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Uploaded byDr.Umang Sharma
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Calcium channel blocker

Calcium channel blockers (CCBs) work by blocking the movement of calcium ions into cardiac and vascular smooth muscle cells. There are three main classes of CCBs: phenylalkylamines like verapamil, benzothiazepines like diltiazem, and dihydropyridines like nifedipine. CCBs cause vasodilation of arteries and relax vascular smooth muscle by inhibiting L-type calcium channels, reducing blood pressure and cardiac workload. Different CCBs have varying effects on heart rate, contractility and conduction. CCBs are used to treat hypertension, angina, arrhythmias and other cardiovascular conditions.

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Calcium channel blockers
continued • Prevent movement of calcium inside myocardial cells and vascular smooth muscle cells Cardiac exitation/contraction coupling↓ vascular smooth muscle relaxation
Chemical Type Chemical Names Brand Names Phenylalkylamines verapamil Calan, Calna SR, Isoptin SR, Verelan Benzothiazepines diltiazem Cardizem CD, Dilacor XR 1,4-Dihydropyridines Nifedipine nicardipine isradipine felodipine amlodipine Adalat CC, Procardia XL Cardene DynaCirc Plendil Norvasc Three Classes of CCBs
Subtypes of Ca channels • L , T, N , P • L Type in cardiac and vascular tissue • N in neuronal tissue.
Continued • L type calcium channel • Subunit-α1,α2,β,gamma,δ
Voltage Gated Calcium Channel
Mechanism of action • Voltage depended L channel plugging- Nefedipine • L channel distortion-Verapamil,Diltiazem
 Increase the time that Ca2+ channels are closed  Relaxation of the arterial smooth muscle but not much effect on venous smooth muscle  Significant reduction in afterload but not preload Effects of CCB
Cardiac cells rely on L-type Ca2+ channels for contraction and for the upstroke of the AP in slow response cells Contractile Cells (atria, ventricle) L-Type Ca2+ Ca2+ Ca2+ Slow Response Cells (SA node, AV node) L-Type Ca2+ Ca2+
Vascular smooth muscle relies on Ca2+ influx through L-type Ca2+ channels for contraction (graded, Ca2+ dependent contraction) L-Type Ca2+
Effects of CCB in LV function LV Performance Reduced Contractility V>N>D Reduced Afterload N>D=V Reflex sympathetic stimulation N>D=V Unchanged Preload Variable HR N↑,V↓,D↓
Differential effects of different CCBs on CV cells AV SN AV SN Potential reflex increase in HR, myocardial contractility and O2 demand Coronary VD Dihydropyridines: Selective vasodilators Non -dihydropyridines: equipotent for cardiac tissue and vasculature Heart rate moderating Mild Peripheral and coronary vasodilation Reduced inotropism Peripheral vasodilation
Effect Verapamil Diltiazem Nifedipine Peripheral vasodilatation    Coronary vasodilatation    Preload 0 0 0/ Afterload    Contractility  0/ / * Heart rate 0/  /0 AV conduction   0 Hemodynamic Effects of CCBs
Agent Oral Absorption (%) Bioavail- Ability (%) Protein Bound (%) Elimination Half-Life (h) Verapamil >90 10-35 83-92 2.8-6.3* Diltiazem >90 41-67 77-80 3.5-7 Nifedipine >90 45-86 92-98 1.9-5.8 Nicardipine -100 35 >95 2-4 Isradipine >90 15-24 >95 8-9 Felodipine -100 20 >99 11-16 Amlodipine >90 64-90 97-99 30-50 CCBs: Pharmacokinetics
 Angina pectoris(prinzmetal)  Hypertension  Treatment of supraventricular arrhythmias - Atrial Fibrillation - Paroxysmal SVT Hypertrophied cardiomyopathy Raynaud phenomenon Widespread use of CCBs
uses • Amlodipine-isolated systolic HF in elderly • PRAISE study-safe in EF>30% • Combination with BB but not in Diabetics and EF<30% • Useful for supraventricular arrythmias,stable angina,Migraine-Verapamil • Atrial fibrillation-Diltiazem • Nimodipine-SAH • Nicardipine-tocolytic agent
Newer and investigational uses • Hypertrophied cardiomyopathy • Cold cardioplegia • PAH • ↓platelet aggregation • Asthma • Achalasia cardia,esophageal spasm • Technique of induced hypotension
Caution • For unstable angina • HF with significant LVD with EF<30%(no) • Conduction defects • WPW syndrome • Hypotension
Contraindication Verapamil Nifedipine Diltiazem Hypotension + ++ + Sinus bradycardia + 0 + AV conduction defects ++ 0 ++ Severe cardiac failure ++ + + Contradications for CCBs
Adverse effects • Bradycardia • Hypotension • Dizziness • Headache • Constipation • Oedema(ankle) • LVD
Drug interactions • Ca channel blocker +inhalation agent=depress SA& AV node,↓BP,↓MAC value • LA + Ca channel blocker= toxicity may be ↑ • NMB+Ca channel blocker=prolong NMB • K solution+ Ca channel blocker=hyperkalemia • Plasma Digoxin level ↑d/t ↓clearence • Verapamil elevate dose of epinephrine producing arrythmia in Halothane use
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