Nonocclusive Mesenteric Ischemia in Cardiogenic Shock: Mechanisms of Splanchnic Hypoperfusion and Strategies for Early Detection

Nonocclusive mesenteric ischemia (NOMI) is an underappreciated and lethal sequelae of cardiogenic shock (CS), forming the bulk of acute mesenteric ischemia in critically ill patients. In the setting of CS, reduced cardiac output, exposure to high doses of vasopressors, and nonpulsatile mechanical circulatory support (MCS) result in a “perfect storm” of hemodynamic insults to the splanchnic circulation. Mortality from NOMI in this population exceeds 70–90%, largely attributable to late diagnosis after irreversible transmural necrosis has already occurred. In this review, we describe the pathophysiology of NOMI in the setting of CS, considering the effects of sympathoadrenergic and renin–angiotensin mediated vasoconstriction, the loss of mesenteric pulsatility due to contemporary MCS, and the gut–heart axis as an enhancer of systemic injury. We address topics such as the under detection of limb ischemia with current imaging modalities, the potential of new markers of gut dysfunction, such as intestinal fatty acid-binding protein and citrulline, and bedside imaging, including contrast-enhanced ultrasound and assessment of portal vein pulsatility. We review strategies for prevention and management, including early MCS escalation, minimizing vasopressor requirements, and careful enteral feeding. Finally, we recognize the need for prospective multicenter registries and AI-based risk stratification to facilitate the diagnosis of this under-recognized condition. Understanding that the gut is not a “mere” bystander in the pathophysiology of CS, but rather a central participant, it may be the gateway to reducing the ongoing high mortality of this syndrome.