Calcium-channel antagonists, principally verapamil and diltiazem, have important antiarrhythmic action by virtue of their effects on the atrioventricular node. By slowing conduction these agents may terminate junctional re-entrant arrhythmias and slow the ventricular rate in atrial fibrillation or atrial arrhythmias. The drugs can be administered by intravenous bolus: verapamil 5-10 mg over 30-60 s, diltiazem 10-20 mg over a similar time period for acute rate control but care should be taken in patients with impaired myocardial function as precipitate drops in blood pressure can occur due to a significant vasodilating effect. Such hypotension may be prevented by immediate prior administration of a bolus of calcium chloride. Caution should also be used in patients with known sinus or atrioventricular nodal disease and especially if the patient is already taking b-blocking agents when administration of a calcium-channel antagonist may produce profound bradycardia and hypotension.
Digoxin and associated preparations are frequently used to control ventricular rate in patients with rapidly conducted atrial arrhythmias, particularly atrial fibrillation. The drug may be ineffective alone and may require addition of other agents, such as b-blocking agents or calcium-channel antagonists, to gain adequate rate control.
In this setting intravenous loading with 0.5 to 1 mg over 24 h followed by maintenance doses of 250 to 375 pg/day is usual. The major problem with digoxin is the narrow therapeutic range with considerable potential for exacerbation of arrhythmia when toxic levels are present. Arrhythmias seen with toxicity include atrial tachycardia with block, junctional tachycardia, ventricular premature beats, ventricular tachycardia, sinus bradycardia, and varying degrees of atrioventricular block. Toxicity may be exacerbated by renal impairment, dehydration, hypokalemia, and old age. Concomitant administration of quinidine, amiodarone, and verapamil all increase digoxin levels. In cases of severe overdose, ventricular arrhythmias may require lidocaine or phenytoin, bradycardia may require temporary pacing, and in extreme cases digoxin-specific antibodies can be administered.
Although digoxin is by far the most widely used cardiac glycoside, its relatively prolonged onset of action (1-5 h) may make it unsuitable in the setting of the critically ill patient. Ouabain and deslanoside are only available as intravenous preparations, but both have a rapid onset of action within 10 to 30 min.
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