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通气调节异常

Author
Douglas C Johnson, MD
Section Editor
Ruth Benca, MD, PhD
Deputy Editors
Helen Hollingsworth, MD
April F Eichler, MD, MPH
Translators
林连君, 主治医师

引言

呼吸系统依靠一套复杂的通气控制系统来确保恰当且足够的通气来供给O2、排出CO2并维持体内酸碱平衡。大脑的呼吸中枢整合来自神经和化学感受器的输入信号,并为呼吸肌提供神经驱动,这一机制保持了上呼吸道通畅性,并驱使胸廓运动以决定通气水平。

由不同疾病[包括慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)、哮喘、Ondine's curse综合征、颈动脉体切除、陈-施呼吸(Cheyne-Stokes respiration, CSR)、黏液性水肿、饥饿和神经肌肉疾病]引起的通气调节异常将总结在此。此外,几种药物对通气和通气调节的影响也将总结在此。通气调节的生理学方面以及通气调节异常患者的评估将单独讨论。 (参见“Control of ventilation”)

慢性阻塞性肺疾病

在COPD及有相似程度气流阻塞的患者中,高碳酸血症的进展并不一致。与血碳酸水平正常且血氧水平相对正常的“红喘型”COPD患者相比,表现为高碳酸血症[CO2潴留,即动脉血二氧化碳分压(arterial carbon dioxide tension, PaCO2)升高]和低氧血症的“紫肿型”患者的呼吸驱动减低[1,2]。

慢性CO2潴留患者的呼吸模式以低潮气量和高呼吸频率(通常≥22次/分)为特点。这种呼吸模式结合通气/血流灌注匹配受损导致死腔通气增加和肺泡通气减少,从而促进CO2潴留[3]。

某些存在高碳酸血症、低氧血症的COPD患者在给氧时出现CO2潴留增加。此类患者的高碳酸血症对呼吸的驱动力和低氧血症对呼吸的驱动力通常均减弱[4]。在吸氧期间,促使CO2潴留的其他因素包括继发于缓解了的代偿性肺血管收缩所导致的通气-灌注分布的恶化[5],以及由于Haldane效应导致的CO2卸载[6]。 (参见“高碳酸血症患者的氧疗”)

                    

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Literature review current through: 2017-06 . | This topic last updated: 2016-01-26.
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