Poisoning from - antihypertensives

Description

Overdose of beta-blockers, calcium channel blockers (CCBs), ACEi/ARBs, or clonidine
Beta-blocker and CCB overdose are the dangerous ones - can cause refractory cardiogenic shock
ACEi/ARB overdose - usually benign (hypotension only); angioedema is a separate reaction, not an overdose phenomenon

Deliberate self-poisoning, often in patients or family members of patients on these drugs
Beta-blocker + CCB co-ingestion is a recognised high-lethality combination

Beta-blockers: beta-1 blockade -> dec HR, dec contractility; membrane-stabilising agents (propranolol, sotalol) -> Na-channel blockade -> wide QRS, seizures
- Sotalol also blocks K+ channels -> QT prolongation, torsades
CCBs:
- Non-dihydropyridines (verapamil, diltiazem) -> dec HR + dec contractility (like beta-blockers)
- Dihydropyridines (amlodipine) -> pure vasodilation, reflex tachycardia at therapeutic dose, but in overdose lose selectivity -> also cause bradycardia/shock
Clonidine: central alpha-2 agonism -> paradoxical presentation - bradycardia + hypotension + CNS/resp depression mimicking an opioid toxidrome (miosis included)

Clinical: bradycardia + hypotension +/- hyperglycaemia (CCB - impaired insulin release) or hypoglycaemia (beta-blocker - impaired glycogenolysis)
ECG - PR prolongation, bradyarrhythmia, wide QRS (membrane-stabilising agents)
Clonidine overdose can look identical to opioid toxicity - respond partially to naloxone in some cases

Resuscitation

IV calcium (calcium chloride or gluconate) - first-line for CCB toxicity, may help beta-blocker toxicity too
High-dose insulin euglycaemic therapy (HIET) - mainstay for refractory CCB and beta-blocker shock
- Improves myocardial contractility via metabolic substrate switch; give with dextrose, monitor glucose and potassium closely
Glucagon - bypasses the beta-receptor, activates adenylate cyclase directly - useful in beta-blocker toxicity
Atropine - often ineffective but reasonable first step for bradycardia
Refractory shock -> IV lipid emulsion, vasopressors, ECMO as a bridge
Sodium bicarbonate for wide QRS from membrane-stabilising agents
Activated charcoal if within 1-2h and airway protected

Hypoglycaemia (beta-blockers) or hyperglycaemia (CCBs) - both markers of severity, not just incidental findings
Non-cardiogenic pulmonary oedema in severe CCB toxicity

Onset can be delayed several hours with sustained-release preparations - observe longer, do not discharge early
Death from refractory cardiogenic shock; ECMO salvage improves survival in severe cases

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