Septic Cardiomyopathy: From Pathophysiology to the Clinical Setting

Abstract

The onset of cardiomyopathy is a common feature in sepsis, with relevant effects on its pathophysiology and clinical care. Septic cardiomyopathy is characterized by reduced left ventricular (LV) contractility eventually associated with LV dilatation with or without right ventricle failure. Unfortunately, such a wide range of ultrasonographic findings does not reflect a deep comprehension of sepsis-induced cardiomyopathy, but rather a lack of consensus about its definition. Several echocardiographic parameters intrinsically depend on loading conditions (both preload and afterload) so that it may be challenging to discriminate which is primitive and which is induced by hemodynamic perturbances. Here, we explore the state of the art in sepsis-related cardiomyopathy. We focus on the shortcomings in its definition and point out how cardiac performance dynamically changes in response to different hemodynamic clusters. A special attention is also given to update the knowledge about molecular mechanisms leading to myocardial dysfunction and that recall those of myocardial hibernation. Ultimately, the aim of this review is to highlight the unsolved issue in the field of sepsis-induced cardiomyopathy as their implementation would lead to improve risk stratification and clinical care.

Clinical implications of endotoxin activity and Polymyxin‐B hemoperfusion in critically ill patients with septic cardiomyopathy: A single‐center, retrospective, observational study

“…In 1989, Suffredini et al 36 demonstrated that endotoxin administration in healthy volunteers caused left ventricular dysfunction, which was similar to the findings of Parker et al 11 in septic patients. The discrepancy with our results may be explained by the potential influence of other mediators beyond endotoxin (e.g., fungal lipoproteins or glucan) in the development of SCM, whose pathophysiology remains mostly unknown 12–14 . Nonetheless, we found that extracorporeal endotoxin removal by PMX‐HP was independently associated with R‐SCM, and this result was in accordance with Vincent et al, 37 who demonstrated cardiac function improvement after this therapy in 17 (47.2%) critically ill patients with abdominal sepsis.…”

“…However, hypotension is a low‐sensitive surrogate of organ perfusion 8,9 and its management relies on the underlying pathophysiological interplay between cardiac function and vascular tone 10 . Since the first description of septic cardiomyopathy (SCM) in 1984, 11 an increasing amount of research has shown that it is frequent, affects both ventricles, and recovers (R‐SCM) in most of the cases 12,13 . Moreover, endotoxin 14 —a membrane component of gram‐negative bacteria, that are the most frequent pathogens isolated in critically ill patients with infection 15 —plays a role of paramount importance in the pathophysiology of SCM 16 and its load can be indirectly measured by the Endotoxin Activity Assay (EAA), 17 whose high levels were directly associated with mortality 18 .…”

Interactions between Gender and Sepsis—Implications for the Future

“…The reported rates of sepsis-associated myocardial dysfunction range from 10% to 70% [ 70 ]. Substantial differences exist between men and women in the prevalence, manifestations and clinical presentation, and outcomes of heart disease [ 71 , 72 ], yet human data on this topic in relation to sepsis remains scarce.…”

Anesthetic management of patients with sepsis/septic shock

“…Cardiac function should be assessed to identify arrhythmias or septic cardiomyopathy. Septic cardiomyopathy, defined as any cardiac dysfunction (left ventricular systolic or diastolic dysfunction or right ventricular dysfunction) unrelated to ischemia ( 15 , 16 ), may be present in a variable percentage of patients, ranging from 10 to 70% ( 15 ), and may significantly contribute to hemodynamic instability and hypoperfusion. Echocardiography has a pivotal role to assess cardiac function.…”

“…Echocardiography has a pivotal role to assess cardiac function. Biomarkers such as troponin or BNP rise in relation to cardiac injury even if different mechanisms of release may be identified during sepsis (e.g., inflammation, myocardial wall stress, and renal impairment) reflecting the severity of critical illness and other organ dysfunctions independent of the cardiac cells' death ( 15 ).…”