Pulmonary Vascular Response to Ventilation Hypercapnia in Man

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Abstract
In the 1st study on 44 patients with little or no airway obstruction and 20 normal men, 5% CO2 breathing produced: significant rise in pulmonary artery pressure (PAP); no significant change in cardiac output; rise in pulmonary vascular resistance; rise in brachial artery pressure (BAP) and no change in wedge pressure (WP). The rise in PAP was more pronounced after 2 min of 10% CO2 breathing in 12 bronchitics. The 2nd study was carried out in 39 bronchitics and 22 normals while breathing 10% CO2 for 1 min and showed that pulmonary vascular response was independent of systemic vascular response, in that BAP rose later and came back earlier to original level during CO2 breathing. In the 3rd study on 26 severe bronchitics and 15 normals, the observed rise in PAP during 10% CO2 breathing was independent of H-ion concentration in the blood since PAP continued to rise even when pH was maintained at air breathing level by i.v. injection of 130 mEq of sodium bicarbonate in 250 cm3 of 5% glucose solution. There was minimal rise in cardiac output, no rise in WP, while PAP and pulmonary vascular resistance rose significantly during ventilation hypercapnia. The responses were pronounced compared with those observed in the 1st study with 5% CO2. The responses might be due to direct action of CO2 on muscular pulmonary arteries.