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Calcium channel blocker
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- 2. continued • Prevent movementof calcium inside myocardial cells and vascular smooth muscle cells Cardiac exitation/contraction coupling↓ vascular smooth muscle relaxation
- 3. Chemical Type ChemicalNames 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
- 4. Subtypes of Ca channels •L , T, N , P • L Type in cardiac and vascular tissue • N in neuronal tissue.
- 5. Continued • L typecalcium channel • Subunit-α1,α2,β,gamma,δ
- 6. Voltage Gated CalciumChannel
- 7. Mechanism of action •Voltage depended L channel plugging- Nefedipine • L channel distortion-Verapamil,Diltiazem
- 8. Increase thetime 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
- 9. Cardiac cells relyon 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+
- 10. Vascular smooth musclerelies on Ca2+ influx through L-type Ca2+ channels for contraction (graded, Ca2+ dependent contraction) L-Type Ca2+
- 11. Effects of CCBin 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↓
- 12. Differential effects ofdifferent 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
- 13. Effect Verapamil DiltiazemNifedipine Peripheral vasodilatation Coronary vasodilatation Preload 0 0 0/ Afterload Contractility 0/ / * Heart rate 0/ /0 AV conduction 0 Hemodynamic Effects of CCBs
- 14. Agent Oral Absorption (%) Bioavail- Ability (%) Protein Bound (%) Elimination Half-Life (h) Verapamil >90 10-3583-92 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
- 15. Angina pectoris(prinzmetal) Hypertension Treatment of supraventricular arrhythmias - Atrial Fibrillation - Paroxysmal SVT Hypertrophied cardiomyopathy Raynaud phenomenon Widespread use of CCBs
- 16. uses • Amlodipine-isolated systolicHF 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
- 17. Newer and investigationaluses • Hypertrophied cardiomyopathy • Cold cardioplegia • PAH • ↓platelet aggregation • Asthma • Achalasia cardia,esophageal spasm • Technique of induced hypotension
- 18. Caution • For unstableangina • HF with significant LVD with EF<30%(no) • Conduction defects • WPW syndrome • Hypotension
- 19. Contraindication Verapamil NifedipineDiltiazem Hypotension + ++ + Sinus bradycardia + 0 + AV conduction defects ++ 0 ++ Severe cardiac failure ++ + + Contradications for CCBs
- 20. Adverse effects • Bradycardia •Hypotension • Dizziness • Headache • Constipation • Oedema(ankle) • LVD
- 21. Drug interactions • Cachannel 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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