• Christian Putensen, Hermann Wrigge, and Rudolf Hering.
• Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany. putensen@uni-bonn.de.de
• Curr Opin Crit Care. 2006 Apr 1; 12 (2): 160-5.

Purpose Of ReviewMechanical ventilation generates an increase in airway pressure and, therefore, in intrathoracic pressure, which may decrease systemic and intraabdominal organ perfusion. Critically ill patients rarely die of hypoxia and/or hypercarbia but commonly develop a systemic inflammatory response that culminates in multiple-organ dysfunction syndrome and death. In the pathogeneses of this syndrome the gastrointestinal tract and liver have received considerable attention.Recent FindingsMechanical ventilation with high positive end-expiratory pressure has been found to decrease splanchnic perfusion. Hepatic arterial buffer response is preserved and an increased hepatic arterial blood flow will compensate the decrease in portal blood flow. Despite an increased cardiac output with an acute moderate increase in arterial PCO2 during protective ventilation it cannot be expected that splanchnic and gut perfusion is improved. In the absence of a significant rise in intraabdominal pressure without impairment in cardiovascular function, splanchnic and gastrointestinal function remained unchanged during short periods of prone positioning. Spontaneous breathing during ventilator support improves systemic blood flow and gastrointestinal and splanchnic perfusion.SummaryIn critically ill patients mechanical ventilation should be adjusted to avoid conditions known to be associated with decreased gastrointestinal and splanchnic perfusion.

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