Blockage of these receptors inhibits relaxation of the smooth muscle in blood vessels and bronchi. Beta-2 receptors are found in bronchial and peripheral vascular smooth muscles, and to a lesser extent, cardiac tissue. Antagonism of these receptors with beta-1 selective blockers (e.g., metoprolol, atenolol, esmolol) results in depressed myocardial contractility, decreased heart rate and blood pressure, and decreased myocardial oxygen consumption. Beta-1 receptors are found primarily in cardiac tissue. They competitively inhibit endogenous catecholamines at beta-adrenergic receptors. In addition, the patient should receive high-dose insulin and dextrose, crystalloid fluids and vasopressor support with norepinephrine.īeta-blockers are widely used medications in the treatment of multiple conditions, including hypertension, dysrhythmias, angina, hyperthyroidism and migraines. Calcium chloride should be administered through a central line. It is reasonable to raise the serum calcium to 14 mg/dL. Although the optimal dosing of calcium is not known, it is recommended to start with 6 grams of calcium chloride followed by a continuous infusion at half that dose. High-dose calcium chloride represents the next step in management. Atropine can be used for bradycardia but in general, does not have a significant effect. Management should begin with good supportive care followed by specific therapy. Hyperglycemia is suggestive of calcium channel blocker overdose in the undifferentiated hypotensive and bradycardic patient. In patients who present with hypotension and bradycardia in overdose, beta-blocker toxicity, sedative-hypnotic drug overdose, and hypoglycemia should also be considered. Verapamil is the most deadly of the calcium channel blockers in overdose as it has profound effects on myocardial contractility and peripheral vasodilation. Calcium channel antagonists block slow calcium channels in the myocardium and smooth muscle leading to vasodilation, decreased cardiac contractility, SA node depression and slowing of AV conduction. Feb 25, 2019: What are the differences in the pharmacological effects and blood levels for THC and CBD when administered orally vs.The patient is suffering from a calcium channel antagonist (verapamil) overdose manifesting with profound bradycardia and hypotension.Please email me with any suggestion at Seger, MD I am interested in any questions you would like answered in the Question of the Week.

This question prepared by: Cosby Arnold MD, UT Emergency Medicine Resident 'Treatment of poisoning caused by beta-adrenergic and calcium-channel blockers.' Am J Health Syst Pharm 63(19): 1828-1835. Goldfrank's toxicologic emergencies 9th edition (McGraw-Hill Education, New York, 2011). 'Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies.' Br J Clin Pharmacol 81(3): 453-461. 'Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity.' Toxicol Rev 23(4): 223-238.

Glucagon may also be considered in other cases of drug-induced bradycardia.ĭeWitt, C.R. Glucagon has a short half-life and the bolus should be followed by a continuous infusion at 3-5 mg/hr. Giving the bolus more quickly increases risk for vomiting. We recommend giving glucagon as a 10 mg bolus over 10 minutes. Glucagon binding to these receptors results in increased adenylyl cyclase activity independent of β-receptor activity. Similar to β-receptors, cardiac glucagon receptors are coupled to Gs proteins. Glucagon, a polypeptide counterregulatory hormone secreted from the pancreatic α-cells, bypasses β-receptors to exert inotropic and chonotropic cardiac effects. β1-receptor antagonism results in decreased calcium entry and, subsequently, decreased inotropy and chronotropy. These receptors normally act through a second messenger system (Gs proteins*) to activate adenyl cyclase (AC) and increase cyclic AMP (cAMP), which results in the influx of intracellular calcium through L-type calcium channels. Beta blockers competitively inhibit myocardial β1 receptors.

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