Abstract：
Objective.Intermittent hypoxia, the primary pathology of obstructive sleep apnea (OSA), causes cardiovascular responses resulting in changes in hemodynamic parameters such as stroke volume (SV), blood pressure (BP), and heart rate (HR). However, previous studies have produced very different conclusions, such as suggesting that SV increases or decreases during apnea. A key reason for drawing contrary conclusions from similar measurements may be due to ignoring the time delay in acquiring response signals. By analyzing the signals collected during hypoxia, we aim to establish criteria for determining the delay time between the onset of apnea and the onset of physiological parameter response.Approach.We monitored oxygen saturation (SpO2), transcutaneous oxygen pressure (TcPO2), and hemodynamic parameters SV, HR, and BP, during sleep in 66 patients with different OSA severity to observe body\'s response to hypoxia and determine the delay time of above parameters. Data were analyzed using the Kruskal-Wallis test, Quade test, and Spearman test.Main results.We found that simultaneous acquisition of various parameters inevitably involved varying degrees of response delay (7.12-25.60 s). The delay time of hemodynamic parameters was significantly shorter than that of SpO2and TcPO2(p< 0.01). OSA severity affected the response delay of SpO2, TcPO2, SV, mean BP, and HR (p< 0.05). SV delay time was negatively correlated with the apnea-hypopnea index (r= -0.4831,p< 0.0001).Significance.The real body response should be determined after removing the effect of delay time, which is the key to solve the problem of drawing contradictory conclusions from similar studies. The methods and important findings presented in this study provide key information for revealing the true response of the cardiovascular system during hypoxia, indicating the importance of proper signal analysis for correctly interpreting the cardiovascular hemodynamic response phenomena and exploring their physiological and pathophysiological mechanisms.
摘要：
目的：间歇性缺氧，阻塞性睡眠呼吸暂停（OSA）的主要病理，导致心血管反应，导致血液动力学参数的变化，如每搏输出量（SV），血压（BP），心率（HR）然而,以前的研究得出了非常不同的结论，如提示在呼吸暂停期间SV增加或减少。从类似测量中得出相反结论的关键原因可能是由于忽略了获取响应信号的时间延迟。通过分析缺氧期间收集的信号，我们旨在建立确定呼吸暂停发作与生理参数反应发作之间延迟时间的标准.
方法。我们监测了氧饱和度(SpO2),经皮氧分压(TcPO2),血流动力学参数SV,HR,BP,66例不同程度OSA患者在睡眠期间观察机体对缺氧的反应并确定上述参数的延迟时间。使用Kruskal-Wallis检验分析数据，Quade测试。和斯皮尔曼测试。
主要结果。我们发现，同时获取各种参数不可避免地涉及不同程度的响应延迟（7.12-25.60秒）。血流动力学参数延迟时间明显短于SpO2和TcPO2(p<0.01)。OSA严重程度影响SpO2、TcPO2、SV、MBP,和HR(p<0.05)。SV延迟时间与呼吸暂停低通气指数呈负相关(r=-0.4831,p<0.0001)。
意义。在消除延迟时间的影响后，应确定真实的身体反应，这是解决从类似研究中得出矛盾结论的关键。本研究中提出的方法和重要发现为揭示缺氧期间心血管系统的真实反应提供了关键信息，指出正确的信号分析对于正确解释心血管血流动力学反应现象和探索其生理和病理生理机制的重要性。
