What is the management of a calcium channel blocker overdose in the emergency department?

Management of Calcium Channel Blocker Overdose in the Emergency Department

Immediately administer intravenous calcium as the first-line antidote while simultaneously initiating high-dose insulin euglycemia therapy (HIET) for any patient presenting with calcium channel blocker overdose and hemodynamic instability. 1

Initial Resuscitation and Assessment

Establish airway, breathing, and circulation following standard BLS/ACLS protocols as your first priority. 1 Secure IV access—preferably central venous access if prolonged therapy is anticipated—and initiate continuous cardiac monitoring with ECG to identify bradycardia, conduction delays (particularly AV blocks), and dysrhythmias. 1

Critical baseline laboratories must include:

• Serum glucose 1
• Potassium 1
• Ionized calcium 1
• Renal function 1

First-Line Pharmacologic Management

Calcium Administration

Administer calcium immediately as the initial antidote for catecholamine-refractory shock. 1 The American College of Cardiology specifically recommends this as first-line therapy. 1

Dosing protocol:

• Initial bolus: 0.3 mEq/kg (equivalent to 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
• Alternative dosing for severe cases: 30-60 mL (3-6 grams) of 10% calcium gluconate IV every 10-20 minutes, or as continuous infusion at 0.6-1.2 mL/kg/hour 2

Monitoring during calcium therapy:

• Monitor serum ionized calcium levels throughout infusion 1
• Avoid severe hypercalcemia (>2× upper limit of normal) 1
• Use continuous ECG monitoring, as even "slow push" administration carries arrhythmia risk 2
• Stop infusion immediately if symptomatic bradycardia occurs or heart rate decreases by 10 beats per minute 2

Administration considerations:

• Calcium gluconate is strongly preferred over calcium chloride for peripheral administration due to less tissue irritation and vein caustic effects 2
• Central venous access is preferred if available 2
• Never mix calcium with vasoactive amines, phosphate-containing fluids, or bicarbonate 2

High-Dose Insulin Euglycemia Therapy (HIET)

HIET should be escalated immediately if myocardial dysfunction persists despite calcium administration. 1 This therapy is reasonable for refractory shock and has emerging evidence as the preferred initial therapy in severe overdoses. 1, 3

HIET dosing protocol:

• Initial bolus: 1 U/kg regular insulin with 0.5 g/kg dextrose 1
• Continuous insulin infusion: 0.5-1 U/kg/hr, titrated to clinical effect (can increase incrementally) 1
• Dextrose infusion: 0.5 g/kg/hr, adjusted to maintain glucose 100-250 mg/dL 1

Critical monitoring for HIET:

• Check glucose every 15 minutes initially during titration phase 1
• Monitor serum potassium every 1-2 hours during HIET 1
• Once stable, glucose monitoring can be reduced to hourly 1

Mechanism: Insulin-mediated active transport of glucose into cells counters the CCB-induced intracellular carbohydrate-deficient state, improving cardiac inotropy. 4

Second-Line Therapies

Glucagon

Consider IV glucagon if first-line therapies fail, though evidence is inconsistent with mixed results in both animal and human studies. 1

Atropine and Pacing

• Consider atropine for symptomatic bradycardia or conduction disturbances, but expect limited efficacy 1
• Use temporary pacing for unstable bradycardia or high-grade AV block WITHOUT significant myocardial dysfunction 1
• Pacing is less effective when significant myocardial depression is present 1

Advanced Rescue Therapies for Refractory Shock

Lipid Emulsion Therapy

Administer intravenous lipid emulsion for refractory shock or periarrest states. 1 This may improve cardiac inotropy through intravascular sequestration of lipophilic CCBs like verapamil. 4

Extracorporeal Membrane Oxygenation (ECMO)

Consider ECMO for refractory shock with significant cardiogenic component or cardiac arrest. 1 Retrospective studies show improved outcomes in drug toxicity-related cardiac arrest with ECMO, and consensus supports ECMO for reversible causes like CCB toxicity. 1

Hemoadsorption/Hemoperfusion

Emerging evidence suggests resin hemoadsorption using styrene bead filters may enhance drug clearance in severe cases, though experience is limited. 5 This represents a potential rescue therapy when conventional measures fail. 5

Cardiac Arrest Management

If cardiac arrest occurs:

• Follow standard ACLS protocols with addition of IV calcium bolus 1
• Consider IV lipid emulsion therapy 1
• Consider ECMO if available 1

Continuous Monitoring Parameters

Throughout treatment, maintain:

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

Critical Pitfalls to Avoid

Do not delay calcium and HIET while waiting for laboratory confirmation—clinical presentation of hypotension and bradycardia in the setting of known or suspected CCB ingestion warrants immediate treatment. 1

Recognize that in high-dose overdoses, CCBs lose receptor specificity—even dihydropyridine CCBs (typically causing peripheral vasodilation) can cause bradycardia and negative inotropy at toxic levels. 6

Avoid rapid calcium administration without ECG monitoring—this can precipitate cardiac arrhythmias and symptomatic bradycardia. 2

Do not rely solely on atropine or pacing—these have limited efficacy in severely poisoned patients and should not delay definitive therapy with calcium and HIET. 1

Prepare for prolonged resuscitation—sustained-release formulations can cause protracted toxicity requiring extended ICU support and consideration for transfer to tertiary centers with ECMO capability. 7