Thirty-three patients with severe head trauma were studied to determine whether the use of positive end-expiratory pressure (PEEP) would cause an increase in intracranial pressure (ICP). Changes in ICP induced by PEEP were then correlated with a panel of physiological variables to try to explain these changes. Mean ICP increased from 13.2 +/- 7.7 mm Hg (+/- standard deviation) to 14.5 +/- 7.5 mm Hg (p less than 0.005) due to 10 cm H2O PEEP, but the eight patients with elevated baseline ICP experienced no significant increase. Cardiac output and venous admixture (Qs/Qt) declined significantly, while central venous pressure, peak inspiratory pressure, functional residual capacity, and arterial pCO2 increased significantly due to PEEP. Blood pressure and cerebral perfusion pressure were unchanged. The change in ICP due to PEEP correlated significantly with a combination of cardiac output, peak inspiratory pressure, Qs/Qt, and changes in blood pressure and arterial pCO2 due to PEEP, indicating that the effect of PEEP on ICP could be largely explained by its effect on hemodynamic and respiratory variables. No patient deteriorated clinically due to PEEP. It is concluded that 10 cm H2O PEEP increases ICP slightly via its effect on other physiological variables, but that this small increase in ICP is clinically inconsequential.

Among 48 pieces of paired frog skins of Rana pipiens in Ringer's solution, 10 pieces showed a strictly monotone decrease in the short circuit current (SCC) following ouabain treatment (10(-4) M). In 9 cases a transient attenuation, and in 27 cases a distinct wave in the ebb of the SCC, was seen. In 2 instances, two waves were seen. Associated with the not-monotone events was a transient rise in electrical skin conductance. The reasons for these mixed skin responses are unknown. One possible reason is considered here: Early during the ouabain action, some of the Na+ entering from the mucosal side is trapped in the skin by electroneutral processes, in keeping with the already known fact that ultimately cellular KCl is partly replaced by NaCl. Computer assisted model studies show how monotone, and not-monotone "transepithelial" net Na+ flux curves can be generated. Essential conditions for the generation of not-monotone Na+ flux curves are: 1. Presence of two distinct "cellular", active Na+ pools in the model. 2. Presence of a loop pathway in which a principal "transepithelial Na+ transport compartment", and a constituent "Na+/K+ maintenance compartment", are connected to each other and to the "extracellular" compartment. The model, then, predicts under which kinetic conditions monotone and not-monotone transepithelial Na+ flux curves will be seen.

Eight infants with intractable respiratory failure were treated with extracorporeal membrane oxygenation. Intractable respiratory failure was defined as alveolar-arterial oxygen gradient of more than 620 torr for six to 12 hours that did not respond to hyperventilation and the use of tolazoline. Infants with overt sepsis, CNS damage, or other debilitating conditions were not considered for extracorporeal membrane oxygenation. Six of the eight infants survived after a mean extracorporeal membrane oxygenation time of 164 hours. Five of the six survivors were normal neurologically and developmentally when examined at 1 year of age.

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