see also:

• calcium channel blockers
• toxicology

• similar in many respects to beta blocker overdose:
• selectivity is lost
• toxicity mainly results from negative inotropy, chronotropy, dromotropy & vasodilatation
  • ⇒ hypotension, bradycardia, AV block, sinus arrest, junctional rhythm, asystole
  • ⇒ nifedipine ⇒ reflex sinus tachycardia
  • ⇒ ventricular arrhythmias are uncommon except for:
    • ⇒ only bepridil has VW class Ia activity
    • ⇒ prolonged QTc, torsades (esp. if hypokalaemia)
• resp. & CNS depressant effects are common but unlike beta blocker OD seizures are uncommon except in children
• does not directly cause end-organ toxicity but via profound hypotension
• unlike beta blocker OD, hyperglycaemia is more likely than hypoglycaemia
• if not slow release then toxicity is only for 24-36hrs
• large Vd > 1-2L/kg make dialysis ineffective
• rapidly absorbed so peak effects occur early if not slow release
• usually require higher than normal dose inotropes but not as high as with beta blocker OD
• mortality is greatest with verapamil as it combines severe myocardial depression with vasodilatation
• children are particularly sensitive:
  • 10mg nifedipine caused death to 14 month old within 3hrs
  • 400mg verapamil (Isoptin) caused death in an 11 month old when became unresponsive at 45min & developed seizures which responded to IV calcium chloride
  • even therapeutic doses of verapamil (Isoptin) have caused cardiovascular collapse & arrest in infants in whom they are C/I

children may have longer elimination half lives for oral verapamil ⇒ importance of GIT decontamination.

• oxygen
• IV access & bloods for glucose, U&E, Ca, Mg +/- ABGs if pt already hypotensive
• cardiac monitoring
• frequent BP measurement
• emesis is C/I as may have rapid decompensation & vomiting-induced vagal tone may exacerbate toxicity
• consider activated charcoal ASAP if recent ingestion
• if sustained release formulations then whole bowel irrigation esp. in pre-symptomatic phase

• if QRS wide or QTc prolonged then consider bepridil or other agent (eg. tricyclic, class Ia) as the cause.

• 1st line:
  • 20ml/kg crystalloid to increase BP prn
  • 1st line now should probably be High Insulin-Dextrose - Euglycaemia Therapy (HIET) as animal studies seem to show this is the only effective Rx.
  • consider boluses of IV atropine children: 0.02mg/kg (min. 0.1mg) adults 0.6-1.2mg (max. 3mg):
    • but short-lived effects & multiple doses may produce anticholinergic toxicity
• 2nd line:
  • isoprenaline infusion (may exacerbate periph. dilatation, thus usually use with dopamine)
  • higher than normal dose inotrope infusions with vasoconstrictor activity:
    • high dose dopamine 5-30mcg/kg/min
    • adrenaline / epinephrine
    • noradrenaline / norepinephrine
  • consider IV calcium:
    • although it helps contractility, effect on bradycardia, AV block & vasodilatation not so good
    • some advocate aggressive doses
    • adults: 10-20ml 10% CaCl2 over 5-10min then infusion 5-10ml/hr
    • children: 0.1-0.3ml/kg 10% CaCl2 over 5-10min then infusion at half bolus dose/hr
    • rapid IV injection may cause:
      • bradycardia, AV block, AV dissociation, junctional tachycardia, VE's, VF
    • take serum Ca level during infusion phase, aiming for [Ca] < 14mg/dL ( …..mM)
• 3rd line:
  • consider temporary pacemaker external or transvenous
  • glucagon infusion
  • amrinone 5mcg/kg/min (but no chronotropy)
• 4th line:
  • peripheral arterial line
  • pulmonary artery catheter to measure cardiac output, etc
  • consider IABP, cardiac bypass
  • High Insulin-Dextrose - Euglycaemia Therapy (HIET)

• if totally asymptomatic for 6hrs post-ingestion of non-slow release preparation then can be discharged home after psych. referral with medical F/U in 24hrs
• otherwise, admit to hospital for at least 24hrs cardiac monitoring
• if hypotensive, etc, admit to ICU