慢性阻塞性肺疾病和肺心病患者血液动力学与循环内皮细胞变化

目的探讨慢性阻塞性肺疾病（ＣＯＰＤ）和肺心病时血循环内皮细胞、血液动力学的变化及意义。方法运用右心导管检查技术和血循环内皮细胞（ＣＥＣ）分离技术，用硫巴比妥法及羟胺法测定血丙二醛（ＭＤＡ）及超氧化物岐化酶（ＳＯＤ）。结果肺心病组肺动脉平均压［（ｍＰＡＰ）３７６±０７５ｋＰａ、血ＣＥＣ数量每０９微升为１６７０±２６５与ＣＯＰＤ组（８４８±２２３）比较，差异有显著性（Ｐ＜０．０１），血ＣＥＣ数量与动脉血氧分压（ＰａＯ２）比较呈显著负相关（ｒ＝０．９４２３，Ｐ＜０．００１），血ＣＥＣ数量与肺动脉压比较呈显著正相关（ｒ＝０．８２７０，Ｐ＜０．００１），肺心病组丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）与ＣＯＰＤ组比较，差异有显著性（Ｐ＜０．０１）。结论缺氧可加重血管内皮细胞损伤     

持续气道正压通气治疗肥胖低通气综合征

目的探讨持续气道正压通气治疗肥胖低通气综合征（ＯＨＳ）的疗效。方法用ＣＰＡＰ（经鼻持续气道正压通气）及ＢｉＰＡＰ（双水平气道正压通气）呼吸机分别对２１例及１４例肥胖低通气综合征患者治疗２个月,比较治疗前后的呼吸紊乱指数（ＡＨＩ）、低通气指数（ＨＩ）、体块指数（ＢＭＩ）、４％的血氧饱和度降低次数（ＯＤＩ４）以及最低血氧饱和度（ｍｉｎＳａＯ２）,并将ＢＭＩ与ＡＨＩ、ＨＩ及ｍｉｎＳａＯ２作相关性分析。结果肥胖低通气患者治疗后ＡＨＩ、ＨＩ、ＢＭＩ、ＯＤＩ４、ｍｉｎＳａＯ２均有明显改善（Ｐ＜００５）;而ＢＭＩ与ＨＩ、及ｍｉｎＳａＯ２的相关性检验无显著性（相关系数分别为ｒ＝０．０３４６８和ｒ＝０．０５５８１,Ｐ＞００５）,提示单纯降低ＢＭＩ并不能有效地改善ＨＩ及ｍｉｎＳａＯ２。结论持续气道正压通气是治疗ＯＨＳ一种无创、有效的措施,且能在短期内明显改善临床症状,提高生活质量。     

细胞释放超氧阴离子自由基含量、超氧化物歧化酶和组织蛋白酶D活力随增龄的变化

目的探讨增龄过程中细胞释放超氧阴离子自由基和超氧化物歧化酶（ＳＯＤ）、组织蛋白酶Ｄ活力的关系。方法用培养不同代次健康人皮肤成纤维细胞，同时测定细胞释放超氧阴离子自由基和ＳＯＤ、组织蛋白酶Ｄ活力并比较其相互关系。结果第８、２０、３６代健康人皮肤成纤维细胞连续培养７天，其细胞释放超氧阴离子自由基量在第２天已显著增高（Ｐ值＜０．０１），且随细胞代次增长而增加；连续培养７天，与培养时间呈正相关（ｒ值＝０．９５７３～０．９７９１，Ｐ值＜０．００１～０．００５）。第３０代细胞连续培养７天，每天测定细胞释放超氧阴离子自由基量、组织蛋白酶Ｄ和ＳＯＤ活力的，前两项指标随培养时间延长而升高，二者呈正相关（ｒ值＝０．９９３，Ｐ值＜０．００１）；细胞ＳＯＤ活力则随培养时间延长而降低，二者呈负相关（ｒ值＝－０．９９３１，Ｐ值＜０．００１）；细胞释放超氧阴离子自由基量与ＳＯＤ活力呈负相关（ｒ值＝－０．９９，Ｐ值＜０．０１），与细胞组织蛋白酶Ｄ活力呈正相关（ｒ值＝０．９９２７，Ｐ值＜０．００１）。结论细胞增龄与其释放自由基与ＳＯＤ、组织蛋白酶Ｄ活力有关。     

夜间经鼻面罩持续正压辅助通气治疗中枢性低通气

报告４例不同原因所致的中枢性低通气病人夜间应用经鼻面罩持续正压通气的疗效反应。４例病人分别于治疗前、吸氧２Ｌ／ｍｉｎ及应用通气治疗后行多导睡眠图检查比较夜间低通气及血氧情况，结果示单纯吸氧不能明显改善低通气次数和低氧情况，最低氧饱和度均＜５０％，低通气指数３例仍＞２０ｂ／ｈ（正常值＜５ｂ／ｈ），另１例为６４ｂ／ｈ；予以持续正压通气机通气治疗，压力调至６～１２ｃｍＨ２Ｏ（１ｃｍＨ＿２Ｏ＝０．０９８ｋＰａ）时，低通气指数及低氧血症明显改善，最低氧饱和度均＞７０％，Ｐ＜０．００１，低通气指数均＜７ｂ／ｈ，Ｐ＜０．０１。结论：夜间应用鼻面罩持续正压通气治疗中枢性低通气的初步结果示疗效显著。     

老年慢性阻塞性肺疾病患者血浆内皮素－1含量与PaO_2、PaCO_2及肺动脉压的关系

目的探讨血浆内皮素－１（ｅｎｄｏｔｈｅｌｉｎ－１，ＥＴ－１）在慢性阻塞性肺疾病（ｃｈｒｏｎｉｃｏｂｓｔｒｕｃｔｉｖｅｐｕｌｍｏｎａｒｙｄｉｓｅａｓｅ，ＣＯＰＤ）中的作用。方法应用放射免疫法测定４３例老年ＣＯＰＤ急性发作期患者和１５名健康对照者血浆ＥＴ－１水平，其中８例肺心病患者行右心微导管检测肺动脉压。结果ＣＯＰＤ患者和肺心病患者的血浆ＥＴ－１含量分别为５．２４±０．５０、５．８０±０．６６ｐｇ／ｍｌ，较健康对照组血浆ＥＴ－１含量（４．６５±０．６５ｐｇ／ｍｌ）明显升高（Ｐ值＜０．０１及０．００１）；血浆ＥＴ－１含量与ＰａＯ２呈显著性负相关（ＣＯＰＤ组：ｒ值＝－０．５８３，Ｐ值＜０．０１；肺心病组：ｒ值＝－０．６２７，Ｐ值＜０．００１），与ＰａＣＯ２呈显著性正相关（ＣＯＰＤ组：ｒ值＝－０．５１４，Ｐ值＜０．０５；肺心病组：ｒ值＝０．５９３，Ｐ值＜０．００１）；ＥＴ－１含量与肺动脉收缩压及平均压均存在正相关（ｒ值＝０．７２７及０．６８１，Ｐ值均＜０．０５）。结论血浆ＥＴ－１参与肺心病肺动脉高压的形成，缺氧和二氧化碳潴留是刺激ＥＴ－１释放的重要原因之一     

高原地区老年慢性肺心病患者夜间睡眠减氧饱和的观察

目的探讨高原老年肺心病患者夜间睡眠减氧饱和及与呼吸功能的关系。方法对３４例高原老年肺心病缓解期患者作了白天血气、血氧饱和度（ＳａＯ２）、肺功能、最大跨膈压（Ｐｄｉｍａｘ）和夜间睡眠脑电图、眼电图、ＳａＯ２连续监测。结果高原老年肺心病患者夜间睡眠快动眼睡眠（ＲＥＭ）和非ＲＥＭ（ＮＲＥＭ）期平均ＳａＯ２（ＭＳａＯ２）和最低ＳａＯ２（ＭｍＳａＯ２）较白天觉醒ＳａＯ２（ＤＳａＯ２）明显降低（均为Ｐ＜００１），以ＲＥＭ期最明显；高碳酸血症组较无碳酸血症组降低明显（Ｐ＜００１或００５）。ＭＳａＯ２与ＤＳａＯ２、１秒钟用力呼气容积（ＦＥＶ１）、７５％、５０％和２５％肺活量最大呼气流量〔Ｖ７５／Ｈｔ（ｍ）、Ｖ５０／Ｈｔ（ｍ）、Ｖ２５／Ｈｔ（ｍ）（Ｈｔ为身高，ｍ为米）〕、Ｐｄｉｍａｘ和ＭｍＳａＯ２与ＤＳａＯ２呈明显正相关（ｒ＝０７３８、０６８７、０７７１、０８８９、０５６８、０８７６、０８２２，均为Ｐ＜００１）。结论高原老年肺心病患者夜间睡眠有明显减氧饱和，尤以ＲＥＭ期最明显，且与肺和膈肌功能损害程度呈正相关     

慢性阻塞性肺疾病患者经皮气管导管短期氧疗研究

我们应用经皮气管导管供氧法对慢性阻塞性肺疾病（ＣＯＰＤ）患者进行２４小时（ｈ）短期氧疗观察，以探讨该法的初步疗效和依从性。对象与方法２０例确诊为ＣＯＰＤ住院患者，动脉血氧分压（ＰａＯ２）均＜５５ｍｍＨｇ（１ｍｍＨｇ＝０．１３３ｋＰａ），随机分为Ｔ组和...     

肺癌患者围术期换气功能的研究

目的研究肺癌患者围术期换气功能的改变规律及影响机制。方法用氧合指数（Ｐ／Ｆ）、动脉肺泡氧分压比（ａ／Ａ）、动脉血氧饱和度５０％的氧分压（Ｐ５０Ｏ２）、动脉血二氧化碳分压（ＰａＣＯ２）４项指标对６８例５０岁以上男性肺癌患者分别于术前、术后即日、１、２、３、７日围术期换气功能进行监测。结果肺癌术后３日内Ｐ／Ｆ、ａ／Ａ较术前显著降低（Ｐ＜０．０１）；ＰａＣＯ２、Ｐ５０Ｏ２术后即日较术前显著增加（Ｐ＜０．０１）；术后２日内全肺切除氧合功能降低大于肺叶切除（Ｐ＜０．０５）；低肺功能患者术后换气及通气功能障碍较肺功能正常者显著（Ｐ＜０．０５）。结论肺癌术后３日换气功能明显减退，尤以氧合功能降低显著。应重点监测氧合功能变化，加强全肺及低肺功能患者的换气功能监测。     

BiPAP呼吸机正压通气治疗COPD合并II型呼吸衰竭临床观察

在常规治疗的基础上采用双水平气道正压（ＢｉＰＡＰ）呼吸机经鼻罩气道正压通气治疗慢性阻塞性肺疾病（ＣＯＰＤ）合并Ⅱ型呼吸衰竭（呼衰）患者２０例（治疗组），并以同期达同样标准的１７例患者仅采用常规治疗做对照组。结果，治疗前后血气分析表明，治疗组ｐＨ、ＰａＯ２的升高及ＰａＣＯ２的降低均较治疗前有非常显著的统计学意义（Ｐ〈０．０１）。对照组则ｐＨ的改变无统计学意义，ＰａＯ２上升其差异非常显著（Ｐ〈０．０１     

慢性阻塞性肺疾病患者睡眠时低氧血症的发生和预测

目的 研究慢性阻塞性肺疾病（ＣＯＰＤ）患睡眠时低氧血症的发生与否及机制。方法对３０例ＣＯＰＤ患白天肺功能、动脉血气及夜间血氧水平与正常对照组（８名）进行比较和分析。结果 ＣＯＰＤ患睡眠时血氧水平较正常人明显下降（Ｐ〈０．０５），尤以快动眼睡眠期（ＲＥＭ期）显，无论夜间平均血氧饱和度（ＭＳａＯ２）还是夜间最低血氧饱和度（ＭｍＳａＯ２），下降程度均明显高于正常人（Ｐ〈０．０５）。从血氧分布情况     

长期无创通气治疗对重叠综合征患者肺功能及夜间血氧的影响

目的 探讨单纯慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者与重叠综合征患者夜间低氧情况及长期呼吸机无创通气治疗对重叠综合征(慢性阻塞性肺疾病患者合并睡眠呼吸暂停低通气综合征)肺功能和血氧的影响.方法 140例稳定期COPD患者均进行夜间氧饱和度监测和肺功能检测,其中重叠综合征患者67例,观察10例重叠综合征患者单纯氧疗和氧疗+呼吸机无创通气治疗前后夜间血氧情况,对5例长期夜间无创通气治疗的重叠综合征患者进行1年动态夜间血氧和肺通气功能监测.结果 10例重叠综合征患者单纯氧疗及氧疗加呼吸机治疗比较,组间在动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、夜间最低氧饱和度(LSaO2)、夜间平均氧饱和度(MSaO2)、血氧饱和度低于90%的时间占总记录时间的百分比(SIT90%)等方面差异有统计学意义(P值均<0.05).长期(1年)无创通气治疗前后肺功能[呼吸峰流量(PEF)、肺活量(FVC)、FVC占预计值%、第1秒用力呼气容积(FEV1)、FEV1占预计值%]及夜间低氧指标(SIT90、MSaO2、LSaO2)明显改善(P值均<0.05).结果 阻塞程度相同的重叠综合征患者夜间低氧比单纯COPD患者严重,长期无创通气治疗可以改善重叠综合征患者肺通气功能及夜间低氧,长期氧疗+无创通气治疗是重叠综合征患者的第一线治疗方案.     

无创机械通气治疗慢性阻塞性肺疾病合并呼吸衰竭

目的　研究无创 Bi- PAP呼吸机治疗慢性阻塞性肺疾病 (COPD)合并呼吸衰竭。方法　 6 2例患者随机分为治疗组 37例 ,持续 Bi- PAP呼吸机治疗 ;对照组 2 5例 ,持续低流量吸氧。两组同时抗感染等常规治疗。观察血气和临床症状变化。结果　治疗 7日后治疗组比对照组其 p H、Pa CO2 、Pa O2 差异具有显著性 (P<0 .0 1)。结论　COPD合并呼吸衰竭患者早期使用 Bi- PAP呼吸机治疗 ,对低氧血症和 CO2 潴留改善明显 ,疗效显著     

Predictors of nocturnal oxygen desaturation in patients with COPD.

The aim of this study was to identify factors which might predict nocturnal desaturation (defined as a fall of > 4% from awake baseline level for > or = 5 min) in normoxic or mildly hypoxic patients with stable COPD [arterial O2 saturation (SaO2) > or = 91%]. The study was prospective in nature, had full ethical approval and was performed in the Respiratory Department of a city teaching hospital. Thirty-three patients [mean (SD) age 67.2 (9) years] with stable COPD [mean (SD) FEV1 36.8 (11.0)% pred.] were recruited via the respiratory outpatient clinics and through the respiratory wards. The following parameters were measured: daytime arterial blood gases; spirometry; lung volumes (helium dilution); single breath CO transfer factor (TLCO and KCO); maximum inspiratory (IMP) and expiratory mouth pressures; pulse oximetry (SpO2) across a 6-min walk test, and SpO2 during sleep. Seventeen patients who experienced nocturnal desaturation had significantly lower mean PaO2 and SaO2, and higher PaCO2 values compared to non-desaturators. There was a positive correlation between mean nocturnal SpO2 and daytime PaO2, SaO2, and minimum exercise SpO2, and a negative correlation between mean nocturnal SpO2 and PaCO2, and FRC. Regression analysis revealed that daytime SaO2 was the only independent predictor of mean nocturnal saturation (accounting for 61% of the variability in the mean nocturnal SpO2). We observed nocturnal desaturation in all patients with a daytime SaO2 < or = 93% but in no patient with SaO2 > or = 95%. We conclude that daytime SaO2 can be used to predict nocturnal desaturation in normoxic or mildly hypoxic patients with stable COPD. Nocturnal desaturation is likely in patients with COPD where daytime SaO2 < or = 93%, and unlikely where daytime SaO2 > or = 95%.     

Evolution of nocturnal oxyhemoglobin desaturation in patients with chronic obstructive pulmonary disease and a daytime PaO2 above 60 mm Hg

We studied 31 clinically stable chronic obstructive pulmonary disease (COPD) patients with a PaO2 greater than or equal to 60 mm Hg using polysomnographic sleep study at baseline (between 1983 and 1986) and at a mean follow-up time of 42.5 months to examine the evolution of rapid-eye-movement (REM) sleep nocturnal oxyhemoglobin desaturation (NOD). Arterial blood gases and spirometry measured at baseline and follow-up were compared with mean nocturnal SaO2 and to other REM sleep SaO2 parameters. We postulated that the onset of NOD would be seen most frequently in those patients with marked derangements of lung mechanics and greater longitudinal deterioration in arterial blood gases. Eight of the subjects developed REM-NOD on follow-up polysomnography. The appearance of REM-NOD was not related, or only minimally so, to initial PaO2, PaCO2, or mean nocturnal SaO2. Upon follow-up, however, the onset of NOD was always associated with deterioration of daytime PaO2 and PaCO2, mainly in those patients with the most severe baseline derangement of spirometry (lung mechanics). On the other hand, one group showed equivalent deterioration in daytime PaO2 and a stable PaCO2 but had less severely deranged baseline mechanics and demonstrated a fall in mean nocturnal SaO2 only. The findings in this latter group indicate that the development of NOD is not purely a result of decreasing daytime PaO2. We conclude that the onset of REM-NOD is mainly related to a severe derangement of lung mechanics with deterioration of resting awake gas exchange (progressive hypoxemia, hypercarbia, and worsening airflow).(ABSTRACT TRUNCATED AT 250 WORDS)     

BiPAP呼吸机治疗呼吸衰竭的疗效观察

目的 探讨BiPAP呼吸机在COPD合并呼吸衰竭的疗效。方法 18例COPD合并Ⅱ型呼吸衰竭患者在常规治疗基础上采用BiPAP呼吸机辅助通气作为治疗组，并取同期达同样标准而采用常规治疗的20例COPD患者作为对照组。结果 两组治疗后动脉血氧分压（PaO2)都明显上升（P＜0．01），但治疗组上升更高；治疗组血二氧化碳分压（PaCO2)比治疗前明显下降，治疗前后相差非常明显（P＜0．01），对照组PaCO2治疗前后相差不显著（P＞0．05）；治疗组临床症状缓解例数也明显多于对照组。结论：用BiPAP呼吸机辅助通气，对COPD合并轻，中度呼吸衰竭疗效肯定, 可降低PaCO2，提高PaO2，减轻症状，有利于呼吸肌疲劳恢复。     

COPD患者经皮血气参数与动脉血气参数的相关性及影响因素的分析

目的研究慢性阻塞性肺疾病（COPD）患者经皮二氧化碳分压（TcPaCO2）、经皮氧分压（TcPO2）及经皮血氧饱和度（SpO2）与动脉血气参数的相关性和影响因素，探讨其临床应用价值。方法测定31例COPD缓解期患者的TcPCO2、TrPO2及SpO2，同步测定动脉血气参数和进行肺功能参数测定。结果①COPD患者经皮血气参数与动脉血气参数间存在线性相关关系，其相关系数和回归方程如下：TcPCO2和PaCO2（Y=3．967＋0．941X，r=0．846，P〈0．001）、TcPO2和PaO2（Y=33．502＋0．716X，r=0．602，P〈0．001）、SpO2和SaO2（Y=7．639＋0．941X，r=0．763，P〈0．001）。②年龄及肺功能参数不是影响COPD患者TcPCO2、TcPO2及SpO2的因素。结论COPD患者经皮血气参数与动脉血气参数间有较好的相关性，经皮血气参数可作为一种无创监测手段应用于临床。     

机械通气治疗老年慢性阻塞性肺疾病合并呼吸衰竭疗效观察

目的观察机械通气对慢性阻塞性肺疾病(chronic obstructive pulmonary diease,COPD)并发Ⅱ型呼吸衰竭的老年患者的治疗作用。方法对66例COPD伴Ⅱ型呼吸衰竭患者进行机械通气治疗。观察上机前后、撤机前后的pH值、PaO2、PaCO2的改变情况。结果机械通气后较通气前动脉血pH值及PaO2均有升高,PaCO2明显下降,差异有显著统计学意义(P0.01)。结论机械通气对COPD并发Ⅱ型呼吸衰竭的老年患者疗效肯定,值得临床应用推广。     

BiPAP呼吸机治疗慢性阻塞性肺疾病合并Ⅱ型呼吸衰竭的疗效观察

目的探讨无创双水平气道正压通气（BiPAP）呼吸机对慢性阻塞性肺疾病（COPD）并发Ⅱ型呼吸衰竭患者的治疗效果。方法将48例COPD并发Ⅱ型呼吸衰竭患者随机分为两组,治疗组28例,采用BiPAP呼吸机加常规治疗;对照组20例,仅采用常规治疗。观察两组患者治疗前后动脉血气分析指标和呼吸频率的变化,以及治疗期间的并发症、治愈率及平均住院时间。结果治疗组患者经BiPAP治疗后,pH、PaO2升高,PaCO2降低,SaO2升高,呼吸频率明显减慢,治疗期间的并发症少,有效率升高,平均住院时间缩短。结论应用BiPAP治疗COPD合并Ⅱ型呼吸衰竭操作简单,效果良好,并发症少,患者易于接受,是一种安全有效的方法。     

Are COPD patients with nocturnal REM sleep-related desaturations more prone to developing chronic respiratory failure requiring long-term oxygen therapy?

BACKGROUND: Nocturnal oxygen desaturations (NOD), especially during REM sleep, have been described in patients with COPD. However, the role of NOD in the evolution of COPD to chronic respiratory failure has not been well studied. OBJECTIVE: The aim of our study was to evaluate whether NOD is a risk factor for the development of chronic respiratory failure in COPD patients. METHODS: We studied 34 consecutive COPD patients with a stable daytime PaO(2) >60 mm Hg over a period of 42 months. We classified patients as desaturators (NOD) when episodic desaturations were found mainly during REM sleep, independently of baseline SaO(2) values. RESULTS: At enrollment 19 patients (55.8%) had NOD. Over the follow-up period, 10 patients (29.4%) were included in a long-term oxygen therapy (LTOT) programme (9 were desaturators). The LTOT was initiated a median time of 22 +/- 6.8 months after enrollment. Patients who were subsequently prescribed LTOT had lower values of FEV(1) at enrollment, with a higher degree of NOD and PaCO(2). Stable respiratory failure developed earlier in patients with NOD: the two enrollment curves for LTOT differed significantly (log-rank test 2.56, p = 0.005). PaCO(2), NOD and FEV(1) were statistically significantly associated, both in univariate and multivariate Cox proportional hazards analyses, with an increased risk of entering a LTOT programme. CONCLUSIONS: We conclude that NOD may represent an independent risk factor for the development of chronic respiratory failure in COPD patients with daytime PaO(2) >60 mm Hg. A larger study is needed to confirm the role of NOD in the natural history of COPD and subsequently to identify the most appropriate therapeutic approach.     

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.