Calcium Channel Blockers
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Calcium channel blockers are a group of medications that use several different mechanisms to disrupt the flow of calcium through calcium channels. They are widely used as antihypertensives and in heart failure, and also have uses as antiarrythmics and in stable angina.

They can be divided into cardioselective (aka ‘second generation’) such as amlodipine, verapamil¬†and felodipine, and non cardioselective, such as diltiazem and nifedipine. The¬†cardioselective agents have greater effect on peripheral smooth muscle and less effect on¬†the myocardium, and thus avoid the negative inotrophic effects of non-selective agents.


Verapamil, diltiazem, nifedipine, amlodipine, felodipine


Calcium channel blockers (sometimes called calcium antagonists) are indicated in:

  • Hypertension
    • Recommended by NICE as first line therapy in patients or 55 or black Africans
    • Can be combined with other agents (usually recommended ACE-inhibitor or ARB)
  • Angina
    • Usually used in conjunction with a beta-blocker
    • Short acting agents (e.g. nifedipine) can cause reflex tachycardia, and are not preferred. Some studies have shown increased mortality when short acting agents are used.
    • Beta-blocker plus calcium channel blocker is more effective than using either agent alone
  • Heart failure
    • Should generally be avoided in systolic heart failure. Nifedipine and diltiazem can have a negative inotropic effect and should be avoided in left systolic dysfunction. It is thought that this negative inotropic effect outweighs the benefits of reduced afterload.
    • Other calcium channel blockers theoretically¬†have beneficial effects in heart failure by reducing peripheral vasoconstriction and therefore the afterload.
  • Some arrythmias
    • Useful in SVTs (superventricular tachyarrythmias) and atrial fibrillation. Usually diltaizem or verapamil¬† are used.


  • Interfere with calcium uptake into cells through the ‘slow calcium channels’
  • These calcium channels are found in the SA and AV nodes. These tissues depend on slow acting calcium currents to develop their action potentials. Fast response myocardial tissues (in the atria, ventricles and accessory pathways) instead depend on sodium channels
  • They are sometimes classified as class IV anti-arrythmics because of their mechanism of action
  • Calcium channel blockers thus block the slow calcium channels, and slow the rate of conduction through the SA and AV nodes
    • In clinical practice, this prolongs the PR interval, and reduces the sinus rate
    • The extent of blockade is dose dependent – the higher the dose, the greater the blockade
  • They also cause peripheral vasodilation, which can then in turn cause activation of the sympathetic nervous system
  • Their effects vary widely depending on the exact calcium channel blockers used, unlike other drugs used for similar purposes – such as beta-blockers. This is due to their different vasodilatory effects, and thus differing sympathetic nervous system activation. Some agents barely activate the sympathetic nervous system at all, whilst other have a stronger effect, which can then counteract their effect on the SA and AV nodes
  • Short acting calcium channel blockers (diltiazem and verapamil) are particularly selective for cardiac muscle, and are strongly negatively inotropic. They reduce cardiac output and slow the heart rate and should be avoided in heart failure.
  • Dihydropyridine calcium channel blockers (e.g. amlodipine, felodipine, nifedipine) tend to affect vascular smooth muscle more than cardiac muscle, and are generally considered safe in heart failure.
  • Abrupt withdrawal of calcium-channel blockers has been known to result in angina due to rebound vasoconstriction


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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