Sepsis-Induced Cardiomyopathy and Acute Respiratory Distress Syndrome

ABSTRACT: Sepsis remains the leading cause of acute respiratory distress syndrome (ARDS) and cardiovascular dysfunction in the ICU. Sepsis-induced cardiomyopathy (SCM) and sepsis-associated ARDS frequently coexist and share overlapping mechanisms, including cytokine-driven injury, endothelial disruption, microvascular dysfunction, and mitochondrial abnormalities. Despite their clinical relevance, these entities are often evaluated in isolation, overlooking the integrated heart-lung interactions that characterize severe sepsis and ARDS. This narrative review synthesizes current evidence on the shared pathophysiology and diagnostic approach to cardiomyopathy and lung injury in sepsis-associated ARDS, emphasizing the physiologic links that unify these syndromes. We review the immunologic, endothelial, and metabolic mechanisms that drive concurrent myocardial depression and alveolocapillary injury, with particular attention to microcirculatory failure, autonomic dysregulation, and mechanical ventilation-associated cardiopulmonary interactions. We then review diagnostic tools, including echocardiography, lung ultrasound, CT imaging, biomarkers, and advanced hemodynamic monitoring, and highlight the impact of integrated assessment on accurate phenotyping and management. Cardiomyopathy and ARDS in sepsis arise from common pathophysiologic drivers and should be understood as a unified cardiopulmonary phenotype rather than isolated organ failures. Early multimodal detection is critical for optimizing management strategies and improving outcomes.