Canine V̇A/Q̇ Distribution Responses to Inhalation Anesthesia and Mechanical Ventilation

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Abstract
The effects of anesthesia produced by halothane (0.7-1.5% end-tidal concentration) vaporized in O2 (21%), balance N2O on distribution of ventilation-perfusion (.ovrhdot.VA/.ovrhdot.Q) ratios, and pulmonary gas exchange were studied in 5 healthy mongrel dogs during both spontaneous (SV) and mechanical (MV) ventilation. Awake control studies (via chronic tracheostomy) with room air breathing in the left or right lateral decubitus position demonstrated normal values for arterial blood P[partial pressure]O2 (98.1 .+-. 4.5 torr, mean .+-. SD) and PCO2 (37.1 .+-. 3.8 torr). Representative distributions derived from multiple tracer inert gas analysis demonstrated minimal or no areas of very low (0.005 < .ovrhdot.VA/.ovrhdot.Q < 0.1) or very high (10.0 < .ovrhdot.VA/.ovrhdot.Q < 100.0) .ovrhdot.VA/.ovrhdot.Q ratios. Shunt (.ovrhdot.VA/.ovrhdot.Q < 0.005) was 0.2 .+-. 0.3% of cardiac output and dead space (.ovrhdot.VA/.ovrhdot.Q > 100.0) was 40.3 .+-. 4.3% of minute ventilation. Studies during anesthesia in the same body position showed no significant development of low .ovrhdot.VA/.ovrhdot.Q areas or shunt. The dispersion of the distribution of blood flow with respect to .ovrhdot.VA/.ovrhdot.Q ratios (represented by SD calculated on a logarithmic scale, log SD) increased from 0.351 .+-. 0.132 awake to 0.449 .+-. 0.033 during anesthesia with SV, and 0.609 .+-. 0.147 with MV. Anesthesia consistently produced very high .ovrhdot.VA/.ovrhdot.Q areas, increased dead space ventilation, or both. As high .ovrhdot.VA/.ovrhdot.Q areas were seen only at the upper extremes (near .ovrhdot.VA/.ovrhdot.Q = 100), they were effectively similar to dead space. Dead space increased to 62.2 .+-. 11.1% of minute ventilation for SV, and 55.2 .+-. 7.0% for MV. This difference was due to smaller tidal volumes during SV. Linear regression of dead space (plus high .ovrhdot.VA/.ovrhdot.Q area) ventilation with respect to tidal volume showed r = -0.777 for SV, and r = -0.693 for MV. In contrast, .ovrhdot.VA/.ovrhdot.Q inequality (log SD blood flow) in the intermediate range (0.1 < .ovrhdot.VA/.ovrhdot.Q < 10.0) showed a positive correlation with tidal volume during anesthesia MV, r = 0.919, but not for awake or anesthesia SV conditions. Arterial PO2 values increased significantly during anesthesia, to 114 .+-. 12.4 torr for SV, and 112 .+-. 7.8 torr for MV, P < 0.005 for both, due reduced O2 consumption rate, r = -0.586, P < 0.01. The .ovrhdot.VA/.ovrhdot.Q inequality in the intermediate range may be produced by altered chest cage and diaphragm motion. In dogs with healthy lungs, this mechanism did not impair arterial oxygenation. Areas of very high .ovrhdot.VA/.ovrhdot.Q and increased dead space ventilation were probably due to redistribution of pulmonary blood flow leading to the presence of essentially unperfused but ventilated lung regions. This may be induced through a pharmacologic mechanism of 1 of the inhalation anesthetic agents, most likely halothane.