THE EFFECT OF HYPOXEMIA ON VENTILATION AND CIRCULATION IN MAN

Publisher Website
Google Scholar
Abstract
Hypoxemia caused by partial CO-poisoning (20-30%) (anemic hypoxemia) elicits little or no respiratory response whereas hypoxemia caused by an alveolar pO2 of about 40 mm. Hg (hypoxic hypoxemia) causes a very pronounced hyper-ventilation both in rest and in work. General O2-lack in the tissues does not evoke a hyperventilation. The O2 tension of the arterial blood, and not its O2 content, is the active factor in causing hyperventilation. The effect is produced through the pO2 of the carotid body (glomus). Both in rest and during work a state of hypoxic hypoxemia, with the O2 in the inspired air low enough to reduce the arterial HbO2 to 70 or 80%, produces an increase in cardiac output above the normal. Furthermore, both in rest and during work a state of anemic hypoxemia (20-30% Hb saturated with CO) has little or no effect on the cardiac output, but increases the pulse rate considerably. Acute Oa-lack in the tissues is not a stimulus for the circulation. A lowered O2 tension of the arterial blood, not a lowered O2 content, is a stimulus for the circulation. The effect probably is produced through the chemoreceptors of the carotid glomus.

This publication has 2 references indexed in Scilit: