• M C Stock, J B Downs, R K Betts, D A Frolicher, M B Howie, and R D Tallman.
• Department of Anesthesiology, College of Medicine, Ohio State University, Columbus.
• Am. Rev. Respir. Dis. 1988 Apr 1; 137 (4): 790-5.

AbstractAcute lung injury causes a restrictive pulmonary defect, decreases lung compliance, and increases the work of breathing. We wished to determine the oxygen cost of the increased elastic work of breathing associated with acute lung injury. Extracorporeal venous circulation with a membrane lung was used to extract CO2 and to induce apnea in 14 anesthetized pigs. Data were collected during 4 experimental states: during spontaneous ventilation and apnea when the animals' lungs were normal, and after acute lung injury developed because of oleic acid administration. Acute lung injury decreased lung compliance from 101 +/- 79 (mean +/- SD) to 52 +/- 25 ml/cm H2O (p less than 0.04), and increased the elastic work of breathing from 700 +/- 590 to 1,060 +/- 630 ml.cm H2O (p = 0.01). During spontaneous ventilation, the increases in total O2 consumption and the O2 cost of breathing caused by acute lung injury were sufficiently small as to be undetectable, and, therefore, less than 3 to 4% of basal O2 consumption despite markedly increased elastic work and ventilatory power requirements. The increase in O2 consumption imposed by acute lung injury was small enough (less than 3 to 4% of total O2 consumption) that it appears to be clinically insignificant.

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