The cardiovascular effects of normobaric hyperoxia in patients with heart rate fixed by permanent pacemaker
The cardiovascular effects of normobaric hyperoxia in patients with heart rate fixed by permanent pacemaker
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DOI：
10.1111/j.1365-2044.2009.06195.x
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发表时间：
2010-02-01
期刊：
影响因子：
10.7
通讯作者：
Kinsella, J.
中科院分区：
文献类型：
--
作者：
Anderson, K. J.;Harten, J. M.;Kinsella, J.
为了研究人类高氧引起的心率和心输出量降低是主要影响还是继发于全身血管阻力的增加，我们以随机、双盲的方式，在呼吸医用空气（吸入 O-2 分数 0.21）或氧气（吸入 O-2 分数 0.80）时以固定速率对 9 名佩戴永久性起搏器的患者进行心脏起搏。采用胸部生物阻抗机测量心率、每搏输出量和血压，并计算心脏指数和全身血管阻力指数。氧气不会导致心脏指数（p = 0.18）、卒中指数（p = 0.44）或血压（p = 0.52）发生变化，但会导致全身血管阻力指数（p = 0.03）小幅增加（5.5%）。这表明高氧没有直接的心肌抑制作用，但先前研究报告的心输出量变化是继发于全身血管阻力变化的。
To investigate whether the established reductions in heart rate and cardiac output with hyperoxia in humans are primary effects or secondary to increases in systemic vascular resistance, we paced the hearts of nine patients with permanent pacemakers at a fixed rate when breathing either medical air (inspired O-2 fraction 0.21) or oxygen (inspired O-2 fraction 0.80) in a randomised, double-blind fashion. A thoracic bio-impedance machine was used to measure heart rate, stroke volume and blood pressure and calculate cardiac index and systemic vascular resistance index. Oxygen caused no change in cardiac index (p = 0.18), stroke index (p = 0.44) or blood pressure (p = 0.52) but caused a small (5.5%) increase in systemic vascular resistance index (p = 0.03). This suggests that hyperoxia has no direct myocardial depressant effects, but that the changes in cardiac output reported in previous studies are secondary to changes in systemic vascular resistance.