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This Article Full Text Full Text (PDF) All Versions of this Article: 585/1/279    most recent jphysiol.2007.137901v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wilson, T. E. Articles by Crandall, C. G. Search for Related Content PubMed PubMed Citation Articles by Wilson, T. E. Articles by Crandall, C. G. Related Collections Integrative

¹ Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, USA
² Department of Anaesthesia, Rigshospitalet
³ Copenhagen Muscle Research Center, University of Copenhagen, Denmark
⁴ Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, TX, USA
⁵ Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA

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.

(Received 3 June 2007; accepted after revision 17 September 2007; first published online 27 September 2007)
Corresponding author C. G. Crandall: Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Avenue, TX 75231, USA. Email: craigcrandall{at}texashealth.org

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				C. G. Crandall, T. E. Wilson, J. Marving, T. W. Vogelsang, A. Kjaer, B. Hesse, and N. H. Secher Effects of passive heating on central blood volume and ventricular dimensions in humans J. Physiol., January 1, 2008; 586(1): 293 - 301. [Abstract] [Full Text] [PDF]