Sepsis-induced myocardial dysfunction: Hemodynamic stability as the cornerstone of anesthetic resuscitation

Sepsis-associated cardiomyopathy (SCM), also known as sepsis-induced myocardial dysfunction (SIMD), is a significant determinant of poor outcomes in septic patients, and the associated cardiac dysfunction correlates closely with increased mortality [1]. Mechanistically, increases in inflammatory mediators and concurrent microcirculatory dysfunction suppress myocardial contractility, further impair right–left ventricular coupling, and make the heart susceptible to pump failure under abnormal loading conditions while diminishing tolerance to changes in intravascular volume [2]. During the initiation of anesthesia and resuscitation, patients are particularly susceptible to circulatory collapse owing to underlying hemodynamic instability and rapid cardiovascular changes during induction [3]. As the disease advances, myocardial dysfunction may progress to a stage where cardiac output becomes inadequate and systemic congestion occurs, culminating in the clinical manifestation of heart failure. Patients with sepsis and concomitant heart failure have higher mortality and are more prone to anesthesia-induced hypotension, yet specific perioperative guidance is lacking [4]. It is worth noting that sepsis-induced heart failure is not exclusively attributable to myocardial dysfunction associated with sepsis. It may also arise from the presence of pre-existing chronic heart failure in conjunction with sepsis, or from the simultaneous occurrence of both conditions during anesthesia, leading to hemodynamic instability. Thus, providing adequate organ perfusion while preventing fluid overload remains a major challenge in perioperative care. Here we describe a precision-based resuscitation strategy incorporating advanced imaging modalities, such as tissue Doppler and speckle-tracking echocardiography, and tailored volume management to preserve hemodynamic equilibrium and improve outcomes in this high-risk cohort.