Table 7.

Literature review

Sl. No.	Author name and type of study	Salient findings	Conclusion
1	Hiraiwa et al. [3]	Non-survivors of SICM episode have a normal EF and unchanged ventricular volume, when contrasted with survivors whose EF was below 40% and mean end-systolic/end-diastolic ventricular volumes were substantially increased with normal SV	RV dysfunction manifests with lethal arrhythmia and circulatory insufficiency independent of the LV systolic function
2	Ognibene et al. [8]	Although volume infusion in patients with sepsis and septic shock induces an increase in PCWP, it does not lead to a substantial increase in LVSWI. LVSWI is a measure of ventricular contractility. The study [16] reports that the administration of vasopressor therapy to patients with septic shock does not have a positive or negative effect on ventricular performance, when given either during or after volume infusion	The serious hemodynamic consequence of sepsis and septic shock includes the markedly abnormal LVSWI in response to volume infusion. This is a consequence of the intrinsic pathogenetic mechanisms of the left ventricle which is noted in the acute stages of sepsis and septic shock, and is manifested prior to depression of LVEF.
3	L’Heureux et al. [10]	The clinical features of SICM are defined as septic, cool extremity phenotype, hemodynamic instability despite vasopressor therapy, failure to respond to a preload challenge, abnormal echocardiogram, cardiac dysrhythmias, low mixed venous oxygen saturation, and elevated cTns	The septal relaxation in TDI is a strong predictor of mortality in patients with septic shock (e’ wave: abnormal <8 cm/s)
4	Grocott-Mason et al. [9]	The pathophysiology of SICM includes overproduction of pro-inflammatory cytokines such as IL-6 and TNF-α, which are crucial in the apoptosis of cardiomyocytes and subsequent injury. The synergistic action of TNF-α and IL-1β induces the release of factors such as nitric oxide, which causes myocardial depression	The cytokines involved with myocardial depression in SICM include endotoxins, which in turn induce mediators such as TNF-α, PAF, and IL-1β. These cytokines cause both acute negative inotropic effects and delayed effects, secondary to the induction of new proteins in the myocardium
5	Baron et al. [12]	SICM patients tend to present with a hyperkinetic profile, associated with tachycardia, supra-normal LVEF, small LV cavity despite massive volume expansion, and a high CI, which are patterns reflecting persistent and profound vasoplegia	100% mortality rate among patients with such a hyperkinetic profile
6	Huang et al. [17]	The meta-analysis reports no convincing evidence that initial low LVEF is associated with better mortality in patients with severe sepsis or septic shock. RVEF and RV dimension were not associated with mortality	LVEF in patients with sepsis could be a reflection of the balance between ventricular function and loading conditions

PCWP, pulmonary capillary wedge pressure; TDI, tissue Doppler imaging; IL-6, interleukin-6; TNF-α, tumor necrosis factor-alpha; PAF, platelet -activating factor.