Calcium-channel Blockers

Calcium channel blocker overdose produces

Non-dihydropyridines (diltiazem, verapamil) are the agents of concern. Dihydropyridine overdose typically causes isolated hypotension with a compensatory tachycardia, although subclass selectivity is lost in massive overdose and myocardial suppression (and bradycardia) can occur.

Epidemiology and Risk Factors

Pathophysiology

  • Direct ↓ inotropy
  • Direct ↓ SVR
  • ↓ Insulin release from β-islet cells
  • ↑ Insulin resistance

Aetiology

Calcium channel blockers:

  • Have high PO absorption
  • Are highly protein bound
  • Hepatically metabolised
  • Include:
    • Phenylalkylamines
      • Greatest cardio-selectivity
      • Include:
        • Verapamil
          • Slow-release preparation
    • Benzothiazepine
      • Mid-range cardioselectivity
      • Include:
        • Diltiazem
    • Dihydropyridines
      • Least cardioselective
      • Include:
        • Amlodipine
        • Felodipine
        • Nimodipine

Clinical Features

Cardiac:

  • Bradyarrhythmias
    • ↓ HR
    • AV nodal blockade
      Full spectrum is possible.
  • Hypotension

Extra-cardiac:

  • ↑ BSL

Unlike calcium channel blockers, β-blockers can also cause bronchospasm, and will typically ↓ the BSL.

Diagnostic Approach and DDx

Investigations

Bedside:

Laboratory:

Imaging:

Other:

Management

  • Give activated charcoal
  • Treat haemodynamics
    Pacing may be required; chemical may be ineffective.
  • High-dose insulin
  • Consider intralipid

Resuscitation:

Calcium Dose Equivalents
Formulation Dose Elemental Ca2+/g
Calcium Gluconate 10mL 2.3mmol
Calcium Chloride 10mL 8.6mmol
  • C
    • Hypotension
      • Fluid resuscitation
      • Calcium
        • 10mL 10% Calcium chloride
        • 30mL 10% Calcium gluconate
        • Infusion can be considered but requires close monitoring
      • Insulin
    • Bradycardia
      • Atropine
        Unlikely to be effective.
      • Cardiac pacing

Specific therapy:

  • Pharmacological
    • Activated charcoal
      • Within 1-hour of immediate release ingestion
      • Any time after sustained release ingestion
        • Consider multiple (Q4H) dosing
    • High-dose Insulin Euglycaemic Therapy
      Overcomes cardiac metabolic starvation that occurs with cardiac toxidromes.
      • ↑ Glucose and lactate uptake by myocardium
      • Positive inotrope without ↑ oxygen demand
      • Initial therapy:
        • 25g 50mL 50% dextrose unless BSL >22mol/L
        • 1 unit/kg IV insulin
      • Continuation:
        • Dextrose 25g/hr, titrated to euglycaemia
          Monitor Q20min for first hour, and hourly thereafter.
        • Insulin at 0.5 unit/kg/hr up to 5unit/kg/hr
        • Insulin dose should be titrated to toxicity, and dextrose dose titrated to maintain euglycaemia
      • Replace potassium if K <2.5mmol/L
      • Cease when clinical resolution of toxicity and ECG abnormalities
    • Intralipid
  • Procedural
  • Physical

Supportive care:

Disposition:

Preventative:

Marginal and Ineffective Therapies

Anaesthetic Considerations

Complications

Prognosis

Key Studies

References

  1. Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.