Clinical implications of septic cardiomyopathy: A narrative review

Abstract

Sepsis is caused by the body's dysregulated response to infection, which can lead to multiorgan injury and death. Patients with sepsis may develop acute cardiac dysfunction, termed septic cardiomyopathy, which is a global but reversible dysfunction of both sides of the heart. This narrative review discusses the mechanistic changes in the heart during septic cardiomyopathy, its diagnosis, existing treatment options regarding severity and course, and emerging treatment approaches. Although no standardized definition for septic cardiomyopathy exists, it is described as a reversible myocardial dysfunction that typically resolves within 7 to 10 days. Septic cardiomyopathy is often diagnosed based on electrocardiography, cardiac magnetic resonance imaging, biomarkers, and direct invasive and noninvasive measures of cardiac output. Presently, the treatment of septic cardiomyopathy is similar to that of sepsis, primarily focusing on acute interventions. Treatments for cardiomyopathy often include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and diuretics. However, because of profound hypotension in sepsis, many cardiomyopathy treatments are contraindicated in patients with septic cardiomyopathy. Substantial efforts have been made to study the pathophysiological mechanisms and diagnostic options; however, the lack of a uniform definition for septic cardiomyopathy is challenging for physicians when considering treatments. Another challenge for physicians is that the treatment for septic cardiomyopathy has only focused on acute intervention, whereas the treatment for other cardiomyopathies has been provided on a long-term basis. A better understanding of the underlying mechanisms of septic cardiomyopathy may contribute to the development of a unified definition of the condition and novel treatment options.

Figure 1.

Pathophysiology and mechanisms of septic myocardial dysfunction. Synopsis of basic pathophysiology and mechanisms of sepsis-induced cardiomyopathy: Septic cardiomyopathy can be caused by several factors, including the release of inflammatory mediators and direct toxic effects of bacteria and their toxins on the myocardium. Additionally, the body’s immune response can cause septic cardiomyopathy, leading to inflammation and damage to the heart muscle. Peripheral vascular beds can become constricted in septic cardiomyopathy, which may be caused by the body’s response to sepsis, causing the release of various mediators, such as catecholamines and cytokines. Restriction of blood flow to the peripheral tissues can lead to organ ischemia, hypoperfusion, and organ failure. Blood vessels may leak, allowing the fluid to escape into the surrounding tissue. This can lead to edema in the peripheral tissues and organs. Myocardial dysfunction can occur in multiple ways during sepsis. For example, the left and/or right ventricles can become impaired during systole or diastole, with or without inadequate cardiac output and oxygen delivery. IL = interleukin, iNOS = induced nitric oxide synthase, PMN = polymorphonuclear cell, TNF = tumor necrosis factor.