Septic cardiomyopathy

Reviewed and revised 11 November 2016


  • Septic cardiomyopathy is a common feature of severe sepsis syndromes and results in impaired intrinsic cardiac contractility
  • First described by Parker et al in 1984
  • Incidence varies in studies, most report 20-60% incidence in the first few days of ICU admission


Proposed mechanisms include

  • cardiac depression due to catecholamine-induced cardiomyocyte toxic effects following excessive sympathetic activation
  • cytokine-mediated impaired contractility (e.g. TNF-alpha, IL1beta)
  • increased cGMP and NO intracellular second messengers
  • sepsis-induced mitochondrial dysfunction
  • increased troponin I phosphorylation resulting in decreased calcium sensitivity
  • release of histones into the circulation

Not due to coronary occlusion! (however, septic cardiomyopathy may be aggravated by co-existent ischaemia)


Characteristic features (Vieillard-Baron, 2011; Sato and Nasu, 2014)

  • rapid onset
  • reversible and leads to full recovery in survivors, usually over 7-10 days
  • left ventricular dilatation with normal or low filling pressure (due to increased LV compliance and EDV and coexistent RV dysfunction)
  • global ventricular dysfunction with decreased ejection fraction (due to ventricular dilatation despite preserved stroke volume)
  • absence of regional dysfunction (distinct from Takotsubo cardiomyopathy and myocardial ischaemia)

Note that

  • cardiac index may not be reduced in vasoplegic patients even if there is significant ventricular dysfunction
    • e.g. the “hyperkinetic profile”: tachycardia, supra-normal LV EF, small LV cavity size and supra-normal cardiac index
  • noradrenaline may unmask septic cardiomyopathy by increasing systemic vascular resistance, causing decreased cardiac output


  • echocardiography is diagnostic
  • exclude other causes of cardiomyopathy (e.g. ischaemic cardiomyopathy, sepsis-induced takotsubo cardiomyopathy)
  • biomarkers
    • troponin
      • correlates with mortality in sepsis, but is not diagnostic of septic cardiomyopathy (Landesberg et al, 2014)
    • BNP
      • likely correlates with critical illness rather than septic cardiomyopathy per se
  • septic screen for the underlying cause
  • low filling pressures and low SVR means PAC is often insensitive for detecting septic cardiomyopathy


  • resuscitation, addressing immediate life threats (e.g. septic shock)
  • seek and treat underlying cause of sepsis (antibiotics and source control)
  • fluid resuscitation if fluid responsive and clinically indicated (avoid fluid overload)
    • positive fluid balance and raised CVP are associated with worse mortality in sepsis (Boyd et al, 2011)
  • vasoactive agents
    • inotropes e.g. dobutamine or adrenaline, if evidence of persistent shock (e.g. hyperlactaemia, oliguria)
    • noradrenaline
      • improves preload and driving pressures for end-organ perfusion (Hamzaoui et al, 2010)
      • vasopressin may be used if unresponsive to noradrenaline
    • levosimendan may avoid catecholamine-related cardiotoxicity (Zangrillo et al, 2015)
    • the benefit of vasoactive agents in terms of patient-orientated outcomes is uncertain
  • negative chronotropic agents (Rudiger and Singer, 2013)
    • Heart rate reduction with ivabradine and beta-blockers have been proposed as beneficial therapies for septic cardiomyopathy
    • They should be viewed as experimental
    • They may myocardial oxygen expenditure and ameliorates diastolic dysfunction. Beta-blockers may additionally reduce local and systemic inflammation and catecholamin toxicity.
  • severe cases may require circulatory support devices (e.g. VA ECMO)
  • seek and treat other complications of sepsis
  • supportive care and monitoring


  • Septic cardiomyopathy usually resolves within 7-10 days in survivors
  • The significance of septic cardiomyopathy as an independent prognostic indicator is uncertain (Huang et al, 2013)
  • the hyperkinetic state in particular is associated with high mortality in one study, but this was not confirmed in a meta-analysis (Huang et al, 2013)
  • impaired intrinsic contractility may be masked by profound vasoplegia, leading to preserved or supra-normal cardiac output
  • dobutamine response (increased cardiac index and oxygen delivery) predicts improved prognosis in septic shock (Kumar et al, 2008)

References and Links


Journal articles

  • Boyd JH, Forbes J, Nakada TA, Walley KR, Russell JA. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Critical care medicine. 39(2):259-65. 2011. [pubmed]
  • Flynn A, Chokkalingam Mani B, Mather PJ. Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms. Heart failure reviews. 15(6):605-11. 2010. [pubmed]
  • Hamzaoui O, Georger JF, Monnet X. Early administration of norepinephrine increases cardiac preload and cardiac output in septic patients with life-threatening hypotension. Critical care (London, England). 14(4):R142. 2010. [pubmed]
  • Huang SJ, Nalos M, McLean AS. Is early ventricular dysfunction or dilatation associated with lower mortality rate in adult severe sepsis and septic shock? A meta-analysis. Critical care (London, England). 17(3):R96. 2013. [pubmed] [free full text]
  • Kumar A, Schupp E, Bunnell E, Ali A, Milcarek B, Parrillo JE. Cardiovascular response to dobutamine stress predicts outcome in severe sepsis and septic shock. Critical Care. 12(2):R35. 2008. [pubmed] [free full text]
  • Landesberg G, Jaffe AS, Gilon D. Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation*. Critical care medicine. 42(4):790-800. 2014. [pubmed]
  • Merx MW, Weber C. Sepsis and the heart. Circulation. 116(7):793-802. 2007. [pubmed] [free full text]
  • Muller-Werdan U, Buerke M, Ebelt H. Septic cardiomyopathy – A not yet discovered cardiomyopathy? Experimental and clinical cardiology. 11(3):226-36. 2006. [pubmed] [free full text]
  • Parker MM, Shelhamer JH, Bacharach SL. Profound but reversible myocardial depression in patients with septic shock. Annals of internal medicine. 100(4):483-90. 1984. [pubmed]
  • Rudiger A, Singer M. The heart in sepsis: from basic mechanisms to clinical management. Current vascular pharmacology. 11(2):187-95. 2013. [pubmed]
  • Sato R, Nasu M. A review of sepsis-induced cardiomyopathy. Journal of intensive care. 3:48. 2015. [pubmed] [free full text]
  • Sevilla Berrios RA, O’Horo JC, Velagapudi V, Pulido JN. Correlation of left ventricular systolic dysfunction determined by low ejection fraction and 30-day mortality in patients with severe sepsis and septic shock: a systematic review and meta-analysis. Journal of critical care. 29(4):495-9. 2014. [pubmed]
  • Vieillard-Baron A. Septic cardiomyopathy. Annals of intensive care. 1(1):6. 2011. [pubmed] [free full text]
  • Zangrillo A, Putzu A, Monaco F. Levosimendan reduces mortality in patients with severe sepsis and septic shock: A meta-analysis of randomized trials. Journal of critical care. 2015. [pubmed]

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Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

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