A calcium channel blocker (CCB) disrupts the movement of calcium (Ca2+) through calcium channels.
Most widespread clinical usage of calcium channel blockers is to treat hypertension.
Calcium channel blockers are considered class-IV antiarrhythmic agents.
Calcium channels are especially concentrated in the sinoatrial and atrioventricular nodes, these agents can be used to decrease impulse conduction through the AV node, thus protecting the ventricles from atrial tachyarrhythmias.
Particularly efficacious in treating elderly patients.
Calcium channel blockers are also frequently used to alter heart rate, to prevent cerebral vasospasm, and to reduce chest pain caused by angina pectoris.
Function by blocking voltage-gated calcium channels (VGCCs) in cardiac muscle and blood vessels. decreasing intracellular calcium leading to a reduction in muscle contraction.
In the myocardium, a decreased calcium available for each beat results in a decrease in cardiac contractility.
In blood vessels, a decreased calcium results in less contraction of the vascular smooth muscle and therefore an increase in arterial diameter, a phenomenon called vasodilation.
Calcium channels are present in the smooth muscle lining blood vessels.
By relaxing the tone of this smooth muscle, calcium channel blockers dilate the blood vessels, leading to their use in treating high blood pressure and angina pectoris.
Calcium channel blockers dilate blood vessels, which increases the supply of blood and oxygen to the heart.
Vasodilation decreases total peripheral resistance, while a decrease in cardiac contractility decreases cardiac output.
Especially effective against large vessel stiffness, one of the common causes of elevated systolic blood pressure in elderly patients.
As blood pressure lowers, the afterload on the heart decreases and so the amount of oxygen required by the heart decreases accordingly, ameliorating symptoms of ischemic heart disease such as angina pectoris.
Unlike beta blockers, do not decrease the responsiveness of the heart to the sympathetic nervous system, allowing blood pressure to be maintained more effectively than do beta blockers.
Because calcium channel blockers result in a decrease in blood pressure, the baroreceptor reflex often initiates a reflexive increase in sympathetic activity leading to increased heart rate and contractility.
To minimize these effects a beta blocker may be combined with a calcium channel blocker.
Ionic calcium is antagonized by magnesium ions in the nervous system, so supplements of magnesium may increase or enhance the effects of calcium channel blockade.
Non-dihydrpyridines CCBs decrease the force of contraction of the myocardium, known as the negative inotropic effect of calcium channel blockers.
Therefore the nondihydropyridine calcium channel blockers, such as verapamil or diltiazem, are to be avoided in individuals with cardiomyopathy.
May slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heat, resulting in a negative chronotropic effect, or a lowering of heart rate.
Can increase the potential for heart block.
The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is required, and lower heart rates have lower cardiac oxygen requirements.
Dihydropyridine calcium channel blockers often used to reduce systemic vascular resistance and arterial pressure.
Dihydropyridine calcium channel blockers are not used to treat angina with the exception of amlodipine, nicardipine, and nifedipine which carry an indication to treat chronic stable angina as well as vasospastic angina, because the vasodilation and hypotension can lead to reflex tachycardia.
Dihydropiridine calcium channel blockers can worsen proteinuria in patients with nephropathy.
CCB class is recognized by “dipine”.
Side effects include: Ankle edema, dizziness, constipation, tachycardia, bradycardia, facial redness, and gingival overgrowth.
Class of drugs metabolized by the CYP3A4 enzyme.
Inhibitors of the CYP3A4 enzyme may result in excessive systemic calcium channel blocker concentration and associated toxicity when used concurrently.
Phenylalkylamine calcium channel blockers are relatively selective for myocardium, can reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina.
Phenylalkylamine calcium channel blockers have minimal vasodilatory effects compared with dihydropyridines.
Phenylalkylamine calcium channel blockers cause less reflex tachycardia, making it a good treatment of angina, where tachycardia can be the most significant contributor to the heart’s need for oxygen.
Phenylalkylamine calcium channel blockers major mechanism of action is causing negative inotropy.
Benzothiazepine calcium channel blockers are an intermediate class between phenylalkylamine and dihydropyridines in their selectivity for vascular calcium channels.
By having both cardiac depressant and vasodilator actions, benzothiazepines are able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines.
Non-dihydropyridine CCB may produce profound toxicity and early decontamination, especially for slow release agents, is essential.
Caution should be taken when using verapamil with a Beta blocker due to the risk of severe bradycardia.
Treatment involves intravenous calcium, atropine, fluids, insulin and inotropes.
Insulin is required because at high doses CCB block the effect of insulin.
Metabolized by CYP3A4 enzyme.
Coadministration with inhibitors of CYP3A4 -erythromycin, antifungals, protease inhibitors, grapefruit juice, raise plasma calcium channel blocker concentrations by up to 500%.
Common side effects include headache, flushing, palpitations, and peripheral edema.