ECHOCARDIOGRAPHIC AND HEMODYNAMIC INDEXES OF LEFT-VENTRICULAR PRELOAD IN PATIENTS WITH NORMAL AND ABNORMAL VENTRICULAR-FUNCTION
ECHOCARDIOGRAPHIC AND HEMODYNAMIC INDEXES OF LEFT-VENTRICULAR PRELOAD IN PATIENTS WITH NORMAL AND ABNORMAL VENTRICULAR-FUNCTION
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DOI：
10.1097/00000542-199408000-00016
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发表时间：
1994-08-01
期刊：
影响因子：
8.8
通讯作者：
BERLIN, JA
中科院分区：
文献类型：
--
作者：
CHEUNG, AT;SAVINO, JS;BERLIN, JA
背景：经食管超声心动图（TEE）用于诊断血容量不足，尽管缺乏验证研究。目的是确定急性分级低血容量对TEE和常规血流动力学决定因素的左心室（LV）前负荷在麻醉患者正常和异常LV function.Methods的影响：来自TEE和血流动力学监测的LV前负荷的决定因素进行了连续测量35例麻醉心脏手术患者无心脏瓣膜病。患者分为两组：左室功能正常（组1，n = 17）和左室壁运动异常（组2，n = 13）。第1组和第2组的患者通过采集6等份血液（每份血液等于其估计血容量（EBV）的2.5%）进行分级血容量减少。第三组患者（组3，n = 5），不进行分级低血容量，进行了研究，以测试时间依赖性的变化。第2组的基线水平显著高于（平均值+/- SD）肺动脉闭塞压（17 +/- 6 vs. 11 +/- 6 mmHg），LV舒张末期面积（23 +/- 5 vs. 18 +/- 4 cm（2）），LV舒张末期壁应力（23 +/- 10 vs. 14 +/- 6 X 10（3）dyne.cm（-2）），和较小的面积变化分数（35 +/- 13 vs. 59 +/- 7%）。在第1组和第2组中，LV舒张末期面积、肺动脉闭塞压和LV舒张末期壁应力响应于EBV的0-15%范围内的失血而线性降低。第3组的测量参数无显著变化。在第1组和第2组中，检测到中心静脉压、肺动脉闭塞压和LV舒张末期面积显著降低，以响应2.5%的EBV缺陷（约1.75 ml.kg（-1））。在第1组和第2组中，左心室舒张末期面积的平均变化（0.3 cm（2）/1.0% EBV缺陷）对等效EBV缺陷的反应相同。相比之下，尽管肺动脉闭塞压下降幅度较大，但第2组的心输出量和左室舒张末期室壁应力的平均变化较小。与组1相比，更大的EBV赤字（7.5%至12.5%比2.5%至5%），需要在组2中引起心输出量，每搏输出量，混合静脉血氧饱和度，和LV舒张末期室壁stress.Conclusions的显着下降：TEE和LV前负荷的血流动力学决定因素检测急性失血引起的LV功能的变化。急性失血导致LV舒张末期面积、肺动脉闭塞压和LV舒张末期室壁应力方向性改变，即使在LV室壁运动异常的患者中也是如此。来自TEE和血液动力学测量的LV舒张末期壁应力的变化对应于急性失血期间发生的心输出量、每搏输出量和混合静脉血氧饱和度的变化。
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 conventional hemodynamic determinants of left ventricular (LV) preload in anesthetized patients with normal and abnormal LV function.Methods: Determinants of LV preload derived from TEE and hemodynamic monitoring were measured serially in 35 anesthetized cardiac surgical patients without valvular heart disease. Patients were stratified into two groups: those with normal LV function (group 1, n = 17) and those with LV wall motion abnormalities (group 2, n = 13). Patients in groups 1 and 2 were 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 hypovolemia, were studied to test for time-dependent changes.Results: Group 2 had a significantly greater baseline (mean +/- SD) pulmonary artery occlusion pressure (17 +/- 6 vs. 11 +/- 6 mmHg), LV end-diastolic area (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 change (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 occurred in group 3. A significant decrease in the central venous pressure, pulmonary artery occlusion pressure, and LV end-diastolic area was detected 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 same 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 stress.Conclusions: TEE and hemodynamic determinants of LV preload detected 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 stress, 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.