Splanchnic ischemia during mechanical ventilation

Background-aim: Positive end-expiratory pressure (PEP ) has been advocated as a prophylactic and therapeutic modality since it improves oxygenation and reopens atelectatic lung injury units. Thus, it is usually added to conventional mechanical ventilation in order to avoid development of post-operation atelectasis. However, high PEP is known to result in diminished cardiac output, decreased venous return and transient ischemia to the abdominal viscera. On the other hand, prolonged gut hypoperfusion of different origin may cause mucosal barrier failure, which is considered an important factor for the initiation and/or perpetuation of bacterial translocation, leading, theoretically in humans, to sepsis. Considering that low PEP may also lead to splanchnic hypoperfusion, we assessed the intestinal and hepatic hemodynamic in two step PEP ventilation. Methods: The hepatic artery, portal vein, and superior mesenteric artery blood flow as well as the hepatic and intestinal mucosal microcirculation, the hepatic tissue pO2 and the intestinal mucosal pH were assessed before and after 5 and 10 cmH2O PEP ventilation, in ten domestic pigs. Results: Statistical analysis revealed a significant decrease (p=0.0001) in all parameters during 5 cmH2O and 10 cmH2O PEP ventilation period in compare to baseline. Hepatic artery exhibited a 20% reduction in 5 cmH2O PEP and a further 15% in 10 cmH2O PEP . Similarly, reductions of 11% and 9% in portal vein, of 15% and 11% in superior mesenteric artery, of 16% and 8% in hepatic microcirculation, and of 29% and 22% in intestinal microcirculation were noticed respectively, while hepatic parenchymal pO2 reached 46% and intestinal mucosa pH fall to 7.29. Conclusion: These findings demonstrate that PEP administration results to the impairment of splanchnic tissue perfusion.