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Critically ill patients are at risk of succumbing to their primary disease or the undesired sequelae associated with their therapy. Although frequently lifesaving, the use of positive airway pressure therapy has numerous undesired physiologic and clinical complications. These complications have their origins in the endotracheal or tracheostomy tube, the positive-pressure ventilation (PPV), or from therapies delivered during the care of mechanical ventilation. Other complications may result from coexisting illness or comorbid conditions. Although not commonly recognized as important effects of PPV or positive end-expiratory pressure (PEEP), alterations in organ functions ought to be recognized and addressed accordingly to reduce morbidity and mortality.
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The interaction between PPV and the gastrointestinal tract in critical setting is a complex one. Gastrointestinal changes are reported frequently in critically ill patients receiving PPV. The true incidence of gastrointestinal complications is not known, but it is reported to be up to 100% for those receiving PPV for more than 3 days. Splanchnic hypoperfusion seems to play a pivotal role in the pathogenesis of these complications, including mucosal damage, motility disorders, and mesenteric ischemia (Fig. 41-1).1 Unlike many other vascular beds, the splanchnic exhibits limited autoregulation when faced with reduction in mean arterial pressure.2 Without altering total blood flow to the organs of the digestive tract, sympathetic stimulation redistributes blood flow to the muscularis of the wall by decreasing mucosal perfusion.3 This poses severe ischemic changes to the mucosal layer because the mucosa is metabolically more active than the muscle layer and is more vulnerable to the destructive effects of a compromised blood supply.
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Mechanical ventilation influences the gastrointestinal function by impacting systemic hemodynamics via high PEEP or potentially injurious ventilator strategies such as a high tidal volume (VT). The effect of PEEP on splanchnic blood flow has been shown in animal models to be dose-dependent.4 PEEP decreases venous return and reduces preload, which in turn reduces cardiac output and results in splanchnic hypoperfusion.5 The reduction of splanchnic blood flow is limited at PEEP levels below 10 cm H2O but it is more pronounced at PEEP levels of 15 to 20 cm H2O.6 In rats, the addition of 10 cm H2O of PEEP resulted in reduction of cardiac output and mesenteric blood flow by 31% and 75%, respectively.7 PEEP also promotes plasma-renin-angiotensin-aldosterone activity, as well as catecholamine release, which limits splanchnic hypoperfusion.4,7 Interestingly, high PEEP levels interfere with mesenteric leukocyte–endothelial interaction. In rats with healthy lungs, 10 mbar of PEEP was associated with an increase in the number of rolling, adherent, and migrated leukocytes when ...