• Catherine M N O'Malley, Robert J Frumento, Berend Mets, Yoshifumi Naka, and Elliott Bennett-Guerrero.
• Department of Anesthesiology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA. co2001@columbia.edu
• Ann. Thorac. Surg. 2003 Jun 1; 75 (6): 1886-91.

BackgroundAbnormal gastric tonometric variables, a surrogate for splanchnic ischemia, occur in approximately 50% of patients at the end of routine cardiac operations and are associated with postoperative morbidity. We sought to determine whether gastric tonometric variables deteriorate after left ventricular assist device insertion and to explore the association between abnormal gastric tonometric variables and vasoconstrictor use.MethodsNineteen patients who had insertion of a left ventricular assist device were enrolled in a prospective, observational study. Automated air tonometry was used to determine the difference between gastric and arterial partial pressure of carbon dioxide (CO2 gap) at five time points perioperatively.ResultsCompared with baseline, systemic blood flow was significantly increased at the end of operation (1.9 +/- 0.6 versus 2.9 +/- 0.7 L x min(-1) x m(-2), p < 0.0001). Tonometric variables, which were normal at baseline, became abnormal in 90% of patients (baseline CO2 gap 4 +/- 2 mm Hg versus end of operation CO2 gap 24 +/- 15 mm Hg, p < 0.0001). Elevated CO2 gaps correlated with larger doses of norepinephrine (r = 0.69, p = 0.001) and vasopressin (r = 0.88, p < 0.0001). Abnormal gastric tonometric variables at the end of operation correlated with postoperative intensive care unit length of stay (r = 0.70, p = 0.0009) and multiple organ dysfunction score (r = 0.64, p = 0.0033).ConclusionsDespite a significant increase in systemic blood flow after left ventricular assist device implantation, abnormal gastric tonometric variables developed and were associated with larger vasoconstrictor dose. These data provide evidence that gastric ischemia can develop independently of changes in systemic blood flow and support the potential role of vasoconstrictors as a cause of splanchnic ischemia.

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