Calcium channel blockers

Last updated: June 2, 2021

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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 [1]
Agents Effects Side effects Indications
Dihydropyridines [2][3]
  • Short-acting : nifedipine, clevidipine, nimodipine
  • Intermediate-acting : nitrendipine, nicardipine, lercanidipine
  • Long-acting : amlodipine, felodipine
  • Benzothiazepines: diltiazem
  • Phenylalkylamines: verapamil, gallopamil

Dihydropyridine CCBs (nifedipine and amlodipine) primarily act on vascular smooth muscles. Nondihydropyridine CCBs (verapamil > diltiazem) primarily act on the heart.

Verapamil mainly acts on Ventricles and Amlodipine mainly acts on Arteries.

All CCBs [4]



Short-acting CCBs (e.g., nifedipine) are not indicated for monotherapy of angina because they cause hypotension and secondary reflex tachycardia, which can worsen cardiac ischemia.

Dihydropyridines [5][6]

Nondihydropyridines [6]

We list the most important adverse effects. The selection is not exhaustive.

All CCBs [10]


Nondihydropyridines [16]

Nondihydropyridine CCBs should not be combined with beta blockers because CCBs can enhance the negative inotropic, chronotropic, and dromotropic effects of beta blockers.

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 [18]

Patients are usually symptomatic but those who present early or have only consumed a small quantity of CCBs may be asymptomatic.

Diagnostics [19]

  • 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 [18]

ECG [20]

May show any of the following associated arrhythmias:

Acute management [21]


Patients with CCB overdose require continuous cardiac monitoring because they can develop severe cardiovascular complications and deteriorate quickly.

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.

Patients on high-dose insulin infusions must have glucose regularly monitored.

Refractory overdose


Consider in all patients who present within the following time frames or who have taken sustained or extended-release preparations.

  1. Katzung B,Trevor A. Basic and Clinical Pharmacology. McGraw-Hill Education ; 2014
  2. Nicardipine. Updated: January 20, 2016. Accessed: November 23, 2017.
  3. Clevidipine. Updated: October 6, 2017. Accessed: November 23, 2017.
  4. Sica DA. Calcium channel blocker-related periperal edema: can it be resolved?. J Clin Hypertens. 2003; 5 (4): p.291–295. doi: 10.1111/j.1524-6175.2003.02402.x . | Open in Read by QxMD
  5. Basile J. The Role of Existing and Newer Calcium Channel Blockers in the Treatment of Hypertension. J Clin Hypertens. 2004; 6 (11): p.621-629. doi: 10.1111/j.1524-6175.2004.03683.x . | Open in Read by QxMD
  6. Ozawa Y, Hayashi K, Kobori H. New Generation Calcium Channel Blockers in Hypertensive Treatment. Curr Hypertens Rev. 2006; 2 (2): p.103-111. doi: 10.2174/157340206776877370 . | Open in Read by QxMD
  7. Calcium Channel Blockers (CCBs). Updated: December 1, 2008. Accessed: April 6, 2017.
  8. Kelley SR, Kamal TJ, Molitch ME. Mechanism of verapamil calcium channel blockade-induced hyperprolactinemia.. Am J Physiol. 1996; 270 (1 Pt 1): p.E96-100. doi: 10.1152/ajpendo.1996.270.1.E96 . | Open in Read by QxMD
  9. Nifedipine. Updated: March 13, 2019. Accessed: September 23, 2019.
  10. Collard CL. Hypertension: Medication update. South Med J. 2001; 94 (11): p.1065-1070.
  11. Nifedipine Disease Interactions. Updated: April 6, 2017. Accessed: April 6, 2017.
  12. Held PH, Yusuf S, Furberg CD. Calcium channel blockers in acute myocardial infarction and unstable angina: an overview. BMJ. 1989; 299 : p.1187. doi: 10.1136/bmj.299.6709.1187 . | Open in Read by QxMD
  13. Marian AJ. Contemporary treatment of hypertrophic cardiomyopathy. Tex Heart Inst J. 2009; 36 (3): p.194-204.
  14. Opie LH. Calcium channel antagonists part IV: Side effects and contraindications drug interactions and combinations. Cardiovasc Drugs Ther. 1988; 2 (2): p.177–189. doi: 10.1007/BF00051233 . | Open in Read by QxMD
  15. Rossi S. Australian Medicines Handbook 2014. Australian Medicines Handbook ; 2014
  16. Calcium-Channel Blockers (CCBs). Updated: March 22, 2015. Accessed: April 6, 2017.
  17. Pre-excitation Syndromes. Updated: May 31, 2016. Accessed: February 13, 2017.
  18. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  19. Olson KR, Erdman AR, Woolf AD, et al. Calcium Channel Blocker Ingestion: An Evidence-Based Consensus Guideline for Out-of-Hospital Management. Clin Toxicol. 2005; 43 (7): p.797-822. doi: 10.1080/15563650500357404 . | Open in Read by QxMD
  20. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. J Am Coll Cardiol. 2019; 74 (7): p.e51-e156. doi: 10.1016/j.jacc.2018.10.044 . | Open in Read by QxMD
  21. St-Onge M, Anseeuw K, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med. 2017; 45 (3): p.e306-e315. doi: 10.1097/ccm.0000000000002087 . | Open in Read by QxMD
  22. Engebretsen KM, Kaczmarek KM, Morgan J, Holger JS. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning.. Clin Toxicol (Phila). 2011; 49 (4): p.277-83. doi: 10.3109/15563650.2011.582471 . | Open in Read by QxMD
  23. Chyka PA, Seger D, Krenzelok EP, Vale JA, American Academy of Clinical Toxicology., European Association of Poisons Centres and Clinical Toxicologists.. Position paper: Single-dose activated charcoal.. Clin Toxicol (Phila). 2005; 43 (2): p.61-87. doi: 10.1081/clt-200051867 . | Open in Read by QxMD
  24. Chakraborty RK, Hamilton RJ. Calcium Channel Blocker Toxicity. StatPearls. 2019 .

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