Calcium channel blocker toxicity


  • Hemodialysis is ineffective
  • Precipitous deterioration is common (esp with verapamil)
  • Nifedipine can kill a child with a single pill
  • Onset of toxicity after overdose is usually seen within the first one to six hours for most CCBs, however verapamil is often more delayed

2 Classes



Clinical Features

Differential Diagnosis

Symptomatic bradycardia


  • Serial ECG
    • PR prolongation (varying degrees of AV block)
      • AV block occurs more commonly with verapamil
    • Bradyarrhythmia
    • Less common presentations include ventricular dysrhythmias and QRS widening, which are more commonly seen in toxicity of membrane-stabilizing beta-blockers (i.e. propranolol)
  • Glucose
  • Chemistry
    • Serum calcium is often normal
    • It is the effect on intracellular calcium in the myocardium and smooth muscle that leads to the toxicity of CCBs
  • Continuous cardiac monitoring


The majority of literature on calcium channel blocker overdose management is low-quality evidence and high-dose insulin and extracorporeal life support have the best evidence; other therapies include calcium, dopamine, norepinephrine, and lipid emulsion therapy may be beneficial but are poorly studied[1]

  • Monotherapy only successful for trivial overdoses

GI decontamination

  • Charcoal
    • 1g/kg (max 50g) x1
    • Consider if present within 1-2hr with delayed-release preparation
  • Consider whole bowel irrigation if sustained or extended-release, esp if the drug is verapamil or diltiazem

IV fluids

  • Initial 20cc/kg bolus especially if source of hypotension is undifferentiated and also possibly hypovolemic or due to Sepsis

High-dose insulin and glucose

  • Mechanism of Action: Insulin has a positive inotropic effect on the heart by improving metabolic support of cardiac tissues during hypotensive shock (cardiac tissues preferentially utilize fatty acid as an energy source during normal condition; under stressed conditions, cardiac tissues rely on glucose metabolism as their primary energy source). Some studies have also demonstrated that high doses of insulin can induce endothelial nitric oxide synthase activity and improve microvascular dysfunction by a vasodila- tory effect in cardiac and pulmonary vasculature
  • Takes 30-60min for effect
  • Glucose:
    • Adult: 50mL of D50W
    • Ped: 2.5mL/kg of D10
  • Insulin bolus 1 unit/kg given with 1amp of D50, then 0.5 – 1 unit/kg/hr continuous infusion
    • Titrate infusion until hypotension is corrected or max 2u/kg/hr
    • Titrate dextrose drip to avoid hypoglycemia
    • initial glucose checks q15 minutes until blood sugar stability established
  • Potassium
    • If <3 administer 20mEq IV

Intravenous lipid emulsion

  • 1.5mL/kg bolus of 20% lipid followed by 0.25mL/kg/minute


  • Norepinephrine is agent of choice
    • Start at 2mcg/min, uptitrate rapidly, goal MAP 65mmHg


  • Adult: 0.5-1mg IV q2-3min to max of 3g
  • Ped: 0.02mg/kg (minimum is 0.1mg)
  • Administer to anyone with symptomatic bradycardia


Avoid if digoxin toxicity is possible

  • Calcium gluconate 3g (30-60mL of 10% soln)
  • Calcium chloride 1-3g IV bolus (10-20mL of 10% soln (requires large IV/central line)
    • Preferred over calcium gluconate because it provides triple the amount of calcium on a weight-to-weight basis [2]
    • Give Calcium 1g Q5min to titrate to BP effect
    • If effect in BP is seen can give as a drip at 10-50mg/kg/hr
    • can safely push serum Calcium levels to 15-18 or even low 20s if patient tolerates (double normal)



  • Admit all symptomatic patients
  • Admit all sustained-release ingestions
  • Discharge if asymptomatic x 6-8hrs

See Also

External Links




  1. St-Onge M, et al. Treatment for calcium channel blocker poisoning: a systematic review. Clin Toxicol 2014 PDF
  2. Tintinalli's 7th Ed.