VENTRICULAR ARRHYTHMIAS

Moderator : Lt Col Brahamjit SinghPresenter : Lt Phuntsho Choden

Arrhythmias that originate in the ventricular myocardium or His Purkinje system include:•Premature ventricular beats•Ventricular tachycardia •Ventricular fibrillation

• Emerge from focus of myocardium and purkinje fibres

• Conduction away from the ventricular focus through the ventricular myocardium is slower than activation of the ventricles over the Purkinje system.

• QRS wide, typically >0.12 s

Premature Ventricular Contraction

• Premature ventricular ectopic beats arising in the diastolic period of preceding sinus beat

• Unifocal• Multifocal• Ventricular Couplets

• Caused by electrical irritability

• Ischemia• Electrolyte imbalances• Drug intoxication

Multiform premature ventricular complexes (PVCs)

The normally conducted QRS complexes exhibit a left bundle branch block contour (arrowhead) and are followed by PVCs with three different morphologies.

Ventricular couplets

• Three or more PVC's in a row (run of V-tach)• They come close to or on top of a preceding T-wave (R on T)• They are frequent (> 30% of complexes) • They are increasing in frequency• PVC's come from different foci ("multifocal" or "multiformed")

May preclude the occurrence of :• Ventricular Tachycardia • Ventricular Fibrillation

PVCs : CLINICAL SIGNIFICANCE

sinus beats Unconverted V-tach r V-fib V-tach

“R on T phenomenon”

time

Fusion beat - note p-wave in front of PVC and the PVC is narrower than the other PVC’s – this indicates the beat is a product of both the sinus node and an ectopic ventricular focus

Capture beat - note that the complex is narrow enough to suggest normal ventricular conduction. This indicates that an atrial impulse has made it through and conduction through the ventricles is relatively normal.

Fusion and capture beats during ventricular tachycardia.

VENTRICULAR TACHYCARDIA

Ventricular Tachycardia (VT)

• Three or more consecutive ventricular ectopic beats at a rate > 100 beats/min

• Originates in the ventricles • Nonsustained < 30secs• Sustained > 30secs• Most patients have significant heart disease

• Coronary artery disease• A previous myocardial infarction• Cardiomyopathy

V1

Ventricular Tachycardia (VT)

• Rates range from 100-250 beats/min• Non-sustained or sustained • P waves often dissociated (as seen here)

SANode

Ventricular Focus

ATRIA AND VENTRICLESACT INDEPENDENTLY

AV Dissociation

Mechanisms of VT

• Reentrant • Reentry circuit (fast and slow pathway) is confined to the ventricles and/or

bundle branches

• Automatic • Automatic focus occurs within the ventricles

• Triggered activity• Early after depolarizations (phase 3)• Delayed after depolarizations (phase 4)

Reentrant

• Reentrant ventricular arrhythmias• Premature ventricular complexes• Idiopathic left ventricular tachycardia• Bundle branch reentry• Ventricular tachycardia and fibrillation when associated with chronic heart

disease:• Previous myocardial infarction• Cardiomyopathy

Automatic

• Automatic ventricular arrhythmias• Premature ventricular complexes• Ischemic ventricular tachycardia• Ventricular tachycardia and fibrillation when associated with acute medical

conditions:• Acute myocardial infarction or ischemia• Electrolyte and acid-base disturbances, hypoxemia• Increased sympathetic tone• Drugs

Automaticity

Abnormal Acceleration of Phase 4

Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.

Triggered

• Triggered activity ventricular arrhythmias• Pause-dependent triggered activity

• Early afterdepolarization (phase 3)• Hypokalemia, TdP

• Polymorphic ventricular tachycardia

• Catechol-dependent triggered activity• Late afterdepolarizations (phase 4)

• Local catecholamines, hypercalcemia • Digitalis intoxication

• Idiopathic right ventricular tachycardia

IDIOVENTRICULAR TACHYCARDIA

• Enhanced inherent idioventricular rhythm• Manifests when the rate equals sinus rate• Characterised by:

• Bizarre QRS complexes or Fusion beats• Rapid idioventricular rate (70-80beats/min)• AV dissociation and capture beats• Absence of pacemaker protection – abolished by faster sinus rhythm

Ectopic ventricular activation

Normal ventricular activation

Fusionbeat

Accelerated Idioventricular Rhythm ( Ventricular Escape Rate, but 100 bpm)

Sinus acceleration

• Hemodynamically well tolerated• Beta blockers and CCBs for prevention• Catheter ablation • No risk of sudden cardiac deaths

ECG Clues Supporting the Diagnosis of Ventricular Tachycardia

• AV dissociation (capture beats, fusion beats)• Concordance of QRS complex in all precordial leads• Frontal plane: LAD with QRS > 140 ms• Precordial leads: RS pattern ; Onset of R to Nadir of S >100ms• RBBB pattern with

- V6 : QS or dominant S- V1 : R > R’- V1 : Monophasic R or biphasic qR or R/S with initial deflection different from

sinus initiated QRS• LBBB pattern with

- Right axis : Negative deflection in V1 > V6- V6 : qR or QS- V1 : R > 40 ms

Monomorphic VT

Polymorphic VT

TORSADES DE POINTES

• ‘Twisting of the points’• Etiology:

• Congenital long QT • Drugs – Quinidine, Phenothiazines • Hypokalemia/ hypomagnesemia • Bradyarrhythmias -3rd degree blocks

ECG Recognition

• QRS morphology continuously changes• Complexes alternates from positive to negative

Mechanism

• Events leading to TdP are:• Hypokalemia• Prolongation of the action potential duration• Early afterdepolarizations• Critically slow conduction that contributes to reentry

Brugada Syndrome

• RBBB + persistent ST elevation in Right precordial leads • Sudden cardiac death• 3 patterns

• Type 1 - J point elevation with ST segment elevation ≥0.2mV followed by Negative T wave

• Type 2 – saddle back configuration of ST elevation >0.2mV – downsloping ST elevation – positive or biphasic T wave not touching baseline

• Type 3 – ST elevation <0.1mV with either of the morphologies

The Brugada Criteria

Morphology Criteria for VT

qRqRAbsent Q

ACUTE MANAGEMENT OF SUSTAINED VT

Hemodynamic decompensation

NO YES

Termination by medical treatment

AMIODARONE

PROCAINAMIDE

SOTALOL

LIDOCAINE

No Response DC Cardioversion

AMIODARONE

15 mg/min over 10 min f/b 1 mg/min for 6 hours f/b 0.5 mg/min for 18 hours.

LONG TERM THERAPYPREVENTION OF RECURRENCE/SUDDEN DEATH

• Asymptomatic Nonsustained

Preserved LV function

• Symptomatic Nonsustained

Preserved LV function

• Symptomatic Nonsustained

LV dysfunction (EF < 0.35)

Need not be treated

Beta blockers

Class IC agentsSotalol

Amiodarone

ICD

LONG TERM THERAPYSECONDARY PREVENTION

Survivors of cardiac arrest/ Sustained VT with hemodynamic compromise

PLUSPoor LV function

ICD IS THE TREATMENT OF CHOICE

Empirical Amiodarone/ Beta blocker is the next best therapy

Implantable Cardioverter Defibrillator

Intracardiac Cardioverter Defibrillator

THANK YOU!