While cardiogenic shock (CS) is classically defined by primary cardiac dysfunction leading to impaired macrocirculatory variables—such as hypotension, reduced cardiac output (CO), and diminished left ventricular ejection fraction—growing evidence highlights the parallel and significant involvement of systemic microcirculatory dysfunction, often manifesting as tissue hypoperfusion. Indeed, most definitions of CS emphasize that it leads to tissue and end-organ hypoperfusion, evidenced in part by “signs of poor peripheral tissue perfusion.” Consequently, the main clinical presentations of CS are wet-cold (∼65%) and dry-cold (∼30%), based on adapted Forrester perfusion/congestion profiles.

Despite advances in CS management, which emphasize rapid restoration of macrocirculatory function, mortality rates remain alarmingly high, often exceeding 40%. Notably, studies have demonstrated that up to 45% of deaths occur in patients with a normalized cardiac index, highlighting a disconnect between macrocirculatory improvement and meaningful clinical recovery.¹ This discrepancy highlights the inadequacy of solely optimizing macrocirculation, suggesting that persistent microcirculatory failure plays a critical role in driving ongoing organ dysfunction and death. While experimental data indicate an initial compensatory microvascular recruitment in the very early stages of CS,² recent investigations reveal that microvascular perfusion is frequently heterogeneously impaired despite restored systemic hemodynamics and that these disturbances are strongly linked to adverse outcomes. Interestingly, cerebral microcirculation appears to be protected in early experimental CS.³

The microcirculation (vessels ≤100 μm), comprising approximately 90% of the total vascular surface area (a far greater extent than arteries and veins of the macrocirculation), is a complex and critical system responsible for balancing tissue oxygen consumption and delivery, and thus, maintaining tissue perfusion.³ Microcirculatory monitoring can be approached through the assessment of lactate levels—an indirect, crude, and imperfect surrogate—as well as by evaluating simple clinical signs at the bedside (Table 1). Capillary refill time (CRT) and the extent of skin mottling provide indirect yet practical information about peripheral perfusion and the adequacy of the microvascular flow. Recent advancements have enabled direct observation of the microcirculation using hand-held vital microscopy, primarily to assess the sublingual microcirculation, making precise “real-time” bedside monitoring a feasible reality.⁴ Other techniques for evaluating microcirculatory function include near-infrared spectroscopy (NIRS) and skin laser Doppler imaging.