Gas phase diffusion does not limit lung volatile anesthetic uptake rate.

Abstract

Inefficiency of lung gas exchange during general anesthesia is reflected in alveolar (end tidal) to arterial (ET-arterial) partial pressure gradients for inhaled gases resulting in an increase in alveolar deadspace. Ventilation-perfusion mismatch is the main contributor to this, but it is unclear what contribution arises from diffusion limitation in the gas phase down the respiratory tree (longtitudinal stratification) or at the alveolar-capillary barrier, especially for gases of high molecular weight (MW) such as volatile anesthetics. The contribution of longtitudinal stratification was examined by comparison of ET-arterial partial pressure gradients for two inhaled gases with similar blood solubility but different molecular weights, desflurane and nitrous oxide (N2O) administered together at 2-3% and 10-15% inspired concentration (FIG) respectively, in seventeen anesthetized ventilated patients undergoing cardiac surgery before cardiopulmonary-bypass. Simultaneous measurements were done of tidal gas concentrations, and arterial and mixed venous blood partial pressures by headspace equilibration, and gas uptake rate calculated using the direct Fick method using thermodilution cardiac output measurement. Adjustment for differences between the two gases in FIG and in lung uptake rate (VG) was made on mass balance principles. A 20% larger ET-arterial partial pressure gradient relative to inspired concentration (PETG-PaG)/FIG for desflurane than for N2O was hypothesized as physiologically significant. Mean (standard deviation) measured (PETG-PaG)/FIG for desflurane was significantly smaller than that for N2O (0.86 (0.37) versus 1.65 (0.58) mmHg, p<0.0001), as was alveolar deadspace for desflurane. After adjustment for the different VG of the two gases, the adjusted (PETG-PaG)/FIG for desflurane remained less than the 20% threshold above that for N2O (1.62 (0.61) versus 1.98 (0.69) mmHg, p=0.028). No evidence was found in measured end-tidal to arterial partial pressure gradients and alveolar deadspace to support a clinically significant additional diffusion limitation to lung uptake of desflurane relative to N2O.