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首页> 外文期刊>Respirology : >Respiratory muscle weakness increases dead-space ventilation ratio aggravating ventilation-perfusion mismatch during exercise in patients with chronic heart failure
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Respiratory muscle weakness increases dead-space ventilation ratio aggravating ventilation-perfusion mismatch during exercise in patients with chronic heart failure

机译:呼吸肌弱势增加了慢性心力衰竭患者运动过程中的死空气通风比加重通气灌注失配

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Background and objective Respiratory muscle weakness causes fatigue in these muscles during exercise and thereby increases dead-space ventilation ratio with decreased tidal volume. However, it remains unclear whether respiratory muscle weakness aggravates ventilation-perfusion mismatch through the increased dead-space ventilation ratio. In ventilation-perfusion mismatch during exercise, minute ventilation versus carbon dioxide production (VE/VCO2) slope 34 is an indicator of poor prognosis in patients with chronic heart failure (CHF). We examined the relationship of respiratory muscle weakness with dead-space ventilation ratio and ventilation-perfusion mismatch during exercise and clarified whether respiratory muscle weakness was a clinical predictor of VE/VCO2 slope 34 in patients with CHF. Methods Maximal inspiratory pressure (PImax) was measured as respiratory muscle strength 2 months after hospital discharge in 256 compensated patients with CHF. During cardiopulmonary exercise test, we assessed minute dead-space ventilation versus VE (VD/VE ratio) as dead-space ventilation ratio and VE/VCO2 slope as ventilation-perfusion mismatch. Patients were divided into low, moderate and high PImax groups based on the PImax tertile. We investigated determinants of VE/VCO2 slope 34 among these groups. Results The low PImax group showed significantly higher VD/VE ratios at 50% of peak workload and at peak workload and higher VE/VCO2 slope than the other two groups (P 0.001, respectively). PImax was a significant independent determinant of VE/VCO2 slope 34 (odds ratio (OR): 0.67, 95% CI: 0.54-0.82) with area under the receiver operating characteristic curve of 0.812 (95% CI: 0.750-0.874). Conclusion Respiratory muscle weakness was associated with an increased dead-space ventilation ratio aggravating ventilation-perfusion mismatch during exercise in patients with CHF.
机译:背景和客观呼吸肌弱效力导致在运动期间这些肌肉中的疲劳,从而增加了潮气量降低的死区空间通风率。然而,仍然尚不清楚呼吸肌弱是否会通过增加的死亡空间通风率加剧通风灌注失配。在运动期间通风灌注失配,微小通风与二氧化碳生产(VE / VCO2)斜坡& 34是慢性心力衰竭(CHF)患者预后不良的指标。我们在运动期间检查了呼吸肌弱点和通风灌注错配的关系,并澄清了呼吸肌弱点是VE / VCO2斜坡的临床预测因子。 34患有CHF的患者。方法在256例补偿患者的乳糖患者中2个月后测量最大吸气压力(PiMax)作为呼吸肌强度为2个月。在心肺运动试验期间,我们评估了微小的死区通风,与VE(VD / VE比率)为死空气通风比和VE / VCO2斜率作为通风灌注失配。患者基于PiMax Tertile分成低,中等和高的帕米达组。我们调查了VE / VCO2斜坡的决定因素。 34这些群体中。结果低PiMax组在峰值工作量的50%和比其他两组(P <0.001分别)的峰值工作量和更高的VE / VCO2斜率下显示出明显较高的VD / VE比率。 Pimax是VE / VCO2斜坡的重要独立决定因素。 34(OTS比率(或):0.67,95%CI:0.54-0.82),接收器的接收器操作特性曲线为0.812(95%CI:0.750-0.874)。结论呼吸道肌肉无力与乳糖患者运动过程中加重通气灌注不匹配的增加有关。

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