Department of Cardiothoracic Anesthesia and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.
Acta Anaesthesiol Scand. 2010 Aug;54(7):814-20. doi: 10.1111/j.1399-6576.2010.02244.x. Epub 2010 May 6.
Recent experimental studies have shown that a norepinephrine-induced increase in blood pressure induces a loss of plasma volume, particularly under increased microvascular permeability. We studied the effects of norepinephrine-induced variations in the mean arterial pressure (MAP) on plasma volume changes and systemic haemodynamics in patients with vasodilatory shock.
Twenty-one mechanically ventilated patients who required norepinephrine to maintain MAP > or =70 mmHg because of septic/postcardiotomy vasodilatory shock were included. The norepinephrine dose was randomly titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, haematocrit, arterial and mixed venous oxygen content and urine flow urine were measured. Changes in the plasma volume were calculated as 100 x (Hct(pre)/Hct(post)-1)/ (1-Hct(pre)), where Hct(pre) and Hct(post) are haematocrits before and after intervention.
Norepinephrine doses to obtain target MAPs of 60, 75 and 90 mmHg were 0.20+/-0.18, 0.29+/-0.18 and 0.42+/-0.31 microg/kg/min, respectively. From 60 to 90 mmHg, increases in the cardiac index (15%), systemic oxygen delivery index (25%), central venous pressure (CVP) (20%) and pulmonary artery occlusion pressure (33%) were seen, while the intrapulmonary shunt fraction was unaffected by norepinehrine. Plasma volume decreased by 6.5% and 9.4% (P<0.0001) when blood pressure was increased from 60 to 75 and 90 mmHg, respectively. MAP (P<0.02) independently predicted the decrease in plasma volume with norepinephrine but not CVP (P=0.19), cardiac index (P=0.73), norepinephrine dose (P=0.58) or urine flow (P=0.64).
Norepinephrine causes a pressure-dependent decrease in the plasma volume in patients with vasodilatory shock most likely caused by transcapillary fluid extravasation.
最近的实验研究表明，去甲肾上腺素引起的血压升高会导致血浆容量减少，尤其是在微血管通透性增加的情况下。我们研究了去甲肾上腺素引起的平均动脉压（MAP）变化对伴有血管舒张性休克的患者的血浆容量变化和全身血液动力学的影响。
共纳入 21 例因败血症/心脏手术后血管舒张性休克而需要去甲肾上腺素维持 MAP≥70mmHg 的机械通气患者。去甲肾上腺素剂量被随机滴定至目标 MAP 为 60、75 和 90mmHg。在每个目标 MAP 时，测量全身血液动力学、血细胞比容、动脉和混合静脉氧含量和尿流量。血浆容量变化通过以下公式计算：100×（Hct（pre）/Hct（post）-1）/（1-Hct（pre）），其中 Hct（pre）和 Hct（post）分别为干预前后的血细胞比容。
获得目标 MAP 为 60、75 和 90mmHg 的去甲肾上腺素剂量分别为 0.20±0.18、0.29±0.18 和 0.42±0.31μg/kg/min。从 60mmHg 增加至 90mmHg 时，心指数（增加 15%）、全身氧输送指数（增加 25%）、中心静脉压（增加 20%）和肺动脉嵌压（增加 33%）增加，而肺内分流分数不受去甲肾上腺素的影响。当血压从 60mmHg 增加至 75mmHg 和 90mmHg 时，血浆容量分别减少了 6.5%和 9.4%（P<0.0001）。MAP（P<0.02）独立预测了去甲肾上腺素引起的血浆容量下降，但 CVP（P=0.19）、心指数（P=0.73）、去甲肾上腺素剂量（P=0.58）或尿流量（P=0.64）均不能预测。
去甲肾上腺素引起伴有血管舒张性休克的患者的血浆容量呈压力依赖性下降，最可能是由跨毛细血管液体外渗引起的。
