Effects of heat and cold stress on central vascular pressure relationships during orthostasis in humans

Abstract

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...

Compression leggings modestly affect cardiovascular but not cerebrovascular responses to heat and orthostatic stress in young and older adults

“…It is well established that the hyperthermic-induced drop in CVP, MAP and peripheral vascular resistance are further reduced during orthostasis (Wilson et al 2002(Wilson et al , 2007). In the current study, this hyperthermicinduced drop in MAP was evident, even when compression leggings were worn.…”

“…This displacement of blood away from the heart creates a regulatory problem, decreasing central blood volume, ventricular filling pressure, stroke volume and subsequently mean arterial blood pressure (MAP) (Crandall et al 2008). Mean arterial pressure can be maintained by increasing heart rate (HR) and myocardial contractility (and thus, Á Q), increasing peripheral vascular resistance, and limiting venous pooling (Wilson et al 2007;Crandall et al 2008). However, sustaining a higher HR under prolonged stress increases the risk of cardiac events, particularly in the elderly (Donaldson et al 2003).…”

Left ventricular systolic and diastolic function during tilt-table positioning and passive heat stress in humans

“…tilt table; systolic function; left ventricle WHOLE BODY PASSIVE HEAT STRESS results in multiple cardiovascular and neural adjustments, including increases in cardiac output (14,17,29), cutaneous vascular conductance (2, 5), splanchnic and renal sympathetic vasoconstriction (15,26,28), and muscle sympathetic nerve activity (6,19). These responses occur in a coordinated effort to redistribute cardiac output to the cutaneous circulation, limit the reduction in blood pressure, and protect against syncope.In the supine heat-stressed individual, left ventricular (LV) end-diastolic volume is significantly reduced compared with normothermic conditions (17,18,34), along with reductions in central blood volume (5) and cardiac filling pressures (3,27,34,37). Despite this significant reduction in preload, stroke volume (SV) is maintained during passive heating (14,15,17,18,23,37), secondary to increased ventricular contractility (2,5,17,18) and ventricular diastolic suction (17, 18).…”

“…In the supine heat-stressed individual, left ventricular (LV) end-diastolic volume is significantly reduced compared with normothermic conditions (17,18,34), along with reductions in central blood volume (5) and cardiac filling pressures (3,27,34,37). Despite this significant reduction in preload, stroke volume (SV) is maintained during passive heating (14,15,17,18,23,37), secondary to increased ventricular contractility (2,5,17,18) and ventricular diastolic suction (17, 18).…”

Influences of Skin and Core Temperature on Cardiovascular Responses during Exercise

“…Additionally, in resting humans Q increases substantially during passive heating, and can approach values upwards of 13 L/min with most of the increase above resting values going to the skin [67]. The rise in Q during passive heating is accomplished primarily by increasing HR; however, it is interesting to note that SV is typically maintained or slightly elevated in these conditions [15,46,69,88]. SBF is influenced not only by temperature, but also by blood pressure.…”