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Calcium channel blockers toxicity

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⚠️ Key Point: Calcium channel blocker (CCB) toxicity is a medical emergency with potentially fatal cardiovascular collapse. Immediate recognition and high-level supportive care are crucial.

🧠 About

CCB toxicity results from overdose of drugs that block voltage-gated L-type calcium channels in cardiac and vascular smooth muscle.
This leads to bradycardia, hypotension, and myocardial depression — the classic triad.
Verapamil and Diltiazem primarily affect the heart; Amlodipine, Felodipine, and Nifedipine act mainly as vasodilators.
Extended-release formulations cause delayed toxicity → observe for ≥12–24 hours.

🔬 Aetiology & Mechanism

Dihydropyridines (Amlodipine, Felodipine, Nifedipine): Potent peripheral vasodilators → hypotension and reflex tachycardia (or paradoxical bradycardia in severe cases).
Non-Dihydropyridines (Verapamil, Diltiazem): Depress SA and AV nodal activity → severe bradycardia, conduction block, and negative inotropy.
Cellular mechanism: Blockade of L-type Ca²⁺ channels ↓ intracellular calcium → ↓ contractility and vascular tone; inhibits insulin release → hyperglycaemia and metabolic acidosis.

🩺 Clinical Features

Severe bradycardia and/or hypotension are the hallmarks.
Collapse, syncope, confusion, or cardiac arrest may occur.
Refractory shock due to vasodilation + myocardial depression.
Hyperglycaemia (useful diagnostic clue).

🧪 Investigations

Laboratory tests: U&E, Mg²⁺, Ca²⁺, glucose, ABG (metabolic acidosis common).
ECG: Continuous monitoring for bradycardia, AV block, or QT changes.
Troponin: Check if ACS suspected.
Glucose: Hyperglycaemia reflects reduced insulin release from pancreatic β-cells.

🩹 Management Overview

💡 Teaching tip: Treatment aims to support perfusion, restore calcium availability, and enhance myocardial metabolism.

Therapeutic Step	Intervention	Rationale / Notes
1️⃣ Resuscitation & Monitoring	Admit to CCU/ICU; establish IV access, cardiac monitoring, frequent BP and glucose checks.	Prevents sudden deterioration and guides titration of therapies.
2️⃣ Circulatory Support	IV crystalloids ± vasopressors (noradrenaline, dopamine if refractory).	Restores preload and counters vasodilatory shock.
3️⃣ Bradycardia	IV Atropine 0.6–1.2 mg repeated as needed (max 3 mg). Temporary pacing if refractory.	Enhances vagal suppression of SA/AV node depression.
4️⃣ Calcium Therapy	10–20 mL of 10% Calcium Gluconate IV over 5–10 min; repeat as needed or give continuous infusion (0.5–1.5 mL/kg/hr).	Increases extracellular Ca²⁺, partially overcoming channel blockade and improving inotropy.
5️⃣ Hyperinsulinaemic Euglycaemic (HIE) Therapy	High-dose insulin infusion (starting 1 U/kg bolus → 0.5–1 U/kg/hr) + IV dextrose; monitor glucose and K⁺.	Insulin enhances myocardial carbohydrate utilisation and contractility; key evidence-based therapy.
6️⃣ Glucagon	3–10 mg IV bolus followed by infusion (3–5 mg/hr) if persistent hypotension or bradycardia.	Stimulates cAMP independent of β-receptors, increasing inotropy and chronotropy.
7️⃣ Lipid Emulsion Therapy	20% Intralipid: 1.5 mL/kg bolus, then 0.25–0.5 mL/kg/min infusion (max 10 mL/kg over 30 min).	“Lipid sink” binds lipophilic drugs like verapamil or amlodipine; used for refractory cases.
8️⃣ Decontamination	Activated charcoal (if within 1 h of ingestion); whole-bowel irrigation for sustained-release preparations.	Reduces further absorption of drug.
9️⃣ Advanced Support	Temporary transvenous pacing, ECMO (Extracorporeal Membrane Oxygenation) if refractory shock.	Bridges to recovery when pharmacological measures fail.

📈 Prognosis

Outcome depends on dose, formulation, and rapidity of intervention.
Verapamil and diltiazem overdoses carry higher mortality than dihydropyridines.
Early initiation of HIE therapy correlates strongly with survival.

🧩 Differential Diagnosis

Beta-blocker overdose (distinguished by normal glucose levels).
Digoxin toxicity.
Severe sepsis or cardiogenic shock.

📚 References

Hyperinsulinaemic Euglycaemia Therapy for Verapamil Poisoning: A Review
NICE Clinical Knowledge Summaries – Poisoning: Calcium Channel Blockers
ToxBase: UK NPIS – Calcium Channel Blocker Overdose
DeWitt CR, Waksman JC. "Pharmacology, pathophysiology, and management of calcium channel blocker and beta-blocker toxicity." Cardiol Clin 2012;30(4):565–79.

In summary, calcium channel blocker overdose causes profound cardiovascular collapse due to depressed calcium-dependent contractility and conduction. The cornerstone of management is early, aggressive supportive therapy — particularly HIE infusion and calcium supplementation — delivered in an intensive care setting.

PLEASE NOTE LEGAL ADVICE: The contents are under continuing development and improvements and may contain errors of omission or fact. Feedback vital and always welcome at drokane at gmail.com. This is not to be used for the assessment, diagnosis or management of patients. It should not be regarded as medical advice. It is only for educational purposes. Please adhere to your local protocols. If you are unwell please seek healthcare advice from your doctor. This does not replace senior or specialist advice. If you do not accept this then please do not use the website. If you need medical advice, please consult a doctor or other appropriate medical professional. If you are a medical professional and you need advice then speak to your senior or colleagues.

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