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odcalciumblockers

calcium channel blocker overdose

general features of toxicity:

  • 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.

Mx of calcium channel blocker toxicity

  • 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

ECG:

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

if hypotension & bradycardia:

  • 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:
    • 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:

disposition:

  • 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
odcalciumblockers.txt · Last modified: 2015/12/31 15:30 (external edit)