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Toxicology – Drugs Causing Bradycardia
Beta-Blockers (e.g., Propranolol)
Beta-blockers reduce sinoatrial (SA) and atrioventricular (AV) nodal conduction, leading to decreased heart rate and, in severe cases, heart block.
Opiates (Poppies)
Opiates increase vagal tone and exert a depressant effect on SA and AV nodal conduction, contributing to bradycardia.
Anticholinesterase Inhibitors
By inhibiting acetylcholinesterase, these agents increase acetylcholine levels, producing a cholinergic toxidrome in which bradycardia is a prominent feature.
Clonidine
Clonidine is a central α₂ receptor agonist that can cause bradycardia along with hypotension and respiratory depression.
Calcium Channel Blockers
These medications impair SA and AV nodal conduction, resulting in decreased heart rate and potential heart block.
Digoxin
Digoxin increases vagal tone while slowing conduction through the SA and AV nodes, leading to bradycardia despite its positive inotropic effects.
Ethanol
At high doses, ethanol can depress cardiac function and contribute to bradycardia.
Treatment
Atropine may be administered to counteract increased vagal tone and raise heart rate. If ineffective, external pacing should be considered. Definitive management involves identifying the causative toxin and administering the appropriate antidote or targeted therapy.
Beta-Blockers (e.g., Propranolol)
Beta-blockers reduce sinoatrial (SA) and atrioventricular (AV) nodal conduction, leading to decreased heart rate and, in severe cases, heart block.
Opiates (Poppies)
Opiates increase vagal tone and exert a depressant effect on SA and AV nodal conduction, contributing to bradycardia.
Anticholinesterase Inhibitors
By inhibiting acetylcholinesterase, these agents increase acetylcholine levels, producing a cholinergic toxidrome in which bradycardia is a prominent feature.
Clonidine
Clonidine is a central α₂ receptor agonist that can cause bradycardia along with hypotension and respiratory depression.
Calcium Channel Blockers
These medications impair SA and AV nodal conduction, resulting in decreased heart rate and potential heart block.
Digoxin
Digoxin increases vagal tone while slowing conduction through the SA and AV nodes, leading to bradycardia despite its positive inotropic effects.
Ethanol
At high doses, ethanol can depress cardiac function and contribute to bradycardia.
Treatment
Atropine may be administered to counteract increased vagal tone and raise heart rate. If ineffective, external pacing should be considered. Definitive management involves identifying the causative toxin and administering the appropriate antidote or targeted therapy.
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