Sampson M G, Grassino K
Am J Med. 1983 Jul;75(1):81-90. doi: 10.1016/0002-9343(83)91171-3.
During hypercapnia-induced hyperventilation, obese patients with a prior history of alveolar hypoventilation appear to have significantly more blunted ventilatory response than simply obese patients who never retained carbon dioxide. In addition, these patients with former obesity-hypoventilation syndrome have decreased neuromuscular responses as measured by way of the mouth occlusion technique when compared with either the patients with simple obesity or normal subjects. The patients with simple obesity appear to have augmented responses in comparison with normal subjects. Simple mechanical considerations and baseline breathing variables failed to distinguish the simple obesity group from the group with former obesity-hypoventilation syndrome. Thus, the decreased neuromuscular responsiveness to carbon dioxide (mouth-occlusion pressure/end-tidal carbon dioxide pressure) among the group with former obesity-hypoventilation syndrome when compared with that in the group with simple obesity is a consequence of a blunted neural (central) drive, and not due to any apparent worse mechanical limitations. The augmented mouth-occlusion pressure/end-tidal carbon dioxide pressure and increased integrated, rectified electromyographic signal of the diaphragm found in the group with simple obesity presumably reflect their attempt to maintain ventilatory homeostasis in the presence of severe respiratory loads. Neuromechanical coupling values, as reflected in the integrated electromyographic signal of the diaphragm versus transdiaphragmatic pressure and mouth-occlusion pressure versus mean inspiratory flow, are identical in the two groups. On the basis of these studies, it would appear that although mechanical loads put all obese patients at a disadvantage, the addition of an acute extra load on the respiratory system produces the obesity-hypoventilation syndrome in those obese persons who have truly blunted central hypercapnic responses.
在高碳酸血症诱发的通气过度期间，既往有肺泡通气不足病史的肥胖患者，其通气反应的减弱程度似乎比从未潴留过二氧化碳的单纯肥胖患者要显著得多。此外，与单纯肥胖患者或正常受试者相比，这些曾患肥胖低通气综合征的患者，通过口阻断技术测量的神经肌肉反应有所降低。与正常受试者相比，单纯肥胖患者似乎有增强的反应。简单的力学因素和基线呼吸变量未能区分单纯肥胖组和曾患肥胖低通气综合征的组。因此，与单纯肥胖组相比，曾患肥胖低通气综合征组对二氧化碳的神经肌肉反应性降低（口阻断压/呼气末二氧化碳分压）是神经（中枢）驱动减弱的结果，而非由于任何明显更差的力学限制。单纯肥胖组中口阻断压/呼气末二氧化碳分压升高以及膈肌综合整流肌电图信号增强，可能反映了他们在存在严重呼吸负荷时试图维持通气稳态。两组中膈肌综合肌电图信号与跨膈压以及口阻断压与平均吸气流量所反映的神经力学耦合值是相同的。基于这些研究，似乎虽然力学负荷使所有肥胖患者处于不利地位，但在呼吸系统上额外增加急性负荷会在那些中枢高碳酸血症反应真正减弱的肥胖者中引发肥胖低通气综合征。
