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Interstitial pulmonary edema accompanying trauma and sepsis is a prime cause of arterial hypoxemia and intrapulmonary shunting (). This hypothesis was tested in 27 patients requiring ventilatory support. Pulmonary extravascular water (PEVW) was measured with the tracers indocyanine green and 131I-antipyrine. Physiologic dead space () was used as an estimate of nonperfused lung, i.e., the volume unavailable to and unmeasurable by tracer methods. Metaraminol infusion abruptly increased from 48.5 to 60.8 percent. PEVW fell from 566 to 219 ml./M.2. Although true lung water was probably unchanged, decreased from 33.9 to 16.4 percent. Isoproterenol produced opposite changes in all parameters. In four hours, furosemide decreased PEVW from 312 to 199 ml./M.2. was unchanged. The data indicate reduction in true lung water but was unaltered. In critically ill patients who died, PEVW = 267 ml./M.2 and = 23.6. With left ventricular failure, PEVW = 274 ml./M.2 but = 16.7. Elevation of the functional residual capacity (FRC) yielded rapid and consistent decreases in . Neither PEVW nor changed. Segmental atelectasis was infrequent by x-ray. Results indicate that shunting is due to perfusion of diffusely collapsed alveolae, most prominent at end-expiration (FRC). Interstitial and intra-alveolar edema, although associated with pulmonary insufficiency, are not primary causes of shunting.
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☆This work was supported by the National Institute of Health, Grant #5-PO1-CM-17366-02-GMP, and the U. S. Army Medical Research and Development Command, Contract DADA17-67-C-7149.
☆☆Presented at the Thirty-fourth Annual Meeting of the Society of University Surgeons, New Orleans, La., Feb. 8–10, 1973.
© 1973 Published by Elsevier Inc.