Abstract

A vagal origin of sudden death has been hypothesised in humans, but it has not yet been clearly demonstrated. Two vagal reflexes have been widely investigated: the diving reflex and the fear-induced central reaction, which are responsible for diving bradycardia and alarm bradycardia, respectively. The latter occurs in humans mainly in the context of emotional presyncope/syncope. A simultaneous occurrence of these two vagal reflexes has been observed in animals that are threatened while diving, and heart rates (HR) as low as two to six beats/min have been reported. In experiments carried out in rats, a high percentage of animals that were stressed before immersion in water died suddenly due to progressive slowing of HR; autopsy revealed no signs of drowning. No animals died if they had not been previously stressed. These data show that vagal sudden death can occur when the vagal cardiac fibres are synergically stimulated by two independent reflexes. In humans, it has been reported that in 10–15% of people who die after falling into water, autopsy reveals little or no water in the lungs. These sudden deaths could be due to vagal overactivity. The development of an adequate laboratory model may improve knowledge of the pathophysiology of this type of vagal sudden death and of its prevention.