Society of University Surgeons| Volume 74, ISSUE 2, P300-306, August 1973

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The independence of pulmonary shunting and pulmonary edema

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      Interstitial pulmonary edema accompanying trauma and sepsis is a prime cause of arterial hypoxemia and intrapulmonary shunting (Math Eq). 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 (Math Eq) was used as an estimate of nonperfused lung, i.e., the volume unavailable to and unmeasurable by tracer methods. Metaraminol infusion abruptly increased Math Eq from 48.5 to 60.8 percent. PEVW fell from 566 to 219 ml./M.2. Although true lung water was probably unchanged, Math Eq 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. Math Eq was unchanged. The data indicate reduction in true lung water but Math Eq was unaltered. In critically ill patients who died, PEVW = 267 ml./M.2 and Math Eq = 23.6. With left ventricular failure, PEVW = 274 ml./M.2 but Math Eq = 16.7. Elevation of the functional residual capacity (FRC) yielded rapid and consistent decreases in Math Eq. Neither PEVW nor Math Eq 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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