**9. Ischemia secondary to low flow state**

Patients with poor cardiac functional status are at risk for splanchnic hypoperfusion secon‐ dary to a number of pre-operative (i.e., pre-existing mesenteric arterial disease), intra-opera‐ tive (i.e., hypotension/tissue hypoperfusion), and post-operative (i.e., low cardiac output) risk factors. Preoperative presence of conditions such as low left ventricular ejection fraction and peripheral vascular disease have been shown to be significant risks for developing post‐ operative gastrointestinal ischemia [32].

Intraoperatively, hypovolemia and use of vasoconstrictors can contribute to splanchnic hypo‐ perfusion [53]. Additionally, patients requiring longer cardiopulmonary bypass times may be at greater risk for developing intestinal hypoperfusion [53]. This may be due to the non-pulsa‐ tile cardiopulmonary bypass flow characteristics, in conjunction with other factors such as the associated hemolysis, inflammatory cascade activation, the use of anticoagulation, the pres‐ ence of hypothermia, and the reduced end-organ perfusion. Further, cardiopulmonary bypass may be associated with increased gastrointestinal permeability and enhanced cytokine release, contributing to microcirculatory dysfunction and mucosal injury [32].

In the postoperative setting, inadequate blood flow to the intestines and subsequent intesti‐ nal ischemia/infarction can be associated with hypotension and/or cardiogenic shock [10]. In one study, patients with renal failure (Creatinine >1.4), prior myocardial infarction, and those requiring intra-aortic balloon pump support were at higher risk of developing mesen‐ teric ischemia secondary to "low flow" state [8]. Prolonged mechanical ventilation requiring high positive end-expiratory pressure (PEEP) can also result in hypotension and impaired cardiac output, leading to splanchnic vasoconstriction and hypoperfusion. Furthermore, high PEEP is associated with activation of the renin-angiotensin-aldosterone system and in‐ creases in catecholamine levels [54]. This, in turn, results in shunting of blood away from the gastrointestinal system, leading to mismatch between oxygen delivery and demand. Persis‐ tent deficit in oxygen delivery then leads to mucosal ischemia and damage. Moreover, dur‐ ing the process of tissue re-perfusion after restoration/normalization of adequate oxygen delivery, the persistent vasoconstrictive state of non-occlusive mesenteric ischemia (NOMI) may be seen [32]. Management of NOMI consists of restoration of adequate circulating intra‐ vascular volume, maintenance of adequate cardiac output, and selective angiographic ap‐ proaches utilizing intra-arterial vasodilating agent infusion therapy [55]. Surgery is reserved for cases requiring resection of necrotic bowel, exploration for suspected perforation, and/or revascularization procedure.
