Microcirculatory dysfunction during cardiac surgery remains heterogeneous and inconclusive in current clinical evidence

Cardiopulmonary bypass (CPB) is a crucial component of cardiac surgery, yet postoperative organ dysfunction remains common despite apparently adequate systemic hemodynamics. This mismatch underscores the importance of the microcirculation, where oxygen delivery and extraction ultimately occur. Increasing evidence suggests that CPB disrupts capillary perfusion through endothelial dysfunction, glycocalyx shedding, inflammation, oxidative stress, hemodilution, functional shunting, and microthromboemboli, thereby causing tissue hypoxia despite normal macro-hemodynamic stability. This review summarizes the physiology of microcirculation and examines the mechanisms by which CPB impairs microvascular function. We also review current tools for microcirculatory assessment, including orthogonal polarization spectral, sidestream dark field, and incident dark field imaging, near-infrared spectroscopy, and circulating biomarkers of endothelial and glycocalyx injury. Although these approaches have improved mechanistic insight, their clinical use remains limited by technical challenges and the lack of standardized endpoints. We further evaluate cardioprotective strategies aimed at preserving microcirculatory function during CPB. These include perfusion and mechanical approaches, ischemic preconditioning, glycocalyx-preserving therapies, and various pharmacologic interventions such as volatile anesthetics, nitric oxide, statins, antioxidants, and antithrombotic agents. Across these domains, preclinical studies often support biologic plausibility, whereas clinical evidence remains heterogeneous and inconclusive and frequently relies on indirect evidence of organ dysfunction rather than direct measures of microvascular perfusion. Important gaps remain in translating findings from experimental models to patients, and greater integration of bedside imaging and biomarkers with biophysiological principles may help establish microcirculation as both a mechanistic endpoint and a therapeutic target in cardiac surgery.