vefstream.blogg.se - Glucagon beta blocker antidote mechanism

Patient presents within 1-2 hours of ingestion (which rarely happens).

(4) Peripheral vasodilators (betaxolol, bucindolol, carteolol, carvedilol, celiprolol, labetalol, nebivolol) may cause hypotension due partially to peripheral vasodilation.

(3) Cardiac potassium channel blockade (acebutolol, sotalol) may prolong the QTc and cause torsade de pointes.

Hypotension can be more severe than one would expect, based solely on the degree of bradycardia.

(2) Cardiac sodium channel blockade (acebutolol, betaxolol, carvedilol, oxprenolol, pindolol, propranolol) – may cause QRS widening and monomorphic VT.

(1) Lipophilic agents (e.g., propranolol) are more likely to enter the brain and cause delirium or seizure.

Higher doses: will affect heart as well (vasodilation combined with bradycardia).

Lower doses: can cause a primarily vasodilatory shock state (hypotension with reflex tachycardia).

However, at high doses they lose selectivity for the vasculature and suppress the myocardium.

Dihydropyridine CCBs (e.g., nifedipine, isradipine, amlodipine, felodipine, nimodipine) initially cause vasodilation.

Presentation is marked by early development of hypotension and bradycardia.

Nondihydropyridine CCBs (verapamil and diltiazem): Cause myocardial suppression more than vasodilation.

Neurologic: Delirium, seizure, coma (may result from brain hypoperfusion, or may be due to lipophilic beta-blockers see below).

💡 In an undefined intoxication with bradycardia and hypotension, the glucose may provide a clue pointing to either CCB or BBl intoxication.

CCB poisoning usually causes hyperglycemia, whereas BBl poisoning may cause hypoglycemia.

Cardiovascular: Bradycardia, hypotension, and shock are common.

Extended-release formulations or sotalol may present later, with deterioration occurring within 24 hours.Ingestion of immediate-release formulations should cause clinical deterioration within ~6-8 hours.Onset of symptoms depends on the medication and formulation:.The high cost and limited availability of glucagon may be the only factors precluding its future clinical acceptance. Glucagon-treated patients should be monitored for side effects of nausea, vomiting, hypokalemia, and hyperglycemia.

The doses of glucagon required to reverse severe beta-blockade are 50 micrograms/kg iv loading dose, followed by a continuous infusion of 1-15 mg/h, titrated to patient response. Because it may bypass the beta-receptor site, glucagon can be considered as an alternative therapy for profound beta-blocker intoxications. This suggests that glucagon's mechanism of action may bypass the beta-adrenergic receptor site. These effects are unchanged by the presence of beta-receptor blocking drugs. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. Atropine and isoproterenol have been inconsistent in reversing the bradycardia and hypotension of beta-blocker overdose. Medical complications of beta-blocker overdose include hypotension, bradycardia, heart failure, impaired atrioventricular conduction, bronchospasm and, occasionally, seizures. The effects of glucagon in reversing the cardiovascular depression of profound beta-blockade, including its mechanism of action, onset and duration of action, dosage and administration, cost and availability, and side effects are reviewed. Two cases of severe beta-blocker overdose are presented that were treated successfully with glucagon therapy.