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End-expiratory thoracic cavity volume (Vthx) was measured in eight volunteers lying supine by three-dimensional X-ray computed tomography using the Dynamic Spatial Reconstructor. Untrapped end-expiratory pulmonary gas volume at functional residual capacity (FRC) was determined by nitrogen clearance. Both measurements were done before and after induction of anesthesia-paralysis. After induction of anesthesia-paralysis, Vthx and FRC were consistently and significantly (P less than 0.01) reduced by 0.28 +/- 0.22 (SD) and 0.59 +/- 0.24 liter, respectively. The reduction of FRC was larger than the reduction of Vthx (delta Vthx) in six of the eight subjects, a finding suggesting that intrathoracic fluid (blood) plus trapped gas volume (Vtt) increased. Changes in Vthx were partitioned into volume changes from the thoracic rib cage (delta Vrc) and from shape and/or position changes of the diaphragm (delta Vdi). delta Vrc contributed significantly (0.17 +/- 0.15 liter, P less than 0.02) to delta Vthx, whereas delta Vdi contributed only in four of the eight subjects. We conclude that delta Vrc, delta Vdi, and delta Vtt contribute to the reduction of FRC after induction of anesthesia-paralysis in humans; the relative contribution of them varies among subjects.

Distributions of ventilation and perfusion relative to Va/Q were determined in seven young healthy volunteers (24-33 yr) while they were either in the supine or right lateral decubitus position. The subjects were studied first awake and then while anesthetized-paralyzed and breathing 30% oxygen and again while breathing 100% oxygen. In the awake state, no statistically significant differences were observed in the distribution of ventilation and perfusion relative to Va/Q between the supine and right lateral decubitus positions or on changing the inspired oxygen concentrations. After induction of anesthesia-paralysis, Va/Q mismatching increased significantly but only small right-to-left intrapulmonary shunts developed. Ventilating the lungs with 100% oxygen further increased the dispersion of blood flow distribution during anesthesia-paralysis; lung units with low Va/Q or right-to-left intrapulmonary shunts (or both) developed. With induction of anesthesia-paralysis and intubation of the trachea, the anatomic dead space was decreased and the alveolar dead space increased.