Fluid extravasation during cardiopulmonary bypass in piglets – effects of hypothermia and different cooling protocols

Authors

  • M. Farstad,

    1. Departments of  1Anaesthesia and Intensive Care and 2Heart Disease, University of Bergen, Haukeland University Hospital, Bergen, Norway
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  • 1 J. K. Heltne,

    1. Departments of  1Anaesthesia and Intensive Care and 2Heart Disease, University of Bergen, Haukeland University Hospital, Bergen, Norway
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  • 1 S. E. Rynning,

    1. Departments of  1Anaesthesia and Intensive Care and 2Heart Disease, University of Bergen, Haukeland University Hospital, Bergen, Norway
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  • 2 T. Lund,

    1. Departments of  1Anaesthesia and Intensive Care and 2Heart Disease, University of Bergen, Haukeland University Hospital, Bergen, Norway
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  • 1 A. Mongstad,

    1. Departments of  1Anaesthesia and Intensive Care and 2Heart Disease, University of Bergen, Haukeland University Hospital, Bergen, Norway
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  • 2 F. Eliassen,

    1. Departments of  1Anaesthesia and Intensive Care and 2Heart Disease, University of Bergen, Haukeland University Hospital, Bergen, Norway
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  • and 2 P. Husby 1

    1. Departments of  1Anaesthesia and Intensive Care and 2Heart Disease, University of Bergen, Haukeland University Hospital, Bergen, Norway
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Abstract

Background: Hypothermic cardiopulmonary bypass (CPB) is associated with capillary fluid leak and edema generation which may be secondary to hemodilution, inflammation and hypothermia. We evaluated how hypothermia and different cooling strategies influenced the fluid extravasation rate during CPB.

Methods: Fourteen piglets were given 60 min normothermic CPB, followed by randomization to two groups: 1: rapid cooling (RC-group) (∼15 min to 28°C); 2: slow cooling (SC-group) (∼60 min to 28°C). Ringer's solution was used as CPB prime and for fluid supplementation. Fluid input/losses, plasma volume, colloid osmotic pressures (plasma, interstitial fluid), hematocrit, serum-proteins and total tissue water (TTW) were measured and fluid extravasation rates calculated.

Results: Start of normothermic CPB resulted in a 25% hemodilution. During the first 5–10 min the fluid level of the reservoir fell markedly due to an intravascular volume loss necessitating fluid supplementation. Thereafter a steady state was reached with a constant fluid need of 0.14 ± 0.04 ml kg−1 min−1. After start of cooling the fluid needs increased in the following 30 min to 0.91 ± 0.11 ml kg−1 min−1 in the RC group (P < 0.001) and 0.63 ± 0.10 ml kg−1 min−1 in the SC-group (P < 0.001) with no statistical between-group differences.

Fluid extravasation rates after start of hypothermic CPB increased from 0.20 ± 0.08 ml kg−1 min−1 to 0.71 ± 0.13 (P < 0.01) and 0.62 ± 0.13 ml kg−1 min−1 (P < 0.05) in the RC- and SC-groups, respectively, without any changes in degree of hemodilution. TTW increased in most tissues, whereas the intravascular albumin and protein masses remained constant with no between group differences.

Conclusion: Hypothermia increased fluid extravasation during CPB independent of cooling strategy. Intravascular albumin and protein masses remained constant. Since inflammatory fluid leakage usually results in protein rich exudates, our data with no net protein leakage may indicate that mechanisms other than inflammation could contribute to fluid extravasation during hypothermic CPB.

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