阻塞性睡眠呼吸暂停低通气综合症与高血压的相关研究

目的 分析伴有高血压的阻塞性睡眠呼吸暂停低通气综合症（oSAHS）的睡眠呼吸障碍特点，并探讨两者之间的关系。方法 对诊断为OSAHS患者中45例高血压和32倒非高血压患者进行基础情况和夜间缺氧程度、睡眠结构和干扰睡眠因素以及OSAHS患者中高血压的危险因素进行分析。结果 高血压组睡眠呼吸暂停低通气指数（AHI）高于非高血压痛组．体重指数（BMI）是引起两组间睡眠呼吸暂停低通气指数（AHI）差异的显著因素。两组间夜间平均Sa02和最低Sa02比较差异无显著性（p〈0．05），睡眠呼吸暂停低通气指数（AHI）是引起夜间缺氧的显著因素。OSAHS患者中高血压病的危险因素是AHI、年龄、BMI。结论 OSAHS伴有高血压的患者的睡眠呼吸障碍程度更重，而夜间低氧血症与高血压无关,但与睡眠呼吸障碍的严重程度有关。年龄、肥胖和睡眠呼吸障碍的严重程度是OSAHS患者中高血压的危险因素。     

阻塞性睡眠呼吸暂停低通气综合征生物力学研究进展

阻塞性睡眠呼吸暂停低通气综合征（obstructive sleep apnea hypopnea syndrome, OSAHS）是一种在睡眠时反复出现咽部塌陷导致呼吸暂停的疾病,其发病机制涉及多个方面。根据人体上气道系统解剖结构与生理学特点,从生物力学角度研究可能诱发睡眠呼吸暂停的各种因素,讨论近年来研究睡眠呼吸暂停的生物力学模型,分析可能导致OSAHS疾病的力学机制,并对OSAHS生物力学今后的研究进行展望。建立上气道生物力学模型是研究OSAHS发病机制的有效方法之一,对OSAHS术前评估和术后预测具有重要的临床意义。     

睡眠呼吸暂停低通气综合征

睡眠呼吸暂停综合征(SAHS)是指在每晚7h睡眠中,呼吸暂停反复发作超过30次或呼吸暂停指数(AHI)超过5次/h的呼吸道疾患[1].根据发病机制不同可以分为阻塞性睡眠呼吸暂停低通气综合征(OSAHS)、中枢性睡眠呼吸暂停低通气综合征(CSAHS)和混合性睡眠呼吸暂停低通气综合征(MSAHS),临床上以OSAHS最常见.OSAHS是指由于上气道塌陷阻塞导致睡眠时反复呼吸暂停和通气不足、打鼾、睡眠结构紊乱和反复微觉醒,频发血氧饱和度下降、白天嗜睡等症状,是一种发病率高、严重影响生活和危及生命的疾病,并发高血压、冠心病、呼吸衰竭、肺心病、糖尿病和脑卒中等,甚至夜间猝死[2].     

云南省昆明地区OSAHS与甲状腺机能减退的相关性

<正>阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)是一种常见的睡眠呼吸障碍疾病,患者在睡眠过程中上气道发生部分或完全阻塞,引起低通气或呼吸暂停。OSAHS在女性中的发病率大约为2%～9%,男性发病率大约为4%～24%[1]。甲状腺机能减退(简称甲减)是因甲状腺激素合成、分泌减少或者组织利用不足     

阻塞性睡眠呼吸暂停低通气综合征与血压变异性的临床研究

目的:通过测定阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血压及脉压(PP),探讨血压变异性与OSAHS之间的关系。方法:OSAHS合并高血压患者99例,根据呼吸暂停低通气指数(AHI)分为轻度、中度和重度OSAHS三组;单纯高血压患者20例作为对照组,比较OSAHS各组及单纯高血压组之间血压变化的特点。结果:重度OSAHS组患者的AHI、体重指数(BMI)、平均血压、非杓型血压所占比例及PP均明显高于轻、中度OSAHS组和单纯高血压组,最低血氧饱和度(SaO2)明显低于轻、中度OSAHS组和单纯高血压组。相关分析结果表明,平均PP与AHI呈正相关;SaO2与平均收缩压、舒张压呈负相关;AHI与平均收缩压呈正相关。结论:OSAHS患者夜间血压出现非杓型模式,血压增高的程度以及非杓型血压所占比例随着OSAHS病情加重而逐渐增高;PP与OSAHS的严重程度密切相关。     

睡眠呼吸暂停/低通气综合征体重指数及睡眠特征分析

睡眠呼吸暂停 /低通气综合征 (ＳｌｅｅｐＡｐｎｅａ/Ｈｙ ｐｏｐｎｅａＳｙｎｄｒｏｍｅ ,ＳＡ/ＨＳ)是一种严重的睡眠呼吸疾病 ,指每晚 7小时睡眠中 ,呼吸暂停反复发作 30次以上 ,每次发作呼吸暂停 10秒以上 ,或睡眠呼吸紊乱指数 (ａｐｎｅａ/ｈｙｐｏｐｎｅａｉｎｄｅｘ ,ＡＨＩ ,即平均每小时的睡眠呼吸暂停 低通气次数 )超过 5次以上。在整个人群中的发病率为 2 %～ 4 % [1] ,中年以后的男性和更年期后的女性发病率增高 ,男性发病率高于女性。ＳＡ/ＨＳ以反复发作的夜间呼吸暂停和低氧血症为主要临床特征 ,患者夜间睡眠质量较差 ,不…     

伴有阻塞性睡眠呼吸暂停低通气综合征的糖尿病患者的临床特点分析

目的：探讨伴有阻塞性睡眠呼吸低通气暂停综合征的糖尿病患者的临床特点,以提高DM与OSAHS两病关系的认识。方法对在2009年1月~2012年12月资料完整的糖尿病患者进行多导睡眠监测,筛选出符合标准的130例患者。根据呼吸暂停低通气指数(AHI)将DM患者分为OSAHS组患者67例;非OSAHS组患者63例。检测血脂、糖代谢等指标并计算胰岛素抵抗指数,比较两组参数的差异。结果OSAHS组的DM患者在体质量指数(BMI)、睡眠呼吸暂停低通气指数(AHI)、最低脉搏容积血氧饱和度(LSpO2)、血清甘油三酯(TG)、糖化血红蛋白(HbA1c)、空腹胰岛素水平(FIns)、胰岛素抵抗指数(HOMA-IR)等参数均高于未伴有OSAHS的DM患者,差异有统计学意义(P<0.05)。 OSAHS组患者血清FIns及HOMA-IR与LSpO2和AHI均存在相关性。OSAHS组高血压和冠心病并发症明显高于非OSAHS组。结论伴有OSAHS的DM患者由于慢性间歇性低氧与IR相关,发生高血压、冠心病的可能性增大,医务工作者应该提高糖尿病患者人群OSAHS的识别。     

血清同型半胱氨酸水平在阻塞性睡眠呼吸暂停低通气综合征和冠心病患者中的变化及其作用

目的:观察血清同型半胱氨酸(Hcy)水平在阻塞性睡眠呼吸暂停低通气综合征(OSHAS)及冠心病(CHD)患者中的变化和作用。方法:收集临床确诊CHD、OSAHS、CHD+OSAHS患者各30例,分别为CHD组、OSAHS组和CHD+OSAHS组。平行检测各组血清Hcy水平及睡眠呼吸监测指标:呼吸暂停低通气指数(AHI)、夜间最低血氧饱和度(SaO2)及平均SaO2,比较各组Hcy水平的差异以及Hcy水平与睡眠呼吸监测指标的相关性。并与30例体检健康者(健康对照组)对比分析。结果:(1)血清Hcy水平:三病例组明显高于健康对照组(P0.01),CHD+OSAHS组明显高于CHD组和OSAHS组(P0.01),CHD组与OSAHS组比较,差异无统计学意义(P0.05)。(2)病例组血清Hcy水平与AHI呈正相关(r=0.64,P0.01),与夜间平均SaO2和夜间最低SaO2均呈负相关(r分别为-0.64、-0.65,P0.01)。结论:血清Hcy水平升高与OSAHS患者SaO2减低有关,可能有利于CHD的发生与发展。     

阻塞性睡眠呼吸暂停低通气综合症的护理体会

目的：通过对阻塞性睡眠呼吸暂停低通气综合症(Obstructive Sleep ApneaHypopnea Syndrome,OSAHS)患者临床资料的回顾性分析,探讨该病的主要危险因素并总结护理经验,从而加强对该疾病的预防和护理。方法对我院自2010年2月~2013年2月收治的135例阻塞性睡眠呼吸暂停低通气综合症患者的临床资料进行回顾性分析。结果135例OSAHS患者在护理人员的精心护理和生活指导下,症状有所缓解,疾病得到有效控制。结论 OSAHS是一种多因素疾病,严重危害人体健康,采取有效的护理干预和生活指导,能够有效改善OSAHS患者睡眠状况,获得自我保健能力,提高生活质量,从而很大程度上改善患者预后情况。     

阻塞性睡眠呼吸暂停低通气综合征外周血IGF-2及其mRNA水平变化的初步研究

目的： 观察阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者胰岛素样生长因子-2（IGF-2）水平的变化,并探讨其与OSAHS及其并发的心血管疾病的关系。方法： 选择40例OSAHS患者作为病例组，20例正常人为对照组，病例组再根据血压水平分为正常血压及高血压组，采用酶联免疫吸附试验( ELISA)检测外周血血清中IGF-2水平，用RT-PCR技术检测受试者外周血单个核细胞胰岛素样生长因子-2mRNA（IGF-2 mRNA）水平,并对病例组中15例呼吸暂停低通气指数（AHI）>40次/h的患者进行经鼻持续气道正压通气（nCPAP）治疗1月后,重复以上过程。结果： OSAHS患者血清IGF-2水平及外周血单个核细胞 IGF-2 mRNA水平明显高于对照组(P<0.05)，并与血压升高水平相关。进一步分析与患者AHI呈正相关，与小于90%血氧饱和度时间占总睡眠时间百分比呈正相关,与呼吸暂停时间占总睡眠时间百分比呈正相关，与平均血氧饱和度、最低血氧饱和度呈负相关。经nCPAP治疗后,重度OSAHS患者血清IGF-2水平及外周血单个核细胞IGF-2 mRNA水平明显降低,差异有显著意义。结论： OSAHS患者IGF-2水平明显增高，增高的IGF-2可能参与OSAHS的病理过程，特别是OSAHS引发心血管疾病的相关病理生理过程。     

Complex sleep apnea syndrome: is it a unique clinical syndrome?

STUDY OBJECTIVES: Some patients with apparent obstructive sleep apnea hypopnea syndrome (OSAHS) have elimination of obstructive events but emergence of problematic central apneas or Cheyne-Stokes breathing pattern. Patients with this sleep-disordered breathing problem, which for the sake of study we call the "complex sleep apnea syndrome," are not well characterized. We sought to determine the prevalence of complex sleep apnea syndrome and hypothesized that the clinical characteristics of patients with complex sleep apnea syndrome would more nearly resemble those of patients with central sleep apnea syndrome (CSA) than with those of patients with OSAHS. DESIGN: Retrospective review SETTING: Sleep disorders center. PATIENTS OR PARTICIPANTS: Two hundred twenty-three adults consecutively referred over 1 month plus 20 consecutive patients diagnosed with CSA. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Prevalence of complex sleep apnea syndrome, OSAHS, and CSA in the 1-month sample was 15%, 84%, and 0.4%, respectively. Patients with complex sleep apnea syndrome differed in gender from patients with OSAHS (81% vs 60% men, p < .05) but were otherwise similar in sleep and cardiovascular history. Patients with complex sleep apnea syndrome had fewer maintenance-insomnia complaints (32% vs 79%; p < .05) than patients with CSA but were otherwise not significantly different clinically. Diagnostic apnea-hypopnea index for patients with complex sleep apnea syndrome, OSAHS, and CSA was 32.3 +/- 26.8, 20.6 +/- 23.7, and 38.3 +/- 36.2, respectively (p = .005). Continuous positive airway pressure suppressed obstructive breathing, but residual apnea-hypopnea index, mostly from central apneas, remained high in patients with complex sleep apnea syndrome and CSA (21.7 +/- 18.6 in complex sleep apnea syndrome, 32.9 +/- 30.8 in CSA vs 2.14 +/- 3.14 in OSAHS; p < .001). CONCLUSIONS: Patients with complex sleep apnea syndrome are mostly similar to those with OSAHS until one applies continuous positive airway pressure. They are left with very disrupted breathing and sleep on continuous positive airway pressure. Clinical risk factors don't predict the emergence of complex sleep apnea syndrome, and best treatment is not known.     

Sleep apnea syndrome: a possible contributing factor to resistant

STUDY OBJECTIVES: There is evidence supporting an association between sleep apnea and hypertension. However, it is not clear if sleep apnea interteres with the pharmacotherapy of hypertension. To investigate this question, we studied the relationship between the effectiveness of anti-hypertensive treatment in reducing blood pressure, and severity of sleep apnea in a large group of apneic patients referred to a sleep disorders centre at St. Michael's Hospital at the University of Toronto. DESIGN: N/A SETTING: N/A PARTICIPANTS: 1,485 adult patients with sleep apnea, as defined by the apnea/hypopnea index (AHI) >10 events/hr, were analyzed. There were 393 who reported using anti-hypertensive medications on a regular basis for more than 6 months. One hundred and eighty-three patients were treated "effectively" (i.e. blood pressure lower than 140/90 mm Hg in the morning and in the evening). Seventy-four patients were treated "ineffectively," defined as blood pressure >140/90 mm Hg in the morning or in the evening. Both groups were compared with respect to clinical and demographic data using analysis of covariance with gender, age, body mass index (BMI), and neck circumference (NC) as covariates. INTERVENTIONS: N/A MEASUREMENTS AND RESULTS: Ineffectively and effectively treated patients were similar in age (57 +/- 9) vs. 57 +/- 10 years, respectively), and had similar body mass index (33.8 +/- 7.4 vs. 33.4 +/- 7.3 kg/m2, respectively). However, ineffectively treated patients had significantly higher apnea/hypopnea index (44 +/- 29 vs. 33 +/- 25 events/hr, p<.0005), despite having similar nocturnal oxygenation (percent of total sleep time spent with oxygen desaturation lower than 90% was 36 +/- 34 vs. 29 +/- 30% in the ineffective and effective groups, respectively). The difference in AHI persisted even after adjusting for age, gender, and body mass index. CONCLUSIONS: Our results demonstrate that hypertensive patients with sleep apnea whose blood pressure responds beneficially to treatment have less severe sleep apnea than those patients whose blood pressure remains elevated despite anti-hypertensive therapy. Since neither obesity nor nocturnal hypoxemia appear to be important determinants of ineffective treatment, we suggest that resistant hypertension may be caused by frequent intermittent sympathetic stimulation.     

Correlation of obstructive sleep apnea hypopnea syndrome with metabolic syndrome in snorers

Though obstructive sleep apnea hypopnea syndrome (OSAHS) and metabolic syndrome (MS) are correlated; the contributing factors for the occurrence of MS in Chinese snorers remain largely undefined. We aimed to investigate the associated pathogenesis of coexistence of OSAHS and MS in Chinese snorers. A total of 144 Chinese habitual snorers were divided into 3 groups, the control group (simple snorers) (n  =  36), the mild OSAHS group (n  =  52) and the moderate-to-severe OSAHS group (n  =  56). The incidence of MS in the moderate-to-severe OSAHS group (26.8%) was significantly higher than that in the control group (8.3%), the mild OSAHS group (11.1%) and all the OSAHS patients (19.45%) (all P < 0.05). Homeostatic model assessment (HOMA) index and proinsulin (PI) were negatively correlated with nocturnal meanSpO₂ and miniSpO₂. Meanwhile, nocturnal SpO₂ were negatively correlated with body mass index, waist and neck circumferences and diastolic blood pressure, but positively correlated with total cholesterol and high-density lipoprotein cholesterol. The study indicated that in Chinese snorers, moderate-to-severe OSAHS was closely associated with MS via nocturnal hypoxemia.     

OSAHS患者自然睡眠期呼吸模式对上气道流场的影响

目的分析阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)患者自然睡眠时平静呼吸和呼吸暂停期不同压力边界条件和呼吸模式对气道内气体的流动和生理状态的影响。方法创建OSAHS患者仰卧位自然睡眠状态,并采集CT数据建立三维上气道有限元模型。临床测量患者睡眠期喉腔压力作为边界条件,考虑鼻吸鼻呼、鼻吸口呼、口吸鼻呼、口吸口呼4种典型呼吸模式进行流体力学仿真。结果睡眠期OSAHS患者的呼吸气流呈非稳定、有涡、双向流动,压力边界以及呼吸模式对气体流动的影响明显。用口呼吸与用鼻呼吸相比,气体的最大流速有所升高,压降主要集中在口腔,吸气时升高约30%,呼气时升高1倍。结论采用OSAHS患者自然睡眠期CT数据建模并以临床喉腔压力作为边界条件进行有限元仿真具有意义,研究结果有助于了解OSAHS患者真实自然睡眠状态下的上气道流场特性。     

Comparison of limited monitoring using a nasal-cannula flow signal to full polysomnography in sleep-disordered breathing

STUDY OBJECTIVES: Evaluate the utility of overnight monitoring limited to nasal cannula airflow and oximetry in the diagnosis of obstructive sleep apnea-hypopnea syndrome (OSAHS). DESIGN: Prospective randomized study, blinded analysis. SETTING: Sleep disorder center, academic institution. PARTICIPANTS: 56 patients with suspected OSAHS, 10 normal volunteers. MEASUREMENTS AND RESULTS: In-laboratory full nocturnal polysomnography (NPSG) and unattended ambulatory study with monitoring of only airflow and oximetry performed in randomized order. Obstructive respiratory events were scored on the full NPSG while visualizing all signals and then rescored on the full NPSG and on the ambulatory study while visualizing only airflow and oximetry signals. Respiratory disturbance indexes (RDI) for the limited studies (RDIFlowNPSG and RDIFlowAmbulatory) were calculated as the sum of the apneas and hypopneas (defined using airflow amplitude and O2 desaturation) divided by the valid flow-signal time. The reference RDIFullNPSG was calculated from the sum of the apneas and hypopneas (defined using flow amplitude, O2 desaturation and electroencephalographic arousal) identified on the full NPSG divided by the total sleep time. RDIFullNPSG was greater than RDIFlowNPSG (bias = 5.6 events per hour) and RDIFlowAmbulatory (bias = 10.9 events per hour), but the differences were mainly in subjects with an RDI > 40 events per hour. The diagnostic sensitivity and specificity for the diagnosis of OSAHS using a cutoff of 18 events per hour were 96% and 93% using the flow signal from the NPSG and 88% and 92% using the flow signal from the ambulatory study performed on a separate night. CONCLUSIONS: In subjects with OSAHS, analysis of the flow signal from a nasal cannula can provide an RDI similar to that obtained in a full NPSG.     

Obstructive sleep apnea and hypertension: are peripheral chemoreceptors involved?

The mechanism of pathogenesis of hypertension in patients with obstructive sleep apnea (OSA) is unknown. Many investigators point to the high sympathetic nervous system activity (SNS) observed in OSA patients. However, there is no clear explanation as to the mechanism for the development of SNS hyperactivity in these patients. A common feature of patients with OSA is repetitive bouts of transient hypoxemia during sleep. Repetitive transient hypoxemia in rats has resulted in hypertension. In OSA patients, resolution of nocturnal hypoxemia with CPAP has corrected nocturnal and diurnal hypertension. Also, exposure to hyperoxia reduces blood pressure and sympathetic activity in OSA patients, but not in normals. These data suggest a significant role of peripheral chemoreceptors in the regulation of vascular tone. We hypothesize that peripheral chemoreceptors significantly contribute to the pathogenesis of hypertension in patients with OSA and that this is associated with chemoreceptor hyperactivity. This implies that correcting the intermittent nocturnal hypoxemia alone may prevent the cardiovascular morbidity associated with obstructive sleep apnea.     

Effect of celiprolol treatment in hypertensive patients with sleep apnea.

The effects of a beta-blocker, celiprolol, on sleep and arterial blood pressure (BP) were evaluated during a single-blind study in seven hypertensive patients with sleep apnea. Diurnal ambulatory BP measurements with an automatic cuff-inflation device and polysomnography with simultaneous Finapres BP recording were performed separately on consecutive days at the end of two 21-day treatment periods involving placebo followed by celiprolol (200 mg/day). Age was 59 +/- 2.5 yr (m +/- sem) and body mass index 33.2 +/- 2.3 kg. m-2. Diurnal ambulatory BP was significantly lower with celiprolol than with placebo (systolic 139 +/- 4 vs 152 +/- 5 mmHg, diastolic 86 +/- 2 vs 96 +/- 2 mmHg). The apnea-hypopnea index was similar under celiprolol and placebo (48 +/- 7.4 vs 53 +/- 7.8, respectively), as were the total sleep time and percent of duration of the different sleep stages. Individual average BP values were significantly lower during REM sleep under celiprolol but remained similar under celiprolol and placebo in the other sleep stages. Variability of nocturnal BP (assessed by the SD of distribution of BP variations) was not affected by celiprolol. In conclusion, celiprolol which decreased daytime BP, did not affect sleep pattern or respiratory disturbances, or nocturnal BP variability related to apnea.     

The Association between the Phenotype of Excessive Daytime Sleepiness and Blood Pressure in Patients with Obstructive Sleep Apnea-Hypopnea Syndrome

Objective Investigate the clinical features and the blood pressure (BP) pattern of the phenotype of excessive daytime sleepiness (EDS) in OSAHS.Methods A total of 508 Chinese adults with suspected OSAHS were referred to our sleep laboratory from October 2009 to May 2012. On the same night of polysomnography (PSG), the levels of blood pressure were measured before sleeping (bedtime BP) and immediately after waking up in the next morning (morning BP). EDS was recognized as Epworth Sleepiness Scale (ESS)≥9. Subjects were classified into four groups based on the apnea-hypopnea index (AHI) from PSG as follows: control (simple snoring) group (control, n=104) with AHI<5; mild group (mild, n=89) with AHI≥5 and <15; moderate group (moderate, n=70) with AHI≥15 and<30; and severe group (severe, n=245) with AHI ≥30. The differences and correlations between BP and PSG parameters in EDS and non-EDS group of OSAHS patients were analyzed.Results In all subjects, ESS was positively correlated with morning diastolic blood pressure (DBP), Mean arterial pressure (MAP) and bedtime DBP (r=0.144, 0.102 and 0.114, respectively, each P value<0.05). In OSAHS patients, ESS was only positively correlated with morning DBP (r=0.137, P<0.05). OSAHS patients with EDS phenotype were younger and were more likely to have the symptom of waking up feeling tired (36.1% vs. 23.2%, p=0.023), who had lower MSaO2, longer SIT90 (the ratio of time of SpO2 below 90% in total sleep time) and higher DBP (bedtime as well as morning). In patients with AHI≥15, ESS was correlated positively with both bedtime and morning DBP after controlling the confounding effects of age, sex, BMI, AHI and nadir nocturnal oxygen saturation( r=0.126,0.143, respectively, both P values<0.05). And in OSAHS patients of EDS phenotype, the bedtime DBP, bedtime MAP, morning DBP, and morning MAP were 3~5 mm Hg higher than that in patients of non-EDS phenotype(P<0.05). In the moderate and severe OSAHS group, patients with EDS phenotype were younger and had a lower mean blood oxygen saturation (MSaO2), longer time of SpO2 below 90% and higher SIT90 than patients with non-EDS phenotype (P<0.05). In hypertensive OSAHS patients, patients with EDS were also younger and had higher micro-arousal index (MiI), as well as higher morning DBP, morning MAP and bedtime DBP than that in non-EDS group (P<0.05).Conclusions EDS in OSAHS patients is a special phenotype, which was characterized by younger age, higher DBP and more severe hypoxic load. This feature is mainly manifested in moderate and severe OSAHS patients. It is very important to identify the phenotype of EDS in patients with OSAHS, who may meet more benefits from effective treatment of OSAHS by correcting the intermittent nocturnal hypoxia and sleep fragmentation.     

Effects of nasal O2 on sleep-related disordered breathing in ambulatory patients with stable heart failure

OBJECTIVE: The purpose of this study was 1) to determine the effects of nasal O2 on periodic breathing, arterial oxyhemoglobin desaturation and nocturnal ventricular arrhythmias in patients with heart failure and 2) determine the characteristics of patients whose periodic breathing will be reversed by O2 administration; our hypothesis was that patients with more severe periodic breathing and desaturation, will respond more favorably to oxygen. DESIGN: Prospective study. SETTING: Referral sleep laboratory of a Department of Veterans Affairs Medical Center. PARTICIPANTS: 36 ambulatory male patients with heart failure whose initial polysomnograms showed periodic breathing with fifteen or more episodes of apnea (A) and hypopnea (H) per hour (AH index, AHI) were treated with nasal O2 during the subsequent full night polysomnography. INTERVENTIONS: Oxygen. MEASUREMENTS AND RESULTS: Arterial blood gases and hydrogen ion concentrations were measured, and cardiac radionuclide ventriculography, Holter monitoring, and polysomnography were done. The studies were scored blindly. Treatment with O2 resulted in a significant reduction in AHI (49+/-19 vs 29+/-29, means+/-SD), central apnea index (28+/-23 vs 13+/-18 per hour), and the percent of total sleep time below an arterial oxyhemoglobin saturation of 90% (23+/-21% vs 0.8+/-2.3%). In spite of virtual normalization of saturation with O2 therapy, the number of ventricular arrhythmias during sleep did not change significantly. In 39% of the patients (14 out of 36), O2 therapy resulted in reversal of central sleep apnea (defined by a reduction in AHI to less than 15/hr). In this group, the AHI decreased by 78% which was significantly (p=0.0001) more than improved (22%) in AHI of the remaining patients (n=22). The main differences between baseline characteristics of the two groups was a significantly higher mean PaCO2 in patients who did respond fully to O2 (39.3+/-5.4 vs 36.1+/-4.2 mm Hg, p=0.03). In both groups, however, O2 administration resulted in significant and similar improvement in arterial oxyhemoglobin saturation (saturation <90%, percent total sleep time 0.1+/-0.3% vs 1+/-3%). CONCLUSION: In patients with stable heart failure, administration of nasal O2 significantly improves periodic breathing and virtually eliminates clinically significant arterial oxyhemoglobin desaturation. The beneficial effects of O2, however, may be modulated by the level of arterial PCO2. Acute O2 therapy has important benefits on sleep apnea and nocturnal arterial oxyhemoglobin desaturation in heart failure patients. Long term benefits of O2 therapy in heart failure and sleep apnea need to be determined.