LV hypokinesia in septic shock was first established by Parker et al, working in the Parillo group. These authors also proposed an original concept to explain the recovery of patients with septic shock. They suggested that survival mainly depends on the ability of the left ventricle to dilate owing to volume loading. In their survivors, despite a severely depressed LVEF, adequate LV stroke output could be maintained through this acute LV dilatation, a compensatory mechanism similar to that operating in chronic congestive cardiac failure. Although our echocardiographic data showed a similar trend in the time-course of LV diastolic dimensions, the extent of LV enlargement in survivors was much smaller than that reported in the study by Parker et al. In our patients who survived, LVEDV increased by approximately 14%, whereas Parker et al reported a 100% increase. In our patients, LV dilatation was therefore limited in response to volume loading, and the progressive increase in stroke output in survivors mainly resulted from a progressive improvement in LVEF. Methodological differences should be considered to explain this discrepancy. Contrast ventriculography, the “gold standard” for LV volume measurements, is not available at the bedside, and other methods suffer from some inaccuracies. more
Transthoracic echocardiography has been validated for LV volume measurements, but generally underestimates LV volumes in comparison with contrast ventriculography, particularly with the single-plane apical four-chamber area-length algorithm used in the present study. Moreover, image quality in patients receiving mechanical ventilation patients is often poor, and 54 of the 114 patients in this cohort were not included because of inadequate endocardial visualization. But this potential limitation will be circumvented in the future by using transesophageal echocardiography, which permits a perfect visualization of endocardial borders in patients receiving mechanical ventilation. Radionuclide angiography provides precise measurements of LVEF that correlate well with values from contrast ventricu-lography. However, this method does not permit direct measurement of LV volumes; combining cardiac output measurement by thermodilution and LVEF by radionuclide angiography, the LV volume calculation performed by Parker et al, may well produce serious inaccuracies. Using the same methodology, Schneider et al found only a 17% LVEDV increase in septic patient responders to volume loading, an LV dilatation far removed from the 100% increase described by Parker et al. Moreover, the minor LV dilatation observed in the present study was expected because pericardial stiffness usually precludes acute LV dilatation despite the amount of fluid used for resuscitation, and a normally filled LV did not have preload reserve because it operates on the steep portion of its pressure-volume relation beyond its optimal filling pressure. In a recent study using transesophageal echocardiography, Poelaert et al did not find any LV dilatation in persistently vasopressor-dependent patients with septic shock.