Time delays between physiological signals in interpreting the body's responses to intermittent hypoxia in obstructive sleep apnea.

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. &#xD;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.&#xD;Main Results. We found that simultaneous acquisition of various parameters inevitably involved varying degrees of response delay (7.12 - 25.60 seconds). The delay time of hemodynamic parameters was significantly shorter than that of SpO2 and TcPO2 (p < 0.01). OSA severity affected the response delay of SpO2, TcPO2, SV, MBP, and HR (p < 0.05). SV delay time was negatively correlated with the apnea-hypopnea index (r = -0.4831, p < 0.0001).&#xD;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.