massive dose of verapamil may cause oedema in the lung with the same mechanism.8 Finally, an interaction between verapamil and inflammatory cytokines may have role in that acute respiratory distress like syndrome can be seen in the course of verapamil overdose.In serum samples of patients with acute respiratory distress syndrome, TNFα and IL1 were shown to be increased.16 17 There have been studies of calcium channel blockers, including verapamil and cytokine release, but the results have been conflicting, probably because of the verapamil concentration used.18 19 High concentrations of verapamil significantly increase IL1 induced expression of endothelial leucocyte adhesion molecule-1 (ELAM-1).18 This mechanism may have a role in the pulmonary oedema seen in verapamil intoxication and needs to be clarified with further studies.Whatever the underlying pathophysiological mechanism is, the important contributory factor is the volume overload because of excessive saline infusion to such patients, especially during the hypotensive period, in emergency units.The mechanisms, mentioned above, probably only makes these patients more prone to the development of pulmonary oedema.Non-cardiogenic pulmonary oedema occurred in 5 of 32 cases (15.6%) with verapamil intoxication reported in the literature, including our two patients.It seems that noncardiogenic pulmonary oedema may occur during the course of verapamil overdose and the patients should be observed closely, up to 72 hours with repeated arterial gas analysis.Pressor therapy/inotropic therapy should be started upon hypotension to overcome the effects of profound peripheral vasodilatation and negative chronotropic and inotropic effects.It must be emphasised that exessive saline infusion should be avoided, as this may exacerbate the pulmonary oedema.If respiratory distress is observed together with hypoxia upon arterial gas analysis, the patient should be intubated immediately and mechanical ventilation instituted.
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Chris G. Downs (2002) studied this question.