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Several factors probably have some role in determining the volume of the effectively ventilated pulmonary capillary bed, including pulmonary blood flow, pulmonary vascular pressures, pulmonary blood volume, alveolar and blood gas tensions, and mechanical effects of ventilation.Others have found that atropine sulfate, 2.0 mg iv, increases cardiac output (1, 2), decreases central venous pressure (1, 2), and affects the distribution of the blood volume as shown by plethysmographic study of extremity venous volume (3). This drug, then, provides an unusual rearrangement of some of the determinants of pulmonary capillary function and, for the present study, was used either alone or in combination with positivepressure breathing or pulmonary vascular engorgement produced by G-suit inflation.This study was carried out to provide further information concerning the interaction of cardiac output, pulmonary vascular pressure, and pulmonary blood volume as determinants of the volume of effectively ventilated capillaries by de-termining the effects of changes in the pulmonary vascular bed produced by atropine, pulmonary engorgement, and positive-pressure breathing on the diffusing and mechanical properties of the lung.

Using a specially designed needle system, pressures were recorded directly from the pleural space in seated normal men. Respiratory pressure changes (ΔP) measured simultaneously from different pleural sites and the esophagus are not the same but become so after a large pneumothorax is produced. Since esophageal ΔP is little affected by a pneumothorax of 2–300 ml, it is suggested that, in the absence of pneumothorax, esophageal ΔP represents a better measure of the over-all elastic behavior of the lung than any local pleural ΔP. In the absence of pneumothorax, ΔP is less in the upper than in the lower chest. This may be an expression of a gradient either of distribution of ventilation or of elastic forces opposing expansion of the lung. In three of four subjects, end expiratory pressure was more positive in the low chest than in the high chest. Acute central vascular engorgement (pressure suit inflation) caused similar changes in esophageal and intrapleural ΔP. These observations confirm the previously observed decrease in lung compliance during acute central vascular engorgement and provide evidence of local differences in respiratory pleural pressure change in man. Submitted on August 20, 1962

Measured by a variety of techniques, the overall ventilation-perfusion relationship of the normal human lung is different in supine and upright positions, and in the upright position, the upper regions of the lung are relatively poorly perfused (1-4). Similarly, pulmonary diffusing capacity (DL) is reduced when normal subjects change from supine to upright positions (5, 6); in the upright position, carbon monoxide absorption is greater in the lower portions of the lung than in the upper portions (7). These differences are probably related to a gravity dependent gradient of perfusion and capillary filling caused by the inability of the normally low pulmonary arterial pressure to provide uniformly adequate perfusion against the hydrostatic gradient that must be present in the pulmonary vascular bed of normal adult humans in an upright position (2,8).The present investigation was undertaken to determine a) whether the normal postural changes in physiologic dead space and diffusing capacity are present in patients in whom the pulmonary vascular pressure should be great enough to insure perfusion of the entire lung in the upright position and b) whether an acute increase in pulmonary vascular pressures affects the arterialalveolar CO2 gradient and alveolar dead space of normal men in an upright position. MethodsThirty-four adult patients having clinical cardiac catheterizations and 20 trained normal subj ects were * Submitted for publication July 8, 1963; accepted September 19, 1963. This study was supported in part by research grants H-6228 and H-4080 from the National Heart Institute, U. S. Public Health Service, Bethesda, Md., and in part by U. S. Air Force contract 33(616) 8378.t Fellow, Indiana Heart Association. used in this study. The patients' surface areas, pulmonary vascular pressures, and diagnoses are listed in Table I. Those patients with mean pulmonary arterial pressure greater than 20 mm Hg are grouped separately and are considered to have pulmonary hypertension. With few exceptions, all patients with pulmonary hypertension had mitral valvular disease. The normal subjects were healthy men whose ages were between 22 and 36 and whose mean surface area was 1.89 ± 0.4 in'. Their pulmonary vascular pressures were assumed to be normal.Tilting was performed on a motor-driven tilt table. Measurements were made in random sequence; subjects were flat or tilted 600 with their heads up. The change in lung volume that occurred during tilting was measured with a bag-in-box spirometer system, in which a steady base line is obtained during spontaneous breathing before and after a change in position, the recorded difference representing the difference in lung volume in the two positions. Measurements of physiologic dead space were begun 15 to 30 seconds after the subjects reached the 600 position. During a different tilt, diffusing capacity was measured 1 minute after reaching the 60°p osition. The effect of acute pulmonary vascular engorgement on alveolar dead space and arterial-alveolar Pco, gradient was studied in...

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