Ventricular Arrhythmias

1. Ventricular Premature Beats (Ventricular Extrasystoles)

Ventricular premature beats are characterized by wide QRS complexes that differ in morphology from the patient’s normal beats. They are usually not preceded by a P wave, although retrograde ventriculoatrial conduction may occur. Unless the latter is present, there is a fully compensatory pause (ie, without change in the PP interval). Bigeminy and trigeminy are arrhythmias in which every second or third beat is premature; these patterns confirm a reentry mechanism for the ectopic beat. Exercise generally abolishes premature beats in normal hearts, and the rhythm becomes regular. The patient may or may not sense the irregular beat, usually as a skipped beat. Ambulatory electrocardiographic monitoring or monitoring during graded exercise may reveal more frequent and complex ventricular premature beats than occur in a single routine ECG. An increased frequency of ventricular premature beats during exercise is associated with a higher risk of cardiovascular mortality, though there is no evidence that specific therapy has a role.

Sudden death occurs more frequently (presumably as a result of ventricular fibrillation) when ventricular premature beats occur in the presence of organic heart disease but not in individuals with no known cardiac disease.

If no associated cardiac disease is present and if the ectopic beats are asymptomatic, no therapy is indicated. If they are frequent, electrolyte abnormalities (especially hypo- or hyperkalemia and hypomagnesemia), hyperthyroidism, and occult heart disease should be excluded. Pharmacologic treatment is indicated only for patients who are symptomatic. Because of concerns about worsening arrhythmia and sudden death with most antiarrhythmic agents, ß-blockers are the agents of first choice. If the underlying condition is mitral prolapse, hypertrophic cardiomyopathy, left ventricular hypertrophy, or coronary disease - or if the QT interval is prolonged - ß-blocker therapy is appropriate. The class I and III agents are all effective in reducing ventricular premature beats but often cause side effects and may exacerbate serious arrhythmias in 5-20% of patients. Therefore, every attempt should be made to avoid using class I or III antiarrhythmic agents in patients without symptoms.

Frolkis JP et al: Frequent ventricular ectopy after exercise as a predictor of death. N Engl J Med 2003;348:781.
Jouven X et al: Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolarizations. N Engl J Med 2000;343:826.

2. Ventricular Tachycardia

Ventricular tachycardia is defined as three or more consecutive ventricular premature beats. The usual rate is 160-240 beats/min and is moderately regular but less so than atrial tachycardia. The distinction from aberrant conduction of supraventricular tachycardia may be difficult. The usual mechanism is reentry, but abnormally triggered rhythms occur. Ventricular tachycardia is either nonsustained (lasting less than 30 seconds) or sustained. It may be asymptomatic or associated with syncope or milder symptoms of impaired cerebral perfusion.

Ventricular tachycardia is a frequent complication of acute myocardial infarction and dilated cardiomyopathy but may occur in chronic coronary disease, hypertrophic cardiomyopathy, mitral valve prolapse, myocarditis, and in most other forms of myocardial disease. Torsade de pointes, a form of ventricular tachycardia in which QRS morphology twists around the baseline, may occur spontaneously in the setting of hypokalemia or hypomagnesemia or after any drug that prolongs the QT interval; it has a particularly poor prognosis. In nonacute settings, most patients with ventricular tachycardia have known or easily detectable cardiac disease, and the finding of ventricular tachycardia is an unfavorable prognostic sign.


A. Acute Ventricular Tachycardia
The treatment of acute ventricular tachycardia is determined by the degree of hemodynamic compromise and the duration of the arrhythmia. The management of ventricular tachycardia in acute infarction has been discussed. In other patients, if ventricular tachycardia causes hypotension, heart failure, or myocardial ischemia, synchronized DC cardioversion with 100-360 J should be performed immediately. If the patient is tolerating the rhythm, lidocaine, 1 mg/kg as an intravenous bolus injection, may terminate it. If the patient is stable and lidocaine is not effective, intravenous procainamide, 20 mg/min intravenously (up to 1000 mg), followed by an infusion of 20-80 ug/kg/min, can be tried. Intravenous amiodarone is often effective when these approaches are not. This formulation is much more bioavailable than the oral form, so more rapid loading can be achieved. It is usually initiated with a rapid loading infusion of 150 mg over 10 minutes, followed by a slow infusion of 1 mg/min for 6 hours and then a maintenance infusion of 0.5 mg/min for an additional 18-42 hours. Supplemental infusions of 150 mg over 10 minutes can be given for recurrent ventricular tachycardia. Bretylium, 5 mg/kg intravenously over 3-5 minutes, repeated after 20 minutes if necessary, followed by an infusion of 1-2 mg/min, is also an alternative. Empiric magnesium replacement (1 g intravenously) may help. Ventricular tachycardia can also be terminated by ventricular overdrive pacing, and this approach is useful when the rhythm is recurrent.

B. Chronic Recurrent Ventricular Tachycardia

1. Sustained ventricular tachycardia -
Patients with symptomatic or sustained ventricular tachycardia in the absence of a reversible precipitating cause (acute myocardial infarction or ischemia, electrolyte imbalance, drug toxicity, etc) are at high risk for recurrence. In those with significant left ventricular dysfunction, subsequent sudden death is common. Several trials, including the Antiarrhythmic Drug Versus Implantable Defibrillator (AVID) and the Canadian Implantable Defibrillator trials, strongly suggest that these patients should be managed with implantable cardioverter-defibrillator devices (ICDs). In those with preserved left ventricular function, the mortality rate is lower and treatment with amiodarone, optimally in combination with a ß-blocker, may be adequate. Sotalol may be an alternative, though there is less supporting evidence. The role of electrophysiologic studies in this group is less clear than was previously thought, but they may help identify patients who are candidates for radiofrequency ablation of a ventricular tachycardia focus. This is particularly the case for arrhythmias that originate in the right ventricular outflow tract (appearing as LBBB with inferior axis on the surface ECG), the posterior fascicle (RBBB, superior axis morphology), or sustained bundle branch reentry. As experience accumulates, it is likely that other forms of ventricular tachycardia will be amenable to radiofrequency ablation.

2. Nonsustained ventricular tachycardia (NSVT) -
NSVT is defined as runs of three or more ventricular beats lasting less than 30 seconds. These may be symptomatic (usually experienced as light-headedness) or asymptomatic. In individuals without heart disease, NSVT is not clearly associated with a poor prognosis. However, in patients with structural heart disease, particularly when they have reduced ejection fractions, there is an increased risk of subsequent symptomatic ventricular tachycardia or sudden death. ß-Blockers reduce these risks in patients who have coronary disease with significant left ventricular systolic dysfunction (ejection fractions

< 35-40%), but if sustained ventricular tachycardia has been induced during electrophysiologic testing, an implantable defibrillator may be indicated. In patients with chronic heart failure and reduced ejection fractions - whether due to coronary disease or primary cardiomyopathy and regardless of the presence of asymptomatic ventricular arrhythmias - ß-blockers reduce the incidence of sudden death by 40-50% and should be routine therapy (see section on Heart Failure).

Although there are no definitive data with amiodarone in this group, trends from a number of studies suggest that it may be beneficial. Other antiarrhythmic agents should generally be avoided because their proarrhythmic risk appears to outweigh any benefit, even in patients with inducible arrhythmias that are successfully suppressed in the electrophysiology laboratory.

Brodsky MA et al: Prognostic value of baseline electrophysiology studies in patients with sustained ventricular tachyarrhythmia: the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial. Am Heart J 2002;144:478
Klein RC et al: Analysis of implantable cardioverter defibrillator therapy in the Antiarrhythmics Versus Implantable Defibrillators (AVID) Trial. J Cardiovasc Electrophysiol 2003; 14:940.
Saliba WI et al: Ventricular tachycardia syndromes. Med Clin North Am 2001;85:267.
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Weinstock J et al: Clinical results with catheter ablation: AV junction, atrial fibrillation and ventricular tachycardia. J Interv Card Electrophysiol 2003;9:275.
Wietholt D et al: Prevention of sustained ventricular tachyarrhythmias in patients with implantable cardioverter-defibrillators - the PREVENT study. J Interv Card Electrophysiol 2003;9:383.
Wilkoff BL et al: Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) trial. JAMA 2002;288:3115.
Young JB et al: Combined cardiac resynchronization and implantable cardioversion defibrillation in advanced chronic heart failure: the MIRACLE ICD Trial. JAMA 2003; 289:2685.

3. Ventricular Fibrillation & Sudden Death

Sudden cardiac death is defined as unexpected nontraumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms. The causative rhythm in most cases is ventricular fibrillation, which is usually preceded by ventricular tachycardia except in the setting of acute ischemia or infarction. Complete heart block and sinus node arrest may also cause sudden death. A disproportionate number of sudden deaths occur in the early morning hours. Over 75% of victims of sudden cardiac death have severe coronary artery disease. Many have old infarctions. Sudden death may be the initial manifestation of coronary disease in up to 20% of patients and accounts for approximately 50% of deaths from coronary disease. When ventricular fibrillation occurs in the initial 24 hours after infarction, long-term management is no different from that of other patients with acute infarction. Other conditions that predispose to sudden death include severe left ventricular hypertrophy, hypertrophic cardiomyopathy, congestive cardiomyopathy, aortic stenosis, pulmonary stenosis, Primary pulmonary hypertension, cyanotic congenital heart disease, atrial myxoma, mitral valve prolapse, hypoxia, electrolyte abnormalities, prolonged QT interval syndrome, and conduction system disease. Late potentials (after the QRS complex) on a signal-averaged surface ECG in patients with prior myocardial infarction may identify a group of patients at risk of ventricular arrhythmias and sudden death.

Unless ventricular fibrillation occurred shortly after myocardial infarction, is associated with ischemia, or is seen with an unusual correctable process (such as an electrolyte abnormality, drug toxicity, or aortic stenosis), surviving patients require evaluation and intervention since recurrences are frequent. Exercise testing or coronary arteriography should be performed to exclude coronary disease as the underlying cause, since revascularization may prevent recurrence. Conduction disturbances should be managed as described in the next section. If prodromal supraventricular arrhythmias or ventricular arrhythmias, such as sustained or nonsustained ventricular tachycardia, are found by ambulatory electrocardiographic monitoring, their elimination by pharmacologic therapy or ablation may prevent further episodes. There is growing consensus that if myocardial infarction or ischemia, other precipitating causes of ventricular fibrillation, or bradyarrhythmias and conduction disturbances are not found to be the cause of the sudden death episode, an implantable defibrillator is the treatment of choice for appropriate patients. In addition, there is evidence from the MADIT II study and other reports that in a patient with a prior myocardial infarction and severe left ventricular dysfunction, prophylactic implantation of a defibrillator reduces the risk of death - though the cost of doing so in all such patients would be very high.

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4. Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm is a regular wide complex rhythm with a rate of 60-120 beats/min, usually with a gradual onset. Because the rate is often similar to the sinus rate, fusion beats and alternating rhythms are common. Two mechanisms have been invoked: (1) an escape rhythm due to suppression of higher pacemakers resulting from sinoatrial and atrioventricular block or from depressed sinus node function; and (2) slow ventricular tachycardia due to increased automaticity or, less frequently, reentry. It occurs commonly in acute infarction and following reperfusion after thrombolytic drugs. The incidence of associated ventricular fibrillation is much less than that of ventricular tachycardia with a rapid rate, and treatment is not indicated unless there is hemodynamic compromise or more serious arrhythmias. This rhythm also is common in digitalis toxicity.

Accelerated idioventricular rhythm must be distinguished from the idioventricular or junctional rhythm with rates less than 40-45 beats/min that occurs in the presence of complete atrioventricular block. Atrioventricular dissociation - where ventricular rate exceeds sinus - but not atrioventricular block occurs in most cases of accelerated idioventricular rhythm.

5. Long QT Syndrome

Congenital long QT syndrome is an uncommon disease that is characterized by recurrent syncope, a long QT interval (usually 0.5-0.7 second), documented ventricular arrhythmias, and sudden death. It may occur in the presence (Jervell syndrome, Lange-Nielsen syndrome) or absence (Romano-Ward syndrome) of congenital deafness. Inheritance may be autosomal recessive or autosomal dominant (Romano-Ward). Specific genetic mutations affecting membrane potassium and sodium channels have been identified and help delineate the mechanisms of susceptibility to arrhythmia.

ß-Blockers are the most effective therapy for congenital long QT syndrome and are often used in conjunction with permanent pacemakers, since low heart rates predispose to ventricular arrhythmias. Agents that prolong the QT (classes Ia, Ic, and III) are contraindicated. ICDs are effective in patients who continue to have life-threatening ventricular arrhythmias while taking ß-blockers. Refractory acute arrhythmic episodes may be treated by local anesthetic block of the left stellate ganglion, and recurrent episodes can be treated by resection of this ganglion as well as of the first three to five thoracic ganglia.

Acquired long QT interval secondary to use of antiarrhythmic agents or antidepressant drugs, electrolyte abnormalities, myocardial ischemia, or significant bradycardia may result in ventricular tachycardia (particularly torsade de pointes, ie, twisting about the baseline into varying QRS morphology). Notably, many drugs that are in some settings effective for the treatment of ventricular arrhythmias prolong the QT interval. Prudence dictates that drug therapy that prolongs the QT interval beyond 500 ms be discontinued.

The management of torsade de pointes differs from that of other forms of ventricular tachycardia. Class I, Ic, or III antiarrhythmics, which prolong the QT interval, should be avoided - or withdrawn immediately if being used. Intravenous ß-blockers may be effective, especially in the congenital form; intravenous magnesium should be given acutely. An effective approach is temporary ventricular or atrial pacing, which can both break and prevent the rhythm.

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Wehrens XH et al: Novel insights in the congenital long QT syndrome. Ann Intern Med 2002;137:981.
Welde AA: Is there a role for implantable cardioverter defibrillators in long QT syndrome? J Cardiovasc Electrophysiol 2002;13(1 Suppl):S110.

Provided by ArmMed Media
Revision date: June 14, 2011
Last revised: by Dave R. Roger, M.D.