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Verapamil Toxicity

Verapamil is a calcium channel blocker (CCB) used as an antiarrhythmetic agent and it is particularly useful in the management of supraventricular tachyarrhythmias. CCB toxicity causes bradycardia, conduction abnormalities, hypotension, and if severe, cardiogenic shock. Some patients may have CNS depression and loss of airway protection reflexes, requiring intubation and mechanical ventilation. Impaired cardiac contractility and peripheral vascular resistance may necessitate pharmacotherapy with cardiotonic and vasoactive drugs.

In addition to resuscitation and supportive care, calcium infusion is the recommended treatment for CCB toxicity. Calcium salts for intravenous use are available as calcium chloride and calcium gluconate. Calcium chloride has 3 times as much elemental calcium as calcium gluconate. Calcium gluconate may be given through a peripheral IV line, but calcium chloride should be given by central venous catheter whenever possible.

 Extracellular calcium concentration is increased to overcome the drug's effects on calcium channels by competitive antagonism and increasing calcium entry through unblocked channels. Ionized calcium levels should be followed because no correction is required for albumin concentration. The therapeutic goal is 2.0 mmol/L for free calcium. To prevent spurious elevations in the measured calcium due to infusion contamination and/or incomplete electrolyte equilibrium, samples should be collected 30 minutes after administration of the calcium chloride bolus.

Singh BN, et al.. Verapamil: a review of its pharmacological properties and therapeutic use. Drugs 1978;15:169–97

Kerns W, et al. Beta-blocker and calcium channel blocker toxicity. Emerg Med Clin North Am 1994;12:365–90.

Hariman RJ et al. Reversal of the cardiovascular effects if verapamil by calcium and sodium: differences between electrophysiologic and hemodynamic responses. Circulation 1979;59:797–804.

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