Calcium channel blockers.ppt

Calcium channel blockers Professor Ian Whyte Hunter Area Toxicology Service Calcium channel blockers Phenylalkylamines verapamil Benzothiazepines diltiazem Dihydropyridines nifedipine, felodipine, nimodipine, nicardipine, amlodipine, lercanidipine Calcium channel blockers Block calcium channels (L-type) in heart and blood vessels prolong depolarisation ↑QRS width block SA and AV node conduction heart block asystole vasodilators cerebral protection Calcium channel blockers Hypotension peripheral vasodilatation and myocardial depression Bradycardia AV and SA node block Antidotes Correction of acidosis Calcium loading Glucagon Insulin-dextrose euglycaemia Atropine Inotropic agents Cardiac pacing Bay K 8644 (calcium channel agonist) Correction of acidosis Correct acidosis to a pH within the normal range L calcium channel function is impaired when the pH falls outside the physiological range acidosis enhances the effect of verapamil and decreases the effect of calcium sodium bicarbonate significantly improved myocardial contractility and cardiac output in a swine model of verapamil poisoning Calcium loading Calcium loading is the most logical and appears to be the most effective agent to use in calcium channel blocker poisoning It is primarily indicated in patients with heart block (who have usually taken verapamil or diltiazem) Glucagon Glucagon is a well-accepted antidote for beta-blocker poisoning The rationale for its use in CCB poisoning is that it activates myosin kinase independent of calcium flux Clinical experience suggests it is less effective in this setting than in beta-blocker poisoning Insulin-dextrose euglycaemia Insulin infusions should be used to treat hyperglycaemia or hyperkalaemia Insulin-dextrose euglycaemia is more effective in animal models than calcium, adrenaline or glucagon Effective in a case series of clinically serious poisonings Hypotension that is refractory to volume loading, correction of acidosis and calcium salts Insulin-E