LV impairment in sepsis is a well known phenomenon and has been regarded as having a significantly higher mortality rate.

Current estimates of LV impairment in sepsis range from 20-70% and RV dysfunction in up to 30%.

Proposed mechanisms:

  • cardiac depression due to catecholamine-induced cardiomyocyte toxic effects following excessive sympathetic activation – may be caused by adrenoreceptor tachyphylaxis.
  • 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.
  • Key – not due to coronary occlusion.

Features:

  • Rapid onset.
  • Lack of coronary occlusion.
  • Inconsistent ECG changes.
  • Complete reversibility in survivors usually over 7-10 days.
  • LV dilatation with normal or low filling pressures (increased compliance/LVEDP or reduced RV function).
  • Decreased ejection fraction.
  • May have normal stroke volume due to profound vasoplegia. Increasing SVR with vasoconstrictors may expose impaired LV function.
  • Absence of RWMAs – in contrast to Takotsubo cardiomyopathy. Caution in patients with previous ischaemic heart disease – look for evidence of chronic infarction.

Prognosis:

  • Usually resolves within 7-10 days.
  • May require inotropy/mechanical support in interim.
  • Although previously thought to be associated with increased mortality its role as an independent risk factor is uncertain – Huang et al, 2013.
  • Dobutamine response predicts improved prognosis in septic shock – Kumar et al, 2008.