Is gastric malperfusion and endotoxemia one motor of the systemic inflammatory response syndrome following cardiac surgery?
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KeywordsCongestive Heart Failure Mitral Valve Cardiac Index Systemic Inflammatory Response Syndrome Gastric Tube
Gastric mucosal acidosis and endotoxemia seems to be responsible for cytokine activation and development of the systemic inflammatory response syndrome (SIRS) in patients with congestive heart failure. In a retrospective study we previously concluded that patients with congestive heart failure (CHF) and a low preoperative cardiac index had a higher incidence of SIRS following cardiopulmonary bypass (CPB) than patients without CHF. In a prospective study we tried to prove our hypothesis that CHF leads to malperfusion of the gut and subsequently to endotoxin release with cytokine activation.
We evaluated one group with low risk for developing SIRS (Group1: coronary artery bypass grafting without CHF) and a high risk group (Group 2: mitral valve surgery with CHF) with 10 patients each for clinical and laboratory signs of SIRS as defined by BONE. Intramucosal gastric pH, endotoxin was detected using a tonometric gastric tube (Baxter Inc.), TNFα and interleukin 6 (IL6) were measured with an ELISA at nine different times pre-, intra- and postoperatively.
Groups were similar with regards to age and sex. Cardiac Index was lower in Group 2 (1.7 ± 0.3 l/min/cm3) than in Group 1 (2.8 ± 0.5 l/min/cm3; P < 0.05). In Group 2 the aortic cross clamping time was longer (Group 1: 59.6 ± 15.2 min, Group 2: 42.7 ± 19.4 min) and norepinephrine requirements for maintenance of vascular resistance were higher (8.2 ± 12.6 mg) than in Group 1 (1.7 ± 2 mg; P < 0.05).
At the end of CPB gastric pH dropped to 7.33 ± 0.34 in Group 2 whereas the other group remained stable between 7.47 and 7.5 (P < 0.05). Endotoxin levels were significantly elevated and significantly higher in Group 2 (37.2 ± 3.2 pg/ml) than in Group 1 (20.6 ± 3.7 pg/ml; P < 0.05) after aortic cross clamp was opened. In Group 1 only in 1 of 3 patients (33%) with gastric acidosis endotoxin was detected, whereas in Group 2 8/9 patients (88%) endotoxemia occurred.
SIRS is more common in patients with CHF undergoing CPB than in others. This seems to be related to a drop of gastric pH as a sign of malperfusion. Consecutively endotoxemia occurs more often and seems to be a trigger of cytokine activation (TNFα, IL6) making higher norepinephrine application necessary. Our study emphasize the role of splanchnic malperfusion and endotoxemia as one mechanism responsible for the development of SIRS.