Fig. 1

Pathophysiology of septic shock and secondary myocardial dysfunction. (a) In the normal condition, cardiac output is adequate to meet the oxygen demand in peripheral tissues. (b) At the very early phase of sepsis, LV ejection fraction (EF) is not impaired (typically LVEF >55 %), but stroke volume (SV) is low because of insufficient cardiac preload due to a high vascular permeability and vasodilation. The compensatory increase in heart rate (HR) is often insufficient to maintain adequate cardiac output. (c) After fluid loading, SV can be recovered especially in the case of survivors while LVEF is temporarily decreased (typically <45 %) in part due to high LVEDV. This indicates that low LVEF may represent preload optimization and good adaptation. (d) During the later phase of sepsis, non-survivors are given more fluid than survivors but, nevertheless, have lower LVEDV suggesting a persistent vascular hyperpermeability and preload deficiency. In these cases, LVEF can be retained in part due to low LVEDV and/or ongoing harmful adrenergic over-stimulation