Eichhorn Lars, Kessler Florian, Böhnert Volker, Erdfelder Felix, Reckendorf Anja, Meyer Rainer, Ellerkmann Richard K
Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Bonn;
Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Bonn.
J Vis Exp. 2016 Dec 22(118):54933. doi: 10.3791/54933.
In case of apnea, arterial partial pressure of oxygen (pO2) decreases, while partial pressure of carbon dioxide (pCO2) increases. To avoid damage to hypoxia sensitive organs such as the brain, compensatory circulatory mechanisms help to maintain an adequate oxygen supply. This is mainly achieved by increased cerebral blood flow. Intermittent hypoxia is a commonly seen phenomenon in patients with obstructive sleep apnea. Acute airway obstruction can also result in hypoxia and hypercapnia. Until now, no adequate model has been established to simulate these dynamics in humans. Previous investigations focusing on human hypoxia used inhaled hypoxic gas mixtures. However, the resulting hypoxia was combined with hyperventilation and is therefore more representative of high altitude environments than of apnea. Furthermore, the transferability of previously performed animal experiments to humans is limited and the pathophysiological background of apnea induced physiological changes is poorly understood. In this study, healthy human apneic divers were utilized to mimic clinically relevant hypoxia and hypercapnia during apnea. Additionally, pulse-oximetry and Near Infrared Spectroscopy (NIRS) were used to evaluate changes in cerebral and peripheral oxygen saturation before, during, and after apnea.
在呼吸暂停的情况下，动脉血氧分压（pO2）降低，而二氧化碳分压（pCO2）升高。为避免对大脑等对缺氧敏感的器官造成损害，代偿性循环机制有助于维持充足的氧气供应。这主要通过增加脑血流量来实现。间歇性缺氧是阻塞性睡眠呼吸暂停患者中常见的现象。急性气道阻塞也可导致缺氧和高碳酸血症。到目前为止，尚未建立足够的模型来模拟人类的这些动态变化。以前针对人类缺氧的研究使用吸入低氧混合气体。然而，由此产生的缺氧与过度通气同时存在，因此更能代表高海拔环境而非呼吸暂停。此外，先前进行的动物实验对人类的可转移性有限，且对呼吸暂停引起的生理变化的病理生理背景了解甚少。在本研究中，健康的人类屏气潜水者被用来模拟呼吸暂停期间临床上相关的缺氧和高碳酸血症。此外，使用脉搏血氧饱和度测定法和近红外光谱法（NIRS）来评估呼吸暂停前、期间和之后大脑和外周血氧饱和度的变化。
