Acute Management

Although direct current cardioversion will terminate most PSVTs, this is rarely necessary, as the vast majority of patients are hemodynamically stable. In stable patients with regular SVTs, vagal maneuvers may be attempted initially (31). If vagal stimuli are unsuccessful in terminating tachycardia, an intravenous (IV) AV-nodal-blocking agent should be administered (see Fig. 10). Adenosine (32) and verapamil appear to be of similar efficacy in terminating PVSTs that require AV-nodal conduction. Adenosine frequently causes flushing, dyspnea, and chest pain, but these symptoms are fleeting because of the extremely short half-life of this agent. The initial dose of adenosine should be a 6-mg iv push, followed by a rapid flush of fluid; 12-mg or higher doses may be given to nonresponders (33). The initial dose through a central line should generally be 3 mg (34). If adenosine is effective in terminating SVT, it is typically effective at the dose that causes transient symptoms of flushing and chest discomfort. Dipyridamole potentiates adenosine effect, and some cardiac transplant patients seem supersensitive to adenosine. Adenosine can trigger bronchospasm in asthmatics. Theoph-ylline and caffeine counteract the effect of adenosine; frequently patients using these agents are refractory to adenosine, or require higher doses. Finally, adenosine may initiate AF in up to 12% of patients—of particular concern when WPW is present or suspected (35).

Verapamil is also frequently used intravenously for the acute termination of PSVT. Verapamil may be particularly beneficial in patients with recurrent or incessant tachycardia because of its longer half-life, but it can also cause hypotension. Negative inotropic effects are also possible in patients with left ventricular dysfunction. Verapamil is typically administered in 2.5-5.0-mg boluses every 5-10 min until PSVT terminates, with careful monitoring of blood pressure and lung exam. Intravenous calcium-channel blockers (or beta-blockers) may be particularly beneficial in patients with atrial tachycardia; AV nodal blockade may allow control of the ventricular rate even when the tachycardia persists. Intravenous diltiazem and beta-blockers may also be effective in terminating PSVT, although data are fewer than with adenosine or verapamil.

Response to pharmacologic therapy is dependent on the mechanism of the arrhythmia. Approximately 90% or more cases of AVNRT or AVRT can be terminated by adequate iv doses of adenosine or verapamil. For the atrial tachyarrhythmias, response rates are typically lower. Only a minority of ectopic atrial tachycardias are terminated with adenosine; those that do terminate with adenosine tend to be catecholamine-dependent (30).

Patients presenting with well-tolerated PSVT that is terminated in the emergency room do not routinely require admission to the hospital. A sinus-rhythm ECG should always be obtained post-termination, in sinus rhythm, to evaluate for WPW. Stable patients can frequently be discharged from the emergency room, with implementation of a long-term treatment plan as described here. Admission to "rule out" myocardial infarction (MI) is of extremely low yield in young patients with recurrent PSVT and no evidence of structural heart disease.

Management of MAT is usually directed at treating the underlying metabolic and pulmonary abnormalities. Potassium and magnesium supplementation may be helpful (36,37). MAT is rarely associated with theophylline or digitalis toxicity. Calcium-channel blockers may help control both the atrial firing rate and AV-nodal conduction. Beta-blockers may have similar activity, but their use is generally limited by the underlying lung disease (38).

Patients with atrial fibrillation (AF) and/or atrial flutter in the setting of WPW syndrome should follow a different treatment algorithm. AV nodal-blocking agents (calcium-channel blockers, beta-blockers, digoxin, adenosine), can shunt conduction over the accessory pathway, accelerating the ventricular rate and increasing the risk of degeneration into VF (39,40). Thus, these agents are contraindicated in pre-excited AF or atrial flutter. Hemodynamically unstable patients should undergo direct current cardioversion for restoration of sinus rhythm. Patients who are hemodynamically stable should be treated with iv procainamide. This agent slows conduction in the accessory pathway as well as the AV node (and atrial and ventricular myocardium), and helps convert AF of short duration to sinus rhythm.

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