Chen, Hsing-Mei MSN, RN; Clark, Angela P. PhD, RN, CNS, FAAN, FAHA
Heart failure (HF) is a gradually disabling and lethal syndrome resulting in a high rate of hospitalizations, morbidity, and mortality.1-4 Approximately 5 million people in the United States are now living with chronic HF, and the epidemic of HF affects other countries as well.5 Heart failure is the final outcome of several cardiovascular diseases, such as ischemic heart disease and hypertension.6 According to American Heart Association,5 people with HF are 6 to 9 times more likely to experience sudden cardiac death than the healthy population. Approximately 20% of patients die within 1 year after being diagnosed with HF.5 Costs of HF care in the United States for 2007 are estimated to be $33.2 billion.5
Heart failure not only impairs patients' physical functioning by causing symptoms related to breathing, sleep, cognition, and activity tolerance but it also increases psychological distress, such as anxiety, feelings of powerlessness, and depression.7-11 Those symptoms and types of psychological distress are viewed as major stressors that affect the health-related quality of life (HRQOL) of patients living with HF.9,11
Sleep disturbance has been reported as the most burdensome symptom for people with HF.10,12,13 Approximately 10% to 70% of patients with HF experience some type of sleep disturbance.14-21 The causes of sleep disturbance include HF symptoms such as orthopnea, paroxysmal nocturnal dyspnea, Cheyne-Stokes respirations, cough, palpitations, fatigue, and nocturia.22-25 In addition, sleep disturbances can disrupt cardiovascular, respiratory, and autonomic regulation, resulting in a high rate of HF morbidity and mortality.26-29 Research has shown that sleep disturbances reduce the HRQOL of HF patients and their overall functional performance, including daily activities, work productivity, social participation, cognitive and mathematic functioning, as well as psychological well-being.15,16,19,30
Although a number of studies have investigated sleep disturbances in patients with HF, the findings documenting prevalence and adverse effects of sleep disturbances are inconsistent across studies.31,32 The purpose of this article is to review the literature regarding sleep disturbances in patients with HF and to highlight findings that are contradictory. Identifying problematic findings may help clinicians and scholars better focus on the prevention of adverse effects of sleep disturbances and the design of interventions for relief.
To identify literature regarding sleep disturbance in HF published from 1966 and 2006, Internet searches were performed using the EBSCO Research Databases, including Academic Search Premier, CINAHL, MEDLINE, Psychology and Behavioral Sciences Collection, and PsycINFO. Keywords included sleep disturbance, sleep disorder, and HF. The following limits were set to the searches: adult, human, and English. Articles were excluded if they primarily focused on trials of the effect of specific drugs on sleep disturbance. Fifty-two articles on sleep in HF were obtained. As each study was reviewed, an additional search of the study's references was performed to identify other sources missed during the EBSCO search. Finally, 47 articles were synthesized for this article.
Sleep Physiology and Pathophysiology
Sufficient sleep is important to the restoration of a damaged myocardium.27 Normally, during non-rapid-eye-movement (NREM) sleep, the reduced metabolic rate increases parasympathetic nervous system tone, decreases sympathetic nervous system activity, and activates baroreflex sensitivity, resulting in decreases in heart rate, blood pressure, stroke volume, cardiac output, and systematic vascular resistance.20,27,33 The greatest relaxation of the cardiac workload occurs during rapid-eye-movement (REM) sleep.20 This cardiovascular autonomic regulation, however, can be interrupted by sleep disturbances (see Figures 1 and 2).27 For example, arousal from sleep may activate sympathetic activity, resulting in catecholamine hypersecretion, vasoconstriction, and increased blood pressure.25,27 As a result, chemosensitivity is destabilized, which further triggers hyperventilation and leads to lower levels of arterial carbon dioxide tension (PaCO2).
When the reduction in PaCO2 reaches the "apnea threshold," sleep apnea is precipitated.24,34 The consequent apnea leads to an increase in PaCO2 and a decrease in arterial oxygen tension (PaO2) with consequent hyperpnea, which lowers PaCO2 and continues the breathing cycle.34 Arousal from sleep has been viewed as an important factor in sustaining the cyclic periodic breathing.24 However, individuals may suffer from hypersomnolence and fatigue because of sleep disruption.24,27 Left ventricular failure with the characteristics of high filling pressure, low cardiac output, and inadequate myocardial perfusion can be worsened by the sympathetic activity and catecholamine release, and by fluctuations of PaO2 and PaCO2.27 Consequently, pulmonary edema can be precipitated, which further triggers the stimulation of pulmonary juxtapulmonary capillary receptors (J-receptors), initiating rapid and shallow breathing, hypotension, and bradycardia.35 Although researchers argue that more studies are needed to support the pathophysiological mechanisms of sleep disturbances and HF, it is evident that sleep disturbances, periodic breathing, apnea-related surges in blood pressure and heart rate, and cardiac ischemia create a vicious cycle that can hinder the restoration of the damaged myocardium and further increase the threat to patients' lives.27,31,33,36
Types of Sleep-Related Breathing Disorders in Heart Failure
Sleep-related breathing disorder is the umbrella term for a variety of sleep disturbances. Patients with HF may suffer from either obstructive sleep apnea syndrome (OSA), central sleep apnea (CSA), or a mixed type of sleep apnea with components of both OSA and CSA (see Figure 3).31,36 In the literature, CSA is commonly described as Cheyne-Stokes respirations with central sleep apnea (CSR-CSA).31,36 When OSA occurs, the upper airway is repeatedly obstructed or partially obstructed during sleep.20,37 In contrast, CSR-CSA involves periodic crescendo-decrescendo breathing separated by periods of apnea lasting at least 10 seconds. It occurs as a result of an absence or a reduction of ventilatory effort during NREM sleep.20,33 CSR-CSA is more likely to occur in HF patients with left ventricular ejection fraction (LVEF) less than 45%.17
Researchers are increasingly interested in finding whether sleep-related breathing disorder contributes to the development of HF or whether HF causes sleep disturbances.27,37 Generally, OSA is identified as a risk factor for HF, whereas CSR-CSA is recognized as a consequence of HF.31,34 Recently, however, there has been increasing interest in the role that HF might play in causing the development of OSA. Two possible mechanisms for the development of OSA are: (1) HF-related periodic breathing could lead to a decrease in muscle tone of the upper respiratory tract and contribute to its collapse; and (2) edema in the soft tissues of the neck and pharynx caused by fluid retention and HF-dependent edema could constrict the upper airway and exacerbate the collapse.27,38
The relationship between sleep-related breathing disorder, oxygen status, and sympathetic activation has been examined. A sample of 301 HF patients with an LVEF less than 40% was used to test the association between daytime systolic blood pressure and the presence of OSA in a cross-sectional study.14 Those with an apnea-hypopnea index (AHI) greater than 10 events per hour during sleep were recognized as sleep-related breathing disorder. The findings showed that 105 (35%) patients with HF had OSA and 121 (40%) had CSA. People with OSA had significantly higher daytime systolic blood pressure and body mass index and a history of snoring, but they had significantly lower SaO2 during sleep than those patients with CSA and no sleep-related breathing disorder. Additionally, subjects with OSA had significantly higher diastolic blood pressure than those with no sleep-related breathing disorder. In contrast, patients with CSA had significantly lower LVEF and PaCO2 but higher AHI than did patients with OSA. After controlling for age, gender, LVEF, SaO2, and body mass index, the study showed that people with OSA were 2.89 times more likely to experience systolic blood pressure greater than 140 mmHg than those without OSA. A single blood pressure measurement, however, might be insufficient for representing the participants' general blood pressure status. Longitudinal studies are needed to ascertain the causal relationship of OSA and high diastolic blood pressure.
Assessment and Diagnosis of Sleep Disturbances
Distinguishing the symptoms of HF, such as lethargy, fatigue, cardiopulmonary intolerance, and paroxysmal nocturnal dyspnea, from the symptoms of sleep disturbances is not easy, especially if the symptoms are caused by sleep-related breathing disorder.24 Nocturnal polysomnography, the gold standard confirmatory laboratory technique in the diagnosis of sleep disturbances, has provided researchers considerable data on sleep disturbances, especially sleep-related breathing disorder.22,24,39 Studies most commonly use the AHI to define sleep-related breathing disorder. The AHI is calculated by adding the number of apnea and hypopnea events during sleep. Apnea is defined as an absence of tidal volume excursion for at least 10 seconds. Hypopnea refers to a greater than 50% reduction in tidal volume for at least 10 seconds with either a decrease of more than 3% to 4% in oxyhemoglobin saturation (SaO2) or associated with an arousal from sleep.14,22,24,33,36,40-42 An AHI of less than 5 obstructive breathing events per hour is defined as normal, 5 to 15 as mild, 15 to 30 as moderate, and more than 30 as severe.37 Sleep-related breathing disorder can be validly and accurately assessed and diagnosed only when the patient is clinically stable.43
Two other common parameters for diagnosing sleep-related breathing disorder are the respiratory disturbance index (RDI) and the arousal index. The RDI is the total number of apneas, all flow hypopneas, and all flow-limitation events regardless of whether oxygen desaturation and arousal occur.42 The RDI is calculated as the number of apneas plus hypopneas divided by the number of hours of sleep.44 An RDI greater than 10 events is considered to be sleep-related breathing disorder.34 Additionally, researchers have proposed that some arousals may occur in non-flow-limitation events; therefore, the arousal index may be a better marker for explaining daytime sleepiness in patients without sleep-related breathing disorder.22,41 The arousal index is calculated by dividing the total number of arousals by the number of hours of sleep.44 The high cost and the necessary laboratory setting for polysomnography, however, may render the test unavailable to many patients and locations.33
In-home sleep studies offer portability and lower costs than overnight sleep studies. A recent review of 18 studies compared characteristics of in-home versus polysomnography testing.45 The costs of home studies ranged from 35% to 88% lower than laboratory studies across a number of countries. However, RDI values on portable sleep studies were 10% lower compared with those obtained in laboratory studies. The mean oxygen saturation values were no different in the 2 settings. They concluded that home sleep studies provide similar diagnostic information and offer a less expensive screening mechanism but may underestimate sleep apnea severity.
Other alternative low-cost approaches to screen for sleep-related breathing disorder, including sleep logs, physical examinations, and sleep questionnaires, are recommended for assessing patients' sleep situations.20 Self-report questionnaires, such as the Epworth Sleepiness Scale46 and the Pittsburgh Sleep Quality Index,47 not only reflect a patient's perspective about sleep and its importance, but also provide information about people who are at high risk for developing or who are experiencing sleep disturbances not due to a sleep-related breathing disorder.48
The Nature of Sleep Complaints in Heart Failure
The nature and prevalence of sleep complaints among people with HF has been investigated. In the EuroHeart survey of 187 patients with HF,49 over 60% of the participants experienced sleep disturbances, including an inability to get to sleep (63%), waking up and having difficulty getting back to sleep (69%), and lacking sufficient refreshing sleep (60%). Similar findings were reported in another study of 84 HF patients with a mean LVEF of 22%.16 When sleep complaints were measured using the16-item Modified Sleep Disorder Questionnaire, approximately 56% of participants reported trouble sleeping.16 The most common symptoms were inability to sleep flat (51%), restless sleep (44%), trouble falling asleep (40%), and awakening early (39%).
In addition to insomnia, people with HF also experience hypersomnolence. In a study of 223 HF participants,15 approximately one-third of the HF participants felt they did not get enough sleep, and another third reported they slept too much. Difficulties in maintaining and initiating sleep were the most commonly reported sleep complaints. The highest frequency of nocturnal awakening was 10, and 25% of participants were awake 1 to 3 hours per night. Approximately 90% of the men and 80% of the women experienced nocturia. About 50% felt sleepy and fatigued during daytime and habitually took a daytime nap.
Redeker and Stein50 examined both subjective and objective characteristics of sleep disturbances in a 2-group comparative study of 59 HF patients and 59 non-HF adults, describing differences in sleep characteristics and excessive daytime sleepiness between the groups. A panel of sleep instruments included a wrist actigraph, sleep diary, the Pittsburgh Sleep Quality Index, and the Epworth Sleepiness Scale. Patients with HF reported more sleep disturbances and poorer objective sleep continuity (sleep undisturbed by frequent awakenings). They were 3 times more likely to report waking too early compared to the control group, yet only 20% ever used sleep medications. Over 44% of the HF group reported excessive daytime sleepiness compared with 19% of the comparison group. These data suggest that patients with HF have insomnia, difficulty maintaining sleep, and significant daytime consequences, which may impact HRQOL and daily functioning.
Brostrom et al23 conducted a qualitative study in which 20 HF patients were interviewed to explore sleep disturbances. They showed that the participants' sleep was influenced by their daily activities, such as gardening; aspects of the HF itself, such as deterioration and side effects of medications; and cardiac symptoms, such as dyspnea, dysrhythmia, and cough. Sleep disturbances caused several adverse effects, including fatigue, listlessness, and loss of temper, and resulted in a perceived need for daytime sleep, seclusion, counseling, and information.23
Health-Related Quality of Life and Sleep-Related Breathing Disorder in Heart Failure
Several studies have shown that HRQOL is lower in people with HF when sleep-related breathing disorder is present. In a study of 14 outpatients with severe HF (mean LVEF <30%) who were waiting for heart transplantation, 3 (21%) were diagnosed with CSA, using the criterion of an AHI greater than 10 per hour.21 Patients with CSA reported poorer HRQOL and intolerance to exercise than those without CSA. Further, age, LVEF, functional class (NYHA class), pulmonary function tests, snoring and hypersomnolence, and witnessed apneas were not significantly different between the 2 groups. Because the sample size was small, confirmation of results is needed.
The effect of sleep-related breathing disorder on HRQOL was investigated in HF patients with an LVEF less than 35% and with an NYHA II or III classification.19 All 51 patients with HF reported exercise intolerance and exertional dyspnea, but only patients with HF and sleep-related breathing disorder had reduced peak oxygen uptake. An AHI of 5 events per hour was used to identify sleep-related breathing disorder. Twenty-six (52%) participants were diagnosed with sleep-related breathing disorder: 12 for CSR-CSA, 5 for OSA, and 9 for mixed sleep apnea. Depressive symptoms, HRQOL, and sleep quality were compared with 10 age-matched healthy adults and 11 patients with OSA. Sleep quality was measured using the 19-item Pittsburgh Sleep Quality Index, which showed that 37% of the patients with HF and sleep-related breathing disorder were poor sleepers. Patients with HF and sleep-related breathing disorder had poorer sleep quality, greater depressive symptoms, and lower total HRQOL compared to healthy adults and HF patients without sleep-related breathing disorder. Three dimensions of HRQOL-physical health, bodily pain, and emotional functioning-showed the greatest impact from HF and sleep-related breathing disorder. Sleep quality, depressive symptoms, and HRQOL were not significantly different among HF patients with different types of sleep-related breathing disorder. Interestingly, the latter 3 variables in patients with HF and sleep-related breathing disorder were similar to those with OSA without HF. The findings suggested that sleep-related breathing disorder adversely affected HRQOL, disturbed sleep itself, and resulted in depressive symptoms in patients with HF.
Sleep-related breathing disorder may occur in patients with mild to moderate HF. Excessive daytime sleepiness, HRQOL, and neurohumoral markers were assessed in 84 HF outpatients who had an overnight recording of respiratory impedance, SaO2, and heart rate using a home-based, wireless monitor.51 Sleep-related breathing disorder was defined as an AHI greater than 15 events per hour. Results showed that the prevalence of sleep-related breathing disorder was 24% in all participants, 15% in participants (n = 53) with LVEF greater than 35%, and 38.7% in those (n = 31) with LVEF less than 35%. The participants with sleep-related breathing disorder had a significantly higher level of B-type natriuretic peptide and urinary noradrenaline levels than those without sleep-related breathing disorder. The more severe the HF, the higher the B-type natriuretic peptide. The authors suggested that the increased sympathetic nervous activation in HF was related to HF rather than the sleep-related breathing disorder. Likewise, in comparison with a normal reference group without HF,52 all domains of HRQOL showed significant impairments for all HF participants except for mental health. There were no significant differences in HRQOL and excessive daytime sleepiness between HF patients with and without sleep-related breathing disorder.
Treatments of sleep-related breathing disorder, including supplementary oxygen, medications, and continuous positive airway pressure (CPAP), have been widely used in clinical practice.6,53 In a randomized trial, Mansfield et al18 examined the effects of CPAP on HRQOL, systolic heart function, sympathetic activity, and blood pressure in patients with HF and OSA. One hundred fifty-six patients with LVEF less than 45% and NYHA of class II to IV were invited to undergo polysomnography. An AHI greater than 5 obstructive events per hour was used to diagnose OSA. Sixty-nine (44%) patients met the criteria for OSA. Compared with a control group of 21 patients, 19 patients in the 3-month overnight nasal CPAP treatment group had significant improvements in LVEF, overnight urinary norepinephrine, AHI, pulse oxygen saturation (SpO2), daytime sleepiness, and HRQOL; however, mean blood pressure, peak oxygen uptake, NYHA class, and body mass index did not significantly change after the CPAP treatment.
Limited studies have examined the relationship between HRQOL and sleep disorders from HF patients' perspective. Brostrom et al15 found that people with HF suffering difficulties in maintaining and initiating sleep, early morning awakenings, and excessive daytime sleepiness reported significantly lower HRQOL compared with patients without sleep difficulties.15 The 3 dimensions of HRQOL most influenced by sleep disturbances were general health, vitality, and social functioning.
Redeker and Hilkert54 examined the extent to which sleep quality, duration, and continuity were relative to mental health and functional performance among 61 patients (39 men and 22 women) with stable systolic HF (LVEF less than 35%). Each participant wore a wrist actigraph to record nocturnal sleep duration, continuity, and daily activities for 3 days while living at home. They found no statistically significant relationships between these sleep variables and age, gender, and comorbidity. However, participants with a higher NYHA class reported poorer sleep quality. Approximately 34% of the patients used sleeping medication at least occasionally. There were small to moderate negative correlations between sleep quality and physical functioning, 6-minute walk distance, and mental functioning. Time in bed was negatively correlated with physical functioning and daytime activity. Longer sleep latency was related to poor physical functioning. After controlling for age, gender, comorbidity, and NYHA class, self-reported sleep quality and actigraph-recorded wake time and wake bout time accounted for 9% to 20% of the variance in the functional performance variables (daytime activity level, 6-minute walk test, SF-36 physical functioning) and mental health. There were no statistically significant relationships between sleep duration and functional performance. The study findings suggested that sleep quality and continuity are more important than quantity of sleep. Perceived sleep quality may be most relevant to mental health, whereas objective data for sleep continuity may be most relevant to functional performance.
Overall, sleep disturbances in people with HF are common, with dyspnea as the most frequent cause of sleep interruption. From the studies examined, up to 70% of the patients with HF had at least 1 sleep complaint.15,16,49 The incidence of sleep disordered breathing (either OSA, CSA, or mixed) ranged from approximately 10% to 60%.14,19,21,37,40,53,55 A diversity of reported sleep complaints was found across studies, although the use of different self-report questionnaires could have caused inconsistent findings. Qualitative research contributed valuable information above that addressed in questionnaires. The most frequently reported complaints of sleep disturbance in patients with HF were daytime sleepiness, inability to sleep flat, difficulties initiating and maintaining sleep, and early awakening.
Many studies overlooked the importance of sleep disturbances in HF when sleep-related breathing disorder was not present, although some studies showed that patients without sleep-related breathing disorder have better sleep quality, fewer depressive symptoms, and better HRQOL than those with HF and sleep-related breathing disorder.14 The evidence, however, is limited and insufficient. From the studies reviewed, less than 50% of the patients with HF were diagnosed with sleep-related breathing disorder,14,17-19,21,40 however, sleep complaints were reported by nearly 70% of the patients with HF.
Differences between the prevalence of sleep-related breathing disorder and the incidence of sleep complaints could be due to: (1) the cutoff point of AHI for diagnosing sleep-related breathing disorder ranged from 5 to 20 events per hour; (2) some researchers used a cutoff point of 5 for RDI, rather the standard criterion of 10; (3) sample sizes varied from 14 to 201 patients in the various studies; (4) criteria for LVEF ranged from less than 35% to less than 55%; and (5) the functional class levels differed in the studies, with some reporting NYHA class I to IV, others including II to III or II to IV. These differences may partially explain the inconsistency of study findings for age, peak oxygen uptake, and dimensions of HRQOL.
Importantly, sleep disturbances could interact to create a cycle that increases perceived severity. For example, patients suffering from low cardiopulmonary tolerance and fatigue might need extra daytime sleep and longer sleep at night to restore energy. Excessive daytime sleep, however, interrupts circadian rhythm and shortens nighttime sleeping, resulting in sleep fragmentation and reduced sleep time and vice versa.29,49
In the Redeker and Hilkert54 study, the finding that sleep duration was not associated with functional performance differs from the view of other researchers that poor sleep duration is a risk factor that affects health and daily functioning.56,57 Sleep duration improves neurocognitive performance and eliminates fatigue during the daytime and sleep debt.56 More research is needed to clarify this area.
Patients with HF and sleep-related breathing disorder who have an AHI of more than 20 events per hour usually experience more sleepiness and fatigue than those with an AHI of less than 20.53 A significant difference, however, was not found by Jahaveri et al.17 Similarly, one study found that an AHI (mean 43.9) was not significantly associated with sleep measures in patients with OSA alone.41 Some researchers have suggested that the total RDI may be a more appropriate marker than AHI in identifying sleep disturbances in patients with sleep-related breathing disorder.22,42
Central sleep apnea was used interchangeably with CSR-CSA in several research studies.14,15,21 That practice raises the issue of whether CSR-CSA should be distinguished from CSA.24,37 Central sleep apnea has a hypercapnic and a hypocapnic form (seeFigure 3), whereas CSR-CSA is a hypocapnic form of CSA but with the additional feature of fluctuation of tidal volume with hyperpneas, hypopneas, and apneas.24,33 The American Academy of Sleep Medicine37 suggested that CSA should be differentiated from CSR-CSA in that there is no periodic crescendo-decrescendo breathing in CSA. Moreover, CSA can occur in healthy adults, whereas CSR-CSA is common in patients with HF. Cheyne-Stokes respirations with central sleep apnea may also be observed during wakefulness in patients with more severe HF.37
Obstructive sleep apnea and CSR-CSA may coexist in patients with HF.37,58 For example, in the Ryan and Bradley55 study, patients with OSA had a pattern of waxing and waning breathing. Furthermore, OSA and CSR-CSA share several features (see Figures 1 and 2), and result in similar adverse effects on HF, although they have different pathophysiologic origins. Both have an adverse effect on a failing myocardium by increasing the left ventricular filling pressure, activating the sympathetic nervous system, increasing cardiac oxygen demand and decreasing myocardial oxygen supply, and by increasing arousals from sleep.27,36 Two common features of sleep-related breathing disorder-intermitted hypoxia and frequent arousals from sleep-further induce excessive daytime sleepiness, insomnia, difficulty initiating and maintaining sleep, light sleep, and early awakening, resulting in fatigue and a worsening of the cardiopulmonary function.31,36 Therefore, a vicious pathophysiological cycle can be created whereby sleep-related breathing disorder causes more severe HF and worsened sleep-related breathing disorder.
Several dissimilarities between OSA and CSR-CSA in HF can be identified: (1) CSR-CSA is more prevalent than OSA14,25,31; (2) OSA has more daytime sleepiness and loud snoring than CSR-CSA22,36,37; (3) witnessed apneas are common in OSA35; (4) hypoxia is less important during CSR-CSA than during OSA14,27; (5) exaggerated negative intrathoracic pressure is a feature of OSA, but not CSR-CSA6,27; (6) CSR-CSA is associated with augmented arrhythmic risk and elevated cardiac mortality17,20,27,31,34; and (7) CSR-CSA is more common in men, but is seldom observed in women.14,27 In contrast, gender might relate to different risk factors for patients with OSA and HF.22 In men with HF, OSA is associated with increasing body mass index, and in women with HF, OSA is associated with increasing age.20
Daytime sleepiness is an important area for HF research. Daytime sleepiness is not only an significant symptom of sleep-related breathing disorder but also an indicator of several severe cardiovascular diseases.27,28,37 In a 4-year cohort study with 5,888 adults, daytime sleepiness was the only sleep disturbance symptom associated with mortality, the incidence of cardiovascular disease morbidity and mortality, myocardial infarction, and HF.28 In the Brostrom et al15 study, approximately half of patients with HF (n = 187) felt sleepiness and fatigue during the daytime.
Daytime sleepiness does not simply affect the quality of life for HF patients, it also impairs sleep for their spouses.15,59 Daytime sleepiness, however, may be misinterpreted as a symptom of HF.31 Systematic assessments are important to identify the sleep problems of individual patients.
Recognition of sleep disorders in the HF population is important in order to guide early diagnostic evaluations for any sleep disorders, including OSA and CSR-CSA, as well as to treat the condition. Obtaining a sleep history in people with HF is an essential step to identify and manage sleep disorders.25,60 Screening for sleep disorders should be routinely performed in this population.36 Nurses can help screen sleep disorders in people with HF by asking specific questions regarding sleep conditions using a list of symptoms of sleep disorders designed by the healthcare team or a self-reported sleep questionnaire, such as the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale. Patients who report sleep difficulties should be referred for further evaluation by sleep experts who may perform confirmatory polysomnography or cardiopulmonary monitoring over time.60
Nurses also play an important role in providing effective interventions for people with HF. To maximize adherence to treatment, nurses educate patients and their families by informing them about the benefits of treatment, for example, improving sleep may improve hemodynamics, functional capacity, and mental health, and may help them to achieve a better HRQOL.54,60 Information regarding treatments including supplemental oxygen, nocturnal nasal CPAP, and adaptive servo-ventilation and sleep practices, such as sleep hygiene and life modifications, can help patients to understand the overall plan of their treatments.36,61 Identifying factors that contribute to patients' sleep difficulties should be done before an intervention is initiated.
Sleep disorders are highly prevalent in people with HF, and can result in negative effects on the progression of HF, creating a vicious cycle that causes both physical and psychological dangers. Sleep disorders are independently associated with worsened HRQOL almost to the same extent as HF. Most research reviewed in this article focused on the pathophysiology of sleep-related breathing disorder. Few studies of the HF patient's perspective about sleep disorders have been done. Inconsistent findings in several studies illustrate the need for continued research exploring the nature of sleep and its effects on health in people living with HF in order to design appropriate interventions.
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