Category: Fundamentals Nitrates (nitroglycerin, isosorbide mononitrate and dinitrate) are used as vasodilators in the treatment of heart failure and ischemic heart disease. They augment coronary blood flow, as well as reducing myocardial oxygen consumption.
Category: Fundamentals Clonidine exerts its effects by binding to pre-synaptic α2-adrenergic receptors in the brain, inhibiting neurons causing decreased norepinephrine release. This can lead to bradycardia, hypotension, decreased mental status, miosis and hypothermia.
Category: Fundamentals Methylene blue in calcium channel blocker poisoning results in decreased production of cyclic guanosine monophosphate and inhibition of endothelial smooth muscle relaxation, causing an increase in systemic vascular resistance.
Category: Fundamentals Methylene blue is an emerging therapy for calcium channel blocker poisoning. Although traditionally used as a reducing agent for the treatment of methemoglobinemia, methylene blue is also a vasoconstrictor.
Category: Fundamentals In calcium channel blocker poisoning, the endocrine system is affected. As calcium influx triggers the release of insulin, patients poisoned with calcium channel blockers are often hyperglycemic.
Category: Fundamentals A unique feature of calcium channel blocker poisoning is endocrine dysfunction. Like many drugs, calcium channel blockers lose specificity in overdose and thus interfere with other calcium channels within the body.
Category: Fundamentals Dihydropyridine calcium channel blocker (such as amlodipine) toxicity often causes reflex sinus tachycardia from peripheral vasodilation. Calcium channel blockade has little effect on ventricular conduction.
Category: Fundamentals Severe calcium antagonism eventually affects multiple organ systems. Hypotension and bradycardia occur early, and other rhythm disturbances which include AV block of all degrees, sinus arrest, AV dissociation, junctional rhythm and asystole.
Category: Fundamentals In calcium channel antagonist overdoses, there are negative effects on heart rate, contractility, conduction and vascular tone, with the exception of dihydropyridine calcium channel blockers, which tend to result in tachycardia even in toxicity.
Category: Fundamentals In cases of calcium channel antagonists overdose, verapamil has the deadliest profile, combining severe myocardial depression and peripheral vasodilation. Both verapamil and diltiazem act on the heart and blood vessels.
Category: Fundamentals Calcium channel antagonists block the slow calcium channels in the myocardium and vascular smooth muscle, leading to coronary and peripheral vasodilation. They also reduce cardiac contractility, depress SA nodal activity and slow AV conduction.
Category: Fundamentals High-dose insulin improves cardiac output significantly in beta-blocker toxicity from an increase in stroke volume more than heart rate. Dosing of high-dose insulin in humans successfully treated ranges from 0.5 to 22 U/kg/hr.
Category: Fundamentals Despite glucagon's longer history for treatment of beta-blocker toxicity, high-dose insulin is a superior therapy. High-dose insulin is not a vasopressor. It is a profound inotrope with vasodilating properties.
Category: Fundamentals Vomiting is a common complication of glucagon, particularly if administered too rapidly, so the airway should be monitored closely to prevent aspiration. With cumulative large doses, glucagon should be diluted in 5% glucose in water.
Category: Fundamentals Glucagon is recommend for beta-blocker overdose for patients with bradycardia or hypotension not responsive to crystalloid fluids, atropine and calcium. Glucagon has a very short (20-minute) half-life, and its effect is often transient.
