Acute volume infusion preserves left ventricular end diastolic volume during combined heat and simulated hemorrhage

Heat stress compromises blood pressure (BP) control during a simulated hemorrhagic challenge, while acute volume loading attenuates this response. This study tested the hypothesis that the mechanism of preserved BP control during heat stress + volume loading is, in part, through preservation of left ventricular end diastolic volume (LVEDV). LVEDV was measured in nine subjects during normothermia (NT), after an increase in pulmonary artery blood temperature of 1.3 ± 0.2 °C (HS; P < 0.05), and after volume infusion (HS + Inf). In each condition, supine LVEDV was assessed via echocardiography, by the Simpson biplane method, prior to and during simulated hemorrhage, evoked via 30 mmHg lower body negative pressure (LBNP). LVEDV was reduced by HS (NT: 148 ± 26 ml, HS: 126 ± 31 ml; P < 0.05), however, this fall was attenuated by HS + Inf (HS + Inf: 133 ± 25 ml; P > 0.05 relative to NT and HS). During simulated hemorrhage, the reductions in LVEDV were similar between NT (45 ± 20 ml) and HS (52± 20 ml), whereas the reduction in LVEDV after volume infusion (22 ± 22 ml) was attenuated relative to NT and HS ( P < 0.05). Importantly, infusion resulted in an LVEDV during LBNP that was significantly elevated (111 ± 26 ml) relative to HS alone (74 ± 25 ml). Improved control of BP following volume infusion during HS occurs in part by attenuating the reduction in LVEDV to a simulated hemorrhagic challenge. Supported by NIH Grant NIH‐HL61388 & HL84072