Guinot Pierre-Grégoire, Longrois Dan, Kamel Said, Lorne Emmanuel, Dupont Hervé
Department of Anaesthesiology and Critical Care, Amiens University Hospital, Place Victor Pauchet, Amiens, France.
INSERM U1088, Jules Verne University of Picardy, Amiens, France.
Crit Care Med. 2018 Jan;46(1):e17-e25. doi: 10.1097/CCM.0000000000002772.
The objectives of the present study were to evaluate, in patients with persistent arterial hypotension in the immediate postcardiac surgery period, the effects of norepinephrine infusion on ventriculo-arterial coupling, its determinants: arterial elastance and end-systolic ventricular elastance, and to test the ability of arterial elastance to end-systolic ventricular elastance ratio to predict stroke volume increases.
Prospective observational study.
Cardiac-vascular surgical ICU.
Twenty-eight postoperative cardiac surgery patients, in whom physicians decided to administer norepinephrine infusion, were included.
Arterial pressure, stroke volume index, cardiac index, indexed total peripheral resistance, arterial compliance, arterial elastance, and end-systolic ventricular elastance, were measured before and after norepinephrine infusion. We estimated ventriculo-arterial coupling by the arterial elastance to end-systolic ventricular elastance ratio and defined stroke volume responders by a stroke volume increase greater than or equal to 15%. Twenty-two of the 28 subjects had altered ventriculo-arterial coupling (1.87 [1.57-2.51] vs 1.1 [1-1.18]). Fifteen of the 28 subjects (54%) were stroke volume responders. At baseline, stroke volume responders had similar arterial pressure, higher indexed total peripheral resistance, arterial elastance, arterial elastance to end-systolic ventricular elastance ratio (2.21 [1.69-2.89] vs 1.33 [1.1-1.56]; p < 0.05), and lower arterial compliance, indexed total peripheral resistance and cardiac index. Norepinephrine significantly increased arterial pressure in all subjects. In stroke volume responders, norepinephrine increased arterial elastance, end-systolic ventricular elastance, cardiac index, and improved arterial elastance/end-systolic ventricular elastance coupling. The baseline arterial elastance to end-systolic ventricular elastance ratio predicted stroke volume responsiveness (area under the curve [95% CI], 0.87 [0.71-1]; p < 0.0001).
In patients with arterial hypotension norepinephrine increased end-systolic ventricular elastance and arterial elastance. The effects of norepinephrine on stroke volume depend on baseline ventriculo-arterial coupling. Although norepinephrine infusion corrects arterial hypotension in all subjects, increase of stroke volume occurred only in subjects with altered ventriculo-arterial coupling.
本研究的目的是评估心脏术后即刻出现持续性动脉低血压的患者中,去甲肾上腺素输注对心室-动脉耦联及其决定因素(动脉弹性和收缩末期心室弹性)的影响,并测试动脉弹性与收缩末期心室弹性比值预测每搏量增加的能力。
前瞻性观察性研究。
心血管外科重症监护病房。
纳入28例心脏术后患者,这些患者经医生决定接受去甲肾上腺素输注。
在去甲肾上腺素输注前后测量动脉压、每搏量指数、心脏指数、外周血管阻力指数、动脉顺应性、动脉弹性和收缩末期心室弹性。我们通过动脉弹性与收缩末期心室弹性比值评估心室-动脉耦联,并将每搏量增加大于或等于15%的患者定义为每搏量反应者。28例受试者中有22例心室-动脉耦联改变(1.87[1.57 - 2.51]对1.1[1 - 1.18])。28例受试者中有15例(54%)为每搏量反应者。基线时,每搏量反应者的动脉压相似,外周血管阻力指数、动脉弹性、动脉弹性与收缩末期心室弹性比值较高(2.21[1.69 - 2.89]对1.33[1.1 - 1.56];p<0.05),而动脉顺应性、外周血管阻力指数和心脏指数较低。去甲肾上腺素使所有受试者的动脉压显著升高。在每搏量反应者中,去甲肾上腺素增加了动脉弹性、收缩末期心室弹性、心脏指数,并改善了动脉弹性/收缩末期心室弹性耦联。基线时的动脉弹性与收缩末期心室弹性比值可预测每搏量反应性(曲线下面积[95%CI],0.87[0.71 - 1];p<0.0001)。
在动脉低血压患者中,去甲肾上腺素增加了收缩末期心室弹性和动脉弹性。去甲肾上腺素对每搏量的影响取决于基线心室-动脉耦联。虽然去甲肾上腺素输注可纠正所有受试者的动脉低血压,但仅在心室-动脉耦联改变的受试者中出现每搏量增加。