Cardiology · USMLE Step 1 and Step 2

Calcium Channel Blockers - Non-Dihydropyridines song

Calcium Channel Blockers: Non-Dihydropyridines, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

Calcium Channel Blockers - Non-Dihydropyridines

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Key points in this song10

Non-dihydropyridine CCBs include verapamil and diltiazem, which act on both cardiac and vascular smooth muscle, distinguishing them from dihydropyridines that are primarily vasodilatory.
Both verapamil and diltiazem block L-type calcium channels in the SA and AV nodes, slowing conduction velocity and decreasing heart rate — making them effective for rate control in atrial fibrillation and atrial flutter.
Verapamil has the greatest negative inotropic and chronotropic effect of all CCBs; diltiazem is intermediate — both are contraindicated in decompensated heart failure and severe LV dysfunction.
Non-dihydropyridine CCBs are contraindicated with beta-blockers in combination due to the risk of complete heart block, severe bradycardia, and asystole.
Verapamil is a first-line agent for terminating PSVT (AV nodal reentrant tachycardia) when vagal maneuvers fail, and is used for rate control in stable narrow-complex tachycardias.
Verapamil causes constipation as its most classic adverse effect due to smooth muscle relaxation in the GI tract — a high-yield USMLE distinguishing feature.
Both verapamil and diltiazem inhibit CYP3A4 and P-glycoprotein, raising serum levels of drugs like cyclosporine, digoxin, and statins — important drug interaction tested on boards.
Non-dihydropyridine CCBs are used in hypertrophic obstructive cardiomyopathy (HOCM) when beta-blockers are contraindicated, as they reduce outflow obstruction by decreasing heart rate and improving diastolic filling.
Verapamil is a treatment option for cluster headache prophylaxis — a classic USMLE cross-system association linking cardiology pharmacology to neurology.
In Wolff-Parkinson-White syndrome with atrial fibrillation, non-dihydropyridine CCBs are contraindicated because blocking the AV node preferentially shunts conduction through the accessory pathway, potentially precipitating ventricular fibrillation.