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Phenylephrine increases cardiac output by raising cardiac preload in patients with anesthesia induced hypotension

机译:通过在麻醉诱导的低血压患者中提高心脏预加载,苯妥肾上腺素增加心输出

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摘要

Induction of general anesthesia frequently induces arterial hypotension, which is often treated with a vasopressor, such as phenylephrine. As a pure -agonist, phenylephrine is conventionally considered to solely induce arterial vasoconstriction and thus increase cardiac afterload but not cardiac preload. In specific circumstances, however, phenylephrine may also contribute to an increase in venous return and thus cardiac output (CO). The aim of this study is to describe the initial time course of the effects of phenylephrine on various hemodynamic variables and to evaluate the ability of advanced hemodynamic monitoring to quantify these changes through different hemodynamic variables. In 24 patients, after induction of anesthesia, during the period before surgical stimulus, phenylephrine 2 mu gkg(-1) was administered when the MAP dropped below 80% of the awake state baseline value for 3min. The mean arterial blood pressure (MAP), heart rate (HR), end-tidal CO2 (EtCO2), central venous pressure (CVP), stroke volume (SV), CO, pulse pressure variation (PPV), stroke volume variation (SVV) and systemic vascular resistance (SVR) were recorded continuously. The values at the moment before administration of phenylephrine and 5(T-5) and 10(T-10)min thereafter were compared. After phenylephrine, the mean(SD) MAP, SV, CO, CVP and EtCO2 increased by 34(13)mmHg, 11(9)mL, 1.02(0.74)Lmin(-1), 3(2.6)mmHg and 4.0(1.6)mmHg at T-5 respectively, while both dynamic preload variables decreased: PPV dropped from 20% at baseline to 9% at T-5 and to 13% at T-10 and SVV from 19 to 11 and 14%, respectively. Initially, the increase in MAP was perfectly aligned with the increase in SVR, until 150s after the initial increase in MAP, when both curves started to dissociate. The dissociation of the evolution of MAP and SVR, together with the changes in PPV, CVP, EtCO2 and CO indicate that in patients with anesthesia-induced hypotension, phenylephrine increases the CO by virtue of an increase in cardiac preload.
机译:通用麻醉诱导经常诱导动脉间低血压,其通常用丙氨酸等血管加压剂处理。作为纯粹的方位点,常规认为吩妥考虑仅诱导动脉血管收缩,从而增加心脏后载但不是心脏预载荷。然而,在具体情况下,苯妥林还可能有助于静脉返回的增加,因此有助于增加心输出(CO)。本研究的目的是描述苯字碱对各种血液动力学变量对各种血液动力学变量的初始时间过程,并评估通过不同血液动力学变量量化这些变化的先进血液动力学监测。在24例患者中,在诱导麻醉后,在手术刺激前的时间内,当地图下降到令人醒着的状态基线值的80%以下时,施用苯字碱2μgkg(-1)。3min。平均动脉血压(MAP),心率(HR),潮端CO2(ETCO2),中央静脉压(CVP),行程体积(SV),CO,脉冲压变化(PPV),行程体积变化(SVV )连续记录系统血管抗性(SVR)。比较此后施用苯妥和5(T-5)和10(T-10)分钟前的值。苯妥杂烩后,平均(SD)图,SV,CO,CVP和ETCO2增加34(13)mmHg,11(9)mL,1.02(0.74)Lmin(-1),3(2.6)mmHg和4.0(1.6 )分别在T-5处的MmHg,而动态预载变量减少:PPV分别在基线下降20%至T-5的9%,分别在T-10的T-10和SVV的13%下降。最初,当两条曲线开始解离时,地图的增加,地图的增加与SVR的增加,直到地图初始增加。地图和SVR的进化的解离,以及PPV,CVP,eTCO2和CO的变化表明,在麻醉诱导的低血压患者中,苯妥氏肾上腺素通过增加心脏预载荷增加。

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