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Conti CR Ventricular arrhythmias: a general cardiologist s assessment of therapies in 2005 Clin Cardiol 2005 Jul;28(7): 314 6 [PMID: 16075822] Morshedi-Meibodi A et al Clinical correlates and prognostic significance of exercise-induced ventricular premature beats in the community: the Framingham Heart Study Circulation 2004 May 25;109(20):2417 22 [PMID: 15148273] O Neill JO et al Severe frequent ventricular ectopy after exercise as a predictor of death in patients with heart failure J Am Coll Cardiol 2004 Aug 18;44(4):820 6 [PMID: 15312865]

The atrial-nodal junction or the nodal-His bundle junctions may assume pacemaker activity for the heart, usually at a rate of 40 60 beats/min This may occur in patients with myocarditis, CAD, and digitalis toxicity as well as in individuals with normal hearts The rate responds normally to exercise, and the diagnosis is often an incidental finding on ECG monitoring, but it can be suspected if the jugular venous pulse shows cannon a waves Junctional rhythm is often an escape rhythm because of depressed sinus node function with sinoatrial block or delayed conduction in the AV node Nonparoxysmal junctional tachycardia results from increased automaticity of the junctional tissues in digitalis toxicity or ischemia and is associated with a narrow QRS complex and a rate usually less than 120 130 beats/min It is usually considered benign when it occurs in acute myocardial infarction, but the ischemia that induces it may also cause ventricular tachycardia and ventricular fibrillation

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VENTRICULAR PREMATURE BEATS (VENTRICULAR EXTRASYSTOLES)

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

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 Torsades 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

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The patient may or may not sense the irregular beat, usually as a skipped beat Exercise generally abolishes premature beats in normal hearts, and the rhythm becomes regular 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 Ambulatory ECG 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

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, or amiodarone 150 mg as a slow intravenous bolus over 10 minutes, followed by a slow infusion of 1 mg/min for 6 hours and then a maintenance

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 hypokalemia 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, -blockers are the agents of first choice If the

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