The Frank-Starling 'law of the heart' is implicated in certain types of orthostatic intolerance in humans. Environmental conditions have the capacity to modulate orthostatic tolerance, where heat stress decreases and cooling increases orthostatic tolerance. The objective of this project was to test the hypothesis that heat stress augments and cooling attenuates orthostatic-induced decreases in stroke volume (SV) via altering the operating position on a Frank-Starling curve. Pulmonary artery catheters were placed in 11 subjects for measures of pulmonary capillary wedge pressure (PCWP) and SV (thermodilution derived cardiac output/heart rate). Subjects experienced lower-body negative-pressure (LBNP) of 0, 15 and 30 mmHg during normothermia, skin-surface cooling (decrease in mean skin temperature of 4.3 ± 0.4• C (mean ± s.e.m.) via perfusing 16• C water through a tubed-lined suit), and whole-body heating (increase in blood temperature of 1.0 ± 0.1• C via perfusing 46 • C water through the suit). SV was 123 ± 8, 121 ± 10, 131 ± 7 ml prior to LBNP, during normothermia, skin-surface cooling, and whole-body heating, respectfully (P = 0.20). LBNP of 30 mmHg induced greater decreases in SV during heating (−48.7 ± 6.7 ml) compared to normothermia (−33.2 ± 7.4 ml) and to cooling (−10.3 ± 2.9 ml; all P < 0.05). Relating PCWP to SV indicated that cooling values were located on the flatter portion of a Frank-Starling curve because of attenuated decreases in SV per decrease in PCWP. In contrast, heating values were located on the steeper portion of a Frank-Starling curve because of augmented decreases in SV per decrease in PCWP. These data suggest that a Frank-Starling mechanism may contribute to improvements in orthostatic tolerance during cold stress and orthostatic intolerance during heat stress.

The prone position may prove beneficial in some cases of hypoxemic respiratory failure, even in awake patients, by avoiding mechanical ventilation and ventilator-associated complications.

Central venous pressure (CVP) provides information regarding right ventricular filling pressure, but is often assumed to reflect left ventricular filling pressure. It remains unknown whether this assumption is correct during thermal challenges when CVP is elevated during skin-surface cooling or reduced during whole-body heating. The primary objective of this study was to test the hypothesis that changes in CVP reflect those in left ventricular filling pressure, as expressed by pulmonary capillary wedge pressure (PCWP), during lower-body negative pressure (LBNP) while subjects are normothermic, during skin-surface cooling, and during whole-body heating. In 11 subjects, skin-surface cooling was imposed by perfusing 16• C water through a water-perfused suit worn by each subject, while heat stress was imposed by perfusing 47• C water through the suit sufficient to increase internal temperature 0.95 ± 0.07• C (mean ± S.E.M.). While normothermic, CVP was 6.3 ± 0.2 mmHg and PCWP was 9.5 ± 0.3 mmHg. These pressures increased during skin-surface cooling (7.8 ± 0.2 and 11.1 ± 0.3 mmHg, respectively; P < 0.05) and decreased during whole-body heating (3.6 ± 0.1 and 6.5 ± 0.2 mmHg, respectively; P < 0.05). The decrease in CVP with LBNP was correlated with the reduction in PCWP during normothermia (r = 0.93), skin-surface cooling (r = 0.91), and whole-body heating (r = 0.81; all P < 0.001). When these three thermal conditions were combined, the overall r value between CVP and PCWP was 0.92. These data suggest that in the assessed thermal conditions, CVP appropriately tracks left ventricular filling pressure as indexed by PCWP. The correlation between these values provides confidence for the use of CVP in studies assessing ventricular preload during thermal and combined thermal and orthostatic perturbations. In supine humans, whole-body heating decreases central venous pressure (CVP) 3-5 mmHg (Rowell et al. 1969;Minson et al. 1998;Crandall et al. 1999;Peters et al. 2000), while skin-surface cooling increases CVP ∼2 mmHg (Cui et al. 2005). These thermally induced changes in CVP are informative as they relate to right ventricular filling pressure, but it is unknown whether CVP reflects pulmonary capillary wedge pressure (PCWP), and thus left ventricular filling pressure, during these thermal challenges.Lower body negative pressure (LBNP) provides a means by which graded responses (i.e. decreases in CVP and PCWP) to an orthostatic stress can be evaluated (Levine et al. 1991). Peters et al. (2000) reported that at 10 mmHg and higher levels of LBNP, CVP was not different between normothermic and heat stressed conditions. Cui et al. (2005) observed increases in CVP during cold stress and that subsequent LBNP-induced decreases in CVP were of similar magnitude during both normothermia and skin-surface cooling conditions. In spite of these informative studies, it is unknown whether changes in right ventricular filling pressure, as indexed by CVP, reflect PCWP during combined thermal and orthostatic stress.CVP does not consistently corr...

In healthy supine humans, the heart is provided with a volume that is sufficient to secure a maximal SV without distending the heart. The implication for individualised goal-directed fluid therapy is that when a maximal SV is established for patients, cardiac pre-load is comparable to that of supine healthy subjects.