Beneficial effects of elevating cardiac preload on left-ventricular diastolic function and volume during heat stress: implications toward tolerance during a hemorrhagic insult

Abstract

Volume loading normalizes tolerance to a simulated hemorrhagic challenge in heat-stressed individuals, relative to when these individuals are thermoneutral. The mechanism(s) by which this occurs is unknown. This project tested two unique hypotheses; that is, the elevation of central blood volume via volume loading while heat stressed would 1) increase indices of left ventricular diastolic function, and 2) preserve left ventricular end-diastolic volume (LVEDV) during a subsequent simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Indices of left ventricular diastolic function were evaluated in nine subjects during the following conditions: thermoneutral, heat stress, and heat stress after acute volume loading sufficient to return ventricular filling pressures toward thermoneutral levels. LVEDV was also measured in these subjects during the aforementioned conditions prior to and during a simulated hemorrhagic challenge. Heat stress did not change indices of diastolic function. Subsequent volume infusion elevated indices of diastolic function, specifically early diastolic mitral annular tissue velocity (E') and early diastolic propagation velocity (E) relative to both thermoneutral and heat stress conditions (P < 0.05 for both). Heat stress reduced LVEDV (P < 0.05), while volume infusion returned LVEDV to thermoneutral levels. The reduction in LVEDV to LBNP was similar between thermoneutral and heat stress conditions, whereas the reduction after volume infusion was attenuated relative to both conditions (P < 0.05). Absolute LVEDV during LBNP after volume loading was appreciably greater relative to the same level of LBNP during heat stress alone. Thus, rapid volume infusion during heat stress increased indices of left ventricular diastolic function and attenuated the reduction in LVEDV during LBNP, both of which may serve as mechanisms by which volume loading improves tolerance to a combined hyperthermic and hemorrhagic challenge.

Keywords: hyperthermia; ventricular filling pressure; ventricular volume.

Fig. 1.

Left ventricular end diastolic volumes (LVEDV) at baseline and at 30 mmHg lower body negative pressure (LBNP) during the three conditions: normothermia, heat stress, and heat stress + volume infusion. Heat stress reduced LVEDV, while volume infusion increased LVEDV, such that it was not different from thermoneutral conditions. LBNP reduced LVEDV in all thermal conditions (P < 0.05), but the magnitude of this reduction was attenuated after volume infusion relative to both thermoneutral and heat stress conditions. †Significantly different relative to the respective heat stress condition (P < 0.05). ¥Significantly different, LVEDV lower relative to respective value prior to LBNP (P < 0.05). ‡Significantly different; magnitude of reduction in LVEDV during LBNP was less relative to reductions in this variable during normothermia (P < 0.05) and heat stress conditions (P < 0.01).