Complexities of cardiomyopathy in septic shock

This review highlights the complex pathophysiology of myocardial dysfunction in septic shock and emphasizes the need for early and repeated hemodynamic assessments to improve outcome.

Septic cardiomyopathy is a complex, dynamic process driven by multiple mechanisms such as direct myocardial depression induced by host immune mediators (e.g., cytokines, nitric oxide) and/or bacterial toxins, and mitochondrial metabolic dysfunction. Recent echocardiography studies have described multiple unique hemodynamic clusters (phenotypes) that correlated with clinical outcomes. Similarly, serial echocardiography findings and mean arterial pressure abnormalities in patients with Streptococcal Toxic Shock Syndrome (StrepTSS) yielded three distinct hemodynamic groups that predicted mortality and morbidity. Because excessive use of fluids and/or vasopressors can be detrimental, especially in patients with microvascular injury or cardiomyopathy, application of the cardiovascular performance criteria of these different phenotypes could better inform management decisions in real time and improve outcome.

Septic cardiomyopathy is a dynamic, multidimensional response of the myocardium to infection involving both normal and dysregulated immune responses in which the measurable changes in myocardial function predict outcomes. This current paradigm mandates that functional parameters of cardiac performance be measured early and repeatedly throughout the disease course using echocardiography to guide treatment and improve outcome.