Physiological insights of exercise hyperventilation in arterial and chronic thromboembolic pulmonary hypertension
Physiological insights of exercise hyperventilation in arterial and chronic thromboembolic pulmonary hypertension
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DOI：
10.1016/j.ijcard.2017.11.023
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发表时间：
2018-05-15
影响因子：
3.5
通讯作者：
Agostoni, Piergiuseppe
中科院分区：
文献类型：
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作者：
Farina, Stefania;Bruno, Noemi;Agostoni, Piergiuseppe
背景资料：肺动脉高压（PH）患者在运动过程中表现出通气量（V-E）相对于二氧化碳排出量（VCO 2）的过度增加，这决定了高V-E/VCO 2斜率。有几种可能的原因，包括死腔通气（V-D）升高，V-E/灌注（Q）不匹配和/或外周或中枢化学感受器活性增强。方法：对18例Ⅰ、Ⅳ组PH患者进行心肺运动试验，并进行每分钟血气分析。计算V-E、肺泡通气量（V-A）和V-D与VCO 2的关系。结果：峰值VO（2）和V-E/VCO 2斜率分别为1.06 +/- 0.24 l/min和39.1 +/- 9.0。在整个练习中，30%的V-E是由于V-D。V-E/VCO 2斜率与V-D/VCO 2斜率显著相关（r = 0.82，p < 0.001），但与V-A/VCO 2斜率不相关（r = 0.3，p = ns）。运动呼气末CO2峰值（PetCO（2））与V-D/VCO 2斜率（r =-0.79，p < 0.001）和V-E/VCO 2斜率（r =-0.91，p < 0.001）相关。死腔（DS）/潮气量和P（动脉-et）CO2升高，无动脉低氧血症，表明V-E/Q不匹配。化学感受器对缺氧的外周反应和中枢CO2反应均增强，外周反应为缺氧和高碳酸血症0.416 +/- 0.402（正常参考值= 0.285 +/- 0.221）l/min/O（2）Sat和0.076 +/- 0.047分别为（0.066 +/- 0.430）l/min/mmHg;中枢高碳酸血症化疗敏感性为4.475 +/- 3.99（2.352 +/- 0.936）l/min/mmHg。结论：DS增加、V-E/ Q失配和化学感受器反应是PH运动过度通气的主要机制。ClinicalTrial.gov NCT 02892981（c）2017 Elsevier B. V.版权所有。
Background: Pulmonary hypertension (PH) patients show, during exercise, an excessive increase in ventilation (V-E) compared to carbon dioxide output (VCO2), determining a high V-E/VCO2 slope. There are several possible causes,including an elevated dead space ventilation (V-D), V-E/perfusion (Q) mismatch and/or an enhanced peripheral or central chemoreceptor activity. We evaluated the causes of exercise hyperventilation in PH patients.Methods: Eighteen group I and IV PH patients underwent cardiopulmonary exercise test with blood gas analysis at every minute. V-E, alveolar ventilation (V-A) and V-D vs. VCO2 relationship were calculated. Resting chemoreceptor sensitivity was analyzed through hypoxia/hypercapnia tests.Results: PeakVO(2) and V-E/VCO2 slopes were 1.06 +/- 0.24 l/min and 39.1 +/- 9.0, respectively. Throughout the exercise, 30% of V-E was due to V-D. V-E/VCO2 slope significantly correlated with V-D/VCO2 slope (r = 0.82, p < 0.001) but not with V-A/VCO2 slope (r = 0.3, p = ns). Peak exercise end-tidal CO2 (PetCO(2)) correlated with V-D/VCO2 slope (r = - 0.79, p < 0.001) and V-E/VCO2 slope (r = - 0.91, p < 0.001). Dead space(DS)/Tidal volume and P(arterial-et) CO2 were elevated without arterial hypoxemia suggesting a high V-E/Q mismatch. Chemoreceptor peripheral response to hypoxia and central CO2 response were both enhanced being peripheral responses to hypoxia and hypercapnia 0.416 +/- 0.402 (normal ref values = 0.285 +/- 0.221) l/min/O(2)Sat and 0.076 +/- 0.047 (0.066 +/- 0.430) l/min/mmHg, respectively; central hypercapnic chemosensitivity was 4.475 +/- 3.99 (2.352 +/- 0.936) l/min/mmHg.Conclusions: Increased DS, V-E/ Q mismatch and chemorecptor response are among the main mechanisms involved in exercise hyperventilation in PH. ClinicalTrial.gov NCT02892981 (c) 2017 Elsevier B.V. All rights reserved.