Calcium Channel Blocker Overdose | Toxicology & Pharmacology | FlyteXCalcium Channel Blocker Overdose
Poisoning:
Calcium‑channel blocker (CCB) overdose - Emergency department guide
Scope and key points
- CCB overdose can cause life‑threatening cardiovascular collapse.
- Verapamil and diltiazem (non‑dihydropyridines) commonly produce profound myocardial depression and conduction block.
- Dihydropyridines (amlodipine, nifedipine) primarily cause vasodilatation but at large overdoses any CCB may depress cardiac function.
- Management is time‑critical: follow standard resuscitation priorities while initiating toxin‑directed therapies early.
- Use TOXBASE/NPIS for agent‑specific guidance and consider early specialist toxicology and critical care involvement.
- Early discussion with an ECMO centre is advised for refractory shock.
Pathophysiology (concise)
- CCBs block L‑type calcium channels in cardiac myocytes, vascular smooth muscle and pancreatic beta cells, causing:
- Negative inotropy and chronotropy, and slowed AV conduction.
- Peripheral vasodilatation and hypotension.
- Inhibition of insulin release → marked hyperglycaemia and impaired myocardial glucose uptake.
- Downstream effects include tissue hypoperfusion, lactic acidosis, acute kidney injury, pancreatitis and rhabdomyolysis.
- Hyperglycaemia and raised lactate are common markers of severity.
Clinical features to recognise
Cardiovascular: hypotension (may be refractory), bradycardia, AV block, cardiogenic shock, arrhythmia, asystole.Metabolic/systemic: marked hyperglycaemia, elevated lactate, metabolic acidosis, CNS depression, nausea/vomiting, ileus.Children are more susceptible; small ingestions can be severe.Co‑ingestion (β‑blockers, digoxin, sedatives) worsens prognosis.Initial ED priorities
- Airway, breathing, circulation: high‑flow oxygen and treat immediate life‑threatening problems first.
- Early intubation for reduced consciousness or impending respiratory failure.
- Establish two large‑bore IV lines and consider...
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