Effects of stabilizing or increasing respiratory motor outputs on obstructive sleep apnea.
Effects of stabilizing or increasing respiratory motor outputs on obstructive sleep apnea.
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稳定或增加呼吸运动输出对阻塞性睡眠呼吸暂停的影响。
DOI：
10.1152/japplphysiol.00064.2013
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发表时间：
2013
期刊：
影响因子：
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通讯作者：
Dempsey,JeromeA
中科院分区：
文献类型：
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作者：
Xie,Ailiang;Teodorescu,Mihaela;Pegelow,DavidF;Teodorescu,MihaiC;Gong,Yuansheng;Fedie,JessicaE;Dempsey,JeromeA
为了确定阻塞性睡眠呼吸暂停（OSA）患者的病理生理特征如何预测旨在稳定或增加呼吸运动输出的治疗的成功，我们研究了26例新诊断的OSA患者[呼吸暂停低通气指数（AHI）42 ± 5次/h，92%为阻塞性呼吸暂停]，这些患者接受了O2补充治疗，一个等二氧化碳再呼吸系统，其中仅在呼吸过度时添加CO2以防止短暂性低碳酸血症，以及一个连续再呼吸系统。我们还测量了每例患者的控制器在正常呼吸下的增益[分钟通气量变化/潮气末Pco 2变化（ΔV时e/Δ PetCO 2）]、CO2储备（正常呼吸-呼吸暂停阈值PetCO 2）和植物增益（Δ PetCO 2/ΔV时e），以及被动上气道闭合压（Pcrit）。等二氧化碳再呼吸后，14/26例患者的AHI降至对照组的31 ± 6%（P< 0.01）（应答者），12/26例患者无显著变化（无应答者）。应答者与无应答者相比，控制器增益更大（6.5 ± 1.7 vs. 2.1 ± 0.2 l·min-1·mmHg-1，P< 0.01），CO2储备更小（1.9 ± 0.3 vs. 4.3 ± 0.4 mmHg，P< 0.01），Pcrit无差异（-0.1 ± 1.2 vs. 0.2 ± 0.9 cmH 2 O，P> 0.05）。在21名CO2储备范围较宽的受试者中，高碳酸再呼吸（+4.2 ± 1 mmHg PetCO 2）使AHI降至对照组的15 ± 4%（P< 0.001）。高氧（SaO 2 ≥ 95-98%）使7/19例OSA患者的AHI降至对照组的36 ± 11%。我们的结论是，通过预防短暂性低碳酸血症来稳定中枢呼吸运动输出，可以预防高化疗敏感性和可塌陷上气道患者的大部分OSA，而通过中度高碳酸血症来增加呼吸运动输出，可以消除大多数化疗敏感性和CO2储备范围更广的患者的OSA。通过高氧降低化疗敏感性对OSA的影响有限且不可预测。
To determine how the obstructive sleep apnea (OSA) patient's pathophysiological traits predict the success of the treatment aimed at stabilization or increase in respiratory motor outputs, we studied 26 newly diagnosed OSA patients [apnea-hypopnea index (AHI) 42 ± 5 events/h with 92% of apneas obstructive] who were treated with O2supplementation, an isocapnic rebreathing system in which CO2was added only during hyperpnea to prevent transient hypocapnia, and a continuous rebreathing system. We also measured each patient's controller gain below eupnea [change in minute volume/change in end-tidal Pco2(ΔV̇e/ΔPetCO2)], CO2reserve (eupnea-apnea threshold PetCO2), and plant gain (ΔPetCO2/ΔV̇e), as well as passive upper airway closing pressure (Pcrit). With isocapnic rebreathing, 14/26 reduced their AHI to 31 ± 6% of control (P< 0.01) (responder); 12/26 did not show significant change (nonresponder). The responders vs. nonresponders had a greater controller gain (6.5 ± 1.7 vs. 2.1 ± 0.2 l·min−1·mmHg−1,P< 0.01) and a smaller CO2reserve (1.9 ± 0.3 vs. 4.3 ± 0.4 mmHg,P< 0.01) with no differences in Pcrit (−0.1 ± 1.2 vs. 0.2 ± 0.9 cmH2O,P> 0.05). Hypercapnic rebreathing (+4.2 ± 1 mmHg PetCO2) reduced AHI to 15 ± 4% of control (P< 0.001) in 17/21 subjects with a wide range of CO2reserve. Hyperoxia (SaO2∼95–98%) reduced AHI to 36 ± 11% of control in 7/19 OSA patients tested. We concluded that stabilizing central respiratory motor output via prevention of transient hypocapnia prevents most OSA in selected patients with a high chemosensitivity and a collapsible upper airway, whereas increasing respiratory motor output via moderate hypercapnia eliminates OSA in most patients with a wider range of chemosensitivity and CO2reserve. Reducing chemosensitivity via hyperoxia had a limited and unpredictable effect on OSA.