• R D Goldfarb, K J Lee, and S W Dziuban.
• Department of Physiology, Albany Medical College, New York 12208.
• Circ. Shock. 1989 Jun 1; 28 (2): 109-19.

AbstractWe 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. One major difference between our studies is the definition of end-systole; we used the time when the ratio of pressure-to-diameter (P/D) in the left ventricle is maximal (P/Dmax), whereas they used the time when the first derivative of pressure is minimal (dP/dtmin). In order to determine if the discrepancy between our conclusions could be explained by the differing definitions of end-systole, data from previous studies were reanalyzed, and the slope of the pressure-diameter relationship at P/Dmax and at dP/dtmin was calculated. Pigs were equipped with instruments to measure left ventricular pressure, short axis diameter, and ECG. Observations during the basal state were obtained 3-7 days after surgery. Chronic endotoxemia was induced by intravenous infusion of S. enteriditis endotoxin via an osmotic minipump at 10 micrograms/kg/hr. During the basal state, the value for the slope of ESPDR at dP/dtmin was lower than the value for the slope of ESPDR at P/Dmax, and there was a good correlation between the two values. During chronic endotoxemia, the slope of ESPDR at dP/dtmin did not change. However, the slope of ESPDR at P/Dmax decreased significantly suggesting that chronic endotoxemia reduced cardiac inotropism. 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.

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