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Vasodepressor syncope is characterized hemodynamically by a sudden fall in total peripheral resistance with little associated change in cardiac output. The failure of the cardiac output to compensate for the fall in peripheral resistance is a striking feature of the fainting reaction. Possible explanations for this phenomenon are the presence of neurogenic myocardial inhibition or markedly limited volume of blood available to the heart. The effects of atropine injections, inflation of antigravity suit, negative pressure breathing, and albumin infusions on the syncopal reaction were studied. Results favor the causative role of limited venous inflow in the cardiac output response.
Weissler et al. (1957) studied this question.
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