SEMPA Clinical Case (12/8/14) Explanation: Clonidine is the most commonly used alpha-2-adrenergic agonist. Stimulation of centrally acting alpha-2-receptors inhibits the release of peripheral catecholamines, resulting in a decrease of heart rate, contractility, and peripheral vascular resistance. Although this ultimately manifests as hypotension and bradycardia, paradoxical hypertension may occur immediately after ingestion due to peripheral alpha-2-adrenergic stimulation. In addition to the hemodynamic effects, clonidine also stimulates the same mu receptor as opioids leading to miotic pupils and lethargy. Digoxin overdose (B) is associated with GI symptoms such as nausea and vomiting. Increased vagal tone can also lead to cardiac dysrhythmias such as severe bradycardia and supraventricular tachycardias with atrioventricular blocks. Hydrocodone (C) is an opioid that will share many of the properties seen in clonidine and is often difficult to distinguish the 2 overdoses. However, clonidine has greater cardiovascular effects and patients with clonidine overdose typically display more significant bradycardia and hypotension compared to overdoses of hydrocodone. However, both will lead to miotic pupils, lethargy, and decreased respirations. As a beta-blocking agent, metoprolol (D) will also cause hypotension and bradycardia. However, it is not a mu receptor agonist; therefore, pupils will be normal in size and the patient should not be lethargic. Beta-blocker poisoning is also associated with hypoglycemia. References: 1. Stolback A, Chanmugam A: Antihypertensive Agent Toxicity, in Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine, A Comprehensive Study Guide, ed 7. New York, McGraw-Hill, 2011, (Ch) 190:p 1273-1275.
Posted on: Tue, 16 Dec 2014 07:42:29 +0000
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