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中度慢性心力衰竭患者在中等强度运动期间心输出量动力学与骨骼肌氧合之间的关系。

The relation between cardiac output kinetics and skeletal muscle oxygenation during moderate exercise in moderately impaired patients with chronic heart failure.

作者信息

Spee Ruud F, Niemeijer Victor M, Schoots Thijs, Wijn Pieter F, Doevendans Pieter A, Kemps Hareld M

机构信息

Department of Cardiology, Máxima Medical Centre Veldhoven, The Netherlands; ICIN, Netherlands Heart Institute, Utrecht, The Netherlands

Department of Cardiology, Máxima Medical Centre Veldhoven, The Netherlands;

出版信息

J Appl Physiol (1985). 2016 Jul 1;121(1):198-204. doi: 10.1152/japplphysiol.00079.2016. Epub 2016 Jun 9.

DOI:10.1152/japplphysiol.00079.2016
PMID:27283909
Abstract

Oxygen uptake (V̇o2) kinetics are prolonged in patients with chronic heart failure (CHF). This may be caused by impaired oxygen delivery or skeletal muscle derangements. We investigated whether impaired cardiac output (Q̇) kinetics limit skeletal muscle oxygen delivery relative to the metabolic demands at submaximal exercise in CHF patients by evaluating the relation between Q̇ kinetics and skeletal muscle deoxygenation. Forty-three CHF patients, NYHA II-III, performed a constant-load exercise test at 80% of the ventilatory aerobic threshold (VAT) to assess V̇o2 kinetics (τV̇o2). Q̇ kinetics (τQ̇) were assessed by a radial artery pulse contour analysis method. Skeletal muscle deoxygenation was assessed by near infrared spectroscopy at the m. vastus lateralis, using the minimal value of the tissue saturation index during onset of exercise (TSImin). Patients were categorized in slow and normal Q̇ responders relative to metabolic demands (τQ̇/V̇o2 ≥1 and τQ̇/V̇o2 <1, respectively), τQ̇ (62 ± 29 s), and τV̇o2 (60 ± 21 s) were significantly related (r = 0.66, P = 0.001). There was a significant correlation between τQ̇ and TSImin in the slow Q̇ responders [rs= -0.57, P = 0.005, n = 22 (51%)]. In conclusion, in moderately impaired CHF patients with relatively slow Q̇ kinetics, central hemodynamics may limit skeletal muscle oxygenation during moderate-intensity exercise.

摘要

慢性心力衰竭(CHF)患者的摄氧量(V̇o2)动力学延长。这可能是由于氧输送受损或骨骼肌紊乱所致。我们通过评估心输出量(Q̇)动力学与骨骼肌脱氧之间的关系,研究了在CHF患者次最大运动时,受损的心输出量动力学是否会限制相对于代谢需求的骨骼肌氧输送。43例纽约心脏协会(NYHA)心功能II - III级的CHF患者,以通气有氧阈值(VAT)的80%进行恒负荷运动试验,以评估V̇o2动力学(τV̇o2)。通过桡动脉脉搏轮廓分析方法评估Q̇动力学(τQ̇)。使用运动开始时组织饱和度指数的最小值(TSImin),通过近红外光谱法在股外侧肌评估骨骼肌脱氧情况。根据相对于代谢需求的情况,将患者分为Q̇反应缓慢组和正常组(分别为τQ̇/V̇o2≥1和τQ̇/V̇o2<1),τQ̇(62±29秒)和τV̇o2(60±21秒)显著相关(r = 0.66,P = 0.001)。在Q̇反应缓慢组中,τQ̇与TSImin之间存在显著相关性[rs = -0.57,P = 0.005,n = 22(51%)]。总之,在Q̇动力学相对较慢的中度受损CHF患者中,中心血流动力学可能会限制中等强度运动期间的骨骼肌氧合。

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