What is the treatment for calcium channel blocker overdose in the Intensive Care Unit (ICU)?

Treatment of Calcium Channel Blocker Overdose in ICU

Initiate high-dose insulin euglycemia therapy (HIET) and intravenous calcium as first-line pharmacologic interventions for calcium channel blocker overdose with hemodynamic instability, while simultaneously providing aggressive supportive care and preparing for ECMO in refractory cases. 1

Initial Stabilization and Assessment

Airway and Circulation Management:

• Establish airway, breathing, and circulation following standard BLS/ACLS protocols 1
• Secure central venous access for prolonged therapy 1
• Institute continuous cardiac monitoring with ECG to identify bradycardia, AV blocks, and dysrhythmias 1
• Place arterial line for continuous blood pressure monitoring in shock states 1

Baseline Laboratory Assessment:

• Obtain serum glucose, potassium, ionized calcium, and renal function immediately 1
• These labs guide initial therapy and must be monitored frequently throughout treatment 1

First-Line Pharmacologic Therapy

Intravenous Calcium (Immediate Administration):

• Administer 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
• For adults in severe toxicity, give 30-60 mL (3-6 grams) of 10% calcium gluconate IV every 10-20 minutes 2
• Follow bolus with continuous infusion of 0.3 mEq/kg per hour (or 0.6-1.2 mL/kg/hour), titrated to hemodynamic response 1, 2
• Monitor serum ionized calcium levels and avoid severe hypercalcemia (>2× upper limit of normal) 1
• Calcium gluconate is preferred over calcium chloride for peripheral administration to minimize vein irritation 2
• Critical caveat: Avoid calcium administration in concomitant digoxin toxicity due to risk of precipitating fatal arrhythmias 3

High-Dose Insulin Euglycemia Therapy (HIET) - Co-First-Line:

• Administer 1 U/kg regular insulin IV bolus with simultaneous 0.5 g/kg dextrose bolus 1
• Start continuous infusion at 0.5-1 U/kg/hr insulin, titrated incrementally to clinical effect 1
• Administer continuous dextrose infusion at 0.5 g/kg/hr, adjusted to maintain glucose 100-250 mg/dL 1
• Monitor glucose every 15 minutes initially during titration phase, then hourly once stable 1
• Monitor serum potassium every 1-2 hours during HIET to detect hypokalemia 1
• HIET improves cardiac inotropy and survival by shifting to carbohydrate metabolism in the setting of decreased insulin secretion from pancreatic calcium channel blockade 3, 4
• Evidence shows improved hemodynamic parameters and lower mortality, though risks include hypoglycemia and hypokalemia 4

Vasopressor Support

Catecholamine Selection:

• Use norepinephrine to increase blood pressure in vasoplegic shock 5
• Use epinephrine to increase contractility and heart rate 5
• Consider dobutamine in the presence of confirmed myocardial dysfunction 5
• Administer fluid resuscitation as long as patient demonstrates fluid responsiveness 5

Second-Line Therapies

For Persistent Hemodynamic Instability:

• Consider IV glucagon for refractory shock, though evidence is inconsistent with mixed results in both animal and human studies 1, 5
• Administer atropine for symptomatic bradycardia or conduction disturbances, but expect limited efficacy 1, 5
• Use temporary cardiac pacing for unstable bradycardia or high-grade AV block WITHOUT significant myocardial dysfunction 1
• Important caveat: Pacing addresses rate but not contractility or vascular tone, so it has limited utility in severe CCB toxicity 1

Advanced Rescue Therapies for Refractory Shock

Intravenous Lipid Emulsion Therapy:

• Administer lipid emulsion for refractory shock or periarrest states 1
• Animal studies show benefit in intravenous verapamil poisoning models but not in oral verapamil models 4
• Human case reports demonstrate variable efficacy 6

Extracorporeal Membrane Oxygenation (ECMO):

• Consider ECMO for shock refractory to pharmacological therapy or cardiac arrest 1, 5
• Retrospective studies show improved outcomes in drug toxicity-related cardiac arrest with ECMO 1
• Consensus supports ECMO for reversible causes like CCB toxicity 1
• ECMO is associated with improved survival in patients with severe shock or cardiac arrest, though risks include limb ischemia, thrombosis, and bleeding 4

Other Mechanical Support:

• Consider intra-aortic balloon counterpulsation or ventricular assist devices for critically hypotensive patients despite maximal therapy 5

Cardiac Arrest Management

If Cardiac Arrest Occurs:

• Follow standard ACLS with addition of IV calcium bolus 1
• Administer IV lipid emulsion therapy 1
• Deploy ECMO if available 1
• Continue high-quality CPR while preparing advanced interventions 1

Critical Monitoring Parameters Throughout Treatment

Continuous Monitoring Requirements:

• Cardiac telemetry for rhythm and conduction abnormalities 1
• Arterial blood pressure monitoring (arterial line preferred) 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
• Serial ECGs to assess for QRS prolongation and conduction abnormalities 5
• Echocardiography to assess cardiac function when available 5

Common Pitfalls and Safety Considerations

Avoid These Errors:

• Do not delay HIET while waiting for calcium response; both should be initiated simultaneously 1
• Stop calcium infusion immediately if symptomatic bradycardia occurs or heart rate decreases by 10 beats per minute 2
• Never mix calcium with phosphate-containing fluids, bicarbonate, or vasoactive amines 2
• Avoid rapid calcium administration to prevent hypotension, bradycardia, and cardiac arrhythmias 2, 7
• Do not rely on atropine or pacing as primary therapy; these have limited efficacy in CCB toxicity 1
• Consult medical toxicologist or specialist for treatment-refractory hypotension 5