Dueck R, Prutow R, Richman D
Department of Anesthesiology, University of California, San Diego.
Anesthesiology. 1991 Jun;74(6):1044-51. doi: 10.1097/00000542-199106000-00012.
We examined the interaction of viral pneumonitis with the respiratory effects of halothane/N2O anesthesia in six tracheostomized sheep. Ventilation-perfusion (VA/Q) distribution, pulmonary artery pressure (PAP), metabolic rate (VO2), and functional residual capacity (FRC) measurements were compared in awake and anesthetized animals before and 1 week after inoculation by tracheal instillation of ovine parainfluenza type-3 (PI-3) virus. Awake shunt (VA/Q less than 0.005) was 0.6 +/- 0.4% (+/- standard deviation [SD]) before, versus 3.9 +/- 2.0% after PI-3 infection (P less than 0.05). Awake arterial O2 tension (PaO2) was 139.9 +/- 14.0 mmHg before and 114.5 +/- 8.7 mmHg after infection (P less than 0.05). Mean PAP increased from 6.0 +/- 1.9 mmHg before to 11.5 +/- 1.6 mmHg after infection (P less than 0.05). Anesthesia shunt increased to 5.7 +/- 2.3% before and 11.2 +/- 3.4% after PI-3 (P less than 0.05 for the change from awake, and P less than 0.05 for a PI-3 anesthesia shunt difference). PAP was not significantly different from awake, either before or after infection. Anesthesia also produced an average 14.8 +/- 3.8% FRC reduction before and 17.4 +/- 6.4% reduction after infection (P less than 0.05 for FRC reduction with anesthesia, not significantly different for PI-3). Three of the six sheep developed shunt at higher FRCs after infection, both awake and during anesthesia; however, the average slope of the shunt/FRC response to anesthesia was unchanged, suggesting that this was not a neurogenic form of auto-PEEP. We therefore conclude that viral infection significantly enhanced the pulmonary effects of anesthesia.
