Increased oxygen consumption after cardiac surgery is associated with the inflammatory response to endotoxemia
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The aim of this study was to determine whether the increase in post-operative oxygen consumption (ΔVO2) in cardiac surgery patients in related to endotoxemia and subsequent cytokine release and whether ΔVO2 can be used as a parameter of post-perfusion syndrome.
Operating room and intensive care unit of a university hospital.
Twenty-one consecutive male patients undergoing elective coronary artery bypass surgery without major organ dysfunction and not receiving corticosteroids.
Measurements and results
Plasma levels of endotoxin, tumor necrosis factor (TNF) and interleukin-6 (IL-6) were measured before, during and for 18 h after cardiac surgery. Oxygen consumption, haemodynamics, the use of IV fluids and dopamine, body temperature and the time of extubation were also measured. Measurements from patients with high ΔVO2 (≥median value of the entire group) were compared with measurements from patients with low ΔVO2 (<median). Patients with high ΔVO2 had higher levels of circulating endotoxin (P=0.004), TNF (P=0.04) and IL-6 (P=0.009) received more IV fluids and dopamine while in the ICU, and were extubated later than patients with low ΔVO2. Several hours after ΔVO2 the patient's body temperature rose, Forward stepwise regression analysis showed that circulating endotoxin and TNF explained 50% of the variability of ΔVO2.
This study demonstrates that patients with high post operative oxygen comsumption after elective cardiac surgery have higher circulating levels of endotoxin, TNF and IL-6 and also have more symptoms of post-perfusion syndrome. Early detection of high VO2 might be used as a clinical signal to improve circulation in order to meet the high oxygen demand of inflammation. In addition, continuous measurement of VO2 provides us with a clinical parameter of inflammation in interventional studies aiming at a reduction of endotoxemia or circulating cytokines.
Key wordsOxygen consumption Endotoxemia Tumor necrosis factor Interleukin-6 Hypermetabolism Post-perfusion syndrome Cardiac surgery
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- 2.Knudsen F, anderson LW (1990) Immunological aspects of cardiopulmonary bypass. J Cardiothorac Vasc Anesth 4:245–258Google Scholar
- 3.Stoutenbeek CP, Oudemans-van Straaten HM (1989) Prevention of the postperfusion syndrome after cardiopulmonary bypass. In: Vincent JL (ed) Update in intensive and emergency medicine. Springer, Berlin Heidelberg New York, pp 378–382Google Scholar
- 10.Kharazmi A, Anderson LW (1988) Endotoxinemia and enhanced generation of oxygen radicals by neutrophils from patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 98: 381–385Google Scholar
- 11.Jansen NJG, Van Oeveren W, Gu Y, Roozendaal KJ, Eysman L, Wildevuur ChRH (1992) Endotoxin release and tumor necrosis factor formation in cardiopulmonary bypass. Ann Thorac Surg 52:744Google Scholar
- 21.Sturk A, Janssen ME, Muylaert FR, Joop K, Thomas LLM, Cate JW ten (1987) Detection of bacterial toxins with limulus amoebocyte lysate test. In: Watson SW, Levin J, Novitsky TJ (eds) Endotoxin testing in blood. Liss, New York, pp 371–385Google Scholar
- 22.Engelberts I, Stephens S, Francot GJM, Linden CJ van der (1991) Evidence for different effects of soluble TNF receptors on various TNF measurements in human biological fluids. Lancet 338: 515–516Google Scholar
- 23.Altman DG (1991) Practical statistics for medical research. Chapman and Hall, Lodon Glasgow New YorkGoogle Scholar
- 24.Vincent JL, Bakker J (1991) The oxygen supply dependency phenomenon is associated with increased blood lactate levels. J Crit Care 6:152–159Google Scholar