Superior vena cava syndrome (SVCS) patients sometimes show signs of obstructive sleep apnea (OSA). However, the mechanism causing hypoxia during sleep in SVCS patients is still uncertain. The aim of this study was to ...Superior vena cava syndrome (SVCS) patients sometimes show signs of obstructive sleep apnea (OSA). However, the mechanism causing hypoxia during sleep in SVCS patients is still uncertain. The aim of this study was to elucidate 1) the changes in central and peripheral respiratory resistance with SVCS, and 2) interpret the mechanism underlying the development of hypoxia during sleep in patients with SVCS related to OSA. Ten SVCS patients related to a neoplasm were recruited for this study. The degree of apnea hypopnea index (AHI) for OSA was evaluated by portable diagnosing device before and after SVCS treatment. We also analyzed the airway resistance and reactance quantitatively in the supine position by Master Screen impulse oscillometry system (MS-IOS?). After SVCS treatment, mean values of AHI were significantly decreased from 30.9 to 16.9 (/hour) (p = 0.001). Central respiratory resistance (R20) also decreased significantly from 0.40 to 0.33 kPa/L/s (p = 0.025) in the supine position. In contrast, peripheral respiratory resistance (R5-R20) and distal capacitive reactance (X5) did not change significantly. It is thought that the exacerbation of OSA due to SVCS is caused by increasing upper airway resistance related to reversible edema of the upper airway mucous or tissue. In contrast, SVCS may not cause peripheral respiratory tract and lung parenchyma edema.展开更多
文摘Superior vena cava syndrome (SVCS) patients sometimes show signs of obstructive sleep apnea (OSA). However, the mechanism causing hypoxia during sleep in SVCS patients is still uncertain. The aim of this study was to elucidate 1) the changes in central and peripheral respiratory resistance with SVCS, and 2) interpret the mechanism underlying the development of hypoxia during sleep in patients with SVCS related to OSA. Ten SVCS patients related to a neoplasm were recruited for this study. The degree of apnea hypopnea index (AHI) for OSA was evaluated by portable diagnosing device before and after SVCS treatment. We also analyzed the airway resistance and reactance quantitatively in the supine position by Master Screen impulse oscillometry system (MS-IOS?). After SVCS treatment, mean values of AHI were significantly decreased from 30.9 to 16.9 (/hour) (p = 0.001). Central respiratory resistance (R20) also decreased significantly from 0.40 to 0.33 kPa/L/s (p = 0.025) in the supine position. In contrast, peripheral respiratory resistance (R5-R20) and distal capacitive reactance (X5) did not change significantly. It is thought that the exacerbation of OSA due to SVCS is caused by increasing upper airway resistance related to reversible edema of the upper airway mucous or tissue. In contrast, SVCS may not cause peripheral respiratory tract and lung parenchyma edema.
