SELF-POISONING WITH ~-BLOCKERS: AN UNCOMMON PROBLEM

The main clinical features of self-poisoning with ~-adrenoceptor blocking drugs are bradycardia, hypotension, low-output cardiac failure and cardiogenic shock. In severe cases the myocardium may become relatively refractory to stimulation, resulting in death in asystole. Because of variations in the pharmacological properties of different ~-blockers, their adverse effects are somewhat unpredictable. Other complicating factors include age, obstructive airways disease, diabetes mellitus, and renal or hepatic insufficiency. Gastric lavage alone is unlikely to prevent serious poisoning unless performed early, owing to the rapid absorption of ~-blockers. Although haemodialysis is unlikely to rid the body of propranolol, it may be possible to dialyse more water-soluble, less protein-bound ~-blockers - but this has not been evaluated. Ideally these patients should have intensive supportive care with facilities for ventilatory support and continuous cardiac monitoring. Transvenous electrical pacing may be useful, and IV atropine should be given to reduce unopposed vagal activity, together with IV isoprenaline (isoproterenol) with the dose monitored according to pulse and BP response. IV glucagon may also be of value if given early. As the effects of ~-blockers outlast their chemical half-life in plasma, intensive care may be needed for several days.

'Individual clinicians are unlikely to gain much experience in treating self-poison­ing with beta-blockers, and hence these emergencies require close collaboration between the cardiologist and the clinical pharmacologist.'

BritiSh Medical Journal l: to I 0 (22 Apr 1978)

INPHARMA 6th May. 1978 p3