THE CARDIAC OUTPUT AND VASCULAR RESPONSE TO TRAUMA.
Rept. no. 8 (Final), 1 Jun 67-31 May 68,
HARVARD MEDICAL SCHOOL BOSTON MASS
Pagination or Media Count:
Clinical observations and animal experiments have delineated the peripheral and pulmonary circulatory alterations encountered in traumatic, postshock, and septic states. Measurements of the caloric expenditure of energy were found not to correlate with the high cardiac outputs and reduced peripheral vascular resistances. The possibilities must be considered of either arteriovenous shunts or of generalized arteriolar dilation secondary to interference with normal oxygen usage and cellular metabolism. A method employing a small dialysis unit was devised to record continuously the dilution curves of beta emitting isotopes injected into the circulation. Employing C 14 urea a reduction of rapidly equilibrated extracellular water was demonstrated after severe shock and during peritonitis. Alterations in cellular membrane diffusion values are also present, which may be responsible for, or secondary to insufficient cellular energy production. A nonspecific inflammatory response of the lung following shock trauma, or sepsis was demonstrated and confirmed experimentally employing induced peritonitis or hypovolemic shock. In the early stages a fibrin containing interstitial edema with a mononuclear leukocyte infiltration is reflected physiologically by mild hypoxemia and uncompensated respiratory alkalosis. Large quantities of stainable fat were present within the mononuclear macrophages. In 10 to 60 of the animal series bacteria were not culturable from lung parenchyma. Focal alveolar collapse is followed subsequently by atelectasis and classical bronchopneumonia. Author
- Medicine and Medical Research