Circulatory shock
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We have reported that cardiac inotropism is reduced in various shock states, most recently during chronic endotoxemia (Lee et al.: American Journal of Physiology 254:H324-H330, 1988) [1]. We based this conclusion upon the alterations observed in the slope of the end-systolic pressure-diameter relationship (ESPDR). Recently, Dietrick and Raymond (Dietrick and Raymond: Surgical Infection Society, 7th Annual Meeting, May, 1987, p 83) [2] have reported that the slope of the end-systolic pressure-wall thickness relationship was augmented in the early stages of sepsis and depressed immediately prior to expiration. ⋯ This conclusion is supported by the findings that chronic endotoxemia reduced steady-state values of percentage diameter-shortening (an estimate of ejection fraction) and stable stroke work at significantly higher end-diastolic diameter. These data indicate that it is possible to calculate differing slopes of ESPDR from the same observations dependent upon the time during the cardiac cycle chosen as end-systole. More importantly, these data suggest that during chronic endotoxemia, ventricular relaxation dynamics may change so that postsystolic shortening becomes more prominent and therefore higher values for the slope of ESPDR using pressure and diameter values at dP/dtmin can be calculated.