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Hypothesis-generating for hypercapnia in vagovagal arrest; prospective human studies required before any practice change.
CARDIAC standstill and ventricular fibrillation constitute major catastrophes that are ever-present threats to the welfare of the patient. Among the suspected factors responsible for cardiac disasters is the so-called vagovagal reflex. Disturbances in the oxygen and carbon dioxide concentrations in the blood due to improper ventilation have been suggested as factors influencing this reflex. Beecher 1 has stated that there is good reason to believe that some of these accidents are due to the accumulation of carbon dioxide, even when the oxygenation of the patient is normal. Sloan 2 has conducted a series of animal experiments in an attempt to elucidate this phase of the problem. He was unable to produce even temporary cardiac arrest by vagal stimulation when the dogs were exposed to normal concentrations of oxygen, and he found that temporary cardiac arrest occurred more frequently during progressive asphyxia (hypoxia and hypercapnia) than during hypoxia alone.
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Benjamin Stewart (1953) studied this question.
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