Introduction

Antiarrhythmic drugs, when used chronically for the prophylaxis of cardiac arrhythmia, have received increasing criticism. Although often efficacious, they may also exacerbate arrhythmia in certain subgroups of patients, resulting in excess mortality. Alternative therapies such as catheter ablation, sophisticated pacing techniques, the implantable cardioverter defibrillator, and arrhythmia surgery have an increasing role in the long-term management of cardiac arrhythmia.

Drugs are still most often used as the first therapeutic modality in the acute management of cardiac arrhythmia. It should be remembered that the ideal antiarrhythmic agent does not exist. Antiarrhythmics are seldom reliably efficacious, have a narrow therapeutic range, often have toxic side-effects, and usually have adverse effects on myocardial contractility and normal impulse formation and conduction.

Cardiac arrhythmias occurring in critically ill patients are often the consequence of non-cardiac states such as sepsis, hypoxia, acid-base imbalance, and electrolyte imbalance, particularly hypokalemia and hypomagnesemia, rather than primary cardiac conditions. Initial management of cardiac arrhythmias should be guided toward correction of underlying abnormalities predisposing to arrhythmia. Furthermore, failure to correct such abnormalities may render attempts to restore sinus rhythm futile. The role of direct current cardioversion should not be forgotten in a patient population likely to be intolerant to antiarrhythmic drugs.

Antiarrhythmic drugs should always be used with caution, particularly in patients with impaired hemodynamics and organ dysfunction. Nonetheless, pharmacological control of pathological arrhythmia may be necessary if the rapid ventricular rate itself is causing hemodymanic compromise. In selecting appropriate antiarrhythmic drugs a number of classifications are available, of which the most widely known is the Vaughan Williams classification based on cellular electrophysiological effects

(Table 1). Such classifications are seldom useful to the clinician, particularly when faced with a patient with unstable hemodynamics and impairment of drug excretion as a consequence of organ dysfunction.

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