top of page

Calcium Channel Blocker Toxicity  

​

​

Background 

​

  • Two main categories of Calcium Channel Blockers (CCBs):

    • Dihydropyridines (e.g. Amlopidine and Felodipine), which preferentially block the L-type calcium channels in the vasculature.  These are strong  vasodilators that have little negative effect upon cardiac contractility or conduction

    • Non-dihydropyridines (e.g. Verapamil and Diltiazem), which selectively block L-type calcium channels in the myocardium.  These are relatively weak vasodilators but have a depressive effect on cardiac conduction and contractility

  • Clinical features of calcium channel blocker toxicity: 

    • Hypotension

    • Bradycardia (with non-dihydropyridines)

    • Usually a clear mental status unless there is significant hypotension and thus reduced cerebral perfusion

    • ECG may show PR interval prolongation and bradycardia

    • Hyperglycemia may result, which is caused by inhibition of calcium-mediated insulin release

​

​

Considerations

 

  • Potentially profoundly unstable cardiovascular status with hypotension and bradycardia

  • If need for emergency surgery, there will be a need for resuscitation and optimization

 

 

Management 

 

  • Consultations with poison control, medical toxicologist, ICU, and cardiology are strongly recommended

  • Admit patient to ICU or high acuity floor with continuous cardiac monitoring

  • Gastrointestinal decontamination is controversial but should be considered if within 2 hours of ingestion or within 4 hours of ingestion of sustained release formulations

  • Replace and correct electrolyte abnormalities and acid-base disorders

  • For severely symptomatic patients, all of the following interventions should be instituted simultaneously:

    • Stabilization of the airway as necessary (avoid induction agents that exacerbate hypotension)

    • Additional IV boluses of isotonic crystalloid

    • IV calcium

    • IV glucagon

    • IV high-dose insulin and glucose

    • IV vasopressor (eg, norepinephrine)

    • IV lipid emulsion therapy

  • For mildly symptomatic patients, start with IV crystalloids and atropine and only move onto the next agent on this list if the prior therapies are ineffective:

    • Additional IV boluses of isotonic crystalloid

    • IV calcium

    • IV glucagon

    • IV high-dose insulin and glucose

    • IV vasopressor (eg, norepinephrine)

    • IV lipid emulsion therapy

​

​

References 

​

bottom of page