AP-HP, Hôpitaux universitaires Paris-Sud, Hôpital de Bicêtre, service de réanimation médicale, Le Kremlin-Bicêtre, F-94270 France.
Inserm UMR S_999, Univ Paris-Sud, Le Kremlin-Bicêtre, F-94270 France.
Crit Care Med. 2019 Apr;47(4):e317-e324. doi: 10.1097/CCM.0000000000003645.
First, to validate bedside estimates of effective arterial elastance = end-systolic pressure/stroke volume in critically ill patients. Second, to document the added value of effective arterial elastance, which is increasingly used as an index of left ventricular afterload.
Prospective study.
Medical ICU.
Fifty hemodynamically stable and spontaneously breathing patients equipped with a femoral (n = 21) or radial (n = 29) catheter were entered in a "comparison" study. Thirty ventilated patients with invasive hemodynamic monitoring (PiCCO-2; Pulsion Medical Systems, Feldkirchen, Germany), in whom fluid administration was planned were entered in a " dynamic" study.
In the "dynamic" study, data were obtained before/after a 500 mL saline administration.
According to the "cardiocentric" view, end-systolic pressure was considered the classic index of left ventricular afterload. End-systolic pressure was calculated as 0.9 × systolic arterial pressure at the carotid, femoral, and radial artery level. In the "comparison" study, carotid tonometry allowed the calculation of the reference effective arterial elastance value (1.73 ± 0.62 mm Hg/mL). The femoral estimate of effective arterial elastance was more accurate and precise than the radial estimate. In the "dynamic" study, fluid administration increased stroke volume and end-systolic pressure, whereas effective arterial elastance (femoral estimate) and systemic vascular resistance did not change. Effective arterial elastance was related to systemic vascular resistance at baseline (r = 0.89) and fluid-induced changes in effective arterial elastance and systemic vascular resistance were correlated (r = 0.88). In the 15 fluid responders (cardiac index increases ≥ 15%), fluid administration increased end-systolic pressure and decreased effective arterial elastance and systemic vascular resistance (each p < 0.05). In the 15 fluid nonresponders, end-systolic pressure increased (p < 0.05), whereas effective arterial elastance and systemic vascular resistance remained unchanged.
In critically ill patients, effective arterial elastance may be reliably estimated at bedside (0.9 × systolic femoral pressure/stroke volume). We support the use of this validated estimate of effective arterial elastance when coupled with an index of left ventricular contractility for studying the ventricular-arterial coupling. Conversely, effective arterial elastance should not be used in isolation as an index of left ventricular afterload.
首先,验证危重病患者床边有效动脉弹性=收缩期末压/每搏量的估计值。其次,记录有效动脉弹性的附加价值,该值越来越多地用作左心室后负荷的指标。
前瞻性研究。
医学 ICU。
配备股动脉(n=21)或桡动脉(n=29)导管的 50 名血流动力学稳定且自主呼吸的患者进入“比较”研究。30 名接受有创血流动力学监测(PiCCO-2;Pulsion Medical Systems,Feldkirchen,德国)的机械通气患者计划进行液体治疗,进入“动态”研究。
在“动态”研究中,在 500ml 生理盐水给药前后获得数据。
根据“心脏中心”观点,收缩期末压被认为是左心室后负荷的经典指标。收缩期末压计算为颈动脉、股动脉和桡动脉水平的 0.9×收缩压。在“比较”研究中,颈动脉张力测量允许计算参考有效动脉弹性值(1.73±0.62mm Hg/mL)。股动脉有效动脉弹性估计比桡动脉估计更准确和精确。在“动态”研究中,液体治疗增加了每搏量和收缩期末压,而有效动脉弹性(股动脉估计)和全身血管阻力没有变化。有效动脉弹性与基础状态下的全身血管阻力相关(r=0.89),并且有效动脉弹性和全身血管阻力的液体诱导变化相关(r=0.88)。在 15 名液体反应者(心指数增加≥15%)中,液体治疗增加了收缩期末压,降低了有效动脉弹性和全身血管阻力(p<0.05 每项)。在 15 名液体无反应者中,收缩期末压增加(p<0.05),而有效动脉弹性和全身血管阻力保持不变。
在危重病患者中,有效动脉弹性可以在床边可靠地估计(0.9×股动脉收缩压/每搏量)。我们支持使用这种经过验证的有效动脉弹性估计值,同时结合左心室收缩性指数来研究心室-动脉耦联。相反,不应单独使用有效动脉弹性作为左心室后负荷的指标。