Improvement of exercise capacity with treatment of Cheyne-Stokes respiration in patients with congestive heart failure

Objectives. The aim of this study was to determine the impact of nasal nocturnal oxygen therapy on respiration, sleep, exercise capacity, cognitive function and daytime symptoms in patients with congestive heart failure and Cheyne-Stokes respiration.Background. Cheyne-Stokes respiration is common in patients with congestive heart failure and is associated with significant nocturnal oxygen desaturation and sleep disruption with arousals. Oxygen desaturations and arousals cause an increase in pulmonary artery pressure and sympathoneural activity and therefore may reduce exercise capacity. Oxygen is an effective treatment of Cheyne-Stokes respiration and should improve exercise capacity in these patients.Methods. The study was designed as a randomized, crossover, double-blind, placebo-controlled trial: 22 patients were assigned to 1 week each of nocturnal oxygen and room air. After each week, polysomnography, maximal bicycle exercise with expiratory gas analysis and trail-making test were performed, and a health assessment chart was completed.Results. Noturnal oxygen significantly reduced the duration of Cheyne-Stokes respiration (162 ± 142 vs. 88 ± 105 min [mean ± SD]; p < 0.005). Sleep improved as evidenced by less stage 1 sleep and fewer arousals (20 ± 13 vs. 15 ± 9/h total sleep time; p < 0.05) as well as more stage 2 and slow-wave sleep; nocturnal oxygen saturation also improved. Peak oxygen consumption during exercise testing increased after oxygen treatment (835 ± 395 vs. 960 ± 389 ml/min; p < 0.05). Cognitive function evaluated by the trail-making test improved, but daytime symptoms in the health assessment chart did not improve significantly.Conclusions. Successful treatment of Cheyne-Stokes respiration with nocturnal nasal oxygen improves not only sleep, but also exercise tolerance and cognitive function in patients with congestive heart failure.     

Respiration and abnormal sleep in patients with congestive heart failure

We investigated the interaction between respiration and sleep in ten male outpatients with severe, stable, maximally treated congestive heart failure (CHF). Cheyne-Stokes respiration (CSR), defined as periodic breathing with apnea or hypopnea, was found in all patients with a mean duration of 120 +/- 87 minutes [50.2 +/- 34.4 percent total sleep time (TST)]. The CSR was found predominantly during stage 1 (20.6 +/- 6.7 percent TST) and stage 2 (25.8 +/- 6 percent TST) NREM sleep and occurred rarely during slow wave sleep (SWS) (1.6 +/- 1 percent TST) and REM sleep (1.6 +/- 0.5 percent TST). All apneas and hypopneas were central. Despite normal awake arterial oxygenation (SaO2) (96.1 +/- 1.6 percent), significant, severe hypoxemia was found during sleep in seven patients with SaO2 less than 90 percent for 9 to 59 percent TST (mean +/- SD, 23 +/- 23 percent TST), and this was significantly related to the duration of CSR (r = 0.66, p less than 0.05). The mean minimum SaO2 for sleep stage was lowest during stage 1 (82.1 percent +/- 2.6 percent) and stage 2 (78.9 percent +/- 2.8 percent) NREM sleep, intermediate during REM sleep (84.5 percent +/- 1.8 percent) and highest during SWS (87.6 percent +/- 2.7 percent). Sleep was disrupted to a variable extent in all patients with a short mean TST (287 +/- 106 minutes), a high proportion of stage 1 sleep (26 +/- 19 percent TST), virtual absence of SWS (5 +/- 7 percent TST) which was found in only four patients, and a high number of sleep stage changes (30 +/- 27/hour) and arousals (28 +/- 25/hour). Arousals occurred predominantly during stage 1 (17 +/- 20/hour) and stage 2 (10 +/- 7/hour) NREM sleep and the majority immediately followed the hyperpneic phase of CSR. The amount of CSR (percent TST) was inversely related to the length of TST (r = -0.73, p less than 0.05), and directly related to the number of sleep stage changes (r = 0.79, p less than 0.01) and the number of arousals (r = 0.66, p less than 0.05). We conclude that in severe, stable CHF, CSR occurs predominantly during light sleep, that despite normal awake arterial oxygen saturation, significant hypoxemia may develop during sleep due to CSR, and that sleep is unstable and disrupted due to frequent arousals caused by the hyperpneic phase of CSR. These sequelae of CSR may be important determinants of the clinical status and outcome of patients with severe CHF.     

稳定期慢性充血性心力衰竭患者睡眠呼吸障碍

目的了解稳定期、已得到良好治疗的慢性充血性心力衰竭(心衰)患者的睡眠呼吸障碍的发生情况及睡眠呼吸障碍对心衰的影响.方法应用多导睡眠监护仪(Polywin1000,RespironicsInc.)对稳定期充血性心衰患者进行监测.结果病人分为两组,Ⅰ组(21例)A-H指数≤15,Ⅱ组(15例,占41.7%)A-H指数》15.Ⅱ组A-H指数为16.8～78.8,平均42.6±15.5,其中阻塞性AHI为11.1±8.4,而中枢性AHI为31.5±9.6.同时,Ⅱ组有着显著多的醒觉指数,为36.8±21.3(Ⅰ组为19.4±11.2),这直接与呼吸暂停及低通气指数有关,并与睡眠中最低血氧饱和度[Ⅱ组(76.7±4.6)%,Ⅰ组(86.5±2.8)%、更低的左心室射血分数[Ⅱ组(24.2±8.8)%,Ⅰ组(31.5±10.6)%]有关.结论稳定期慢性充血性心衰患者有着很高的严重的睡眠呼吸障碍的发生率,主要为伴中枢性睡眠呼吸暂停的周期性呼吸.睡眠呼吸障碍的发生与严重的夜间氧合血红蛋白饱和度的下降及过多的觉醒有关.严重的未经治疗的睡眠呼吸障碍可能影响左心室功能,并能加剧充血性心衰患者的死亡.     

Nocturnal periodic breathing in primary pulmonary hypertension.

Cheyne-Stokes respiration is frequently observed in congestive heart failure. Among other factors, prolongation of circulation time, hypocapnia and hypoxia are thought to underlie this sleep-related breathing disorder. Primary pulmonary hypertension (PPH) is also characterized by reduced cardiac output and blood gas alterations. Therefore, the aim of the present study was to determine whether a nocturnal periodic breathing (PB) occurs in PPH. A total of 20 consecutive patients with PPH who had been admitted for pharmacological investigation of pulmonary vasoreactivity were investigated by lung function testing, right heart catheterization and full-night attended polysomnography. PB was detected in six patients (30%) (mean +/- SEM: apnoea/hypopnoea index 37 +/- 5 h(-1); arterial oxygen saturation was <90% during 56 +/- 6.5% of total sleep time). The patients with PB had more severe haemodynamic impairment than those without. They also had a more marked reduction in the pulmonary diffusion capacity and greater arterial hypoxia. PB was markedly improved or even eradicated by nasal oxygen during the night. Periodic breathing occurs in patients with advanced primary pulmonary hypertension and can be reversed by nocturnal nasal oxygen. The clinical and prognostic significance of periodic breathing in primary pulmonary hypertension needs to be determined by further studies.     

Influence of Low-Flow Oxygen Supply on Sleep Architecture in Patients with Severe Heart Failure (NYHA III-IV) and Cheyne-Stokes Respiration

Patients suffering from severe heart failure may develop breathing pattern disorders during sleep, especially in the form of Cheyne-Stokes respiration. Results may be severe disturbances in sleep architecture and worsening of hemodynamics and of prognosis of these patients. Causes of the periodic breathing disorders are probably hypocapnia, hypersensitivity of respiratory control centers, hypoxemia, and prolonged blood circulation time. This study examined the influence of different concentrations of continously administered oxygen during the nighttime on breathing pattern disorders, oxygen saturation, and sleep architecture in 65 patients with severe heart failure (NYHA III–IV). Fifty-two of 65 patients showed an improvement of sleep architecture. Total sleeping time increased significantly (p < 0.01). Fragmentations of sleep by arousals decreased (p < 0.01); time of random eye movement (REM) sleep and non–REM sleep III and IV increased significantly.     

Effects of home oxygen therapy on patients with chronic heart failure

OBJECTIVES: Dyspnea on exertion and/or hypoxemia due to nocturnal respiratory disturbance may occur in patients with stable chronic congestive heart failure. Such patients with respiratory disorder during sleep have a poor prognosis. The effects of treatment with home oxygen therapy on patients with congestive heart failure are unclear when symptoms are stable at rest. This study investigated the effects of home oxygen therapy on patients with stable chronic congestive heart failure. METHODS: Thirty-three patients with stable chronic congestive heart failure(New York Heart Association functional class II-IV) and hypoxemia during exercise or sleep were treated with oxygen above the level of 90% SaO2. The following factors were compared before and after home oxygen therapy: Subjective minimal capacity on exercise(metabolic equivalents: METs) before and 1 month after patients first became aware of dyspnea on effort using the specific activity scale(SAS); SaO2 at rest before and 1 month after; and frequency of admission during 1 year due to deterioration of heart failure. RESULTS: After home oxygen therapy, SAS improved from 2.5 +/- 0.9 to 3.3 +/- 1.0 METs(p < 0.0001), and SaO2 at rest improved from 92.8 +/- 2.5% to 96.3 +/- 1.6%(p < 0.0001). The frequency of admission was decreased from 1.3 +/- 1.2 to 0.8 +/- 1.2 times(p = 0.03). CONCLUSIONS: Home oxygen therapy is effective for improving the symptoms and activity of daily life in patients with chronic heart failure. Home oxygen therapy may prevent the deterioration of heart failure.     

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.     

Underestimation of nocturnal hypoxemia due to monitoring conditions in patients with COPD

STUDY OBJECTIVES: COPD patients run a risk of developing nocturnal oxygen desaturation. When evaluating patients with nocturnal hypoxemia, an unfamiliar hospital environment and the monitoring equipment may cause sleep disturbances. It was hypothesized that increased sleep disruption will lead to fewer instances of desaturation during a night of monitoring. DESIGN:The following forms of monitoring were evaluated prospectively on 3 nights for each patient: oximetry at home; polysomnography (PSG) at home; and PSG in the hospital. SETTING: Department of Pulmonology, Rijnstate Hospital Arnhem, The Netherlands. PATIENTS: Fourteen stable COPD patients (7 men; median age, 71.5 years; age range, 59 to 81 years; FEV(1), 32.5% predicted; FEV(1) range, 19 to 70% predicted) participated in the study. All subjects had significant instances of nocturnal arterial oxygen desaturation. Those patients with a sleep-related breathing disorder or cardiac failure were excluded from the study. MEASUREMENTS AND RESULTS: The mean nocturnal arterial oxygen saturation (SaO(2)) level was higher during PSG monitoring at home (89.7%; range, 77 to 93%) than during oximetry monitoring (88.5%; range, 80 to 92%) [p < 0.025]. The fraction of time spent in hypoxemia (ie, SaO(2) < 90%) was lower during PSG monitoring at home (40.8%; range, 5 to 100%) than during oximetry monitoring (59.9%; range, 6 to 100%) [p < 0.01]. Desaturation time (DeltaSaO(2) > 4%) was lower during PSG monitoring at home (22.1%; range, 3 to 63%) during PSG monitoring at home than during oximetry monitoring (50.4%; range, 4 to 91%) [p < 0.01]. A correction for actual sleep during PSG monitoring reduced the differences between PSG monitoring at home and oximetry monitoring, although a difference in the desaturation time remained (PSG monitoring at home, 31.9% [range, 2 to 75%]; oximetry monitoring, 50.4% [range, 4 to 91%]) [p = 0.041]. A comparison of sleep architectures for nights when PSG was being monitored showed a higher arousal index in the hospital than at home (PSG monitoring in the hospital, 5.6 arousals per hour [range, 2 to 16 arousals per hour]; PSG monitoring at home, 2.5 arousals per hour [range, 1 to 6 arousals per hour]) [p < 0.025], but no differences in SaO(2) levels were found between PSG monitoring at home and PSG monitoring in the hospital. CONCLUSION: The artifacts due to sleep-monitoring equipment may cause an underestimation of the degree of nocturnal hypoxemia in COPD patients. The addition of an unfamiliar environment causes more sleep disruption, but this does not affect nocturnal SaO(2) levels further.     

The role of high-frequency jet ventilation in the treatment of Cheyne-Stokes respiration in patients with chronic heart failure

BACKGROUND: Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) is common in patients with severe cardiac failure. Various modes of positive airway pressure have been suggested as treatments.The authors hypothesized that high frequency jet ventilation (HFJV) can improve central sleep apnea in patients with chronic heart failure. METHODS: Eleven subjects with stable, optimally treated chronic heart failure and Cheyne-Stokes respiration were tested untreated and on four treatment nights in random order: nasal oxygen (4 L/min), continuous positive airway pressure (CPAP) (mean 9.3 cm H(2)O), bilevel positive airway pressure (BiPAP)(mean 12.0/5.3 cm H(2)O), or HFJV(60 approximately 80 breaths per minute) during polysomnography (EMBLA, Flaga, Reykjavik, Iceland). RESULTS: The apnea-hypopnea index (AHI) declined from 30.9 +/- 8.3/h in untreated night to 23.6 +/- 6.6/h oxygen night and 18.5 +/- 5.0/h CPAP, 14.3 +/- 3.9/h BiPAP, and 20.1 +/- 4.1/h HFJV (all P < 0.001 versus control). There was no significant difference between the AHI of HFJV and that of CPAP (P = 0.541). Arousal index decreased from 31.4+/-13.2/h untreated to 25.0 +/- 7.1/h oxygen and 13.6 +/- 4.7/h CPAP, to 13.7 +/- 4.9/h BiPAP and 14.4 +/- 4.7/h HFJV. HFJV had the similar effect to the other therapeutic groups in arousal index (P > 0.05). There were large increases in slow-wave and rapid eye movement (REM) sleep with HFJV. All subjects preferred HFJV to CPAP. CONCLUSIONS: One night of therapy with HFJV improved nocturnal breathing pattern and sleep quality in patients with Cheyne-Stokes respiration in chronic heart failure. HFJV therapy for sleep and breathing were the same as those during a nasal CPAP night. A long-term study of the effect of HFJV on cardiovascular function is needed.     

Heart failure and central respiratory dysregulation. Cheyne-Stokes respiration during sleep in advanced left heart failure

Central sleep apnoea, especially Cheyne-Stokes respiration, is found in 45 to 66% of patients with congestive heart failure (CHF) in functional classes NYHA II to IV. Cheyne-Stokes breathing cycles are characterised by central apnoeas, followed by a crescendo--like increase of tidal volume into hyperventilation and a subsequent decline of tidal volume, ending in another central apnoea. Cheyne-Stokes respiration has been shown to be a poor prognostic factor for patients with CHF. Apnoeas and hypopnoeas cause marked oxygen desaturation and rises of carbon dioxide concentrations in the blood. The resumption of breathing is frequently associated with arousals, which might cause daytime symptoms like fatigue and sleepiness as well as persistent activation of the sympathetic nervous system. Elevated concentrations of catecholamines increase cardiac work, adversely affecting cardiac function. Serum catecholamines are known to augment the chemoreceptor susceptibility for carbon dioxide. This might be one reason for the permanent mild hyperventilation found in these patients during wakefulness. Increased chemoreceptor responsiveness destabilises the feedback control of breathing, and hyperventilation below the apnoeic threshold grows more likely. Other contributing factors for the development of Cheyne-Stokes respiration include alterations in the control of breathing during sleep and the increased circulation time between the lung and chemoreceptors in CHF patients. The feedback regulation of breathing might be less dampened since carbon dioxide levels are reduced in these patients. Treatment includes nCPAP, but in many cases this is poorly tolerated in patients with central sleep apnoea. Future approaches to Cheyne-Stokes respiration might focus on improving ventilatory pattern and pharmacological manipulation of carbon dioxide receptor susceptibility.     

Effect of triazolam on sleep and arterial oxygen saturation in patients with chronic obstructive pulmonary disease

We compared the effects of a placebo with 0.125 and 0.25 mg of triazolam (Halcion) on sleep quality, oximetry, and respiratory events during sleep in ten stable outpatients with chronic obstructive pulmonary disease. The subjects had a forced expiratory volume in 1 s ranging from 17% to 76% of the predicted value (mean +/- SD, 38.1% +/- 19%) and a waking arterial oxygen pressure from 46 to 84 mm Hg (mean +/- SD, 67 +/- 12 mm Hg). Polysomnography was done on three nights within a two-week period after the patients received on a "blinded" basis either placebo or 0.125 or 0.25 mg of triazolam. Triazolam produced improvements in total sleep duration, time spent in stage 2 nonrapid eye movement (NREM) sleep, and subjective of sleep quality. For most patients, there was a nighttime drop in arterial oxygen percentage of saturation (SaO2) in the placebo condition, but triazolam did not cause a significant worsening, of the mean SaO2, minimum SaO2, or the number of apneic and hypopneic events. Across all experimental conditions, we documented little desaturation during wakefulness (mean low, 87.2% +/- 10.2%), more during NREM sleep (mean low, 83.2% +/- 12.6%), and most desaturation in REM sleep (mean low, 80.1% +/- 15.7%). We conclude that single-night use of triazolam improved the quality and duration of sleep in patients with chronic obstructive pulmonary disease. In patients without severe waking hypoxemia and without carbon dioxide retention, triazolam did not increase either nocturnal hypoxemia or respiratory events during sleep.     

The incidence,pathophysiology, treatment and prognosis of Cheyne-Stokes breathing disorder in patients with congestive heart failure

DEFINITION: Cheyne-Stokes respiration is a breathing disorder characterized by recurrent central sleep apneas, mainly during sleep, alternating with a crescendo-decrescendo pattern of tidal volume. PATHOPHYSIOLOGY AND PROGNOSIS: The pathophysiology of Cheyne-Stokes respiration, involving the cardiovascular, pulmonary and sympathetic nervous systems, is still not well understood. Although 50% of moderate to severe congestive heart failure patients suffer from significant Cheyne-Stokes respiration, studies been undertaken to determine the prevalence of this phenomenon and its implications regarding patients' life expectancy and quality of life were conducted only in recent years. Other studies suggest that Cheyne-Stokes respiration has a negative prognostic value upon congestive heart failure patients. TREATMENT: Novel therapeutic approaches have been attempted in order to treat Cheyne-Stokes respiration; they include oxygen delivery, various pharmaceutical treatments aimed to stabilize the ventilatory system and other pharmaceutical treatments aimed to improve the left ventricular ejection fraction. However, none of them was effective. OBJECTIVES: This review summarizes some of the current knowledge regarding Cheyne-Stokes respiration pathophysiology, prevalence, prognostic implication and available treatments.     

Cardiac resynchronization therapy improves central sleep apnea and Cheyne-Stokes respiration in patients with chronic heart failure

OBJECTIVES: We studied the effects of cardiac resynchronization therapy (CRT) on heart failure (HF) patients with central sleep apnea (CSA). BACKGROUND: Patients with advanced HF often suffer from CSA with Cheyne-Stokes respiration. Cardiac resynchronization therapy improves myocardial function and exercise capacity in HF patients with conduction disturbances. The relationship between CRT and CSA is currently unknown. METHODS: Twenty-four patients (7 females; 62 +/- 11 years) with HF, a reduced left ventricular ejection fraction (24 +/- 6%), and left bundle branch block (QRS duration 173 +/- 22 ms) received a CRT device. The number of apneas and hypopneas per hour (apnea-hypopnea index [AHI]) and minimal oxygen saturation (SaO2min) were quantified by cardiorespiratory polygraphy. Fourteen patients showed CSA (AHI >5/h), and 10 patients had an AHI <5/h without CSA. Subjective sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI). Data were evaluated before and after 17 +/- 7 weeks of CRT. RESULTS: In patients with CSA, CRT led to a significant decrease in AHI (19.2 +/- 10.3 to 4.6 +/- 4.4, p < 0.001) and PSQI (10.4 +/- 1.6 to 3.9 +/- 2.4, p < 0.001) without Cheyne-Stokes respiration and to a significant increase in SaO2min (84 +/- 5% to 89 +/- 2%, p < 0.001). There was no significant change in AHI (1.7 +/- 0.7 to 1.5 +/- 1.6), PSQI (2.4 +/- 0.5 to 2.6 +/- 0.9), and SaO2min (90 +/- 2% to 91 +/- 1%) in patients without CSA. CONCLUSIONS: Cardiac resynchronization therapy leads to a reduction of CSA and to increased sleep quality in patients with HF and sleep-related breathing disorders. This may have prognostic implications in patients receiving CRT.     

Breathing during sleep in patients with interstitial lung disease

Patients with interstitial lung disease (ILD) have a rapid shallow breathing pattern while awake that is thought to be due to activation of lung reflexes. We wondered whether sleep would result in changes in respiratory control and thus cause hypoxemia and poor sleep quality. Eleven patients with ILD (5 men and 6 women) and 11 age- and sex-matched control subjects were studied during sleep. Sleep quality was worse in patients with ILD, with more time in Stage 1 (33.7% of total sleep time (TST) versus 13.5%) and less time in REM sleep (11.8 versus 19.9% TST) than found in control subjects, and more fragmentation of sleep (13.7 +/- 3.1 arousals/h and 24.3 +/- 6.0 sleep stage changes/h versus 6.9 +/- 1.0 and 12.7 +/- 1.4, respectively). Patients with ILD with awake SaO2 less than 90% had greater abnormalities in sleep structure than did those with SaO2 greater than 90%. The incidence of apneas and hypopnea periods in patients with ILD was low (apnea plus hypoventilation index of 1.3 +/- 0.45 versus 2.9 +/- 0.82 in control subjects, p = NS). Oxygen saturation dropped during REM sleep in patients, especially in those with more severe awake hypoxemia. Expiratory time (Te), inspiratory time (Ti), and their sum (Ttot) were shorter in the patients, whereas Ti/Ttot was the same as in control subjects. No systematic changes during sleep were seen in these variables. The variability of inspiratory volume index, Ti, Te, and Ti/Ttot was similar to that in control subjects, and was lowest during NREM sleep. The incidence of snoring was comparable in patients and control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of nocturnal oxygen therapy on outcome measures in patients with chronic heart failure and cheyne-stokes respiration.

BACKGROUND: The effects of nasal oxygen (O(2)) supply at night using conventional home oxygen therapy (HOT) equipment on quality of life (QOL) and sleep-disordered breathing (SDB) were evaluated in patients with congestive heart failure (CHF). Nasal nocturnal O(2) therapy not only stabilizes SDB but also reduces sympathetic activity, and improves exercise capacity in patients with CHF. However, the effects of oxygen on the cardiac function and QOL of heart failure patients have not been fully elucidated. METHODS AND RESULTS: Fifty-six patients with CHF (New York Heart Association class II - III, left ventricular ejection fraction (LVEF) 相似文献   

Noninvasive pressure preset ventilation for the treatment of Cheyne-Stokes respiration during sleep.

Cheyne-Stokes respiration (CSR) during sleep is common in patients with congestive heart failure (CHF). This pattern of breathing fragments sleep, leading to daytime symptoms of sleepiness and fatigue. It was hypothesized that by controlling CSR with noninvasive pressure preset ventilation (NPPV), there would be a decrease in sleep fragmentation and an improvement in sleep quality. Nine patients (eight males, one female; mean +/- SD 65 +/- 11 yrs) with symptomatic CSR diagnosed on overnight polysomnography (apnoea/hypopnoea index (AHI) 49 +/- 10 x h(-1), minimum arterial oxygen saturation (Sa,O2, 77 +/- 7%) and CHF (left ventricular ejection fraction 25 +/- 8%) were studied. After a period of acclimatization to NPPV (variable positive airway pressure (VPAP) II ST, Sydney, NSW, Australia and bilevel positive airway pressure (BiPAP), Murraysville, PA, USA), sleep studies were repeated on therapy. NPPV almost completely abolished CSR in all patients with a reduction in AHI from 49 +/- 10 to 6 +/- 5 x h(-1) (p<0.001). Residual respiratory events were primarily due to upper airway obstruction at sleep on-set. Arousal index was markedly decreased from 42 +/- 6 to 17 +/- 7 x h(-1) (p <0.001). Sleep architecture showed a trend toward improvement with a reduction in stage 1 and 2 (79 +/- 7% during the diagnostic night versus 72 +/- 10% during NPPV, (p=0.057)), whilst sleep efficiency, slow-wave sleep (SWS), and rapid eye movement (REM) were not altered. Controlling Cheyne-Stokes respiration with noninvasive pressure preset ventilation resulted in reduced arousal and improved sleep quality in the patients with congestive heart failure. Noninvasive pressure preset ventilation should be considered a potential therapy for Cheyne-Stokes respiration in congestive heart failure in those patients who do not respond or fail to tolerate nasal continuous positive airway pressure therapy.     

Improvement in Cheyne-Stokes respiration following cardiac resynchronisation therapy.

The effect of standard cardiac resynchronisation therapy (CRT) on the severity of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure was studied. It was hypothesised that CRT, through its known beneficial effects on cardiac function, would stabilise the control of breathing and reduce CSR. Twenty-eight patients who were eligible for CRT and receiving optimised medical treatment for congestive heart failure were referred for overnight polysomnography, including monitoring of thoracic and abdominal movements to identify CSR and obstructive sleep apnoea events. Patients underwent repeat polysomnography after 6 months of CRT to re-evaluate sleep quality and sleep-disordered breathing. Twelve of the 28 patients had significant CSR (43%); 10 patients had a successful implantation and underwent repeat polysomnography a mean+/-SD 27+/-7 weeks after continuous biventricular pacing. Six of the 10 patients experienced a significant decrease in CSR severity following CRT, associated with correction of congestive heart failure-related hyperventilation and hypocapnia. Circulation time, oxygen saturation, frequency of obstructive apnoeas and sleep quality did not change. In conclusion, cardiac resynchronisation therapy is associated with a reduction in Cheyne-Stokes respiration, which may contribute to improved clinical outcome in patients treated with cardiac resynchronisation therapy.     

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     

Nocturnal efficiency and tolerance of a demand oxygen delivery system in COPD patients with nocturnal hypoxemia.

OBJECTIVES: We compared the efficacy of the standard nasal cannula and the demand oxygen delivery system (DODS) during sleep in patients with COPD. SUBJECTS: Twenty patients with moderate or severe COPD were included in the study. METHODS: Four consecutive polysomnographic recordings were performed under the following conditions: DODS powered by compressed air (night 1 [N1]); oxygen delivered with a nasal cannula alone (night 2 [N2]); oxygen delivered through a DODS (night 3 [N3]); and oxygen delivered with nasal cannula alone (night 4 [N4]). Oxygen flow rates with and without DODS were adjusted the day before the first night so that the resulting transcutaneous arterial oxygen saturation (SaO2) was > or = 95%. The following parameters were evaluated each night: apnea-hypopnea index, nocturnal SaO2, total oxygen saving, and several neurophysiologic parameters. RESULTS: The oxygen saving with the DODS was, on average, 60%. All parameters obtained during N2 and N4 (oxygen alone) were identical. The percentage of total recording time spent at SaO2 > or = 95% was comparable between N2 ([mean +/- SD]; 69+/-32%) and N3 (61+/-31%) (difference is not significant [NS]), as was the time spent at SaO2 between 90% and 95% (N2, 29.8+/-31%; N3, 35.9+/-27%; NS) and < 90% (N2, 0.75+/-2.6%; N3, 2.5+/-8.6%; NS). Although the mean response time was not significantly different between N2 and N3, two patients experienced a substantial increase in response time with an SaO2 < 90% on the DODS. The DODS device did not induce any difference in the percentage of time spent in rapid eye movement (REM) sleep (N2, 12.3+/-8.7%; N3, 16.4+/-7.8%; NS) or non-REM sleep (N2, 87.7+/-8.7%; N3, 83.7+/-7.9%; NS). Non-REM distribution in stage 1-2 sleep and in stage 3-4 sleep was comparable between N2 and N3. Similarly, no difference was observed for the sleep efficiency index (N2, 71+/-15%; N3, 69.6+/-14%; NS). Differences between sleep onset latency times were NS. CONCLUSIONS: In a majority of moderate to severe COPD patients, the use of a DODS device does not induce any significant alteration of nocturnal neurophysiologic and ventilatory profiles. However, the presence of nocturnal desaturation in a few patients justifies the need to systematically perform a ventilatory polygraphic recording when prescribing a DODS device.     

Polysomnographic characteristics in patients with Prader-Willi syndrome

To evaluate the occurrence of sleep-disordered breathing and to clarify the characteristics of sleep among patients with Prader-Willi syndrome (PWS). Overnight continuous EEG-polysomnographic studies were performed in 30 patients with PWS (16 males and 14 females; mean age, 7.4 +/- 4.1 years; age range, 1-19 years) unselected for sleep disturbance. The baseline arterial oxygen saturation (SpO2) was 96.6 +/- 0.6%, with a nadir of 77.2 +/- 10.2%. The rapid eye movement (REM) latency was 67.4 +/- 30.0 min. The percent of total sleep time spent in sleep stages 1, 2, slow wave, and REM were 13.1 +/- 8.2%, 41.9 +/- 10.5%, 21.5 +/- 9.4%, and 21.1 +/- 5.7%, respectively. The respiratory disturbance index (RDI) was 5.8 +/- 3.7/hr and desaturation index (DI) was 8.1 +/- 7.3/hr, respectively. Age-adjusted BMI was associated with more severe hypoxemia during sleep (baseline SpO2, r = -0.53, P < 0.01; nadir SaO2, r = -0.65, P < 0.01; RDI, r = 0.37, P < 0.05; DI, r = 0.53, P < 0.01) and more sleep disruption (arousal index, r = 0.46, P < 0.01). There were no significant associations between gender or genotype pattern (deletion vs. uniparental disomy) and the results of polysomnography. Sleep hypoxemia and sleep disruption are more prevalent in patients with PWS than in normal children. Obesity in these patients is associated with more severe sleep-disordered breathing.