Intended for healthcare professionals

Letters

Overdose with calcium channel blockers

BMJ 1994; 308 doi: https://doi.org/10.1136/bmj.308.6944.1639 (Published 18 June 1994) Cite this as: BMJ 1994;308:1639
  1. N A Buckley,
  2. I M Whyte,
  3. A H Dawson
  1. Department of Clinical Pharmacology and Toxicology, Locked Bag 7, Hunter Regional Mail Centre, NSW 2310, Australia.

    EDITOR, - John Kenny's editorial on overdose with calcium channel blocking drugs made several statements that could be misinterpreted with potentially serious results.1 Calcium channel blockers had similar effects in overdose despite differing therapeutic effects. A range of similar adverse effects have been reported in case reports, but death, and life threatening complications such as heart block and refractory hypotension, are much more common with verapamil than diltiazem.2,3 Similarly, these effects are more common with diltiazem than nifedipine (and presumably other dihydropyridines).2,3 This mirrors their relative effects on cardiac conduction in therapeutic doses. There have been no deaths formally reported with nifedipine poisoning alone.3 Most nifedipine poisonings will respond to supportive treatment with intravenous fluids. Verapamil, in contrast, frequently causes profound bradycardia and hypotension and warrants aggressive and intensive therapy.

    We agree that the initial treatment of choice is calcium, but the suggestion that four doses of 1 g (or 20 mg/kg) at 15-20 minute intervals is the maximum safe dose and that calcium concentrations should be monitored (presumably to avoid hypercalcaemia) will often lead to failure of this treatment. An analysis of reports of patients failing to respond to calcium reveals either that the doses given are not mentioned or that the total dose given was in the order of 1-3 g.4 Surely the aim of calcium treatment in this situation is to overcome a competitive blockade of calcium channels in the cardiac conducting system. The degree of hypercalcaemia that is required will depend on the level of calcium channel blocker and its relative effect on these tissues. This can be easily monitored with the electrocardiogram. Thus, our approach to calcium channel blocker poisoning with cardiac conduction problems is to give 1 g of calcium salts every 2-3 minutes until the block is reversed. The maximum dose of calcium we have used has been 30 g over 12 hours, and the highest calcium concentration we have observed has been 5.94 mmol/l (23.8 mg/dl).4 We have found no adverse effects attributable to this treatment.5 In our experience, the few patients who do not respond to such a regimen do not respond to any other treatment including glucagon, isoprenaline, dopamine, noradrenaline, and pacing. These may all be worth trying, but our experience is that patients who are truly refractive to calcium therapy are, unfortunately, refractory to all other treatments. This has been supported by animal work done in our laboratory - calcium given in sufficient doses was able to reverse all the cardiovascular toxicity associated with calcium channel blocker overdose.6

    The severity of this poisoning warrants thorough gastrointestinal decontamination. For sustained release calcium channel blocker preparations, whole bowel lavage with polyethylene glycol is, in our experience, far more effective than charcoal with an osmotic cathartic4 (and also does not cause intravascular volume depletion) and should be used routinely.

    References