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(Circulation. 1969;39:639.)
© 1969 American Heart Association, Inc.

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Effects of Breathing 10 Per Cent Carbon Dioxide on the Pulmonary Circulation of Human Subjects

K. H. KILBURN M.D.¹; T. ASMUNDSSON M.D.¹; R. C. BRITT M.D.¹; R. CARDON M.D.¹

¹ From the Department of Internal Medicine, Duke University Medical Center and Durham Veterans Administration Hospital, Durham, North Carolina.

The effects on the pulmonary circulation of breathing 10% CO₂ for 10 to 20 min were studied in five eucapnic and 11 convalescing hypercapnic patients to recreate the CO₂ tensions which they had experienced during respiratory failure. Right heart catheterization permitted measurements of pulmonary arterial and wedge pressures and obtaining samples of mixed venous blood. Breathing CO₂ increased mean pulmonary arterial pressures from 33 to 50 mm Hg (52%); pulmonary arterial wedge pressures were unchanged, and cardiac output increased only 22%. In three hypercapnic and two eucapnic subjects reduction of blood hydrogen ion levels by rapid infusion of 120 to 135 mEq NaHCO₃ during CO₂ breathing did not lower pulmonary arterial pressure significantly, nor raise cardiac output. Neither vascular pressures nor cardiac outputs changed during oxygen breathing. Larger increases in cardiac output, which were produced by exercise, raised pulmonary artery pressure only half as much as breathing 10% CO₂ did. Therefore, pulmonary vascular resistance (PVR) that was elevated to an average of 4.8 mm Hg/L/min at rest while breathing air was increased to 6.5 mm Hg/L/min during CO₂ breathing (P<0.01). In contrast, PVR was unchanged (4.6 mm Hg/L/min) during exercise. This difference between PVR while breathing CO₂ and during exercise was statistically significant (P<0.02). Restoration of the pH of the blood toward normal by the infusion of bicarbonate during breathing of CO₂ raised the pulmonary arterial pressure. The five eucapnic subjects showed similar changes during CO₂ breathing and exercise, although their base-line values were significantly different. The differences were due, at least in part, to lower Paco₂. This evidence suggests that CO₂ acts on pulmonary arterioles and capillaries that are exposed to alveolar gases to increase the pulmonary vascular impedance.

Key Words: Cardiac output • Acidosis • Pulmonary hypertension • Exercise • Pulmonary function • Cor pulmonale

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