Although left ventricular (LV) junction appears altered by severe hemorrhagic shock (HS), the mechanisms of this dysfunction have been difficult to characterize. Depression in the LV function curve could be caused by altered diastolic or systolic function. It has been difficult to assess the systolic function, but the use of the rate and load independent index of contractility, Emax (the slope of the end-systolic pressure-dimension relationship), offers a new approach to the quantification of systolic mechanical performance. Emax and the LV diastolic pressure-strain relationship were measured in 15 chronically instrumented dogs by sonomicrometric and micromanometric techniques. Gradual LV unloading was obtained from transient vena caval occlusion. After control study, each dog underwent 2 hours of HS (mean aortic pressure 40 mm Hg), followed by reinfusion of all shed blood. Upon reinfusion, Emax was not decreased; however, all dogs had a significant decrease in LV compliance. During the next 4 days, the LV compliance of the eight survivors progressively returned toward control, while Emax remained stable. All seven nonsurvivors demonstrated progressive loss of LV compliance, and Emax was significantly decreased prior to death. Cardiac contractility appeared improved immediately after shock, but a consistent decrease in compliance was observed. Reversal of abnormal diastolic function was demonstrated in all survivors and progressive depression in all nonsurvivors. Depression in systolic function was observed only in nonsurvivors immediately prior to death.
|Original language||English (US)|
|Number of pages||9|
|State||Published - Aug 1983|
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