Calcium Channel Blockers (CCBs)

What are the three classes of calcium channel blockers

Phenylalkylamines, Benzothiazepines, Dihydropyridines

Which CCBs act on both cardiac and vascular smooth muscle

Verapamil and Diltiazem

Which CCBs act mainly on vascular smooth muscle

Dihydropyridines (e.g., amlodipine, nifedipine)

What are the general indications for CCBs

Hypertension, angina, arrhythmias, subarachnoid hemorrhage, Raynaud’s disease, migraines

What is the mechanism of CCBs

Block L-type calcium channels → ↓ intracellular Ca²⁺ → vasodilation and reduced cardiac contractility

What does blocking L-type calcium channels do

Reduces peripheral resistance, heart rate, and myocardial oxygen demand

What are the types of calcium channels

L-type (heart, vessels), T-type (heart), N-type (neurons), P-type (Purkinje neurons)

What does verapamil inhibit

Binding of diltiazem and dihydropyridines to the calcium channel

Which CCBs reduce oxygen demand

Verapamil and diltiazem (↓ chronotropy and inotropy)

How do CCBs reduce total peripheral resistance

Relax vascular smooth muscle → arteriolar dilation → ↓ afterload

Which CCBs are used as antiarrhythmics

Verapamil and diltiazem

How do CCBs act as antiarrhythmics

Block slow inward Ca²⁺ channels in SA and AV nodes → ↓ conduction velocity

what are the indications for verapamil

Angina, post-IM and preventing arrhythmias

what medications are dosed chronologically at bedtime to release during early morning BP surge

Covera-HS and Verelan-PM (Verelen ER can be sprinkled on food; do not chew)

What are the three generations of dihydropyridines

1st: nifedipine, 2nd: nicardipine, isradipine, felodipine, 3rd: amlodipine

Why use controlled-release nifedipine

To reduce reflex tachycardia and extend duration

What is clevidipine used for

Ultra-short acting IV CCB for acute hypertension

What is the onset and duration of clevidipine

Onset ~2 min, duration ~15 min

What is nimodipine used for

Cerebral vasospasm prophylaxis due to high lipid solubility

What is the formulation of clevidipine

IV oil-in-water emulsion with soybean oil, glycerin, and egg yolk phospholipids

What is the half-life of amlodipine

30–50 hours

What is the dosing for amlodipine

2.5, 5, or 10 mg once daily

What are contraindications for amlodipine

Hypotension, sick sinus syndrome, AV block, severe LV dysfunction

What are common adverse effects of amlodipine

Peripheral edema, flushing

What are adverse effects of verapamil

Constipation, edema, gingival hyperplasia

Why avoid verapamil in heart failure

It decreases heart rate and contractility, worsening cardiac output

What are drug interactions with verapamil

↑ digoxin and cyclosporine levels; CYP3A4 substrate; inhibits P-gp

What are adverse effects of diltiazem

Edema, AV block, bradycardia, headache, dizziness, rash, constipation

What are drug interactions with diltiazem

↑ digoxin and cyclosporine levels; CYP3A4 substrate

Which CCBs have the strongest peripheral vasodilation

Dihydropyridines (especially nifedipine)

Which CCBs affect SA and AV node conduction

Verapamil and diltiazem

What is the effect of CCBs on coronary arteries

Vasodilation → improved oxygen delivery

What is the effect of CCBs on heart rate

Verapamil and diltiazem ↓ HR; dihydropyridines may cause reflex ↑ HR

What is the effect of CCBs on contractility

Verapamil and diltiazem ↓ contractility; dihydropyridines have minimal effect

What is the effect of CCBs on arrhythmias

Verapamil and diltiazem suppress supraventricular arrhythmias

What is the therapeutic use of verapamil

Angina, arrhythmias, hypertension

What is the therapeutic use of diltiazem

Angina, arrhythmias, hypertension

What is the therapeutic use of dihydropyridines

Hypertension, angina, Raynaud’s, migraines

What is the adverse effect profile of 2nd gen dihydropyridines

Flushing, edema, reflex tachycardia