Department of Anaesthesiology and Intensive Care Medicine, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Department of Clinical Physiology, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Acta Anaesthesiol Scand. 2019 Nov;63(10):1337-1345. doi: 10.1111/aas.13454. Epub 2019 Aug 19.
In this observational study, the effects of norepinephrine-induced changes in mean arterial pressure (MAP) on right ventricular (RV) systolic function, afterload and pulmonary haemodynamics were studied in septic shock patients. We hypothesised that RV systolic function improves at higher doses of norepinephrine/MAP levels.
Eleven patients with septic shock requiring norepinephrine after fluid resuscitation were included <24 hours after ICU arrival. Study enrolment and insertion of a pulmonary artery catheter was performed after written informed consent from the next of kin. Norepinephrine infusion was titrated to target mean arterial pressures (MAP) of 60, 75 and 90 mmHg in a random sequential order. At each target MAP, strain-and conventional echocardiographic-and pulmonary haemodynamic variables were measured. RV afterload was assessed as effective pulmonary arterial elastance, (E ) and pulmonary vascular resistance index, (PVRI). RV free wall peak strain was the primary end-point.
At highest compared to lowest norepinephrine dose/MAP level, RV free wall peak strain increased from -19% to -25% (32%, P = .003), accompanied by increased tricuspid annular plane systolic excursion (22%, P = .01). At the highest norepinephrine dose/MAP, RV end-diastolic area index (16%, P < .001), central venous pressure (38%, P < .001), stroke volume index (7%, P = .001), mean pulmonary artery pressure (19%, P < .001) and RV stroke work index (15%, P = .045) increased, with no effects on PVRI or E . Cardiac index did not change, assessed by thermodilution (P = .079) and echocardiography (P = .054).
Higher doses of norepinephrine to a target MAP of 90 mm Hg improved RV systolic function while RV afterload was not affected.
在这项观察性研究中，我们研究了去甲肾上腺素引起的平均动脉压（MAP）变化对脓毒性休克患者右心室（RV）收缩功能、后负荷和肺血液动力学的影响。我们假设 RV 收缩功能在更高剂量的去甲肾上腺素/MAP 水平下会改善。
在 ICU 到达后 24 小时内，纳入了 11 名需要去甲肾上腺素进行液体复苏的脓毒性休克患者。在获得家属的书面知情同意后，进行研究登记和肺动脉导管插入。以 60、75 和 90mmHg 的目标平均动脉压（MAP）顺序进行去甲肾上腺素输注滴定。在每个目标 MAP 时，测量应变和传统超声心动图及肺血液动力学变量。RV 后负荷评估为有效肺动脉弹性（E）和肺血管阻力指数（PVRI）。RV 游离壁峰值应变是主要终点。
与最低去甲肾上腺素剂量/MAP 水平相比，RV 游离壁峰值应变从-19%增加到-25%（32%，P=0.003），同时三尖瓣环平面收缩期位移增加（22%，P=0.01）。在最高去甲肾上腺素剂量/MAP 时，RV 舒张末期面积指数（16%，P<0.001）、中心静脉压（38%，P<0.001）、每搏量指数（7%，P=0.001）、平均肺动脉压（19%，P<0.001）和 RV 每搏功指数（15%，P=0.045）增加，但对 PVRI 或 E 没有影响。通过热稀释法（P=0.079）和超声心动图（P=0.054）评估的心输出量没有变化。
目标 MAP 为 90mmHg 时更高剂量的去甲肾上腺素可改善 RV 收缩功能，而 RV 后负荷不受影响。
