What is the treatment for a calcium channel blocker overdose?

Treatment of Calcium Channel Blocker Overdose

Immediately administer intravenous calcium as the first-line antidote, followed by high-dose insulin euglycemia therapy (HIET) for refractory shock, with ECMO reserved for patients who fail all pharmacologic interventions. 1

Initial Resuscitation and Assessment

• Establish airway, breathing, and circulation following standard BLS/ACLS protocols 1, 2
• Initiate continuous cardiac monitoring with ECG to identify bradycardia, AV blocks (especially with verapamil/diltiazem), and dysrhythmias 1, 2
• Secure IV access immediately; place central venous access if prolonged therapy is anticipated 1, 2
• Obtain baseline labs: serum glucose, potassium, ionized calcium, and renal function 1, 2
• Consider activated charcoal (1-2 g/kg) if presentation is within 1-2 hours of ingestion and airway is protected 2

Common pitfall: Many clinicians fail to recognize that patients may not have a perfusing blood pressure at presentation and delay CPR initiation 3

First-Line Pharmacologic Therapy

Intravenous Calcium (Immediate Administration)

Administer calcium immediately for catecholamine-refractory shock, as it directly counteracts the calcium channel blockade. 1, 2

• Initial bolus: 0.3 mEq/kg (0.6 mL/kg of 10% calcium gluconate OR 0.2 mL/kg of 10% calcium chloride) IV over 5-10 minutes 1
• Continuous infusion: 0.3 mEq/kg per hour, titrated to hemodynamic response 1
• Monitor serum ionized calcium levels throughout; avoid severe hypercalcemia (>2× upper limit of normal) 1
• Calcium was efficacious in reversing cardiac conduction depression and increasing blood pressure in prospective case series 4

High-Dose Insulin Euglycemia Therapy (HIET)

HIET is the most effective therapy for restoring hemodynamic stability and improving survival in severe CCB toxicity; escalate if myocardial dysfunction persists despite calcium. 1, 2

• Initial bolus: 1 U/kg regular insulin IV with simultaneous 0.5 g/kg dextrose 1, 2
• Continuous infusion: 0.5-1 U/kg/hr insulin (can increase incrementally based on response) 1, 2
• Dextrose infusion: 0.5 g/kg/hr, adjusted to maintain glucose 100-250 mg/dL 1
• Critical monitoring: Check glucose every 15 minutes initially during titration, then hourly once stable 1, 2
• Monitor potassium every 1-2 hours during HIET to prevent hypokalemia 1
• Systematic review found HIET associated with improved hemodynamic parameters and lower mortality, though risks include hypoglycemia and hypokalemia 5

Second-Line Vasopressor Support

• Dopamine was efficacious in increasing blood pressure in prospective case series 4
• Norepinephrine improved hemodynamic parameters and survival without documented severe side effects 5
• Atropine for symptomatic bradycardia has limited efficacy (only 25% response rate in case series), but reasonable to attempt 1, 4
• Glucagon has inconsistent evidence with mixed results in animal and human studies; consider if first-line therapies fail 1, 5

Cardiac Pacing

• Use temporary pacing for unstable bradycardia or high-grade AV block WITHOUT significant myocardial dysfunction 1
• Critical caveat: Pacing is ineffective when myocardial contractility is severely depressed, which is common in CCB overdose 1

Advanced Rescue Therapies for Refractory Shock

Lipid Emulsion Therapy

• Administer IV lipid emulsion for refractory shock or periarrest states 1
• If cardiac arrest occurs, add IV lipid emulsion to standard ACLS with calcium bolus 1
• Animal studies showed improved hemodynamics with IV verapamil poisoning, but not with oral verapamil models 5

Extracorporeal Membrane Oxygenation (ECMO)

Consider ECMO for shock refractory to all pharmacological interventions, particularly with significant cardiogenic component or cardiac arrest. 1, 2

• Retrospective studies show improved outcomes in drug toxicity-related cardiac arrest with ECMO 1
• Consensus supports ECMO for reversible causes like CCB toxicity 1
• Systematic review found ECMO associated with improved survival in severe shock or cardiac arrest, though risks include limb ischemia, thrombosis, and bleeding 5

Emerging Therapies

• Levosimendan (calcium sensitizer) improved hemodynamics in two case reports of severe CCB overdose refractory to conventional therapy 6
• Hemoadsorption/hemoperfusion with styrene resin filters showed temporal relationship with shock resolution in a 2024 case report, with significant amlodipine elimination detected 7

Critical Monitoring Parameters

• Continuous cardiac telemetry for rhythm and conduction abnormalities 1, 2
• Blood pressure monitoring with arterial line preferred for shock states 1, 2
• Serum glucose every 15 minutes initially, then hourly once stable 1, 2
• Serum potassium every 1-2 hours during HIET 1
• Ionized calcium levels during calcium infusions 1, 2

Essential Consultation

Promptly consult a medical toxicologist or poison control center (1-800-222-1222) for all CCB overdoses to guide therapy and ensure access to advanced interventions. 2

Key clinical distinction: Dihydropyridines (amlodipine, nifedipine) primarily cause peripheral vasodilation, while non-dihydropyridines (verapamil, diltiazem) cause more cardiac manifestations including AV nodal block 3, 4. However, in overdose, all CCBs lose receptor specificity and can cause both vasoplegic and cardiogenic shock 3.