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AJP - Heart and Circulatory Physiology, Vol 260, Issue 3 702-H712, Copyright © 1991 by American Physiological Society
ARTICLES |
K. R. Walley and D. J. Cooper
Pulmonary Research Laboratory, St. Paul's Hospital, University of British Columbia, Vancouver, Canada.
To determine the causes of impaired left ventricular function during hypovolemic shock we measured diastolic and end-systolic pressure-volume relationships and hemodynamics. Left ventricular pressure (Millar catheter) and volume (3 ultrasonic crystal pairs) were measured in six open-chest, chloralose-morphine anesthetized, juvenile pigs. After baseline measurements, the pigs were bled and maintained at a mean aortic pressure of 50 cmH2O for 7 +/- 1 h. After resuscitation with all shed blood, left ventricular function was markedly impaired as indicated by increased end-diastolic pressure (20.3 vs. 8.7 cmH2O at baseline, P less than 0.05), decreased aortic pressure (36% of baseline, P less than 0.01), and decreased stroke volume (50% of baseline, P less than 0.01). Systolic contractility was increased (P less than 0.05), but diastolic compliance was greatly reduced due to decreased diastolic maximum (52% of baseline, P less than 0.01) and equilibrium volumes (57% of baseline, P less than 0.01). We conclude that impaired left ventricular function during hypovolemic shock is due entirely to increased diastolic stiffness. These results can theoretically be accounted for by a 20% reduction in myocardial muscle length with no change in muscle stress-strain characteristics. This may be the physiological expression of morphologically observed myocardial "zonal lesions" of hypovolemic shock.
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