Chest
Volume 93, Issue 3, March 1988, Pages 471-475
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The Effects of Hypoxemia on Cardiac Output: A Dose-Response Curve

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To establish a dose-response curve for the effects of isocapnic hypoxemia on cardiac output (CO), we studied 20 healthy men, aged 20 to 34 years, using a tight-fitting face mask and an isocapnic partial rebreathing system (a modified anesthesia machine). We blended oxygen and hypoxic gas to achieve arterial oxygen saturations (SaO2) of 80, 85, and 90 percent; subjects also breathed 100 percent oxygen and room air (RA). Target SaO2 and end-tidal carbon dioxide were continuously monitored using an ear oximeter and CO2 gas analyzer. Subjects experienced the five SaO2 measurements in random order. CO was measured noninvasively at approximately two-minute intervals, using continuous-wave Doppler echocardiography. Mean cardiac output increased with increasing hypoxemia from 6.84 L/min at FIO2 1.0 to 8.44 L/min at SaO2 80 percent (p <0.0005); the increase was entirely due to increased heart rate. We concluded that cardiac output increases significantly in a dose-response manner in response to acute isocapnic hypoxemia in normal persons.

Section snippets

Subjects

We studied 20 normal young men (aged 20 to 34 years). All subjects gave written, informed consent to the experimental protocol, which was approved by the Human Investigations Committee of the University of Kentucky College of Medicine. All subjects were nonsmokers.

Induction and Measurement of Hypoxemia

After a baseline period of at least ten minutes, during which the subjects breathed room air through a face mask, hypoxemia was induced by a modification of the partial rebreathing method of Severinghaus et al.16 We have developed a

Cardiac Output

The dose-response curve for the effect of hypoxemia on cardiac output measured with continuous wave Doppler echocardiography is shown in Figure 3 and Table 1. Cardiac output increases as SaO2 falls from 99 to 80 percent. Compared with room air, the mean increases in CO at 85 percent and 80 percent SaO2 were 13 percent and 20 percent, respectively. As expected, comparable increases also occurred in cardiac index (cardiac output/body surface area), with increasing hypoxemia (Table 1). Means of

DISCUSSION

The findings of this work are that cardiac output rises in a dose-dependent fashion with increasing hypoxemia in healthy men and that there is a significant increase in cardiac output compared to baseline with SaO2 of 85 percent and 80 percent. Further, this increase is due primarily to increased heart rate. There is minimal change in blood pressure, suggesting that systemic vascular resistance decreases. The time course of cardiovascular response to hypoxemia is brisk, with all but one subject

ACKNOWLEDGMENT

Claudine Moffet provided technical assistance. We are grateful to N. K. Burki, M.D., for his ideas and critical review and to John Reeves, M.D., for his encouragement.

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Supported by a grant from the American Lung Association of Kentucky.

Manuscript received Au~t 7; revision accepted September 29.

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