阻塞性睡眠呼吸暂停综合征患者清醒状态时肺动脉高压形成的危险因素分析

目的探讨阻塞性睡眠呼吸暂停综合征(OSAS)患者清醒状态时肺动脉高压形成的相关危险因素。方法15例OSAS患者,右颈内静脉置SwanGanz导管测肺动脉压(PAP),同步行多导睡眠图监测,测肺通气功能[用力呼吸容积(FVC)占预计值的百分比,第1秒钟用力呼吸容积(FEV1.0)占预计值的百分比]、呼吸驱动[低氧通气反应以Δ口腔内阻断压(P0.1)/Δ脉搏血氧饱和度(SpO2)来表示;高碳酸通气反应以ΔP0.1/Δ呼气末CO2分压(PETCO2)来表示]、Hb等指标,行血气分析,对所测指标行多因素相关分析、多元逐步回归分析。结果(1)15例OSAS患者清醒状态时的PAP为(20.39±11.04)mmHg(1mmHg=0.133kPa),睡眠时平均最大PAP为(37.93±19.20)mmHg;其中8例PAP正常,7例PAP升高(PAP≥20mmHg);与PAP正常者相比,PAP升高者的体重指数(BMI)、PaCO2、Hb增高,而FVC占预计值的百分比、PaO2降低。(2)清醒状态时平均PAP与睡眠中平均最大PAP(β=0.35,标准误为0.10,R2=0.89,P=0.006)、PaCO2(β=0.72,标准误为0.27,R2=0.94,P=0.022)关系最为密切;而PaCO2、PaO2、BMI、快动眼睡眠的ΔPAP/ΔSpO2是与睡眠中平均最大PAP关系最密切的因素,并建立回归方程:y'=-152.70+1.92PaCO2+1.37BMI+0.67PaO2+16.29快动眼睡眠的ΔPAP/ΔSpO2。结论OSAS患者PAP升高与呼吸暂停引起的日间CO2升高和低氧、FVC、BMI、快动眼睡眠的低氧等有关,与暂停指数未表现明显关系。

The analysis of risk factors correlated to pulmonary hypertension in obstructive sleep apnea syndrome patients during awake state

OBJECTIVE: To investigate the development of pulmonary hypertension in obstructive sleep apnea syndrome (OSAS) patients and to analyze the correlated factors. METHODS: Pulmonary arterial pressure was monitored by right cardiac catheterization in 15 OSAS patients, and simultaneously polysomnography was performed. Blood gas analysis and lung function were also measured. RESULTS: Pulmonary arterial pressure at awake state was correlated positively to mean maximal pulmonary pressure during sleep, body mass index (BMI) and hemoglobin (Hb), but negatively to PaO2, the percent predicted forced vital capacity (FVC% pred). Compared with OSAS patients without pulmonary hypertension, the BMI, PaCO2, and Hb of OSAS patients with pulmonary hypertension increased significantly, while FVC% pred and PaO2 decreased. Stepwise linear regression indicated that pulmonary arterial pressure at awake state was closely correlated with mean maximal pressure during sleep (beta = 0.35, standard error 0.10, R(2) = 0.89, P = 0.006) and PaCO2 (beta = 0.72, standard error 0.27, R(2) = 0.94, P = 0.022), and mean maximal pulmonary arterial pressure during sleep was closely correlated to PaCO2, BMI, PaO2 and the ratio of arterial pressure and oxygen concentration during rapid eye movement sleep (RDeltaPAP/DeltaSpO2). The regression equation was y' = -152.70 + 1.92 PaCO2 + 1.37 BMI + 0.67 PaO2 + 16.29 RDeltaPAP/DeltaSpO2. CONCLUSION: Pulmonary arterial pressure increasing in OSAS patients is induced mainly by hypercapnia and hypoxia at day time, and related to forced ventilation capacity, BMI and the ratio of pulmonary arterial pressure and oxygen concentration variation during rapid eye movement sleep. There was no obvious relation between pulmonary arterial pressure and apnea index.