Department of Rehabilitation, Kitasato University Hospital, Sagamihara, Japan.
Department of Cardiovascular Medicine, Kitasato University Graduate School of Medical Sciences, Sagamihara, Japan.
Respirology. 2019 Feb;24(2):154-161. doi: 10.1111/resp.13432. Epub 2018 Nov 14.
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/VCO ) 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/VCO slope > 34 in patients with CHF.
Maximal inspiratory pressure (PI ) 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/VCO slope as ventilation-perfusion mismatch. Patients were divided into low, moderate and high PI groups based on the PI tertile. We investigated determinants of VE/VCO slope > 34 among these groups.
The low PI group showed significantly higher VD/VE ratios at 50% of peak workload and at peak workload and higher VE/VCO slope than the other two groups (P < 0.001, respectively). PI was a significant independent determinant of VE/VCO 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).
Respiratory muscle weakness was associated with an increased dead-space ventilation ratio aggravating ventilation-perfusion mismatch during exercise in patients with CHF.
呼吸肌无力导致运动时肌肉疲劳，从而使死腔通气量增加，潮气量减少。然而，呼吸肌无力是否通过增加死腔通气量加重通气-灌注不匹配仍不清楚。在运动时的通气-灌注不匹配中，分钟通气量与二氧化碳产量的斜率（VE/VCO ）>34 是慢性心力衰竭（CHF）患者预后不良的指标。我们研究了呼吸肌无力与运动时死腔通气量和通气-灌注不匹配的关系，并阐明了呼吸肌无力是否是 CHF 患者 VE/VCO 斜率>34 的临床预测指标。
在 256 例代偿性 CHF 患者出院后 2 个月，测量最大吸气压力（PI ）作为呼吸肌力量。在心肺运动试验中，我们评估了分钟死腔通气量与 VE（VD/VE 比值）作为死腔通气量比值和 VE/VCO 斜率作为通气-灌注不匹配。根据 PI 三分位将患者分为低、中、高 PI 组。我们研究了这些组中 VE/VCO 斜率>34 的决定因素。
低 PI 组在 50%峰值工作量和峰值工作量时的 VD/VE 比值明显较高，且 VE/VCO 斜率也高于其他两组（P<0.001，分别）。PI 是 VE/VCO 斜率>34 的显著独立预测因子（比值比（OR）：0.67，95%可信区间：0.54-0.82），其受试者工作特征曲线下面积为 0.812（95%可信区间：0.750-0.874）。
呼吸肌无力与 CHF 患者运动时死腔通气量增加有关，加重了通气-灌注不匹配。
