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.