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We have measured the partial pressure of isoflurane simultaneously in inspired gas (PIiso), end-expired gas (PE'iso), mixed-expired gas (PEiso), arterial (Paiso) and mixed venous blood (Pviso) in six patients (aged 57-79 yr) anaesthetized with nitrous oxide, oxygen and isoflurane before surgery and after PE'iso had been stable for at least 15 min. We related these changes to the various indices of pulmonary maldistribution to determine if they were sufficient to explain reported differences between PE'iso and Paiso. Alveolar deadspace dilution of end-expired gas was calculated for carbon dioxide and this dilution factor used to calculate the "ideal" alveolar Piso (PAiso) from the observed inspired and end-expired concentrations. Shunt fraction was measured for oxygen and then used to calculate the partial pressure of isoflurane in the pulmonary end-capillary blood (Pc'iso) from the partial pressure in arterial and mixed venous blood. Mean (SE) values were: PIiso 0.69 (0.05) kPa; PE'iso 0.52 (0.04) kPa; PAiso 0.50 (0.04) kPa; Pc'iso 0.38 (0.04) kPa; Paiso 0.35 (0.03) kPa and Pviso 0.22 (0.02) kPa; Paiso: PE'iso 0.66 (0.02) kPa. The mean "ideal" alveolar to pulmonary end-capillary Piso difference was 0.12 (0.01) kPa and highly significant (P < 0.001). Paiso was substantially less than PE'iso but, for isoflurane, the difference was reasonably constant (range 0.14-0.22 kPa). The difference was attributable in part to the effects of shunt and deadspace, but also a failure of equilibration of isoflurane between the alveolar gas and pulmonary end-capillary blood. It is likely to be different for other anaesthetics. We conclude that, while PE'iso may adequately reflect Paiso for isoflurane, it cannot be assumed that the relation between end-expiratory gas and arterial partial pressures is the same for all anaesthetics.

Rats were exposed to 100% oxygen for up to 60 h to determine early changes in lung permeability leading to the development of pulmonary edema. The time course of development of increased solute flux was assessed by the clearance of 99mTc-labeled diethylenetriamine pentaacetate (99mTc-DTPA) from the lung and the accumulation of 125I-labeled albumin (125I-albumin) in the lung. These end points were related to the development of pulmonary edema by the measurement of the wet-to-dry weight ratio of the lung and the weight of fluid in the pleural cavity. No significant changes occurred until 48 h of hyperoxia, when sharp increases in both indexes of lung permeability and wet-to-dry weight ratio occurred. By 60 h of exposure, pleural effusions had developed. The volume of this effusion was significantly correlated to both 99mTc-DTPA clearance and 125I-albumin flux.

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