Han J N, Stegen K, Simkens K, Cauberghs M, Schepers R, Van den Bergh O, Clément J, Van de Woestijne K P
Laboratory of Pneumology, U.Z. Gasthuisberg, Katholieke Universiteit Leuven, Belgium.
Eur Respir J. 1997 Jan;10(1):167-76. doi: 10.1183/09031936.97.10010167.
The breathing pattern of 399 patients with hyperventilation syndrome (HVS) and/or with anxiety disorders and that of 347 normal controls was investigated during a 5 min period of quiet breathing and after a 3 min period of voluntary hyperventilation. The diagnosis of HVS was based on the presence of several suggestive complaints occurring in the context of stress, and reproduced by voluntary hyperventilation. Organic diseases as a cause of the symptoms were excluded. The anxiety disorders were diagnosed by means of an abbreviated version of the Anxiety Disorders Interview Schedule (ADIS). There was a large overlap between the two diagnoses. Simply breathing via a mouthpiece and pneumotachograph made end-tidal CO2 fractional concentration (FET,CO2) decrease progressively both in hyperventilators and in patients with anxiety disorders, but not in normals. At the start of the measurement the FET,CO2 was not different between patients and healthy subjects. In patients < or = 28 yrs, the decrease of FET,CO2 resulted from a higher tidal volume, and in patients > or = 29 years from an increase in frequency. After voluntary hyperventilation, the recovery of FET,CO2, was delayed in patients, due to a slower normalization of respiratory frequency in females and in older males, and of tidal volume in younger males, and also due to less frequent end-expiratory pauses. When breathing was recorded first by means of inductive plethysmography (Respitrace), the progressive decline of FET,CO2 seen in patients was not observed: from the onset of the recording, FET,CO2 was reduced in patients. It did not change further when, immediately afterwards, the subject switched to mouthpiece breathing. The finding that breathing through a mouthpiece induces hyperventilation in patients and that recovery of FET,CO2 is delayed after voluntary hyperventilation, suggests that the respiratory control system is less resistant to challenges (mouthpiece or voluntary hyperventilation) in those patients. On the other hand, the lower values of FET,CO2 measured during recording by means of a Respitrace probably result from a challenge, prior to the recordings, induced by the fitting of the measuring device to the patient. This unsteadiness of breathing characterizes patients with hyperventilation syndrome and those with anxiety disorders, but is not sufficiently sensitive to be used for individual diagnosis.
对399例患有通气过度综合征(HVS)和/或焦虑症的患者以及347名正常对照者在安静呼吸5分钟期间和自主通气过度3分钟后进行了呼吸模式研究。HVS的诊断基于在应激情况下出现的几种提示性症状,并通过自主通气过度再现。排除了作为症状原因的器质性疾病。焦虑症通过焦虑症访谈量表(ADIS)的简化版进行诊断。这两种诊断之间有很大重叠。无论是通气过度者还是焦虑症患者,仅通过咬嘴和呼吸流速仪呼吸都会使呼气末二氧化碳分数浓度(FET,CO2)逐渐降低,但正常对照者不会。在测量开始时,患者和健康受试者的FET,CO2并无差异。在年龄≤28岁的患者中,FET,CO2的降低是由于潮气量增加,而在年龄≥29岁的患者中则是由于频率增加。自主通气过度后,患者的FET,CO2恢复延迟,这是因为女性和老年男性的呼吸频率、年轻男性的潮气量恢复正常的速度较慢,并且呼气末暂停也较少。当首先通过感应式体积描记法(Respitrace)记录呼吸时,未观察到患者中出现的FET,CO2逐渐下降情况:从记录开始,患者的FET,CO2就已降低。当受试者随后立即切换为咬嘴呼吸时,它没有进一步变化。通过咬嘴呼吸会导致患者通气过度,并且自主通气过度后FET,CO2恢复延迟,这一发现表明这些患者的呼吸控制系统对挑战(咬嘴或自主通气过度)的抵抗力较低。另一方面,通过Respitrace记录期间测得的较低FET,CO2值可能是由于在记录之前测量设备安装到患者身上所引发的挑战所致。这种呼吸不稳定是通气过度综合征患者和焦虑症患者的特征,但对个体诊断的敏感性不足。