The respiratory system is commonly affected in severe hypoperfusion. Respiratory failure is often due to increased respiratory workload and impairment of diaphragmatic function. Hypoxemia and increased respiratory efforts associated with an increase in minute volume are typical; thus the O 2 needs of the respiratory muscles are increased at the very time that O2 supply is limited. In these circumstances, type II respiratory failure may complicate hypotension. Delayed respiratory failure in hypotension may also be due to acute respiratory distress syndrome following injury to the lung's microcirculation. Hypotension also depresses renal blood flow and glomerular perfusion rate. The compensatory release of catecholamines and angiotensin II also decreases renal blood flow by inducing constriction of afferent arterioles. Ultimately, renal hypoperfusion is followed by acute tubular necrosis and renal failure. In severe hypotension, blood flow is directed away from the intestine and liver towards the heart and brain. Thus the liver and gut may be early sites of tissue damage. These organs are uniquely sensitive in reperfusion injury.
In the liver, hypoxic damage leads to attenuated metabolic and synthetic function, with the latter including a decreased generation of proteins and coagulation factors. Gut injury is often followed by ileus or submucosal hemorrhage. Although it was previously assumed that inadequate gut perfusion may cause barrier failure, allowing translocation of bacteria and bacterial fragments into the circulation, it now appears that bacterial translocation does not cause bacteremia but is a source of activation of systemic inflammatory processes (Dejtch...efal 1996).
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