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  • Review Article
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Pathophysiology of sepsis-induced cardiomyopathy

Nature Reviews Cardiology volume 18, pages 424–434 (2021)Cite this article

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Abstract

Sepsis is the life-threatening organ dysfunction caused by a dysregulated host response to infection and is the leading cause of death in intensive care units. Cardiac dysfunction caused by sepsis, usually termed sepsis-induced cardiomyopathy, is common and has long been a subject of interest. In this Review, we explore the definition, epidemiology, diagnosis and pathophysiology of septic cardiomyopathy, with an emphasis on how best to interpret this condition in the clinical context. Advances in diagnostic techniques have increased the sensitivity of detection of myocardial abnormalities but have posed challenges in linking those abnormalities to therapeutic strategies and relevant clinical outcomes. Sophisticated methodologies have elucidated various pathophysiological mechanisms but the extent to which these are adaptive responses is yet to be definitively answered. Although the indications for monitoring and treating septic cardiomyopathy are clinical and directed towards restoring tissue perfusion, a better understanding of the course and implications of septic cardiomyopathy can help to optimize interventions and improve clinical outcomes.

Key points

  • Advances in diagnostic techniques have increased the sensitivity of detection of myocardial abnormalities in patients with sepsis but have increased uncertainty about how sepsis-induced cardiomyopathy should be defined.

  • The variability in definitions of septic cardiomyopathy poses challenges in linking these abnormalities to therapeutic strategies and relevant clinical outcomes.

  • Sophisticated methodologies have helped to elucidate the mechanisms of septic cardiomyopathy, but the degree to which these mechanisms are adaptive remains uncertain.

  • The indications for monitoring and treating septic cardiomyopathy are clinical and aimed at tissue perfusion.

  • A better understanding of the course and implications of septic cardiomyopathy can help to optimize interventions and improve clinical outcomes.

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Fig. 1: Pathophysiology of sepsis-induced cardiomyopathy.
Fig. 2: Potential physiological implications of systolic dysfunction and downregulation of mitochondrial function in sepsis-induced cardiomyopathy.

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Authors and Affiliations

  1. Hackensack Meridian School of Medicine, Hackensack University Medical Center, Hackensack, NJ, USA

    Steven M. Hollenberg

  2. Bloomsbury Institute of Intensive Care Medicine, Division of Medicine, University College London, London, UK

    Mervyn Singer

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  1. Steven M. Hollenberg
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S.M.H. wrote the manuscript, and M.S. reviewed and edited the article before submission.

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Correspondence to Steven M. Hollenberg or Mervyn Singer.

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Nature Reviews Cardiology thanks K. Werdan and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

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Glossary

Fluid resuscitation

Administration of intravenous fluids to restore intravascular volume.

Global longitudinal strain

(GLS). GLS is a parameter derived from speckle tracking echocardiography that expresses longitudinal shortening. GLS is calculated by convention as final length minus baseline length divided by baseline length as a percentage, and so left ventricular (LV) shortening yields a negative strain.

Arterial elastance

A representation of the change in pressure for a given change in arterial volume on an LV pressure–volume loop. Arterial elastance is usually estimated as end-systolic pressure divided by stroke volume.

End-systolic elastance

A measure of the net arterial load exerted on the ventricle. LV end-systolic elastance is usually estimated clinically as LV end-systolic pressure divided by end-systolic volume, although this is a simplification.

Lusitropic effects

Effects related to the rate of relaxation of the LV myocardium. Lusitropy is correlated with calcium reuptake into the sarcoplasmic reticulum, which is an energy-dependent process.

Immunoparesis

Excessive downregulation of immune function, often in response to a previous inflammatory stimulus.

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Hollenberg, S.M., Singer, M. Pathophysiology of sepsis-induced cardiomyopathy. Nat Rev Cardiol 18, 424–434 (2021). https://doi.org/10.1038/s41569-020-00492-2

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