Determination of vascular waterfall phenomenon by bedside measurement of mean systemic filling pressure and critical closing pressure in the intensive care unit.
Determination of vascular waterfall phenomenon by bedside measurement of mean systemic filling pressure and critical closing pressure in the intensive care unit.
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DOI：
10.1213/ane.0b013e318247fa44
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发表时间：
2012-04
影响因子：
5.7
通讯作者：
Jansen JR
中科院分区：
文献类型：
--
作者：
Maas JJ;de Wilde RB;Aarts LP;Pinsky MR;Jansen JR
平均全身充盈压(PMSF)可在床边通过测量中心静脉压(PCV)和心输出量(CO)在吸气保持动作时确定。临界关闭压(PCC)可以用测量动脉压(Pa值)和CO的相同方法来确定。如果PCC&>PMSF，那么就有一个血管瀑布。在这项研究中，我们通过测定床边的PMSF和PCC来评估瀑布的存在及其对血管阻力计算的影响。对10例心脏手术后机械通气患者进行吸气屏气动作，一过性增加PCV，降低Pa值和CO至四个不同的稳态水平。每个患者的PCV和CO值被绘制在静脉回流曲线上，以确定PMSF。同样，通过绘制动脉压和心输出量的心输出量曲线来确定PCC。对每例患者用0.5g L胶体扩容前后进行测量，计算血管阻力。对于每个患者，PCV和CO的四个测量值与Pa值和CO的测量值之间呈线性关系。基线PMSF值为18.7±4.0(Mean±SD)mm Hg，与PCC45.5±11.1 mm Hg有显著差异(p<；0.0001)。PCC和PMSF的差值为26.8±10.7 mm Hg，提示存在全身血管瀑布。扩容后PMSF(2 6.3±3.2)mm Hg、PCC(5 1.5±9.0)mm Hg、CO(5.5±1.8)−·min-1增加(P<0.0 5)。动脉(PCC上游)和静脉(PMSF下游)的血管阻力分别为8.27±4.45和2.75±1.23−·min·L−1，两者之和(11.01 mm Hg.min·L−1)与全身血管总阻力(16.56±8.57 mm Hg.min·L)相比差异有统计学意义(p=0.005)。动脉阻力与总阻力相关。心脏手术患者的血管压力梯度提示存在血管瀑布现象，这不受CO的影响。因此，全身血管总阻力的测量在评估全身血管舒缩张力时可能变得无关紧要。
Mean systemic filling pressure (Pmsf) can be determined at the bedside by measuring central venous pressure (Pcv) and cardiac output (CO) during inspiratory hold maneuvers. Critical closing pressure (Pcc) can be determined using the same method measuring arterial pressure (Pa) and CO. If Pcc > Pmsf there is then a vascular waterfall. In this study we assessed the existence of a waterfall and its implications for the calculation of vascular resistances by determining Pmsf and Pcc at the bedside. In 10 mechanically ventilated postcardiac surgery patients inspiratory hold maneuvers were performed, transiently increasing Pcv and decreasing Pa and CO to four different steady-state levels. For each patient values of Pcv and CO were plotted in a venous return curve to determine Pmsf. Similarly, Pcc was determined with a ventricular output curve plotted for Pa and CO. Measurements were performed in each patient before and after volume expansion with 0.5 l colloid and vascular resistances were calculated. For every patient the relationship between the four measurements of Pcv and CO and of Pa and CO was linear. Baseline Pmsf was 18.7±4.0 (mean±SD) mmHg and differed significantly from Pcc 45.5±11.1 mmHg; (p<0.0001). The difference of Pcc and Pmsf was 26.8±10.7 mmHg, indicating the presence of a systemic vascular waterfall. Volume expansion increased Pmsf (26.3±3.2 mmHg), Pcc (51.5±9.0 mmHg) and CO (5.5±1.8 to 6.8±1.8 l·min−1). Arterial (upstream of Pcc) and venous (down-stream of Pmsf) vascular resistance were 8.27±4.45 and 2.75±1.23 mmHg·min·l−1; the sum of both (11.01 mmHg·min·l−1) was significantly different from total systemic vascular resistance (16.56±8.57 mmHg·min·l−1, p=0.005). Arterial resistance was related to total resistance. Vascular pressure gradients in cardiac surgery patients suggest the presence of a vascular waterfall phenomenon, which is not affected by CO. Thus measures of total systemic vascular resistance may become irrelevant in assessing systemic vasomotor tone.