolerated, intravenous amiodarone may
be given as a bolus, followed by a continuous infusion.
 Intravenous lidocaine can be used but may depress left
ventricular function, causing hypotension or acute heart failure.
 Treatment of underlying cause:
 Hypokalaemia, hypomagnesaemia, acidosis and hypoxaemia
should be corrected.
Contd
 Prevention
 Beta-blockers are effective at preventing VT by reducing
ventricular automaticity.
 Amiodarone can be added if additional control is needed.

 Class Ic anti-arrhythmic drugs should not be used for prevention of

VT in patients with coronary artery disease or heart failure
because they depress myocardial function and can be pro-
arrhythmic (increase the likelihood of a dangerous arrhythmia).
 In patients at high risk of arrhythmic death (e.g. those with poor left
ventricular function, or where VT is associated with haemodynamic
compromise), the use of an implantable cardiac defibrillator is
recommended.
 Rarely, surgery (e.g. aneurysm resection) or catheter ablation can
be used to interrupt the arrhythmia focus or circuit in patients with
VT associated with a myocardial infarct scar.
Polymorphic VT & Torsades de Pointes (TdP)

 Definitions
 Polymorphic ventricular tachycardia (PVT) is a form
of ventricular tachycardia in which there are
multiple ventricular foci with the resultant QRS
complexes varying in amplitude, axis and
duration.
 The commonest cause of PVT is myocardial
ischaemia.
Contd
 Torsades de pointes (TdP) is a specific form of
polymorphic ventricular tachycardia occurring in the
context of prolonged ventricular repolarization (QT
prolongation).
 It has a characteristic morphology in which the QRS
complexes “twist” around the isoelectric line.
 For TdP to be diagnosed, the patient has to have
evidence of both PVT and QT prolongation.
 Bidirectional VT is another type of polymorphic VT,
most commonly associated with digoxin toxicity.
Causes of long QT interval and torsades de pointes

•Drugs
 Bradycardia •Disopyramide, flecainide (and other
 Bradycardia class Ia, Ic anti-arrhythmic drugs,
compounds other
factors that cause •Sotalol, amiodarone (and other class III
anti-arrhythmic drugs)
torsades de pointes
 Electrolyte •Amitriptyline (and other tricyclic
disturbance antidepressants)

 Hypokalaemia •Chlorpromazine (and other

 Hypomagnesaemia phenothiazines)
 Hypocalcaemia
•Erythromycin (and other macrolides) …
and many more
Contd
 Congenital syndromes
 Long QT1: gene affected KCNQI: K+ channel, 30–35%
 Long QT2: gene affected HERG: K+ channel, 25–30%

 Long QT3: gene affected SCNSA: Na+ channel, 5–10%

 Long QT4–12: rare

Pathophysiology of TdP
 A prolonged QT reflects prolonged myocyte
repolarization due to ion channel malfunction.
 During periods of sinus rhythm, the ECG will usually
show a prolonged QT interval (> 0.43 s in men, >
0.45 s in women when corrected to a heart rate of
60/min).
 This prolonged repolarization period also gives rise
to early after-depolarisations (EADs).
Contd
 EADs may manifest on the ECG as tall U waves; if
these reach threshold amplitude they may manifest
as premature ventricular contractions (PVCs).
 TdP is initiated when a PVC occurs during the
preceding T wave, known as ‘R on T’ phenomenon.
 The onset of TdP is often preceded by a sequence
of short-long-short R-R intervals, so called “pause
dependent” TDP, with longer pauses associated with
faster runs of TdP.
Clinical Significance
 TdP is often short lived and self terminating, however can be
associated with hemodynamic instability and collapse.
 TdP may also degenerate into ventricular fibrillation (VF).
 QT prolongation may occur secondary to multiple drug
effects, electrolyte abnormalities and medical conditions;
these may combine to produce TdP, e.g. hypokalaemia may
precipitate TdP in a patient with congenital long QT
syndrome.
 Recognition of TdP and the risk of TdP allows the instigation
of specific management strategies (e.g. magnesium,
isoprenaline, overdrive pacing, etc.)
Electrocardiographic Pearls
 The ECG shows rapid irregular complexes that oscillate from
an upright to an inverted position and seem to twist around
the baseline as the mean QRS axis changes.
 During short runs of TdP or single lead recording the
characteristic “twisting” morphology may not be apparent.
 Bigeminy in a patient with a known long QT syndrome may
herald imminent TdP.
 TdP with heart rates > 220 beats/min are of longer
duration and more likely to degenerate into VF.
 Presence of abnormal (“giant”) T-U waves may precede TdP
Torsades de pointes

A bradycardia with a long QT interval is followed by polymorphic

ventricular tachycardia that is triggered by an R on T ectopic.
Torsades de Pointes

Frequent PVCs with ‘R on T’ phenomenon trigger a run of

polymorphic VT which subsequently begins to degenerate to VF.
QT is difficult to see because of artefact but appears slightly
prolonged (QTc ~480ms), making this likely to be TdP.
This combination of mildly prolonged QTc and frequent PVCs /
bigeminy is commonly seen in acute myocardial ischaemia and is
high-risk for deterioration to PVT / VF.
TdP secondary to hypokalaemia

Sinus rhythm with inverted T waves, prominent U waves and a long Q-U
interval due to severe hypokalaemia (K+ 1.7)
A premature atrial complex (beat #9 of the rhythm strip) lands on the
end of the T wave, causing ‘R on T’ phenomenon and initiating a
paroxysm of polymorphic VT.
Because of the preceding long QU interval, this can be diagnosed as
TdP.
 Torsades de Pointes

Sinus rhythm, or possibly ectopic atrial rhythm (biphasic / inverted P waves in

lead II).
Prolonged QTc interval of 540 ms (greater than half the R-R interval).
Ventricular ectopics with ‘R-on-T’ phenomenon; the second PVC initiates a run of
TdP.
NB. See how the arterial line pressure waveform (lower tracing) is affected by the
dysrhythmia. There is a reduced volume pulse during the first PVC as the heart has
less time to fill. Subsequently the cardiac output drops away to almost nothing
during the run of TdP – this is likely to result in syncope or cardiac arrest.
Long QT
Long QT syndrome subtypes have different triggers, which
are important when counselling patients

Adrenergic stimulation (e.g. exercise) is a common trigger in long QT type 1,

Auditory Stimulation :a sudden noise (e.g. an alarm clock) may trigger arrhythmias in long
QT type 2.
Sleep /rest: Arrhythmias are more common during sleep in type 3.
Management
 Acute Treatment
 Treatment should be directed at the underlying cause.
 Intravenous magnesium (8 mmol over 15 mins, then 72
mmol over 24 hrs) should be given in all cases.
 Atrial pacing will usually suppress the arrhythmia
through rate-dependent shortening of the QT interval.
 Intravenous isoprenaline is a reasonable alternative to
pacing but should be avoided in patients with the
congenital long QT syndromes.
Contd
 Long Term Treatment:
 Long-term therapy may not be necessary if the
underlying cause can be removed.
 Beta-blockers are effective at preventing syncope in
patients with congenital long QT syndrome.
 Some patients, particularly those with extreme QT
interval prolongation (> 500 ms) or certain high-risk
genotypes should be considered for implantation of a
defibrillator.
 Left stellate ganglion block may be of value in patients
with resistant arrhythmias.
Brugada Syndrome
 The Brugada syndrome is a related genetic
disorder that may present with polymorphic VT or
sudden death.
 It is characterised by a defect in sodium channel
function and an abnormal ECG (right bundle branch
block and ST elevation in V1 and V2 but not usually
prolongation of the QT interval).
 The only known effective treatment is an
implantable defibrillator.
ECG Features
Types of Brugada
contd
References

http://ecg.utah.edu/lesson/
http://lifeinthefastlane.com
Davidson medicine Text book
http://emedicine.medscape.com/article/159075-clinical
Thanks