Papp L A, Klein D F, Gorman J M
Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY.
Am J Psychiatry. 1993 Aug;150(8):1149-57. doi: 10.1176/ajp.150.8.1149.
The purpose of this article is to offer a comprehensive, data-based explanation of the relationship between hyperventilation and panic disorder linking CO2 hypersensitivity, cognitive/behavioral factors, and the respiratory effects of antipanic pharmacologic and psychological treatments.
The authors conducted a computerized search of MEDLINE for relevant articles.
Some panic patients have a chronic, subtle respiratory disturbance. Acute hyperventilation is neither necessary nor sufficient for panic to occur. Respiratory abnormalities in panic patients may adaptively aim at coping with a hypersensitive CO2 chemoreceptor system. Pharmacologic panicogens also stimulate the respiratory system, causing hyperventilation. Triggering this hypersensitive respiratory control mechanism may incite panic. Antipanic medications may reset the receptor threshold. Misattribution and catastrophic interpretation of somatic symptoms or the sense of loss of control may contribute to panic symptoms. Behavioral interventions such as desensitization or breathing retraining may block the full-blown attack. Cognitive strategies through cognitive control of respiration may supplement and accentuate these interventions.
Panic disorder may be due to an inherently unstable autonomic nervous system, coupled with cognitive distress.
本文旨在基于数据，全面阐释过度换气与惊恐障碍之间的关系，将二氧化碳超敏反应、认知/行为因素以及抗惊恐药物和心理治疗的呼吸效应联系起来。
作者对MEDLINE进行了计算机检索以查找相关文章。
一些惊恐障碍患者存在慢性、轻微的呼吸紊乱。急性过度换气对于惊恐发作既非必要条件也非充分条件。惊恐障碍患者的呼吸异常可能是为了适应性地应对超敏的二氧化碳化学感受器系统。药物性惊恐诱发剂也会刺激呼吸系统，导致过度换气。触发这种超敏的呼吸控制机制可能引发惊恐。抗惊恐药物可能会重置感受器阈值。对躯体症状或失控感的错误归因和灾难性解读可能会导致惊恐症状。诸如脱敏或呼吸再训练等行为干预可能会阻止全面发作。通过对呼吸进行认知控制的认知策略可能会补充并强化这些干预措施。
惊恐障碍可能是由于内在不稳定的自主神经系统，再加上认知困扰所致。
