Breathlessness, anxiety, and respiratory physiology.
Breathlessness, anxiety, and respiratory physiology.
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呼吸困难、焦虑和呼吸生理学。
DOI：
10.1097/00006842-199811000-00005
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发表时间：
1998
影响因子：
3.3
通讯作者：
Thomas,AJ
中科院分区：
文献类型：
--
作者：
Strohl,KP;Thomas,AJ
呼吸困难是与化学驱动相关的感知的产物，呼吸的努力，以及呼吸输出与呼吸时产生的压力和流量的匹配（1，2）。虽然呼吸的基本驱动力位于脑干，但这些“呼吸中心”的神经通路穿过丘脑，然后到达皮层。这些通路被假定为呼吸和其他信息的有意识的感觉。同样，感觉皮层也有一些通路直接或间接地与脑桥和延髓形成突触，这些通路可能会影响呼吸，甚至在言语等活动中（暂时）超越呼吸驱动。还可以通过上呼吸道和胸壁呼吸肌运动单位的运动外流来改变通气（潮气量和频率）。最后，肌肉本身可以产生即将疲劳的传入信号。即使在其他方面健康的个体中，呼吸驱动也有两到四倍的变化。这种变异中的一些可以通过遗传背景来解释，然而，这种复杂性状的调节位点是未知的。我们和其他人已经表明，各种各样的经历，包括儿童早期的条件，可能会调节呼吸驱动（3）。呼吸控制系统中的所有这些元素在解释呼吸急促、呼吸短促、空气饥饿和窒息的呼吸感觉的研究中都很重要。1993年，Klein（4）提出了”窒息假警报理论”，认为二氧化碳超敏反应是解释惊恐发作和其他焦虑症的统一因素，这些焦虑症的部分特征是，呼吸道疾病其中一个假设是存在一个”错乱的电路”和一个特定的区域，这种二氧化碳传感器，这导致了刻板的恐慌反应。这个有趣的假设为实验研究提供了结构。自1993年以来，几个在动物研究中研究呼吸神经控制的小组已经确定了细胞二氧化碳传感器广泛分布在大脑中，但到目前为止，还没有脑干区域被确定为负责呼吸行为，除了恐慌发作或窒息反应。我们的观点是，在目前，一个特定的解剖位置不能指定为”窒息。"
Breathlessness is a product of perceptions related to chemical drive, the effort of breathing, and the matching of respiratory output to the pressure and flow produced when one takes a breath (1, 2). Although a basic drive to breathe is located in the brainstem, there are neural pathways from these" respiratory centers" that travel through the thalamus and then to the cortex. These pathways are postulated to transduce respiratory and other information for conscious sensation. Likewise, there are pathways from the sensory cortex that synapse directly and indirectly on the pons and medulla and may act to shape the breath or even override (temporarily) respiratory drive during activities such as speech. Ventilation (tidal volume and frequency) can be modified additionally through motor outflow to the motor units of the respiratory muscles of the upper airway and chest wall. Finally, the muscles themselves, can produce afferent signals of impending fatigue. There are two-to four-fold variations in respiratory drive found even in otherwise healthy individuals. Some of this variation can be accounted for by genetic background, however, the site (s) for modulation of this complex trait is (are) unknown. We and others have shown that a variety of experiences, including early childhood conditions, may modulate respiratory drive (3). All of these elements in the respiratory control system are important in the interpretation of studies of respiratory sensations of breathlessness, shortness of breath, air hunger, and suffocation.In 1993, Klein (4) proposed a" suffocation false alarm theory" that suggested carbon dioxide hypersensitivity as a unifying factor in explaining panic attacks and other anxiety disorders that are characterized, in part, by respiratory symptomatology. One of the postulates is the existence of a" deranged circuitry" and a specific region for this carbon dioxide sensor, which results in a stereotypic panic response. This interesting hypothesis provided structure for experimental investigation. Since 1993, several groups investigating the neural control of breathing in animal studies have identified cellular carbon dioxide sensors to be widely distributed in the brain (5), but as of yet there is no brainstem region that has been identified as responsible for respiratory behavior, aside from panic attacks or suffocation responses. Our point is that, at the present time, a specific anatomic location cannot be assigned for" suffocation."