Ventricular tachycardia termination

Ventricular tachycardia is a series of three or more consecutive VPDs at a rate of greater than 100 bpm. Ventricular tachycardia is defined as non-sustained if it lasts less than 30 seconds and terminates spontaneously sustained VT lasts greater than 30 seconds and does not terminate spontaneously, but rather requires therapeutic intervention for termination. 

FIGURE 6-11. Decision algorithm for termination of hemody-namically stable ventricular tachycardia. 

Cardiopulmonary arrest in adults usually results from arrhythmias. The most common arrhythmias are ventricular fibrillation (VF) and pulseless ventricular tachycardia (PVT), often in patients after myocardial infarction (MI) or pulmonary embolism (PE). In children, cardiopulmonary arrest is often the terminal event of progressive shock or respiratory failure. 

Pharmacology Bretylium tosylate inhibits norepinephrine release by depressing adrenergic nerve terminal excitability, inducing a chemical sympathectomy-like state. Bretylium blocks the release of norepinephrine in response to neuron stimulation. Peripheral adrenergic blockade causes orthostatic hypotension but has less effect on supine blood pressure. It has a positive inotropic effect on the myocardium. Pharmacokinetics Peak plasma concentration and peak hypotensive effects are seen within 1 hour of IM administration. However, suppression of premature ventricular beats is not maximal until 6 to 9 hours after dosing, when mean plasma concentration declines to less than 50% of peak level. Antifibrillatory effects occur within minutes of an IV injection. Suppression of ventricular tachycardia and other ventricular arrhythmias develops more slowly, usually 20 minutes to 2 hours after parenteral administration. 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

Magnesium sulfate may be effective in terminating refractory ventricular tachyarrhythmias, particularly polymorphic ventricular tachycardia. DigitaUs-induced arrhythmias are more likely in the presence of magnesium deficiency. Magnesium sulfate can be administered orally, intramuscularly, or, preferably, intravenously,... 

Lidocaine is the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. However, routine prophylactic use of lidocaine in this setting may actually increase total mortality, possibly by increasing the incidence of asystole, and is not the standard of care. Most physicians administer IV lidocaine only to patients with arrhythmias. 

Supraventricular tachycardia is the major arrhythmia indication for verapamil. Adenosine or verapamil are preferred over older treatments (propranolol, digoxin, edrophonium, vasoconstrictor agents, and cardioversion) for termination. Verapamil can also reduce the ventricular rate in atrial fibrillation and flutter. It only rarely converts atrial flutter and fibrillation to sinus rhythm. Verapamil is occasionally useful in ventricular arrhythmias. However, intravenous verapamil in a patient with sustained ventricular tachycardia can cause hemodynamic collapse. 

Lidocaine Sodium channel (INa) blockade Blocks activated and inactivated channels with fast kinetics does not prolong and may shorten action potential Terminate ventricular tachycardias and prevent ventricular fibrillation after cardioversion IV first-pass hepatic metabolism reduce dose in patients with heart failure or liver disease Toxicity Neurologic symptoms... 

As noted above, the antiarrhythmic drugs can modify impulse generation and conduction. More than a dozen such drugs that are potentially useful in treating arrhythmias are currently available. However, only a limited number of these agents are clinically beneficial in the treatment of selected arrhythmias. For example, the acute termination of ventricular tachycardia by lidocaine or supraventricular tachycardia by adenosine or verapamil are examples in which antiarrhythmic therapy results in decreased morbidity. In contrast, many of the antiarrhythmic agents are now known to have lethal proarrhythmic actions, that is, to cause arrhythmias. 

An 86-year-old woman was given adenosine 12 mg intravenously for sustained supraventricular tachycardia, which terminated but was followed by atrial fibrillation and paroxysmal ventricular tachycardia (24). Cardioversion was unsuccessful, but normal sinus rhythm was obtained with procainamide. This followed an anteroseptal myocardial infarction. 

In a prospective study of 187 episodes of tachycardia in 127 unselected patients adenosine was given in an average dose of 9.7 mg (28). In 108 cases, adenosine induced transient ventricular extra beats or non-sustained ventricular tachycardia after successful termination of supraventricular tachycardia more than half had a right bundle branch block morphology that suggested that the dysrhythmias had originated from the inferior left ventricular septum. 

The authors proposed that amiodarone had modulated the threshold of induction and/or termination of ventricular tachycardia. 

Shimoshige S, Uno K, Miyamoto K, Nakahara N, Wakabayashi T, Tsuchihashi K, Shimamoto K, Murakami H. Amiodarone modulates thresholds of induction and/or termination of ventricular tachycardia and ventricular fibrillation—a case of VT with previous myocardial infarction. Ther Res 2001 22 861-6. 

Griffith MJ, Linker NJ, Garratt CJ, Ward DE, Camm AJ. Relative efficacy and safety of intravenous drugs for termination of sustained ventricular tachycardia. Lancet 1990 336(8716) 670-3. 

ChaugWT, LiuLC, Yen RE, Huang PJ. Persistent myocardial ischemia after termination of dipyridamole-induced ventricular tachycardia by intravenous aminophylUne scintigraphic demonstration. J Formos Med Assoc 2000 99(3) 264-6. 

Sustained ventricular tachycardia is defined as consecutive premature ventricular contractions lasting more than 30 seconds. Nonsustained ventricular tachycardia (VT) usually self-terminates and lasts for less than 30 seconds. The acute treatment of SuVT depends on the hemodynamic stability and symptoms of the patient. Unstable patients should receive immediate cardioversion. If patients are stable with mild symptoms, they can be treated with IV antiarrhythmics. 

Most but not all forms of recurrent ventricular tachycardia occur in patients with extensive heart disease. Ventricular tachycardia occurring in a patient without heart disease is sometimes referred to as idiopathic ventricular tachycardia and may take several forms. " Fascicular tachycardia arises from a fascicle of the left bundle branch (usually posterior) and usually is not associated with severe underlying heart disease. Calcium channel blockers (but not adenosine) are effective in terminating an acute episode of fascicular ventricular tachycardia. Ventricular outflow tract tachycardia (usually originating from the right ventricular outflow tract and thus abbreviated RVOT) originates from near the pulmonic valve (or uncommonly the aortic) and also occurs in patients with normal LV without discernible cardiac disease. Unlike other forms of ventricular tachycardia, RVOT... 

Gorgels A, van den Dool A, Hofs A, et al. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol 1996 78 43-46. 

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