Exploring the mechanisms and management of sepsis-related cardiac dysfunction

Sepsis-related cardiac dysfunction (SRCD) represents a critical determinant of both acute mortality and long-term cardiovascular morbidity in sepsis survivors. Sepsis-related cardiac dysfunction denotes the spectrum of acute, non-ischemic myocardial impairment occurring in the setting of sepsis, ranging from subclinical myocardial injury detected by biomarkers or strain imaging to overt systolic or diastolic dysfunction, right-ventricular predominance, and, rarely, sepsis-associated cardiogenic shock; SRCD may be transient in many patients but can also seed persistent cardiac vulnerability. Moving beyond the historical view of reversible septic cardiomyopathy, contemporary evidence reveals a heterogeneous syndrome encompassing systolic, diastolic, and right ventricular impairment, often with subclinical myocardial injury. This review synthesises recent mechanistic advances, highlighting mitochondrial dysfunction, dysregulated immune-cardiac crosstalk, and programmed cell death pathways as central drivers. We discuss the limitations of conventional ejection fraction-based assessment and advocate for multimodal phenotyping incorporating strain imaging, tissue characterisation, and novel biomarker panels. Despite current management being anchored in hemodynamic support, emerging mechanism-based strategies, including immunomodulation, metabolic resuscitation, and cell death inhibition, offer promising avenues for precision therapy. The integration of multi-omics data and machine learning may help refine the classification of sepsis cardiomyopathy into biologically coherent endotypes, guiding future trials and personalised care. Ultimately, a shift from syndrome-level to endotype-guided management is imperative to improve both acute outcomes and long-term cardiovascular health in sepsis survivors.