Calcium channel blockers (CCBs) are drugs that bind to and block L-type calcium channels, which are the predominant calcium channels in the myocardium and vascular smooth muscles. By blocking these channels, CCBs cause peripheral arterial vasodilation (leading to a drop in blood pressure) and myocardial depression (leading to negative chronotropic, inotropic, and dromotropic effects on the myocardium). CCBs are classified into two major groups according to the main site of action: Dihydropyridines (e.g., nifedipine, amlodipine) are potent vasodilators, and nondihydropyridines (e.g., verapamil) are potent myocardial depressants. Diltiazem, a common nondihydropyridine, has moderate vasodilatory and myocardial depressant effects. Nondihydropyridines are also categorized as class IV antiarrhythmic drugs and are used in the treatment of supraventricular arrhythmias. The most common indications for CCB use are arterial hypertension and stable angina. The main side effects of dihydropyridines are caused by vasodilation (e.g., headache, peripheral edema); those of nondihydropyridines are caused by myocardial depression (e.g., bradyarrhythmias, atrioventricular block). CCBs are contraindicated in patients with preexisting cardiac conduction disorders, symptomatic hypotension, and/or acute coronary syndrome.
|Overview of calcium channel blockers |
|Dihydropyridines || |
- CCBs bind to and block L-type calcium channels in cardiac and vascular smooth muscle cells; → decreased frequency of Ca2+ channel opening in response to cell membrane depolarization; → decreased transmembrane Ca2+ current
Effects of decreased Ca2+ influx
- Vascular smooth muscle relaxation; → vasodilation → decreased peripheral vascular resistance → decreased afterload → decreased blood pressure
- Decreased cardiac muscle contractility (negative inotropic action) → decreased cardiac output → decreased blood pressure
- Decreased SA node discharge rate (negative chronotropic action); → decreased heart rate (bradycardia) → decreased cardiac output → decreased blood pressure
- Decreased AV node conduction (negative dromotropic action) → termination of
- Dihydropyridines act mainly on vascular smooth muscle. The order of potency is nifedipine/amlodipine followed by the nondihydropyridines verapamil and diltiazem.
- Nondihydropyridines act mainly on the heart. The order of potency is verapamil > diltiazem > amlodipine/nifedipine.
Verapamil mainly acts on Ventricles and Amlodipine mainly acts on Arteries.
All CCBs 
- Arterial (esp. amlodipine )
- Stable angina: for patients with contraindications for beta blockers or who are not responsive to beta blockers
- (Prinzmetal angina)
- Diffuse esophageal spasm
- (e.g., nifedipine, felodipine)
- ; (e.g., nimodipine; , nicardipine) to prevent secondary vasospasm
- Gestational hypertension
- Hypertensive urgency/hypertensive emergency (e.g., nicardipine, clevidipine)
- Supraventricular arrhythmias (verapamil and diltiazem ;)
- hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy) (
Effects due to vasodilation
- Peripheral edema (esp. amlodipine)
- Headaches, dizziness
- Facial flushing, feeling of warmth
- Reflex tachycardia: a condition of tachycardia secondary to a decrease in blood pressure (esp. nifedipine)
- Gingival hyperplasia
- Benzothiazepines: similar to those of the other CCB classes, but milder
We list the most important adverse effects. The selection is not exhaustive.
All CCBs 
- Hypertrophic obstructive cardiomyopathy (HOCM) 
- Severe stenotic heart valve defects 
- Preexisting cardiac conduction disorders
- Combination with beta blockers: risk of AV block, bradycardia, and/or decreased cardiac contractility
Phenylalkylamines (e.g., verapamil), which primarily affect the calcium channels of the heart, are contraindicated in cases of heart failure because of their negative effect on myocardial contractility.
We list the most important contraindications. The selection is not exhaustive.
Clinical features 
Patients are usually symptomatic but those who present early or have only consumed a small quantity of CCBs may be asymptomatic.
- Respiratory: respiratory depression (including apnea), pulmonary edema
- Gastrointestinal: nausea and vomiting
- Central nervous system: confusion, lethargy, and coma
- Diagnosis is based on clinical observation and a thorough history
- Determine the time of intake, type, amount, and preparation (extended-release vs. immediate-release) of the drug.
- Assess for risk of self harm.
- Any ingestion exceeding the maximum therapeutic dosage is usually clinically relevant.
Laboratory tests 
May show any of the following associated arrhythmias:
Acute management 
- Assess hemodynamic stability.
- Hemodynamically unstable: combination therapy for stabilization (e.g., IV fluids, calcium, atropine, vasopressors)
- Hemodynamically stable or asymptomatic patients: 24 hours of inpatient observation
- All patients
Hemodynamically unstable patients
Management is complicated and specialists should be involved early. A combination of therapies is frequently required and should be tailored to the predominant symptoms.
- IV fluids
- Evidence of myocardial dysfunction
- Symptomatic bradycardia or conduction disorders: atropine
- Shock: vasopressor therapy
Patients on high-dose insulin infusions must have glucose regularly monitored.
- Escalating high-dose insulin therapy while maintaining euglycemia and normokalemia 
- Lipid emulsion therapy 
- Consider transcutaneous pacing in patients with unstable bradycardia or high-grade AV block.
- Consider VA-ECMO if available for patients in refractory shock and significant myocardial dysfunction.
Consider in all patients who present within the following time frames or who have taken sustained or extended-release preparations.