Emergency Medicine · Toxicology
The facts most likely to be tested
Press 1–5 to rate · ↑↓ to navigate
Beta-blocker overdose classically presents with bradycardia, hypotension, and hypoglycemia, distinguishing it from calcium channel blocker overdose which causes hyperglycemia.
Glucagon is the first-line antidote, directly stimulating adenylyl cyclase to raise cAMP and bypass the blocked beta receptor.
For refractory shock, high-dose insulin euglycemia therapy (HIET) is the gold-standard inotrope.
Lipophilic propranolol uniquely causes seizures, coma, and QRS widening from sodium channel blockade, treated with sodium bicarbonate.
The first diagnostic step is a fingerstick glucose, followed by a mandatory 12-lead ECG for AV blocks and QRS prolongation.
Atropine is often ineffective for the bradycardia; refractory lipophilic toxicity may require intravenous lipid emulsion (ILE).
Patients are at high risk for asystole and refractory shock, requiring aggressive ICU-level resuscitation.
Vignette unlocked
A 47-year-old man is brought to the ED after an intentional ingestion of his propranolol prescription. He is lethargic with a heart rate of 38/min and blood pressure of 76/44 mmHg. Fingerstick glucose is 48 mg/dL and an ECG shows a junctional bradycardia. He receives atropine and IV fluids with no improvement in his heart rate or blood pressure.
Which of the following is the most appropriate next step in management?
Glucagon
Glucagon is the first-line antidote for beta-blocker overdose because it stimulates adenylyl cyclase independently of the beta receptor, increasing cAMP to restore inotropy and chronotropy. Atropine is frequently ineffective, and the accompanying hypoglycemia is a classic clue that distinguishes beta-blocker from calcium channel blocker toxicity.
Full handout
High yield triage
Etiology / Epidemiology
Life-threatening toxicologic emergency resulting from intentional self-harm or accidental pediatric ingestion of beta-adrenergic antagonists.
Clinical Manifestations
Classic presentation features bradycardia, hypotension, and hypoglycemia, with severe cases progressing to cardiogenic shock.
Diagnosis
Clinical diagnosis supported by an ECG showing AV blocks and a fingerstick blood glucose to evaluate for classic hypoglycemia.
Treatment
Glucagon is the first-line antidote, followed by high-dose insulin euglycemia therapy (HIET) for refractory shock.
Prognosis
High risk for asystole and refractory shock, requiring aggressive ICU-level resuscitation and monitoring.
Full handout
Epidemiology & Etiology
Most commonly results from intentional self-harm in adults or accidental ingestion in pediatrics. Frequently involves co-ingestion of other cardioactive drugs, particularly calcium channel blockers. Represents a life-threatening toxicologic emergency with a high mortality rate if unrecognized.
Pertinent Anatomy
Beta-1 receptors are concentrated in the myocardium and cardiac conduction system (SA/AV nodes). Beta-2 receptors are located in bronchial smooth muscle, peripheral blood vessels, and the liver/pancreas.
Pathophysiology
Competitive antagonism of beta-adrenergic receptors blunts G-protein coupled activation of adenylyl cyclase, decreasing intracellular cAMP. This reduces intracellular calcium, leading to profound decreases in myocardial inotropy, chronotropy, and dromotropy. Blockade of hepatic beta-2 receptors inhibits glycogenolysis, causing hypoglycemia. Highly lipophilic agents like propranolol cross the blood-brain barrier, directly causing central nervous system depression.
Clinical Manifestations
The classic presentation is profound bradycardia and hypotension unresponsive to standard resuscitation. Patients may exhibit wheezing due to beta-2 mediated bronchospasm. The presence of hypoglycemia is a classic distinguishing feature. Propranolol toxicity uniquely presents with seizures, coma, and QRS widening due to concomitant sodium channel blockade.
Diagnosis
Primarily a clinical diagnosis based on history and toxidrome. The first diagnostic step is a fingerstick blood glucose to identify hypoglycemia. An immediate 12-lead ECG is mandatory to evaluate for sinus bradycardia, AV blocks, or QRS prolongation. Serum drug levels are available but are never used to guide acute management.
Treatment
Initial stabilization requires ABCs and large-volume IV crystalloids. While atropine is given for bradycardia, it is often ineffective. Glucagon is the first-line antidote because it directly stimulates adenylyl cyclase, bypassing the blocked beta-receptor to increase cAMP. For refractory hypotension, high-dose insulin euglycemia therapy (HIET) is the gold-standard inotrope. Propranolol-induced QRS widening requires sodium bicarbonate, and refractory lipophilic drug toxicity may require intravenous lipid emulsion (ILE).
Prognosis
Early mortality is driven by refractory cardiogenic shock and asystole. Sotalol overdose carries a specific delayed risk of QT prolongation and torsades de pointes. Patients require continuous cardiac monitoring in an ICU until asymptomatic for at least 24 hours.
Differential Diagnosis
1. Calcium channel blocker overdose: Presents identically with bradycardia and hypotension but classically features hyperglycemia instead of hypoglycemia.
2. Digoxin toxicity: Features GI distress, yellow-green halos in vision, and scooped ST segments on ECG.
3. Clonidine overdose: Presents with bradycardia and hypotension but uniquely includes miosis and respiratory depression.
4. Organophosphate poisoning: Bradycardia accompanied by profound SLUDGE syndrome hypersecretions and fasciculations.