Nygren A, Thorén A, Ricksten S-E
Department of Cardiothoracic Anesthesia and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden.
Acta Anaesthesiol Scand. 2009 May;53(5):581-8. doi: 10.1111/j.1399-6576.2008.01900.x. Epub 2009 Feb 23.
Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery.
Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) > or = 60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained.
The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous-hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin.
Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction.
低至中等剂量的血管加压素已被用于治疗脓毒症或心脏手术后儿茶酚胺依赖性血管舒张性休克。我们评估了血管加压素对心脏手术后血管舒张性休克患者空肠黏膜灌注、胃-动脉二氧化碳分压梯度以及整体内脏氧供需关系的影响。
纳入8例机械通气患者，这些患者因脓毒症/心脏术后血管舒张性休克及心脏手术后多器官功能衰竭而依赖去甲肾上腺素维持平均动脉压（MAP）≥60 mmHg。血管加压素以1.2、2.4和4.8 U/h的剂量依次输注30分钟。同时降低去甲肾上腺素剂量以维持MAP在75 mmHg。在血管加压素的每个输注速率下，获取有关全身血流动力学、空肠黏膜灌注、空肠黏膜血细胞比容和红细胞速度（激光多普勒血流仪）以及胃-动脉二氧化碳分压梯度（胃张力测定法）和内脏氧及乳酸摄取（肝静脉导管）的数据。
随着血管加压素剂量增加，心脏指数、每搏量指数和全身氧输送降低，全身血管阻力和全身氧摄取显著增加，而心率或整体氧消耗未发生变化。空肠黏膜灌注降低，动脉-胃-黏膜二氧化碳分压梯度增加，而血管加压素输注速率增加未影响内脏氧或乳酸摄取或混合静脉-肝静脉氧饱和度梯度。
对心脏手术后依赖去甲肾上腺素的血管舒张性休克患者输注低至中等剂量的血管加压素会引起肠道和胃黏膜血管收缩。
