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Dynamic evaluation of fluid shifts during normothermic and hypothermic cardiopulmonary bypass in piglets
Author(s) -
Heltne J. K.,
Koller M.E.,
Lund T.,
Bert J.,
Rynning S. E.,
Stangeland L.,
Husby P.
Publication year - 2000
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.2000.441006.x
Subject(s) - cardiopulmonary bypass , medicine , anesthesia , hypothermia , hematocrit , hemodynamics , interstitial fluid , cardiac output
Background: Edema, generalized overhydration and organ dysfunction commonly occur in patients undergoing open‐heart surgery using cardiopulmonary bypass (CPB) and induced hypothermia. Activation of inflammatory reactions induced by contact between blood and foreign surfaces are commonly held responsible for the disturbances of fluid balance (“capillary leak syndrome”). We used an online technique to determine fluid shifts between the intravascular and the interstitial space during normothermic and hypothermic CPB. Methods: Piglets were placed on CPB (fixed pump flow) via thoracotomy in general anesthesia. In the normothermic group (n=7), the core temperature was kept at 38°C prior to and during 2 h on CPB, whereas in the hypothermic group (n=7) temperature was lowered to 28°C during bypass. The CPB circuit was primed with acetated Ringer’s solution. The blood level in the CPB circuit reservoir was held constant during bypass. Ringer’s solution was added when fluid substitution was needed (falling blood level in the reservoir). In addition to invasive hemodynamic monitoring, fluid input and losses were accurately recorded. Inflammatory mediators or markers were not measured in this study. Results: Cardiac output, s‐electrolytes and arterial blood gases were similar in the two groups in the pre‐bypass period. At start of CPB the blood level in the machine reservoir fell markedly in both groups, necessitating fluid supplementation and leading to a markedly reduced hematocrit. This extra fluid need was transient in the normothermic group, but persisted in the hypothermic animals. After 2 h of CPB the hypothermic animals had received 7 times more fluid as compared to the normothermic pigs. Conclusion: We found strong indications for a greater fluid extravasation during hypothermic CPB compared with normothermic CPB. The experimental model using the CPB‐circuit reservoir as a fluid gauge gives us the opportunity to study further fluid volume shifts, its causes and potential ways to optimize fluid therapy protocols.