Sleep disordered breathing in the elderly

Sleep-disordered breathing, especially obstructive sleep apnea (OSA), has a high prevalence among the elderly, where it may present with atypical symptoms. Untreated OSA can reduce quality of life and have adverse health consequences. Effective treatment is available, so all physicians treating the elderly should be aware of the clinical presentation, diagnostic methods, and treatment options for OSA.     

老年人慢性充血性心力衰竭稳定期的睡眠呼吸障碍

目的　了解稳定期、已得到良好治疗的老年慢性充血性心力衰竭患者睡眠呼吸障碍的发生情况及其对心力衰竭的影响。　方法　应用多导睡眠监护仪对 42例老年稳定期充血性心力衰竭患者进行监测。以呼吸紊乱指数 (AHI) 15作为界值 ,AHI >15者为睡眠呼吸障碍组 ,19例 ;AHI≤ 15者为对照组 ,2 3例。　结果　睡眠呼吸障碍组AHI为 18 3～ 84 1,平均 48 6± 16 3,其中阻塞性者AHI为 10 7± 9 2 ,而中枢性者AHI为 37 9± 10 5。与对照组比较 ,睡眠呼吸障碍组有着显著高的醒觉指数 (分别为 17 6± 12 1和 37 3± 2 2 4 )。同时 ,有着更低的睡眠中最低血氧饱和度〔分别为(81 2± 6 8) %和 (6 7 8± 8 2 ) %〕、更低的左心室射血分数〔(32 4± 10 3) %和 (2 4 5± 8 6 ) %〕。　结论　老年稳定期慢性充血性心力衰竭患者有着很高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 (陈 施呼吸 )。睡眠呼吸障碍的发生与严重的夜间氧合血红蛋白的脱饱和过多的醒觉有关。严重的未经治疗的睡眠呼吸障碍可能影响左心室功能 ,并能加剧老年充血性心力衰竭患者的死亡。     

Sleep disordered breathing in neurologic disorders

Wakefulness, NREM sleep, and REM sleep are accompanied by specific changes in breathing control, which arise from the interaction of automatic (metabolic, involuntary) and behavioural (voluntary and involuntary control systems. Considering the complexity in the neuroanatomy and neurophysiology of breathing control, it is not surprising that neurologic disorders are frequently accompanied by sleep disordered breathing. An introduction on pathophysiology, clinical features, diagnosis, and treatment of sleep disordered breathing in such diseases as stroke, epilepsy, dementia, spinal cord disease, polyneuropathies, and myopathies is presented.     

Sleep disordered breathing and hypertension.

Patients with sleep apnea may be at increased risk for cardiovascular disease. Recently, the link between hypertension and sleep apnea has been strengthened by findings of two large epidemiologic studies. Neurohumoral and hemodynamic responses to repetitive episodes of hypoxemia and apnea may offer a pathophysiologic basis for patients with sleep apnea having an increased risk for hypertension. Sympathetic, humoral, and cellular responses to sleep apnea over the long term may cause vascular dysfunction and consequent hypertension. These responses may be exacerbated by sleep deprivation, which occurs commonly in patients with sleep apnea because of poor sleep architecture. Patients with sleep apnea are often obese and may be predisposed to weight gain. Hence, obesity may further contribute to cardiovascular risk in this patient population. Alleviation of sleep disordered breathing may be accompanied by lower blood pressure in hypertensive patients with sleep apnea.     

Sleep disordered breathing and driving risk

Obstructive sleep apnea syndrome leads to an increased risk of motor vehicle accidents through multiple pathways. Sleep apnea and motor vehicle crashes are common, and motor vehicle collisions are the leading causes of death amongst accidents. Therefore, the clinician charged with the care of apneic patients must address the issue of safe driving. Some recent evidence reveals that driving simulator technology may discriminate apneic drivers from control drivers as well as those apneics at a lesser risk for automobile crashes. This same tool demonstrates an improvement in driving capabilities to baseline when patients with sleep apnea are treated with nasal continuous positive airway pressure and that this improvement may occur rapidly. The prevention of driving accidents in patients with sleep apnea appears cost effective. Educating the patient with sleep apnea about sleepy driving and objective documentation of treatment efficacy are important in reducing the likelihood of accidents.     

Sleep disordered breathing: management update

The term sleep disordered breathing encompasses a spectrum of abnormalities, including snoring, obstructive sleep apnoea (OSA), central sleep apnoea (CSA), respiratory‐related arousals and hypoventilation. This review focuses on both OSA and CSA. It provides a clinical update of recent advances in the diagnosis, management and prognosis of these two conditions. An increasing array of treatment modalities, particularly for OSA, broadens the opportunity for personalised therapy tailored to the individual patient.     

Sleep disordered breathing in primary care medicine

Primary care medicine plays a key role in the delivery of health care. Sleep disorders medicine is a new specialty and standard medical school curricula do not contain any or only very little training in sleep medicine. Unrecognized and therefore untreated sleep disorders account for a large loss of human life and socio-economic damage. Recognition of sleep disorders, in particular sleep-disordered breathing at the primary care level is thus a major element in health care delivery. The objective of this study was to assess the occurrence of the risk of sleep-disordered breathing (SDB) in a large primary care population. 852 primary care patients received a validated questionnaire which contained items based on signs and symptoms of SDB, periodic limb movement disorder (PLMD), and insomnia. A polygraphically validated algorithm was used to identify patients with a high suspicion of having sleep disordered breathing. Based on this algorithm 20% of the study participants had a high risk for SDB, 18.5% of PLMD and 25% of insomnia. Most commonly daytime sleepiness and fatigue was associated in patients with a positive likelihood of SDB, PLMD, and insomnia. Fifty percent of all primary care patients reported to snore while 31% of snorers reported to snore every night. SDB was twice as common in men than in women and associated with a significantly higher body mass index. A popular validated scale to assess the degree of daytime sleepiness, the Epworth sleepiness scale, was not always useful to document the degree of daytime sleepiness. We conclude that SDB, PLMD, and insomnia are very frequent sleep disorders in primary care patients yielding the need to include assessment of these sleep disorders in the medical history of primary care physicians.     

Sleep disordered breathing in chronic obstructive pulmonary disease

We prospectively studied sleep disordered breathing in 50 consecutive patients (39 males) with chronic obstructive pulmonary disease (COPD) with chronic respiratory failure (CRF) (n=33) and without CRF (n=17) by performing polysomnography. Patients with CRF had a lower mean nocturnal oxygen saturation (SaO2 %) (88.6+/-6.7 vs. 96.3+/-0.8; p=0.0001) and a lower minimal nocturnal SaO2 (73.6+/-12.0 vs. 84.3+/-7.3; p=0.002) compared to those without CRF, suggesting that patients with CRF tend to have more severe drops in nocturnal SaO2. Patients with CRF also had a lower FEV1 (% predicted) (p=0.01) and PEFR (% predicted) (p=0.031) compared to those without CRF suggesting an indirect relation to the oxygen saturation. Other pulmonary functions were comparable between both the groups. Among patients with and without CRF, the total sleep time (minutes); the rapid eye movement (REM) stage (% of total sleep time); the non-rapid eye movement (NREM) stage (% of total sleep time) were comparable (p=NS). Only three of the 50 patients with COPD had a significant (>5) apnea-hypopnea index (AHI) (total no. of apneas + total no. of hypopneas/ total sleep time [(hours) = AHI] and these three patients had a mean BMI = 27.7 which was higher than the mean BMI of the whole group (21.1). The AHI was comparable in patients with and without respiratory failure. Multiple regression analysis revealed a positive correlation between AHI and the neck circumference (r=0.41; p=0.005) and BMI (r=0.31; p=NS). There was a small but statistically insignificant negative correlation between AHI and neck length (r= -0.28; p=NS). We conclude that, BMI per se contributes to the AHI and nocturnal desaturation in patients with COPD.     

Sleep disordered breathing in patients with chronic obstructive pulmonary disease

Sleep-related disordered breathing (SDB) and its influence on desaturation were examined in stable COPD patients with waking SpO2 > 90%. With respiratory inductance plethysmography, thoracic-abdominal respiratory movements for all events with more than 4% desaturation were analyzed in 26 patients. Types of SDB were confirmed by full polysomnography. Irregular breathing induced desaturation, while stable respiration continued during some desaturation events. Three types of altered ventilation were observed: hypoventilation, paradoxical movement and periodic breathing. An unusual type of paradoxical movement, with normal airflow despite progressive desaturation, was observed in REM sleep. Patients were divided into desaturation (15 patients) and non-desaturation (11 patients) groups. Daytime arterial blood gas, lung function values, and 6-min walking distance did not differ. Awake, mode, maximum and minimum nocturnal SpO2 were lower in the desaturation group. SDB-induced desaturation events in the desaturation group were more frequent (9.2+/-3.5 vs. 1.8+/-2.2 times), a greater SpO2 decrease (11.4+/-7.1% vs. 5.2+/-2.1%) and longer duration (73.2+/-34.8 vs. 18.8+/-39.0 min). Patterns of SDB in the desaturation group were hypoventilation (74.4+/-23.4%), paradoxical movement (10.2+/-14.5%), periodic breathing (12.1+/-18.3%) and unclassified (5.8+/-11.2%). These results reveal that lower SpO2 and SDB influence nocturnal desaturation in stable COPD patients.     

Sleep complaints and sleep disordered breathing in hemodialysis patients.

BACKGROUND: The objective of the study was to determine the prevalence of sleep complaints and of sleep disordered breathing (SDB) in hemodialysis patients not selected for sleep complaints and to determine the effect of hemodialysis on SDB. The feasibility of home recording of sleep related respiration in these patients was also studied. METHODS: The patients completed a questionnaire and parameters of SDB were examined in the home setting on nights following dialysis and nights following no dialysis with the Edentrace II Recording System. RESULTS: Six (46%) of 13 patients had sleep complaints. Symptoms suggestive for sleep apnea syndrome were found in four (31%) of these 13 patients. In three (75%) of these four patients SDB was found. Sleep related respiration was monitored in 15 patients. Registrations satisfactory for interpretation were obtained in all patients. SDB was observed in five (33%) of these 15 patients. There were no significant differences in parameters of SDB between nights following dialysis and nights following no dialysis. CONCLUSIONS: Home recording of sleep related respiration in hemodialysis patients is feasible. Sleep complaints and SDB are common in these patients. No clinically significant differences in SDB were found between nights following dialysis and nights following no dialysis.     

Sleep disordered breathing and its treatment in congestive heart failure

Sleep disordered breathing (SDB) is a common problem with adverse cardiorespiratory, endocrinological, and endothelial effects. Recent studies demonstrate an even higher prevalence of SDB in congestive heart failure (CHF) than in a randomly selected population, with up to 40% and 11% having Cheyne Stokes respiration-central sleep apnoea and obstructive sleep apnoea-hypopnoea syndromes, respectively. Randomised controlled trials of nocturnal respiratory support for SDB associated with CHF for up to three months demonstrate significant benefits in terms of improvements in left ventricular ejection fraction, markers of sympathetic system activity, and quality of life. Further randomised controlled trials of larger scale and longer duration are required to establish the role and benefit of this intervention for the treatment of this debilitating condition. The evidence for the higher prevalence of SDB in CHF, its pathogenesis, its pathophysiological consequences, and the emerging benefits of respiratory support are reviewed.     

Sleep disordered breathing and risk factors for cardiovascular disease

Patients with sleep disordered breathing (SDB) are at increased risk for cardiovascular disease including hypertension, angina, myocardial infarction, and stroke. Neurohumoral and hemodynamic responses to untreated sleep apnea are likely mechanisms that produce functional and structural changes within the cardiovascular system. Obesity, higher blood pressure, and advancing age, which are common characteristics of patients with SDB, contribute to the overall risk for cardiovascular disease. Recent studies indicate that OSA is associated with or aggravates other risk markers for cardiovascular disease. These factors include leptin, C-reactive protein, homocysteine, and insulin resistance syndrome. Elevations in C-reactive protein and glucose intolerance may be correlated with the severity of SDB. The impact of alleviating SDB on these cardiovascular risk factors has not been fully elucidated. Regardless, assessment of overall cardiovascular risk in patients with sleep apnea is warranted to identify those individuals that are high-risk who require immediate attention and intervention or in those that should be treated more aggressively.     

Sleep disordered breathing and cognitive function in a retirement village population.

Sleep disordered breathing (SDB) may be associated with cognitive dysfunction in non-demented elderly people. A random sample of 96 retirement village residents were given both neuropsychological assessment and overnight sleep monitoring with a portable microprocessor based system (Vitalog PMS-8). Respiratory disturbance index (RDI) was calculated as the number of apnoeas and hypopnoeas per hour of sleep. RDI was not associated with 'memory', 'verbal', and 'motor' factors identified from the analysis of cognitive tests, but was associated with the 'cerebral efficiency' factor (R2 = 0.21, p less than 0.0001). Seventy-three subjects had repeat neuropsychological tests, median time to follow-up being 17 months. Baseline RDI did not predict changes in scores on the two factors identified from the second analysis. We conclude that mild to moderate disturbance of breathing during sleep is not associated with cognitive dysfunction in non-demented subjects.