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. 2007 Sep 27;585(Pt 1):279–285. doi: 10.1113/jphysiol.2007.137901

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

T E Wilson 1, C Tollund 2, C C Yoshiga 2,3, E A Dawson 2,3, P Nissen 2, N H Secher 2,3, C G Crandall 4,5
PMCID: PMC2375461  PMID: 17901119

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 correlate with other central vascular pressures, mixed venous oxygenation or indices of central blood volume in healthy individuals and those with clinical conditions (Perko et al. 1994; van Lieshout et al. 2003; Magder 2005; Reinhart & Bloos, 2005). Yet, Fu et al. (2004) observed similar reductions in CVP and PCWP during LBNP in normothermic men and women. This latter finding indicates that at least while healthy young subjects are normothermic, CVP appropriately tracks PCWP. However, this relationship between CVP and PCWP can be uncoupled by environmental conditions (e.g. hypoxia) and anaesthetics (e.g. isoflurane) partially mediated through the autonomic nervous system (Heerdt et al. 1998; Kerbaul et al. 2004; Huez et al. 2005). Since thermal stress is a potent autonomic stimulant (Rowell 1990) and its effects on the pulmonary vasculature are largely unknown (Johnson et al. 1996), the effects of differing thermal conditions on the relationships between these vascular pressures need to be evaluated prior to CVP being used as a surrogate for PCWP. Accordingly, this project tests the hypothesis that during an orthostatic stress induced by LBNP, CVP tracks PCWP during both skin-surface cooling and whole-body heating.

Although the effects of differing thermal conditions on CVP have been described (Rowell et al. 1969; Minson et al. 1998; Crandall et al. 1999; Peters et al. 2000; Cui et al. 2005), the findings are equivocal whether whole-body heating alters PCWP or pulmonary artery pressure (PAP) (Johnson et al. 1996). Moreover, it is unknown whether PCWP or PAP are affected by skin-surface cooling. In both cases, if PCWP tracks CVP, it would be expected that PCWP would increase during a cold stress and decrease during a heat stress. Thus, the secondary purpose of this study was to test the hypothesis that heat stress decreases PAP and PCWP, whereas these vascular pressures will be increased during skin-surface cooling.

Methods

Subjects

Eleven male subjects participated in this study; physical characteristics of subjects were mean age of 28 ± 4 years, height of 186 ± 11 cm and weight of 83 ± 11 kg (mean ± s.d.). Subjects were not taking medications and were free of any known cardiovascular, metabolic or neurological diseases. Written informed consent was obtained from all subjects before participating in this study. The study procedures were approved by the Ethics Committee of Copenhagen and all experiments were performed in accordance with the Declaration of Helsinki.

Measures

Heart rate was determined via electrocardiography and arterial blood pressure was measured from a brachial artery catheter. Mean CVP and PAP were obtained upon integration of the respective pressure waveforms from a pulmonary artery catheter. PCWP was measured during 5 s end-expiratory breath hold from integrating the pressure waveform following careful inflation of the balloon of the pulmonary artery catheter and confirmation of a successful wedge. For each stage at least two PCWP measurements were obtained and averaged. Cardiac output was measured via thermodilution of cooled isotonic saline repeated 2–4 times per stage. Internal temperature was measured from a pulmonary artery blood thermistor. Skin temperature was indexed from the weighted average of the six thermocouples attached to the skin (Taylor et al. 1989).

Protocol

Subjects were familiarized with the experimental procedures and were instrumented with skin thermocouples and ECG electrodes. Subjects were then fitted to a two-piece water-perfused suit and placed in the supine position in a LBNP chamber. A two-piece suit (upper and lower halves) were used for this protocol to improve the seal of the LBNP chamber to the subject and reduce air leaking and associated skin cooling during LBNP. The suit covered the entire body except for the head, hands and feet. While in this position, a 1.1 mm catheter (20G) was placed in the brachial artery of the left arm and a flow-directed pulmonary arterial catheter (93 A-831H-7.5F, Baxter Healthcare Corporation, Irvine, CA, USA) was introduced through the basilic vein of the left arm and advanced into the pulmonary artery (van Lieshout et al. 2005). With the balloon inflated, the catheter was advanced to the pulmonary wedge position, which was confirmed by the presence of characteristic pressure waveforms. Measurements of PAP were completed with the balloon deflated and measurements of CVP were made from the proximal port of the catheter. All measurements were confirmed via inspection of the respective waveforms. Pressures were referenced to atmospheric pressure via uniflow pressure transducer (Baxter Healthcare Corporation) zeroed at 5 cm below the sternal angle, and connected to a pressure monitoring system (Dialogue 2000, IBC-Danica, Copenhagen, Denmark). The catheter lumens were flushed with isotonic saline at a rate of 3 ml h−1.

Throughout instrumentation as well as during normothermic data collection, neutral temperature water (34°C) was perfused through the suit. After baseline data collection, LBNP was engaged at 15 mmHg and then immediately followed this data collection by 30 mmHg. These levels of LBNP were selected because of the high incidence of orthostatic intolerance with higher levels of LBNP during similar heat stress conditions (Wilson et al. 2006). Measurements (i.e. CVP, PAP, PCWP and cardiac output) began after 3 min of LBNP. Because of the nature of obtaining an adequate PCWP and multiple thermodilution cardiac outputs, the exact duration of LBNP varied slightly from subject to subject, with the typical duration being ∼15 min per LBNP stage. Following completion of normothermic data collection, LBNP was turned off and a recovery period ensued. This was followed by 20 min of skin-surface cooling by perfusing 16°C water through the tube-lined suit. The level of skin-surface cooling was chosen to be as cool as possible without evoking shivering (Durand et al. 2004). If pre-shivering tonus was observed, water temperature was increased slightly to abate this response. After this 20 min period, baseline cold stress data were obtained followed by 15 and 30 mmHg LBNP. LBNP was then turned off, and after a recovery period, whole-body heating began by perfusing 46°C water through the tube-lined suit until blood temperature increased ∼1.0°C from the temperature nadir. The temperature change from the nadir was used because temperature decreases during the onset of heat stress, especially when preceded by cooling (Wilson et al. 2002; White et al. 2003). Upon achieving close to the desired blood temperature increase, the temperature perfusing the suit was slightly reduced to attenuate the rate of rise of blood temperature during the ensuing data collection period. Baseline heat stress data were obtained followed by data collection during 15 and 30 mmHg LBNP.

Data analysis

Data were acquired at a minimum of 50 Hz throughout experimental procedures by a data acquisition system (Biopac, Santa Barbara, CA, USA). Pulmonary and systemic vascular conductances were calculated via:

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To determine if the change in vascular pressures were similar between thermal conditions and across LBNP, data were analysed via two-way repeated measures ANOVA. If a significant main effect or interaction was identified, Student–Newman–Keuls post hoc analysis was performed. Linear regression analysis was performed to determine the relationships between the decrease in CVP and the decrease in PAP and PCWP during LBNP for each thermal condition. The α-level for all statistical analyses was set at 0.05. Results are reported as means ± s.e.m.

Results

Prior to any thermal perturbations, blood and mean skin temperatures were 36.6 ± 0.1 and 34.5 ± 0.2°C, respectively. Skin-surface cooling reduced mean skin temperature by 4.3 ± 0.3°C and systemic vascular conductance (95.2 ± 2.3 to 80.8 ± 2.7 ml min−1 mmHg−1) while increasing blood temperature by 0.17 ± 0.03°C and mean arterial pressure (87 ± 1 to 95 ± 1 mmHg); all P < 0.001. Skin-surface cooling resulted in small decreases in heart rate (58 ± 3 to 53 ± 3 beats min−1, P < 0.01) and cardiac output (7.6 ± 0.6 to 6.9 ± 0.7 l min−1, P < 0.01) but did not change stroke volume (125 ± 7 to 122 ± 8 ml, P = 0.49) or pulmonary vascular conductance (1.78 ± 0.03 to 1.71 ± 0.04 l min−1 mmHg−1, P = 0.27). No shivering was observed or identified by the subjects throughout the cooling procedure. Whole-body heating increased mean skin temperature by 3.4 ± 0.3°C and blood temperature 0.95 ± 0.07°C. Whole-body heating increased heart rate (to 76 ± 5 beats min−1), cardiac output (to 10.7 ± 0.5 l min−1), and systemic vascular conductance (to 133.3 ± 2.4 ml min−1 mmHg−1; all P < 0.001). Whole-body heating slightly reduced mean arterial pressure (to 84 ± 1 mmHg; P < 0.01) and did not significantly change stroke volume (to 135 ± 7, P = 0.11) or pulmonary vascular conductance (to 1.72 ± 0.02 l min−1 mmHg−1, P = 0.26).

Significant main effects were observed for thermal condition in CVP, PAP and PCWP (all P < 0.001). Prior to LBNP, mean CVP during normothermia was 6.3 ± 0.2 mmHg, increased with skin-surface cooling to 7.8 ± 0.2 mmHg, and decreased with whole-body heating to 3.6 ± 0.1 mmHg (all P < 0.05). Mean PAP followed a similar pattern as CVP, being 14.0 ± 0.3, 15.3 ± 0.3 and 12.8 ± 0.2 mmHg during normothermia, skin-surface cooling and whole-body heating, respectively (all P < 0.05). Mean PCWP during normothermia was 9.5 ± 0.3 mmHg, increased with skin-surface cooling to 11.1 ± 0.3 mmHg, and decreased with whole-body heating to 6.5 ± 0.2 mmHg (all P < 0.05). Representative tracings of CVP, PAP and PCWP during normothermia, skin-surface cooling and whole-body heating can be observed in Fig. 1.

Figure 1.

Figure 1

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Representative pressure waveforms during thermal stress A, representative tracings of pulmonary artery pressure (PAP) and central venous pressure (CVP) during normothermia, skin-surface cooling and whole-body heating. B, representative tracing of pulmonary capillary wedge pressure (PCWP) during the same thermal conditions. Variables in A are time sequenced with each other but not to PCWP in B.

Statistical analyses revealed main effects for thermal condition and LBNP for CVP, PAP and PCWP (all P < 0.001). An interaction between thermal condition and LBNP was observed for CVP (P < 0.001) and PAP (P = 0.002), while there was a tendency for an interaction between thermal condition and LBNP for PCWP (P = 0.052). Such interactions suggest that the magnitude of the reduction in these vascular pressures during LBNP may be influenced by the thermal status of the individual. However, the relationship of LBNP-induced decreases between CVP, PAP and PCWP were similar in magnitude and slope within each thermal condition (Fig. 2).

Figure 2.

Figure 2

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Effect of lower body negative pressure (LBNP) on central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP) and pulmonary artery pressure (PAP) during normothermia, skin-surface cooling and whole-body heating Significant main effects were observed between CVP, PCWP and PAP and across LBNP for all thermal conditions.

LBNP of 15 and 30 mmHg progressively decreased CVP and PCWP, and these decreases were correlated (all P < 0.001; Fig. 3). The strength of the correlation between CVP and PCWP was high in both normothermia (r = 0.93, PCWP = 1.1 × CVP + 2.3) and skin-surface cooling (r = 0.91, PCWP = 1.1 × CVP + 2.6) conditions, but decreased slightly during whole body heating (r = 0.81, PCWP = 1.1 × CVP + 2.1, all P < 0.001). Although each thermal condition resulted in different y-intercepts of the CVP to PCWP relationships, the slopes of these relationships were similar. When data were pooled across all thermal conditions and level of LBNP, highly correlated relationships emerge between CVP and PCWP (r = 0.92, PCWP = 1.1 × CVP + 2.3, P < 0.001; Fig. 2). Similar to CVP and PCWP, LBNP decreased PAP during normothermia (to 9.9 ± 0.4 and 6.5 ± 0.3 mmHg for 15 and 30 mmHg of LBNP), skin-surface cooling (to 12.5 ± 0.4 and 8.9 ± 0.3 mmHg for 15 and 30 mmHg of LBNP), and whole-body heating (to 9.0 ± 0.2 and 6.9 ± 0.3 mmHg for 15 and 30 mmHg of LBNP). When data were pooled across all thermal conditions a high correlation was observed between CVP and PAP (r = 0.85, PAP = 1.1 × CVP + 6.9, P < 0.001).

Figure 3.

Figure 3

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Regression analysis between central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) at baseline and two lower body negative pressures (LBNP; 15 and 30 mmHg) The strength of relationships and regression equations were r = 0.93, PCWP = 1.1 × CVP + 2.3 for normothermia; r = 0.91, PCWP = 1.1 × CVP + 2.6 for skin-surface cooling; r = 0.81, PCWP = 1.1 × CVP + 2.1 for whole-body heating; and r = 0.92, PCWP = 1.1 × CVP + 2.3 when all thermal conditions are combined (all P < 0.001). The black line refers to the line of identity and the grey lines refer to 95% confidence interval

Discussion

The major findings of this study are: (1) skin-surface cooling increases CVP, PAP and PCWP; (2) whole-body heating decreases CVP, PAP and PCWP; and (3) during an orthostatic challenge, decreases in CVP are correlated with decreases in PCWP during all thermal conditions. Pooled data (i.e. combining normothermia, skin-surface cooling and whole-body heating during LBNP) suggest that the change in CVP appropriately tracks changes in PCWP. Combined, these data provide evidence that regardless of the thermal condition of the individual, 15 and 30 mmHg LBNP causes similar changes in right and left ventricular filling pressures as referenced from CVP and PCWP.

These data provide insight into central vascular pressure changes during cold exposure of healthy subjects independent of confounders such as water immersion and volume infusion. Skin-surface cooling increased CVP to a similar magnitude relative to what we previously observed (Cui et al. 2005) and also increased PAP and PCWP (1.6 and 1.3 mmHg, respectively). These increases in vascular pressures are probably due to vasoconstriction that results in peripheral displacement of blood volume into the large veins. Consistent with this hypothesis, Cai et al. (2000) observed increases in thoracic blood volumes (as indexed from electrical impedance) during cold air exposure, thus supporting a centralization of blood volume, although this observation is not routinely observed by others (Durand et al. 2004; Cui et al. 2005). Skin-surface cooling increases PAP and decreases pulmonary vascular conductance in anaesthetized pigs (Kornberger et al. 1995). We did not observe a decrease in pulmonary vascular conductance (or increase in pulmonary vascular resistance) in the present study, given the lack of a large affect of cooling on cardiac output coupled with parallel increases in both PAP and PCWP. Skin-surface cooling did not increase cardiac output, which confirms prior findings where alternate methods to measure cardiac output were used (Raven et al. 1980; Raven et al. 1981; Durand et al. 2004). Changes in cardiac output in response to cold stress are variable (Stocks et al. 2004), but are strongly related to increases in metabolic rate associated with shivering (Muza et al. 1988). Therefore, perhaps due to the absence of shivering in the present protocol, it is not surprising that cardiac output did not increase in the present protocol.

A key finding of the present investigation is that the reduction in CVP (2.7 mmHg) during whole-body heating was almost identical to the reduction in PCWP (3.0 mmHg). The primary mechanism for decreases in these vascular pressures is an increase in cutaneous vascular conductance and cutaneous blood volume and possible decreases in effective circulatory volume (Deschamps & Magder, 1990, 1994; Gonzalez-Alonso et al. 2004), in combination with an ∼40% increase in cardiac output. Heat stress-induced decreases in CVP can be associated with reductions in thoracic admittance, used as an index of central blood volume (Cai et al. 2000), although the effects of heat stress on central blood volume remains unresolved (Rowell 1986).

In the current study we did not observe significant increases in pulmonary vascular conductance during whole-body heating. Although cardiac output increased by ∼3 l min−1 with heating, the pressure gradient between PAP and PCWP also increased, resulting in an absence of an effect of heat stress on pulmonary vascular conductance. The widening of this pressure gradient was primarily due to a greater reduction in PCWP (3.0 mmHg) relative to the reduction in PAP (1.2 mmHg) during heating. A lack of a change in pulmonary vascular conductance with heat stress is in contrast to previous studies (el-Sherif et al. 1970; Tonnesen et al. 1987). However, the majority of these previous studies were obtained during clinical procedures from non-healthy, and in some cases in anaesthetized, humans. In contrast to pulmonary vascular conductance, systemic vascular conductance increased during whole-body heating, as shown by a large increase in cardiac output coupled with small decreases in arterial and central venous pressures.

Orthostatic stress, induced via LBNP, decreased CVP in a graded manner in all thermal conditions. We observed similar rates of decrease in CVP between normothermia and skin-surface cooling conditions between 0 and 30 mmHg of LBNP, which corroborates previous observations (Cui et al. 2005). The current study extends these observations by finding similar LBNP-induced decreases in PAP and PCWP between normothermia and skin-surface cooling. A statistical interaction between thermal condition and LBNP for central vascular pressures was identified during whole-body heating. Compared with normothermia and skin-surface cooling, the rate of decrease in CVP during LBNP was attenuated when subjects were heat stressed, probably due to CVP already being low prior to beginning LBNP in this thermal condition. Consistent with this observation, Minson et al. (1999) observed similar CVPs at the end of a 60 deg head-up tilt test when young subjects were normothermic and whole-body heated, despite beginning at a lower supine CVP during heating; however, Peters et al. (2000) observed that once LBNP was engaged absolute CVPs were very similar at each LBNP between these thermal conditions. Nevertheless, important to the purpose of this study are the observations that changes in CVP are similar to changes in PCWP during LBNP regardless of thermal condition (Fig. 2).

Orthostatic tolerance is decreased during heat stress and improved during cold stress (Rowell 1986; Wilson et al. 2002; Durand et al. 2004). In addition to reductions in CVP and PCWP, orthostatic stress also decreases central blood volume and cardiac output (Levine et al. 1991; Cai et al. 2000; Harms et al. 2003; van Lieshout et al. 2005). If prior to the orthostatic challenge CVP and PCWP are reduced, as occurs during whole-body heating, then it is likely that further decreases in these pressures due to the orthostatic stress will compromise ventricular filling and possibly stroke volume. The opposite is probably the case for skin-surface cooling. That is, increases in CVP and PCWP due to cooling may preserve ventricular filling and stroke volume thereby attenuating the reduction in CVP and stroke volume during an orthostatic challenge, as we have previously reported (Cui et al. 2005).

LBNP-induced decreases in CVP and PCWP correlated during normothermia and skin-surface cooling conditions (r > 0.90); although the strength of this relationship was high, it was less strong (r = 0.81) during whole-body heating. The reason for a lower correlation coefficient during heat stress may be related to an attenuated range over which CVP and PCWP could decrease during LBNP, given that prior to LBNP CVP and PCWP are reduced by heat stress compared with normothermia and skin-surface cooling (Fig. 2). Nonetheless, when data were pooled across all thermal conditions, the overall tracking ability of CVP for PCWP was robust (r = 0.92). Combined, these data provide support of CVP as an acceptable surrogate for left ventricular preload, as indexed from PCWP, during thermal and orthostatic stress.

Acknowledgments

The authors would like to express their appreciation to Chester A. Ray for his help and support. This research project was funded in part by grants and awards from the National Heart, Lung, and Blood Institute (C.G.C.: HL-61388, HL-67422 and HL-84072), American College of Sports Medicine (T.E.W.), and Aase & Ejnar Danielsens Fund (N.H.S.).

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