it is difficult to explain how successful resuscitation is possible after 40 minutes' submersion.2 The reduced oxygen requirement in profound hypothermia has been suggested by some authors as the mechanism by which tissue viability is maintained in these circumstances,2 but this alone is an incomplete explanation, as for the submerged body to cool to a degree at which oxygen requirements are sufficiently reduced, heat transfer by mass flow-that is, circulation -must be present (a dead body cools relatively slowly). The degree of cooling encountered in our cases can be explained only by the fact that circulation was maintained for some or all of the period of submersion. The persistence of cardiac activity during such a prolonged period of apnoea supports the hypothesis that some protective mechanism may be present. We do not know whether ventricular fibrillation was present before resuscitative efforts were started and must concede that these efforts alone may have initiated the arrhythmia.Our cases show yet again that successful resuscitation is possible after long periods of immersion and emphasise the importance of performing electrocardiography early in the immersion incident, preferably at the accident site, before death is pronounced.

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ABSTRACr The mechanism by which airway cooling induces airflow obstruction in asthmatic subjects has not yet been established. Using a pair of isocapnic hyperventilation challenges, with a 40-minute interval, we looked for the presence of a refractory period in 19 asthmatic patients (aged 9-18 years). The subjects fell into two groups. The eight in the "non-refractory" group showed less than a 25% reduction in response to the second challenge, but the 11 in the "refractory" group showed at least a 35 % reduction. Twelve subjects also performed a hyperventilation challenge after cholinergic blockade with inhaled ipratropium bromide. In five, in whom no refractoriness after hyperventilation was seen, there was a significant protection from cholinergic blockade (p < 0.05). In these a vagal (cholinergic) reflex seems likely. The remaining seven, who had a refractory period, received no significant protection from cholinergic blockade and therefore no evidence for the presence of any cholinergic mechanism. We conclude that two mechanisms are responsible for hyperventilation-induced asthma, one of which is a vagal reflex while mediator release may be the other.