Verapamil (Calan/Verelan) is an oral and intravenous non-dihydropyridine calcium channel blocker (CCB) which is more selective for L-type calcium channels on cardiac muscle than vascular smooth muscle. In comparison, dihydropyridine CCBs like nicardipine and clevedipine cause more vasodilation.

Electrical conduction through the sinoatrial (SA) and atrioventricular (AV) nodes relies on the movement of calcium ions. CCBs like verapamil inhibit the influx of calcium to slow conduction (decrease dromotropy, cool word right?!) namely through the AV node. This prolongs the refractory period between conduction cycles and can slow the ventricular rate in patients with supraventricular tachycardias.

Due to its mechanism, verapamil also reduces cardiac contractility (inotropy) and heart rate (chronotropy) which can potentially induce atrioventricular block. Constipation is also a side effect associated with verapamil.

Admittedly in my clinical practice, I can’t remember the last time I wrote or administered verapamil in the operating room or ICU especially since most of my patients have baseline cardiac impairment. Nevertheless, it’s important to know how the spectrum of CCBs affect the “pump” (heart) and “plumbing” (vasculature) to varying degrees.

Drop me a comment below with questions! 🙂

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