Sato F, Nishimura M, Shinano H, Saito H, Miyamoto K, Kawakami Y
First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Circulation. 1997 Jul 1;96(1):274-81.
In patients with obstructive sleep apnea syndrome (OSAS), there are cyclic fluctuations in heart rate (HR), that is, bradycardia during apnea followed by abrupt tachycardia on resumption of ventilation. Although a previous study suggested that the degree of bradycardia observed during central apnea at high altitude was determined by individual hypoxic chemosensitivity of the carotid body, it is not known whether this is true for subjects with obstructive sleep apnea syndrome.
First, we examined apnea-associated HR changes in II subjects with OSAS and analyzed the relationship of the HR change during apnea (delta HR, defined as the difference between the values at the beginning and the end of apnea) and apnea-induced nadir SaO2 in each subject. Second, we conducted an apnea-simulation study in 7 subjects to examine whether the individual pattern of delta HR could be simulated while they held their breath under different levels of arterial oxygenation. The delta HR was highly variable among subjects: 2 showed an increase in HR during apnea, 6 a decrease, and the other 3 a borderline-type response. The slope factor of the nadir of the SaO2-delta HR line obtained from each subject had a significant correlation with the HR change during breath-holding conducted under normoxia (Spearman's rank correlation coefficient, rs = 69, P < .05) or hypoxia (rs = .81, P < .05) but not under hyperoxia. Finally, we evaluated hypoxic chemosensitivity of the carotid body by measuring the ventilatory response to isocapnic progressive hypoxia in all subjects. The magnitude of the ventilatory response ranged from 0.05 to 1.89 L.min-1.%SaO2 fall-1 and showed a significant correlation with the slope factor of the nadir of the SaO2-delta HR line (rs = -.64, P < .05).
The intersubject variation of the HR changes during sleep apnea can be explained in large part by individual hypoxic chemosensitivity of the carotid body regardless of the type of apnea.
在阻塞性睡眠呼吸暂停综合征（OSAS）患者中，心率（HR）存在周期性波动，即呼吸暂停期间出现心动过缓，恢复通气后随即出现突然的心动过速。尽管先前的一项研究表明，在高海拔地区中枢性呼吸暂停期间观察到的心动过缓程度由颈动脉体的个体低氧化学敏感性决定，但对于阻塞性睡眠呼吸暂停综合征患者是否也是如此尚不清楚。
首先，我们检查了11名OSAS患者呼吸暂停相关的心率变化，并分析了每名患者呼吸暂停期间的心率变化（δHR，定义为呼吸暂停开始和结束时的值之差）与呼吸暂停诱发的最低血氧饱和度（SaO2）之间的关系。其次，我们对7名受试者进行了呼吸暂停模拟研究，以检查在不同动脉氧合水平下屏气时，个体的δHR模式是否可以被模拟。受试者之间的δHR变化很大：2名受试者在呼吸暂停期间心率增加，6名受试者心率降低，另外3名受试者表现为临界型反应。从每名受试者获得的SaO2-δHR线最低点的斜率因子与常氧（Spearman等级相关系数，rs = 0.69，P < 0.05）或低氧（rs = 0.81，P < 0.05）但不是高氧状态下屏气期间的心率变化有显著相关性。最后，我们通过测量所有受试者对等碳酸渐进性低氧的通气反应来评估颈动脉体的低氧化学敏感性。通气反应的幅度范围为0.05至1.89 L·min-1·%SaO2下降-1，并且与SaO2-δHR线最低点的斜率因子有显著相关性（rs = -0.64，P < 0.05）。
无论呼吸暂停类型如何，睡眠呼吸暂停期间心率变化的个体间差异在很大程度上可由颈动脉体的个体低氧化学敏感性来解释。
