Department of Anaesthesiology and Intensive Care Medicine, Institute of Clinical Sciences at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Section of Cardiothoracic Anaesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden.
Acta Anaesthesiol Scand. 2021 Feb;65(2):220-227. doi: 10.1111/aas.13710. Epub 2020 Oct 5.
Arterial haematocrit (Hct) has been shown to decrease after anaesthesia induction, most probably because of an increased plasma volume (PV). The primary objective was to quantify change in PV if mean arterial pressure (MAP) was kept at baseline level or allowed to decrease to 60 mm Hg. Our secondary objective was to evaluate underlying mechanisms of this response.
Twenty-four coronary artery bypass patients were randomized to a higher (90 mm Hg, intervention group) or lower (60 mm Hg, control group) MAP by titration of norepinephrine. During the experimental procedure, no fluids were administered. Baseline PV was measured by I-albumin and the change in PV was calculated from the change in Hct. Changes in MAP, plasma I-albumin, colloid osmotic pressure, albumin, Mid Regional-pro Atrial Natriuretic Peptide (MR-proANP) and endothelial glycocalyx components were measured from baseline to 50 minutes after anaesthesia induction.
The MAP during the trial was 93 ± 9 mm Hg in the intervention group and 62 ± 5 mm Hg in the control group. PV increased with up to 420 ± 180 mL in the control group and 45 ± 130 mL in the intervention group (P < .001). Albumin and colloid osmotic pressure decreased significantly more in the control group. MR-proANP increased in the control group but no shedding of the glycocalyx layer was detected in either of the groups.
Allowing mean arterial pressure to fall to 60 mm Hg during anaesthesia induction, increases the plasma volume due to reabsorption of interstitial water, with no ANP-induced degradation of the endothelial glycocalyx.
麻醉诱导后动脉血细胞比容(Hct)会降低,这很可能是由于血容量(PV)增加所致。主要目的是量化平均动脉压(MAP)保持在基线水平或允许下降至 60mmHg 时 PV 的变化。我们的次要目标是评估这种反应的潜在机制。
24 例冠状动脉旁路患者随机分为较高(90mmHg,干预组)或较低(60mmHg,对照组)MAP 通过去甲肾上腺素滴定。在实验过程中,不给予液体。基线 PV 通过 I-白蛋白测量,Hct 的变化计算 PV 的变化。从基线到麻醉诱导后 50 分钟测量 MAP、血浆 I-白蛋白、胶体渗透压、白蛋白、中间区 pro 心房利钠肽(MR-proANP)和内皮糖萼成分的变化。
试验期间,干预组的 MAP 为 93±9mmHg,对照组为 62±5mmHg。对照组的 PV 增加了 420±180mL,而干预组的 PV 增加了 45±130mL(P<.001)。对照组白蛋白和胶体渗透压显著下降。对照组 MR-proANP 增加,但两组均未检测到糖萼层脱落。
在麻醉诱导期间允许平均动脉压降至 60mmHg 会因间质水的再吸收而增加血容量,而没有 ANP 诱导的内皮糖萼降解。