ECHOCARDIOGRAPHIC AND HEMODYNAMIC INDEXES OF LEFT-VENTRICULAR PRELOADIN PATIENTS WITH NORMAL AND ABNORMAL VENTRICULAR-FUNCTION

Background: Transesophageal echocardiography (TEE) is used to diagnose hypovolemia despite the lack of validation studies. The objective was to determine the effects of acute graded hypovolemia on TEE and conve ntional hemodynamic determinants of left ventricular (LV) preload in a nesthetized patients with normal and abnormal LV function. Methods: De terminants of LV preload derived from TEE and hemodynamic monitoring w ere measured serially in 35 anesthetized cardiac surgical patients wit hout valvular heart disease. Patients were stratified into two groups: those with normal LV function (group 1, n = 17) and those with LV wal l motion abnormalities (group 2, n = 13). Patients in groups 1 and 2 w ere subjected to graded hypovolemia produced by collecting 6 aliquots of blood, each equal to 2.5% of their estimated blood volume (EBV). A third group of patients (group 3, n = 5), not subjected to graded hypo volemia, were studied to test for time-dependent changes. Results: Gro up 2 had a significantly greater baseline (mean +/- SD) pulmonary arte ry occlusion pressure (17 +/- 6 vs. 11 +/- 6 mmHg), LV end-diastolic a rea (23 +/- 5 vs. 18 +/- 4 cm(2)), LV end-diastolic wall stress (23 +/ - 10 vs. 14 +/- 6 X 10(3) dyne.cm(-2)), and smaller fractional area ch ange (35 +/- 13 vs. 59 +/- 7%) In groups 1 and 2, the LV end-diastolic area, pulmonary artery occlusion pressure, and LV end-diastolic wall stress decreased linearly in response to blood loss in the range of 0- 15% of the EBV. No significant changes in the measured parameters occu rred in group 3. A significant decrease in the central venous pressure , pulmonary artery occlusion pressure, and LV end-diastolic area was d etected in response to a 2.5% EBV deficit (approximately 1.75 ml.kg(-1 )) in groups 1 and 2. The mean change in LV end-diastolic area (0.3 cm (2)/1.0% EBV deficit) in response to equivalent EBV deficits was the s ame in groups 1 and 2. In contrast, the mean change in cardiac output and LV end-diastolic wall stress was less in group 2 despite a greater decrease in pulmonary artery occlusion pressure. Compared to group 1, a greater EBV deficit (7.5% to 12.5% vs. 2.5% to 5%) was required in group 2 to cause a significant decrease in the cardiac output, stroke volume, mixed venous oxygen saturation, and LV end-diastolic wall stre ss. Conclusions: TEE and hemodynamic determinants of LV preload detect ed changes in LV function caused by acute blood loss. Acute blood loss caused directional changes in LV end-diastolic area, pulmonary artery occlusion pressure, and LV end-diastolic wall stress even in patients with LV wall motion abnormalities. Changes in LV end-diastolic wall s tress, derived from both TEE and hemodynamic measurements corresponded to changes in cardiac output, stroke volume, and mixed venous oxygen saturation that occurred during acute blood loss.