Journal of Applied Physiology, Vol 64, Issue 5 1908-1915, Copyright © 1988 by American Physiological Society
Diaphragmatic energetics and blood flow during pulmonary edema and hypotension
F. S. Rutledge, S. N. Hussain, C. Roussos and S. Magder
Royal Victoria Hospital, Department of Medicine, Montreal, Quebec, Canada.
We studied the role of O2 supply and demand factors for producing
diaphragmatic failure in a canine model of cardiogenic shock with pulmonary
edema. We produced pulmonary edema with oleic acid and then hypotension
with cardiac tamponade and followed the animals until respiratory failure
began, which was defined by a 50% fall in frequency of breathing and
diaphragmatic pressure-time index (PTI; cmH2O.s-1.min-1) with no decrease
in the diaphragmatic electromyogram. Regional blood flows were measured
with radiolabeled microspheres. Diaphragmatic O2 consumption (VO2 di)
(ml.min-1.100 g-1) was determined from the diaphragmatic blood flow (Qdi)
and the arterial and phrenic venous O2 contents. With oleic acid-induced
pulmonary edema, PTI Qdi, and VO2 di increased from control of 101.7 +/-
31.7, 17 +/- 1.8, and 0.81 +/- 0.11, respectively, to 187.2 +/- 27.6, 42.2
+/- 7.2, and 3.32 +/- 0.35 (P less than 0.05). With tamponade, PTI did not
change (186.7 +/- 60.0), whereas VO2 di increased further to 3.98 +/- 0.98
(P less than 0.05) due to increased O2 extraction and no significant change
in Qdi (32.8 +/- 4.0). As fatigue developed, VO2 di decreased to 2.30 +/-
0.23 due to the combined effects of small declines in Qdi and the arterial
O2 content but remained higher than control even though the energy demands
returned to control values. In conclusion, when cardiogenic shock is added
to pulmonary edema VO2 di and energy output do not increase further and
eventually fall.
