Inefficiency of lung gas exchange during general anesthesia is reflected in alveolar (end-tidal) to arterial (end-tidal–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 (longitudinal stratification) or at the alveolar–capillary barrier, especially for gases of high molecular weight such as volatile anesthetics.
The contribution of longitudinal stratification was examined by comparison of end-tidal–arterial partial pressure gradients for two inhaled gases with similar blood solubility but different molecular weights: desflurane and nitrous oxide, administered together at 2 to 3% and 10 to 15% inspired concentration (FiG), respectively, in 17 anesthetized ventilated patients undergoing cardiac surgery before cardiopulmonary bypass. Simultaneous measurements were done of tidal gas concentrations, of arterial and mixed venous blood partial pressures by headspace equilibration, and of 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 end-tidal–arterial partial pressure gradient relative to inspired concentration (PetG – PaG)/FiG for desflurane than for N2O was hypothesized as physiologically significant.
Mean (SD) measured (PetG – PaG)/FiG for desflurane was significantly smaller than that for N2O (0.86 [0.37] vs. 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] vs. 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 nitrous oxide.
Inefficiency of gas uptake and elimination in the lung is reflected by development of partial pressure gradients between expired alveolar (end-tidal) gas and arterial blood
These arise mainly from variation of alveolar ventilation–perfusion ratios across the lung, but longitudinal partial pressure gradients down the respiratory tree due to diffusion limitation may possibly also contribute, especially for larger molecules such as volatile anesthetics
The hypothesis that the end-tidal to arterial partial pressure gradient for desflurane would be larger than that for nitrous oxide was tested in 17 patients inhaling a mixture of desflurane and nitrous oxide, which have similar effective blood–gas partition coefficients but a fourfold difference in molecular weight
Raw measurements of end-tidal to arterial partial pressure gradients, relative to inspired concentration, were smaller for desflurane
After adjustment for the higher rate of lung gas uptake for desflurane at the time of measurement, no difference was found in end-tidal to arterial partial pressure gradients