Marked bradycardia suggests a number of cardiac toxins, and in the presence of hypotension may lead to coma. Propranolol and oxprenolol can also directly cause coma (without hypotension).

Opioids, organophosphates, barbiturates, and chloral hydrate are more likely also in this setting.

Bradycardias suggest propranolol or severe TCA poisoning.

Tachycardia may be commonly due to anticholinergic effects (TCAs, neuroleptics), tissue hypoxia (CO, organochlorines), hypoglycaemia ( insulin), acidosis (toxic alcohols and glycols), nicotinic effects (organophosphates) and arrhythmias (TCAs, thioridazine, etc.).

Most other proconvulsant poisonings will lead to tachycardia due to anticholinergic effects or sympathetic stimulation.

Tachycardia may occur with most of these syndromes and is of little diagnostic value. The absence of tachycardia makes LSD, mescaline or hallucinogenic mushrooms more likely.

Bradycardias suggest propranolol or severe TCA poisoning.

Most other proconvulsant poisonings will lead to tachycardia due to anticholinergic effects or sympathetic stimulation.

All of these drugs will lead to a mild tachycardia initially. Severe poisoning with TCAs may lead to bradycardia (with an abnormal ECG) and bradycardia also occurs in carbamazepine poisoning.

Tachycardia is likely with all drugs that cause tissue hypoxia, shock, or seizures:

• Sympathomimetic drugs
• Carbon monoxide
• Tricyclic antidepressants
• Cellular poisons (e.g. cyanide)

Bradycardia prior to the tachyarrhythmia suggests torsade de pointes and a lack of adrenergic or anticholinergic effects making propranolol, digoxin, antiarrhythmic drugs, and non-sedating antihistamines more likely.

Most other tachyarrhythmias will be preceded by sinus tachycardia.