Heart Failure Reviews

, Volume 15, Issue 6, pp 605–611

Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms

Authors

  • Anthony Flynn
    • CardiologySt. Louis University Hospital
  • Bhalaghuru Chokkalingam Mani
    • Department of MedicineThomas Jefferson University Hospital
    • Department of Medicine, Advanced Heart Failure and Cardiac Transplant Center at the Jefferson Heart InstituteJefferson Medical College of Thomas Jefferson University
Article

DOI: 10.1007/s10741-010-9176-4

Cite this article as:
Flynn, A., Chokkalingam Mani, B. & Mather, P.J. Heart Fail Rev (2010) 15: 605. doi:10.1007/s10741-010-9176-4

Abstract

Cardiac dysfunction is a well-recognized complication of severe sepsis and septic shock. Cardiac dysfunction in sepsis is characterized by ventricular dilatation, reduction in ejection fraction and reduced contractility. Initially, cardiac dysfunction was considered to occur only during the “hypodynamic” phase of shock. But we now know that it occurs very early in sepsis even during the “hyperdynamic” phase of septic shock. Circulating blood-borne factors were suspected to be involved in the evolution of sepsis induced cardiomyopathy, but it is not until recently that the cellular and molecular events are being targeted by researchers in a quest to understand this enigmatic process. Septic cardiomyopathy has been the subject of investigation for nearly half a century now and yet controversies exist in understanding it’s pathophysiology. Here, we discuss our understanding of the pathogenesis of septic cardiomyopathy and the complex roles played by nitric oxide, mitochondrial dysfunction, complements and cytokines.

Keywords

CardiomyopathySepsisNitric oxideComplementsCytokineMyocardial depression

Copyright information

© Springer Science+Business Media, LLC 2010