Splanchnic ischemia during mechanical ventilation

Abstract

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.