阻塞性睡眠呼吸暂停综合征患者睡眠状态下呼吸中枢控制功 …

目的 探讨阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）患者上气道阻塞与睡眠状态下呼吸中枢控制功能的低下是否有关，方法 通过经鼻气管插管建立鼻咽通气道测定了１６例重度ＯＳＡＳ患者在清楚状态，非快动眼（ＮＲＥＭ）Ｉ＋Ⅱ睡眠期，Ⅲ＋Ⅳ睡眠期，快速眼（ＲＥＭ）睡眠期的口腔阻断压（Ｐ０．１）低氧反应指标（△Ｐ０．１／△ＳａＯ２，△ＶＥ／△ＳａＯ２）及高二氧化碳反应指标（△Ｐ０．１／△ＳａＯ２，△ＶＥ／△ＳａＯ２）。     

经鼻持续性气道正压对阻塞性睡眠呼吸暂停综合征患者呼吸中枢驱动性的影响

为了解经鼻持续性气道正压（ｎＣＰＡＰ）通气治疗对阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）患者呼吸中枢驱动性的影响，研究了２０例无二氧化碳（ＣＯ＿２）储留的ＯＳＡＳ患者（Ｏ组）及２０例单纯鼾症患者（Ｓ组）夜间睡眠前后呼吸方式及口腔阻断压（Ｐ＿（０．１））的改变，并观察了ｎＣＰＡＰ治疗对ＯＳＡＳ，患者呼吸方式及Ｐ＿（０．１）的影响。结果显示：Ｏ组患者睡前的Ｐ＿（０．１）、呼吸频率、有效吸气阻抗明显高于Ｓ组，潮气量则显著低于Ｓ组。ｎＣＰＡＰ治疗组患者经一夜睡眠后的Ｐ＿（０．１）、每分通气量、潮气量、呼吸频率等较睡前显著增高。经ｎＣＰＡＰ治疗后Ｏ组的呼吸紊乱指数较治疗前明显降低，夜间最低氧饱和度明显提高，Ｐ＿（０．１）较睡前则无明显升高。提示ＯＳＡＳ患者睡前的呼吸中枢驱动性高于单纯鼾症患者，其呼吸形式为浅快呼吸；经过一夜睡眠后，其呼吸中枢驱动水平较睡前明显增高，呼吸形式更为浅快；ｎＣＰＡＰ治疗可以有效地解除睡眠呼吸暂停及其继发的低氧血症，从而逆转睡眠前后呼吸方式和呼吸中枢驱动性的改变。     

阻塞性睡眠呼吸暂停综合征患者鼻阻力变化

目的探讨阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）患者鼻阻力的变化在睡眠呼吸暂停发病机制中的作用。方法对３０名正常人、３０例鼾症、６０例ＯＳＡＳ患者在进行多导睡眠监测的基础上,行鼻阻力检测。结果轻、中度ＯＳＡＳ组鼻阻力为（１．０６±４．２５）Ｐａｓ／ｍｌ,重度ＯＳＡＳ组鼻阻力为（２．２９±９．７４）Ｐａ·ｓ／ｍｌ,鼾症组鼻阻力为（０．７１±０．３１）Ｐａ·ｓ／ｍｌ,均明显高于正常对照组（０．４０± ０．１３）Ｐａ· ｓ／ｍｌ（Ｐ＜０．０１）,鼻阻力与鼾声指数呈正相关（ｒ＝０．２５８,Ｐ＜０．０１）,但鼻阻力与睡眠呼吸紊乱指数（ＡＨＩ）、醒觉次数、最低血氧均无相关关系。结论鼾症、ＯＳＡＳ患者鼻阻力增加,可能与ＯＳＡＳ的发病有关。     

阻塞性睡眠呼吸暂停综合征与高血压病：附240例监测报告

对２４０例患者行整夜多导睡眠图监测及睡前、醒后肘部血压测定，呼吸紊乱指数（ＡＨＩ）＞５的１００例为阻塞性睡眠呼吸暂停综合征组（ＯＳＡＳ组），１４０例ＡＨＩ≤５的为对照组，发现ＯＳＡＳ组由睡前血压１７．６±３．０／１１．８±１．９ｋＰａ（１３２．３±２２．５／８８．２±１４．６ｍｍＨｇ）至醒后血压１９．７±３１／１３．１±２．２ｋＰａ（１４７．８±２３．４／９８．６±１６．２ｍｍＨｇ）明显增高（Ｐ＜０．００１），较对照组睡前血压１５．５±１．５／１０．５±１．０ｋＰａ（１１６．２±１１．６／７８．４±７．６ｍｍＨｇ），醒后血压１５．０±１．５／１０．５±１．３ｋＰａ（１１２．４±１１．２／７８．６±１０．０ｍｍＨｇ）明显升高（Ｐ＜０．００１），ＯＳＡＳ组最低血氧饱和度６０．６±１８．２％较对照组８６．２±５．０％明显降低（Ｐ＜０．００１），ＯＳＡＳ组６８％确诊为高血压病，且ＯＳＡＳ经有效治疗后血压也下降接近正常或部分下降，提示ＯＳＡＳ患者夜间反复呼吸暂停引起的低氧血症可能是部分高血压病原因之一。     

睡眠呼吸紊乱患者的警觉性测定

目的检测几种临床常见的睡眠呼吸紊乱患者的警觉性是否受损。方法前瞻性地对因疑诊而接受全晚睡眠监测的患者,在监测前（傍晚）和监测后（早上）,利用电脑模拟开车试验,以碰撞障碍物的百分率,衡量其警觉性。以等级方差分析检验各组间早晚平均碰撞率（％Ｈｍ）的差异,并将％Ｈｍ与睡眠监测有关参数作等级相关分析。结果正常人和按诊断分组后患者的％Ｈｍ［以中位数（范围）表示］为：正常人（１１名）０．６（０～２．５）;睡眠鼾症（７例）１．１（０．２～２．０）;阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ,２２例）２．２（０．２～７．７）;中枢性睡眠呼吸暂停综合征（ＣＳＡＳ,６例）２．７（０．９～５．４）。除睡眠鼾症组外,各组患者％Ｈｍ均高于正常人（Ｐ＜０．０５）。正常、睡眠鼾症及ＯＳＡＳ三组合并分析表明：％Ｈｍ与睡眠累计低血氧饱和度时间％有相关性（ｒ＝０．４１,Ｐ＜０．０５）而与呼吸停顿／低呼吸指数和觉醒指数无明显相关（ｒ分别为０．２２和０．１０,Ｐ＞０．０５）。结论ＯＳＡＳ和ＣＳＡＳ患者的警觉性下降,睡眠鼾症患者的警觉性大致正常。警觉性受损可能与睡眠时缺氧有关     

经鼻持续气道正压通气治疗阻塞性睡眠呼吸暂停综合征的远期效果

目的探讨经鼻持续气道内正压通气（ＣＰＡＰ）治疗阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）的远期效果。方法报告１９８７～１９９５年在家坚持长期应用ＣＰＡＰ治疗的ＯＳＡＳ有完善多导睡眠图（ＰＳＧ）监测记录对比的１８例患者及其临床治疗的效果。结果（１）应用ＣＰＡＰ治疗后，ＯＳＡＳ症状消除。（２）１３例（７２％）患者复查ＰＳＧ参数改善，１８例停用ＣＰＡＰ治疗后ＰＳＧ复查，最长呼吸暂停时间从６６±２１秒缩短至４３±２４秒（Ｐ＜０．０５）；呼吸紊乱指数从６６±１６降低至２８±２０（Ｐ＜０．００１）；最低血氧饱度（ＳａＯ２）从５３％±１９％提高至７５％±１１％（Ｐ＜０．００１）。（３）治疗前、后１８例患者体重、血压改变不明显，１２例合并高血压的患者６例（５０％）血压恢复到正常范围。结论ＣＰＡＰ治疗ＯＳＡＳ有效，长期坚持治疗呼吸暂停引起的低氧血症、最长呼吸暂停时间改善，临床症状减轻或消除。其机制可能与患者呼吸调节功能改善有关     

经鼻持续性气道正压对阻塞性睡眠呼吸暂停综合征患者呼吸中…

为了解经鼻持续性气道正压通气治疗对阻塞性睡眠呼吸暂停综合片患者呼吸中枢驱动性的影响，研究了２０例无二氧化碳潴留的ＯＳＡＳ患者及２０例单纯鼾症患者夜间睡眠前后呼吸方式及口腔阻断压的改变，并观察了ｎＣＰＡＰ治疗对ＯＳＡＳ患者呼吸方式及Ｐ０．１的影响。     

阻塞性睡眠呼吸暂停综合征患者肺功能与夜间低氧血症的关系

目的探讨睡眠呼吸暂停综合征（ＳＡＳ）患者体位及肥胖因素引起的肺功能改变与夜间低氧血症的关系。方法选择确诊为ＳＡＳ患者３４例，分别于坐位和仰卧位检查肺功能和血气分析，整夜多导睡眠仪监测。肺功能、血气指标和理想体重％（ＩＢＷ％）分别与呼吸暂停指数（ＡＩ）、＜９０％Ｔ（ＳａＯ２低于９０％时间占总睡眠时间百分比）进行相关分析。结果患者由坐位改为仰卧位，ＰａＯ２、肺活量（ＶＣ％）、补呼气量（ＥＲＶ）、功能残气量（ＦＲＣ％）、残气容积（ＲＶ％）、肺总量（ＴＬＣ％）均出现有统计学意义的降低。ＡＩ与仰卧位ＶＣ％、ＴＬＣ％呈正相关。＜９０％Ｔ与坐位ＰａＯ２、ＥＲＶ呈负相关。ＩＢＷ％与坐、仰卧位ＶＣ％和ＥＲＶ呈负相关，与坐位ＦＲＣ呈负相关。ＩＢＷ％与＜９０％Ｔ呈正相关。结论伴有肥胖的ＯＳＡＳ患者，体位改变及肥胖因素影响患者肺功能，加重呼吸暂停时的低氧血症     

口腔矫正器治疗阻塞性睡眠呼吸暂停综合征的临床观察

目的探讨口腔矫正器对３６例阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）患者的临床疗效。方法制作“下颌前移型”矫正器让３６例ＯＳＡＳ患者在睡眠时配戴,用多导睡眠图监测患者治疗前后呼吸紊乱指数（ＡＨＩ）、夜间最低血氧饱和度（最低ＳａＯ２）与最长呼吸暂停时间（Ｔ）,用ｔ检验进行统计学比较。结果使用口腔矫正器后患者的ＡＨＩ明显降低（Ｐ＜００５）,最低ＳａＯ２亦有明显改善（Ｐ＜００５）,Ｔ明显缩短（Ｐ＜００５）。结论口腔矫正器能使上气道增宽,使下颌稳定于一个前伸位置,舌和软腭前移,增加睡眠时的有效通气量,改善睡眠质量,是治疗ＯＳＡＳ的一个有效的辅助手段。     

阻塞性睡眠呼吸暂停患者睡眠时高血压的发生

目的明确阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）患者清醒及睡眠时血压变化情况及对其影响的相关因素。方法１３例ＯＳＡＳ患者在桡动脉内留置导管监测血压并同步进行夜间睡眠多导生理仪连续记录，部分患者观察吸氧或经鼻（面）罩持续正压通气（ＮＣＰＡＰ）的治疗效果。结果（１）ＯＳＡＳ患者白天高血压发生率为４６％（６／１３）；白天无高血压的患者夜间一过性高血压发生率为８６％（６／７）；（２）ＯＳＡＳ患者夜间血压增高与低氧血症和呼吸暂停时间有关，与呼吸暂停指数（ＡＩ）无相关性（Ｐ＞０．０５）；（３）２例ＯＳＡＳ患者经吸氧治疗后，夜间血压波动仍存在，高血压未得到纠正；４例ＯＳＡＳ患者经ＮＣＰＡＰ治疗后，夜间血压波动消失。结论白天无高血压的ＯＳＡＳ患者夜间可反复出现一过性血压增高；ＯＳＡＳ患者夜间血压增高与低氧血症、呼吸暂停时间有关，但低氧血症不是引起夜间血压增高的主要因素；单纯吸氧不能纠正ＯＳＡＳ患者夜间血压增高，ＮＣＰＡＰ是纠正ＯＳＡＳ患者夜间血压增高的较好方法。     

Treatment effects on carbon dioxide retention in patients with obstructive sleep apnea-hypopnea syndrome

OBJECTIVES: This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2) retention. METHODS: We recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their awake PaCO(2). Five patients were hypercapnic (PaCO(2), > or = 45 mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio of the change in minute ventilation [DeltaV(E)] to the change in arterial oxygen saturation [DeltaSaO(2)] and the ratio of the change in mouth occlusion pressure over the first 100 ms of inspiration against an occluded airway [DeltaP(0.1)] to DeltaSaO(2)) and hypercapnic responses (DeltaV(E)/DeltaPCO(2) ratio and DeltaP(0.1)/DeltaPCO(2) ratio) were tested during wakefulness before treatment in all 10 patients, and before and during treatment (at 2, 4, and 6 weeks) with pressure support in the hypercapnic group. RESULTS: Hypercapnic patients had lower mean (+/- SD) DeltaV(E)/DeltaSaO(2) ratio than eucapnic patients (-0.17 +/- 0.04 vs -0.34 +/- 0.04 L /min/%SaO(2), respectively), lower mean DeltaP(0.1)/DeltaSaO(2) ratio (-0.04 +/- 0.02 vs -0.14 +/- 0.03 cm H(2)O/%SaO(2), respectively), and lower DeltaP(0.1)/DeltaPCO(2) ratio (0.23 +/- 0.1 vs 0.49 +/- 0.1 cm H(2)O/mm Hg, respectively) [p < 0.05]. After receiving noninvasive ventilation treatment, the hypercapnic and hypoxic responses of the hypercapnic patients increased. At 4 to 6 weeks, values for both responses had increased to within the normal range and PaCO(2) had fallen to < 45 mm Hg, while weight was unchanged. CONCLUSIONS: Depressed chemoresponsiveness plays a role that is independent of obesity in the development of CO(2) retention in some OSAHS patients, and it may be a response to sleep-disordered breathing.     

阻塞性睡眠呼吸暂停低通气综合征患者睡眠时的呼吸中枢反应性与夜间低氧血症的关系

目的　探讨阻塞性睡眠呼吸暂停低通气综合征 (OSAHS)患者夜间低氧血症与呼吸中枢反应性的关系。方法　应用动态脉搏容积血氧饱和度 (SpO2 )仪定量分析了 2 4例白天二氧化碳分压(PaCO2 )≥ 4 5mmHg(高CO2 组 ,1mmHg=0 133kPa)及 39例PaCO2 <4 5mmHg(等CO2 组 )的OSAHS患者夜间低氧血症的严重程度。进一步应用重复呼吸法测定了其中 15例患者 (等CO2 组 11例 ,高CO2 组 4例 )睡眠状态下呼吸中枢的低氧及高CO2 反应性。结果　 6 3例患者的睡眠呼吸暂停低通气指数 (AHI)平均为 (5 4± 2 1)次 /h ;夜间动态SaO2 监测发现高CO2 组与等CO2 组比较 ,每小时氧减饱和4 %以上的次数 (ODI4)为 (43± 2 3)次 /hvs (2 9± 18)次 /h ;SaO2 <90 %的时间占总睡眠时间的百分数(SIT90 )为 (39± 32 ) %vs(15± 18) % ,高CO2 组均较等CO2 组高 ;而睡眠时的最低SaO2 (LSaO2 )为 (5 6± 18) %vs (6 6± 16 ) % ,平均SaO2 (MSaO2 )为 (86± 12 ) %vs(93± 5 ) % ,均较等CO2 组低 (P <0 0 1) ,提示其夜间缺氧程度更重。在清醒状态下 ,高CO2 组及等CO2 组患者的高CO2 反应 (ΔP0 1/ΔPaCO2 )、低氧反应 (ΔP0 1/ΔSaO2 )、口腔阻断压 (P0 1)差异均无显著性 (P >0 1)。进入非快动眼睡眠 (NREM)及快动眼睡眠 (REM)后 ,高CO2 组     

Determinants of chronic hypercapnia in Japanese men with obstructive sleep apnea syndrome

STUDY OBJECTIVE: To identify the determinants of chronic hypercapnia (ie, PaCO(2), > or = 45 mm Hg) in men with obstructive sleep apnea syndrome (OSAS) without airflow obstruction. DESIGN: An analysis was conducted of 143 male patients with OSAS, which had been diagnosed by polysomnography (PSG), who had been referred to a university hospital. Patients were classified as hypercapnic (ie, PaCO(2), > or = 45 mm Hg) and normocapnic (ie, PaCO(2), < 45 mm Hg), and obese (ie, body mass index [BMI], > or = 30 kg/m(2)) or nonobese (ie, BMI, < 30 kg/m(2)). Patients with airflow obstruction (ie, FEV(1)/FVC ratio, < 70%) were excluded from the study. Baseline clinical characteristics, pulmonary function, PSG data, and blood gas data were compared between hypercapnic and normocapnic patients. Correlations between PaCO(2) and several anthropometric, respiratory, and polysomnographic variables were determined by stepwise multiple regression analysis. RESULTS: Fifty-five patients (38%) were hypercapnic. Hypercapnic patients were younger and heavier, and had more abnormalities on pulmonary and PSG testing. Stepwise multiple regression analysis revealed that the PaCO(2) level was influenced significantly by the mean level of arterial oxygen saturation (SaO(2)) during sleep and by the percent of vital capacity (%VC) (R(2) = 0.430; p < 0.0001), indicating that 43% of the total variance in the PaCO(2) could be explained by the mean SaO(2) and %VC in hypercapnic patients. In contrast, only 13% of the total variance in the PaCO(2) was accounted for by the mean SaO(2) and BMI in normocapnic patients (R(2) = 0.134; p = 0.0034). The mean SaO(2), %VC, and PaO(2) were selected as independent variables for predicting the PaCO(2) in obese patients. These variables explained 41% of the total variance in the PaCO(2) (R(2) = 0.407; p < 0.0001), whereas the mean SaO(2) only accounted for 13% of the total variance in PaCO(2) levels in nonobese patients (R(2) = 0.134; p = 0.0064). CONCLUSION: Nocturnal desaturation and restrictive pulmonary impairment play major roles in determining the PaCO(2) in hypercapnic and obese OSAS patients without airflow obstruction.     

Incidence of nocturnal desaturation while breathing oxygen in COPD patients undergoing long-term oxygen therapy

STUDY OBJECTIVE: It is suggested that oxygen flow be increased by 1 L/min during sleep in COPD patients undergoing long-term oxygen therapy (LTOT) in order to avoid nocturnal desaturations. The purpose of this study was to investigate the occurrence of nocturnal desaturations while breathing oxygen in COPD patients receiving LTOT. SETTING: Inpatient/university hospital. PATIENTS: We studied 82 consecutive COPD patients. Their functional characteristics were as follows (mean +/- SD): FVC, 2.15 +/- 0.69 L; FEV(1), 0.87 +/- 0.33 L; PaO(2), 51.6 +/- 5 mm Hg; and PaCO(2), 47 +/- 8 mm Hg. MEASUREMENTS: Overnight pulse oximetry (PO) was performed twice: (1) while breathing air and (2) while breathing supplemental oxygen assuring satisfactory diurnal resting oxygenation (mean PaO(2) during oxygen breathing, 67 +/- 6 mm Hg; mean arterial oxygen saturation [SaO(2)] during oxygen breathing, 93%). RESULTS: PO performed while patients were breathing air showed a mean overnight SaO(2) of 82.7 +/- 6.7%. Patients spent 90% of the recording time with an SaO(2) of < 90%. While breathing oxygen, 43 patients (52.4%) remained well oxygenated. Their mean overnight SaO(2) while breathing oxygen was 94.4 +/- 2.1%, and time spent with saturation < 90% was 6.9 +/- 8.6%. Thirty-nine patients (47.6%) spent > 30% of the night with an SaO(2) of < 90% while breathing supplemental oxygen. Their mean overnight SaO(2) while breathing oxygen was 87.1 +/- 4.5%, and time spent with an SaO(2) of < 90% was 66.1 +/- 24.7% of the recording time. Comparison of ventilatory variables and daytime blood gases between both groups revealed statistically significantly higher PaCO(2) on air (p < 0.001) and on oxygen (p < 0. 05), and lower PaO(2) on oxygen (p < 0.05) in the group of patients demonstrating significant nocturnal desaturation. CONCLUSIONS: We conclude that about half of COPD patients undergoing LTOT need increased oxygen flow during sleep. Patients with both hypercapnia (PaCO(2) > or = 45 mm Hg) and PaO(2) < 65 mm Hg while breathing oxygen are most likely to desaturate during sleep.     

肺移植对5例慢性阻塞性肺疾病患者肺功能的影响

目的研究单肺移植手术治疗慢性阻塞性肺疾病(COPD)对呼吸生理及肺功能的影响。方法5例患者均为Ⅳ级COPD男性患者,年龄51～63岁。术前2周测定患者用力肺活量(FVC)、第一秒用力呼气容积(FEV1)、FEV1/FVC、最大通气量(MVV)、残气容积(RV)、肺总量(TLC)、残总比(RV/TLC)、深吸气量(IC)、胸腔气体容积(TGV)、呼气峰流量(PEF)、总气道阻力(Rawtotal)、肺一氧化碳弥散量(DLCO)、每升肺泡容积肺一氧化碳弥散量(DLCO/V·A)、6分钟行走距离(6MWD)、动脉血氧分压(PaO2)、肺泡气动脉血氧分压差[P(Aa)O2]、动脉血氧饱和度(SaO2)、动脉血二氧化碳分压(PaCO2)及平均肺动脉压(mPAP)等参数。术后2个月再行上述测定。结果5例患者术前2周、术后2个月检测的参数为MVV(23.6±5.8)、(71.6±21.8)L,FEV1(0.68±0.21)、(1.85±0.46)L,FEV1/FVC(37.4±8.3)、(75.6±13.9)%,PaO2(60.0±9.1)、(86.2±2.9)mmHg(1mmHg=0.133kPa),SaO2(90.0±4.6)%、(96.8±0.5)%及mPAP(31.2±5.5)、(16.6±1.8)mmHg,均有显著改善(P均<0.05);3例患者IC[(1.16±0.26)、(1.83±0.35)L]、TGV[(6.52±0.27)、(4.52±0.29)L]、RV[(5.12±0.39)、(3.20±0.32)L]、RV/TLC[(71.0±5.6)、(51.3±2.5)%]及Rawtotal[(6.62±0.99)、(2.48±0.87)cmH2O·L-1·s-1]改善显著(P均<0.05);4例患者PEF[(1.65±0.40)、(3.92±1.63)L/s]、DLCO[(8.5±3.0)、(21.0±6.2)ml·min-1·mmHg-1]及6MWD[(46.8±14.7)、(246.8±51.9)m]也显著增加(P均<0.05);FVC[(1.85±0.40)、(2.45±0.49)L]、TLC[(7.19±0.15)、(6.26±0.73)L]、DLCO/V·A[(2.90±1.50)、(5.41±0.87)L·min-1·mmHg-1]、P(Aa)O2[(37.6±16.3)、(17.8±6.3)mmHg]及PaCO2[(44.6±7.7)、(37.4±3.4)mmHg]有所改善,但差异无统计学意义(P均>0.05)。结论COPD患者肺移植术后肺通气、气道阻力、残气、弥散、运动耐力及气体交换功能均明显改善。     

Effects of acetazolamide and furosemide on ventilation and cerebral blood volume in normocapnic and hypercapnic patients with COPD

STUDY OBJECTIVES: Effects of chronic metabolic alkalosis and acidosis and their relation to central chemoregulation may differ between normocapnic and chronic hypercapnic patients with COPD. The relationship between responses of inspired ventilation (VI), mouth occlusion pressure (P(0.1)), and cerebral blood volume (CBV), to short-term changes in arterial PCO(2) was measured. PATIENTS AND METHODS: Seventeen patients with chronic hypercapnia and COPD (PaCO(2) > 6.0 kPa) and 16 normocapnic patients with COPD (PaCO(2) < or = 6.0 kPa) [FEV(1) 27% predicted] were studied under baseline metabolic conditions and after 1 week of treatment with oral furosemide, 40 mg/d, or acetazolamide, 500 mg/d. Hypercapnia (change in end-tidal carbon dioxide > 1 kPa) was induced by administering adequate amounts of carbon dioxide in the inspired air. CBV was measured using near-infrared spectroscopy. RESULTS: Compared with baseline metabolic condition, chronic metabolic acidosis and alkalosis did not change ventilatory (Delta VI/Delta PaCO(2)) and cerebrovascular (Delta CBV/Delta PaCO(2)) reactivity. Base excess (BE) decreased by 6.8 +/- 1.1 mEq/L and 6.9 +/- 1.6 mEq/L, respectively, in the normocapnic and chronic hypercapnic COPD groups during metabolic acidosis, resulting in a not-quite-significant leftward shift of both the ventilatory and cerebrovascular carbon dioxide response curve. BE increased by 2.3 +/- 1.2 mEq/L and 1.2 +/- 1.3 mEq/L, respectively, during chronic metabolic alkalosis in both COPD groups, without concomitant shift. Poor correlations between ventilatory and cerebrovascular carbon dioxide responsiveness (Delta CBV/Delta PaCO(2) and Delta VI/Delta PaCO(2), Delta CBV/Delta PaCO(2) and Delta P(0.1)/Delta PaCO(2), respectively) were found irrespective of baseline, respiratory condition, and induced metabolic state. CONCLUSIONS: Normocapnic and chronic hypercapnic COPD patients have the same ventilatory and cerebrovascular carbon dioxide responsiveness irrespective of induced metabolic state.     

Daytime pulmonary hypertension in patients with obstructive sleep apnea syndrome

The frequency of daytime pulmonary hypertension (PH) in patients with obstructive sleep apnea syndrome (OSAS) has not been well established and its mechanisms are still under debate. We have thus performed right heart catheterization, in addition to standard spirography and arterial blood gas measurements, in a series of 46 consecutive patients in whom OSAS was firmly diagnosed by whole-night polysomnography. Only 9 of the 46 patients (20%) had PH defined by a mean resting pulmonary arterial pressure (Ppa) greater than or equal to 20 mm Hg. Among the patients without resting PH, 14 had exercising PH (defined by a Ppa greater than 30 mm Hg during 40-watt, steady-state exercise). Patients with resting PH differed from the others by a lower daytime PaO2 (60.8 +/- 7.6 versus 76.2 +/- 9.4 mm Hg; p less than 0.001), a higher daytime PaCO2 (44.6 +/- 4.2 versus 38.0 +/- 4.0 mm Hg; p less than 0.001), and lower VC and FEV1 (p less than 0.001). There was no difference between the 2 groups with regard to apnea index (62 +/- 34 versus 65 +/- 40) or the lowest sleep SaO2 (59 +/- 21 versus 66 +/- 18%) or the time spent in apnea. For the group as a whole, there was a good correlation between Ppa and daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), and FEV1 (r = -0.52; p less than 0.001), but there was no significant correlation between Ppa and the apnea index, the lowest sleep SaO2, or the time spent in apnea.(ABSTRACT TRUNCATED AT 250 WORDS)     

慢性阻塞性肺疾病患者静息能量与呼吸力学及气体交换关系的研究

目的　探究慢性阻塞性肺疾病 (COPD)患者静息能量消耗 (REE)与肺通气功能、呼吸驱动及呼吸肌功能间的关系。方法　用canopy法间接测定 2 6例COPD患者和 2 1例健康对照者的REE、氧耗量 ( VO2 )、二氧化碳产生量 ( VCO2 )及呼吸商 (RQ)。同时测静息肺通气功能、口腔阻断压(P0 1)、最大吸气压 (PIMAX)及最大呼气压 (PEMAX) ,并进行动脉血气分析。结果　 (1)COPD组患者REE实测值 [(15 77 6 9± 311 31)kcal/d]较健康对照组 [(1388 2 9± 194 89)kcal/d]高 (P <0 0 5 ) ;PIMAX[(44 5 3± 10 6 0 )mmHg]较健康对照组 [(71 4 3± 2 2 34)mmHg]低 (P <0 0 1) ,P0 1/PIMAX(0 0 6 8± 0 0 2 6 )较健康对照组 (0 0 39± 0 0 14 )高 (P <0 0 5 ) ;第 1秒钟用力呼气容积 (FEV1)占预计值的百分比 [(5 0 4 6± 2 1 35 ) % ]、动脉血氧分压 (PaO2 ) [(77 72± 8 84 )mmHg]、动脉血氧饱和度(SaO2 ) [(92 5 4± 2 5 5 ) % ]均较健康对照组低 (P <0 0 1) ;心率 [(83 4 6± 11 36 )次 /min]较健康对照组 [(6 9 71± 5 73)次 /min]高 (P <0 0 5 )。 (2 )相关分析显示 ,COPD组REE实测值与身高、体重、体重指数、P0 1/PIMAX及心率呈正相关 (r分别为 0 5 7、0 6 5、0 6 2、0 4 1、0 5 1) ,与FEV1占预计