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Abstract
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.
). 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.To read this article in full you will need to make a payment
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References
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Article info
Footnotes
☆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.
Identification
Copyright
© 1973 Published by Elsevier Inc.
