Caille Vincent, Jabot Julien, Belliard Guillaume, Charron Cyril, Jardin François, Vieillard-Baron Antoine
Centre Hospitalier Universitaire Ambroise Paré, 92104, Boulogne Cedex, France.
Intensive Care Med. 2008 Jul;34(7):1239-45. doi: 10.1007/s00134-008-1067-y. Epub 2008 Mar 20.
To determine the effects of passive leg raising (PLR) on hemodynamics and on cardiac function according to the preload dependency defined by the superior vena cava collapsibility index (DeltaSVC).
Forty patients with shock, sedated and mechanically ventilated, were included. Transesophageal echocardiography was performed. At baseline (T1), two groups were defined according to DeltaSVC. Eighteen patients presenting a DeltaSVC > 36%, an indicator of preload dependency, formed group 1, whereas 22 patients (group 2) exhibited a DeltaSVC < 30% (not preload-dependent). Measurements were then performed during PLR (T2), back to baseline (T3), and after volume expansion (T4) in group 1 only. At T1, DeltaSVC was significantly higher in group 1 than in group 2, 50 +/- 9% and 7 +/- 6%, respectively. In group 1, we found a decrease in DeltaSVC at T2 (24 +/- 9%) and T4 (17 +/- 7%), associated with increased systolic, diastolic and arterial pulse pressures. Cardiac index also increased, from 1.92 +/- 0.74 (T1) to 2.35 +/- 0.92 (T2) and 2.85 +/- 1.2 l/min/m(2) (T4) and left ventricular end-diastolic volume from 51 +/- 41 to 61 +/- 51 and 73 +/- 51 ml/m(2). None of these variations was found in group 2. No change in heart rate was observed.
Hemodynamic changes related to PLR were only induced by increased cardiac preload.
根据上腔静脉塌陷指数(DeltaSVC)定义的前负荷依赖性,确定被动抬腿(PLR)对血流动力学和心脏功能的影响。
纳入40例休克、接受镇静和机械通气的患者。进行了经食管超声心动图检查。在基线(T1)时,根据DeltaSVC定义了两组。18例DeltaSVC>36%(前负荷依赖性指标)的患者组成第1组,而22例患者(第2组)DeltaSVC<30%(非前负荷依赖性)。然后仅在第1组的PLR期间(T2)、恢复到基线时(T3)和容量扩充后(T4)进行测量。在T1时,第1组的DeltaSVC显著高于第2组,分别为50±9%和7±6%。在第1组中,我们发现T2(24±9%)和T4(17±7%)时DeltaSVC降低,同时收缩压、舒张压和动脉脉压升高。心脏指数也增加,从1.92±0.74(T1)增加到2.35±0.92(T2)和2.85±1.2 l/min/m²(T4),左心室舒张末期容积从51±41增加到61±51和73±51 ml/m²。第2组未发现这些变化。心率未观察到变化。
与PLR相关的血流动力学变化仅由心脏前负荷增加引起。