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1 Joint Cardio-Respiratory Service, Royal Victoria Hospital and Montreal Children's Hospital, McGill University, Montreal, Canada
The effect of changes in ventilation and carbon dioxide tension on cardiac output was studied in seven normal human subjects in the supine posture using a dye dilution method. Voluntary hyperventilation of room air with resultant hypocapnia invariably produced an increase in cardiac output (mean, 38 ml blood/ liter increase in ventilation). Voluntary hyperventilation with maintenance of CO2 tension at near normal levels resulted in a smaller increase in cardiac output (mean, 15 ml/liter). Hyperventilation produced by the inhalation of 8.4% CO2 produced no change in cardiac output within the first 2 min but an increase thereafter. The response of the cardiac output to hyperventilation is thus largely determined by the carbon dioxide content of the inspirate. The manner in which this takes place is uncertain. The higher cardiac output response at 2 min with hypocapnia may be partly the result of respiratory alkalosis. It might also be related to the increase in respiratory mechanical work per liter ventilation associated with the fall in CO2. The reason for the late rise of cardiac output with hypercapnia is unknown.
Submitted on May 14, 1962
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