Effect of posture on pulmonary dead space in man

Abstract

Physiologic dead space was determined in the supine and upright postures by simultaneous sampling and subsequent analysis of arterial blood and expired gas for Pco2. In seven normal men there was invariably a higher dead space in the upright than in the supine position. The difference averaged 83 ml and was statistically significant (S.E. 25 ml and P < 0.01). The ratio of dead space to tidal volume also invariably increased on assuming the upright posture. Evidence is presented for believing that most of the change in physiologic dead space resulted from a change in alveolar dead space. Estimated changes in the ratio of alveolar dead space to alveolar tidal volume suggest that approximately one seventh of the total number of alveoli became nonperfused on changing from the supine to the erect posture. These findings are consistent with bronchospirometric and hemodynamic evidence that the apex of the lung is virtually nonperfused in the resting human subject in the upright posture. Submitted on November 12, 1958

Gas Exchange in the Normal Lung : Experimental studies on the effects of positive end-expiratory pressure and body position

“…They concluded that the regional differences in V/Q ratio were less in all subjects and positions than those found in upright man, indicating that V and Q are generally better matched in the other positions. This is in accordance with observations that the alveolar-arterial O 2 tension differences (A -a)O 2 were smaller in the supine than in upright position (Riley et al, 1959). Since the 1960s distribution of perfusion and ventilation has been explained by the effect of gravity on regional perfusion pressure and regional lung compliance (West and Dollery, 1960).…”

Ventilation.

“…Minute volume and tidal volume can also be divided into separate contributions from the alveoli and from the conducting airways or 'dead-space ': j-E = V~A + V~D j.VT = VA+ VD Normal dead space is about 150 ml and represents 20-30% of tidal volume at rest (Fowler, 1948;Riley, Permutt, Said, Godfrey, Cheng, Howell & Shephard, 1959). It increases only slightly during exercise, when it constitutes a smaller proportion of tidal volume (Jones, McHardy, Naimark & Campbell, 1966).…”

The Effect of Changes in the Pulmonary Vascular Bed Produced by Atropine, Pulmonary Engorgement, and Positive-Pressure Breathing on Diffusing and Mechanical Properties of the Lung*

“…When CL was determined during G-suit inflation, the subjects breathed into a recording spirometer so placed that they were able to observe their respiratory ex- (17,18). Arterial Pco2 and the Pco, of mixed expired gas were determined with a Pco2 electrode system.3 VD(phyS) was determined by the method of Riley and co-workers (19) in seated subjects before and 10 minutes after administration of atropine.…”