Ventricular Tachycardia

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Contents 1 More Specific Terms 2 Introduction 3 Etiology 4 Clinical-manifestations 5 Diagnostic-procedures 6 Complications 7 Management 8 More General Terms 9 References

More Specific Terms

• monomorphic ventricular tachycardia
• polymorphic ventricular tachycardia
• sustained ventricular tachycardia
• ventricular fibrillation (V Fib)
• ventricular flutter

Introduction

• Ventricular tachycardia (VT) is defined as a series or 3 or more wide QRS complexes occuring at a rate >100/min resulting from depolarization originating in the ventricles.It is the most frequently encountered life-threatening arrhythmia. Left untreated, VT may deteriorate into ventricular fibrillation.

Etiology

• re-entry ( monomorphic)
• increased automaticity
• myocardial infarction
• drug toxicity
• electrolyte abnormalities
• cardiomyopathy
• infiltrative diseases

• amyloidosis
• sarcoidosis

• infectious diseases

• viral myocarditis or cardiomyopathy
• Chagas' disease
• Lyme disease

• congenital diseases

• inborn errors of metabolism
• long QT syndrome

• inflammatory diseases

• systemic lupus erythematosus
• rheumatoid arthritis

• malignancies

• primary
• metastatic

• idiopathic

Clinical-manifestations

• patients may be asymptomatic
• palpitations
• neck pounding ( AV dissociation)
• dyspnea
• light-headedness
• angina
• syncope & near-syncope

Diagnostic-procedures

• electrocardiogram

• wide QRS >120 ms with bizarre morphology
• ventricular rate >100/min
• p waves dissociated from QRS complex
• T-waves opposite in polarity to major QRS deflection
• EKG features that favor ventricular tachycardia over supraventricular tachycardia with aberrancy (i.e. bundle-branch block)

• AV dissociation
• presence of capture or fusion beats
• left axis deviation
• QRS duration >140 ms
• precordial concordant of the major QRS deflection
• factors favoring ventricular tachycardia (VT) vs right bundle branch block ( RBBB)

• monophasic or biphasic QRS complexes in V1
• left axis deviation
• R/S ratio of <1 in V6

• factors favoring ventricular tachycardia (VT) vs left bundle branch block ( LBBB)

• R in V1 or V2 >30 ms in duration
• any Q in V6
• onset of QRS to nadir of S >60 ms in V1 or V6
• notching of the downstroke of S in V1 or V2

• electrophysiologic testing after restoration of sinus rhythm

Complications

• non- sustained ventricular tachycardia within 48 hours of myocardial infarction does not confer additional risk
• non- sustained ventricular tachycardia within the first year after myocardial infarction outside of that 48 hour window is associated with increased mortality [2]

Management

• sustained ventricular tachycardia

• hemodynamic instability

• immediate DC synchronized cardioversion

• stable patient, chemical cardioversion

• preserved heart function

• procainamide*
• sotalol or other beta-blocker
• amiodarone# 150 mg IV over 10 minutes
• lidocaine 0.5-0.75 mg/kg IV push

• poor LV ejection fraction

• amiodarone# 150 mg IV over 10 minutes
• lidocaine 0.5-0.75 mg/kg IV push
• then DC synchronized cardioversion

• prolonged QT interval

• treat as torsades de pointes

• IV infusion of above agents may be indicated for recurrent sustained VT
• avoid adenosine & calcium channel blockers

• treat ischemia, correct electrolytes
• follow-up after restoration of sinus rhythm

• search for ischemia

• myocardial perfusion study
• coronary angiography

• catheter ablation if indicated by electrophysiologic testing
• implantable cardiac defibrillator
• high risk of sudden death
• workup should be conducted as an inpatient

• non- sustained ventricular tachycardia

• asymptomatic non- sustained ventricular tachycardia

• no proven antiarrhythmic treatment
• implantable defibrillator if post- MI, LVEF < 35%, & VT inducible during electrophysiologic testing

• symptomatic non- sustained ventricular tachycardia

• beta-blockers 1st line
• Ca+2-channel blocker may be used if structurally normal heart
• amiodarone & sotalol have been used
• class 1c antiarrhythmics ( flecainide, propafenone) limited to patients with coronary artery disease
• radiofrequency ablation if drug therapy fails

• medical treatment does not diminish mortality [2]

• * procainamide is the agent of choice for chemical cardioversion except in the setting of acute MI or digoxin toxicity; in these cases, lidocaine remains the agent of choice [2]
• # amiodarone not effective [4]

More General Terms

• ventricular arrhythmia
• wide complex tachycardia

References

1. Manual of Medical Therapeutics, 28th ed, Ewald & McKenzie (eds), Little, Brown & Co, Boston, 1995, pg 147-48
2. Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 15 American College of Physicians, Philadelphia 1998, 2006, 2009
3. American Heart Association
4. Marill KA et al, Amiodarone is poorly effective for the acute termination of ventricular tachycardia Ann Emerg Med 2006; 47:217 PMID: [1]
   - Tomlinson DR et al, Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: Is bolus dose amiodarone an appropriate first-line treatment? Emerg Med J 2008, 25:15 PMID: [2]

ventricular tachycardia (VT)