Acute left ventricular ejection fraction changes in Sepsis: Clinical predictors, management, and hospital outcomes

Sepsis causes systemic vasodilation and sympathetic activation, potentially increasing left ventricular ejection fraction (LVEF), while acidosis and cellular dysfunction may decrease it. The effects of sepsis on LVEF and its predictors remain underexplored.

In this IRB-approved retrospective cohort study, we analyzed consecutive ICU patients with sepsis who had transthoracic echocardiograms before and during sepsis. Patients were categorized into four groups based on baseline LVEF (normal vs. reduced <50 %) and LVEF change during sepsis (unchanged/increased vs. decreased). Patients with STEMI or significant valvular disease were excluded.

The aim of this study is to investigate acute LVEF changes in sepsis and assess their predictors and associated outcomes.

Of 216 included patients (39.4 % female, mean age 65±14.5 years), 64.5 % with low baseline LVEF and 74.4 % with normal baseline LVEF had unchanged or increased LVEF during sepsis. LVEF decreased in 35.4 % and 25.6 % of these groups, respectively (p = 0.180). LVEF decline was associated with a history of coronary artery disease (p = 0.003), atrial fibrillation (p = 0.015), and right ventricular dysfunction (p < 0.001). This group also had higher BNP (p < 0.001), lower blood pressures (p = 0.013), and increased vasopressor needs (p < 0.001). However, LVEF decline was not associated with differences in-hospital mortality (p = 0.862) or length of stay (p = 0.472).

Acute changes in LVEF during sepsis appear to be influenced by the severity of sepsis and underlying cardiac comorbidities. BNP may serve as a marker for acute LVEF changes. Importantly, acute changes in LVEF do not appear to influence outcomes such as mortality or hospital length of stay.