Sleep is essential to optimal health and performance.

Transcription

1 Journal of Cardiovascular Nursing Vol. 19, No. 6S, pp S67 S Lippincott Williams & Wilkins, Inc. The Heart of Sleep Sleep-Disordered Breathing and Heart Failure Robin J. Trupp, MSN, RN, APRN, BC, CCRN, CCRC Heart failure is associated with high rates of hospitalization and mortality as well as great economic burden in the United States. Recent data show that a high percentage of patients with depressed left ventricular ejection fractions suffer from sleep-disordered breathing, contributing to this incidence of morbidity and mortality. Since the signs and symptoms associated with sleep disorders do not differ significantly from chronic heart failure signs and symptoms, detection and recognition of sleep-disordered breathing is a clinical challenge. Thus clinicians frequently fail to recognize it as a possible contributor to the development of heart failure or as a consequence of the disease. This article discusses sleep, sleep-disordered breathing, its effects and consequences on the cardiovascular system, strategies for identifying at-risk individuals, and treatment options. KEY WORDS: central sleep apnea, Cheyne-Stokes respirations, heart failure, obstructive sleep apnea, sleep-disordered breathing Sleep is essential to optimal health and performance. Yet sleep deprivation is endemic in Western societies, with most individuals getting less than 7 hours of sleep per night. 1 The consequences of either acute or chronic sleep deprivation include altered alertness, impaired concentration, and delayed reaction times that can result in daytime somnolence, cognitive impairment, or motor vehicle accidents. While considered part of the normal aging process, daytime sleepiness can also indicate more serious health problems. Still sleep disorders frequently go unrecognized. Heart failure (HF) is a progressive, unrelenting syndrome, triggered initially by a fall in left ventricular performance that quickly results in activation of at least four neurohormonal vasoconstrictor systems. These vasoconstrictor systems exert a direct adverse effect on the myocardium, contributing to ventricular hypertrophy and dilation and thus to the progression of HF. Heart failure continues to increase in both incidence and prevalence, affecting more than 5 million Americans. 2 As a result, healthcare utilization is high, making HF a great economic Robin J. Trupp, MSN, RN, APRN, BC, CCRN, CCRC PhD student, The Ohio State University, Columbus, Ohio. Corresponding author Robin J. Trupp, MSN, RN, ACNP, BC, CCRN, CCRC, 8640 Craigston Court, Columbus, OH ( trupp.3@osu.edu). burden. Recent data have shown that 40% to 50% of HF patients suffer from some form of sleepdisordered breathing (SDB), far exceeding the 2% to 4% rate in the general population. 3 If untreated, SDB can result in worsened outcomes for these patients. 4 Diagnosing and subsequently treating SDB have shown dramatic improvements in HF patient outcomes. 5 8 Background The word sleep comes from the Latin word somnos. Sleep is regulated by a number of mechanisms, including circadian rhythm. Resulting from a body clock within the hypothalamus that is synchronized with environmental periods of light and dark, circadian rhythm regulates wakefulness and sleep. Melatonin, the hormone of darkness, is released in response to changes in light and inhibits histamine, dopamine, norepinephrine, and serotonin secretion, preventing arousal. Both cortisol and growth hormone levels vary according to the sleep cycle. Thus, refreshing sleep results from synchrony with the circadian rhythm and the environment. When misaligned, such as in jet lag or night-shift work, sleep gets disrupted and negatively affects the immune and neurohormonal systems. S67

2 S68 Journal of Cardiovascular Nursing November/December 2004 Sleep consists of 2 distinct stages: nonrapid eye movement (NREM) and rapid eye movement (REM). NREM makes up 80% to 85% of total sleep time and has 4 stages, beginning with stage 1 (light sleep) and progressing to the deeper sleep found in stages 3 and 4. It is during stages 3 and 4 that parasympathetic tone increases, resulting in reduced heart rate, stroke volume, and blood pressure and a concomitant reduction in cardiac output, systemic vasculature resistance, and myocardial oxygen workload. Respiratory control is driven primarily by metabolism during NREM sleep. The deepest level of relaxation occurs during REM, which follows NREM sleep. REM sleep is essential to waking up feeling rested and refreshed. During the transition from NREM to REM sleep, respiration becomes more dependent on behavioral factors and less on metabolism. 9 Rapid eye movement sleep is associated with variable, and frequently increased, blood pressure, heart rate, and respirations due to increased sympathetic and decreased parasympathetic nerve activities. During REM, the body is essentially paralyzed, but the brain remains very active. Atonia of the nondiaphragmatic respiratory muscles leads to reduced ventilatory effort and decreased hypoxemia. Vivid dreams occur during REM. Progression through NREM stages 1 to 4 occurs in cycles (4 6 per night), each lasting approximately 90 to 110 minutes, before entering REM sleep. Rapid eye movement sleep is followed by more stage 2 NREM before resuming the progression toward deeper sleep. Arousals during the middle of the night usually last 3 to 14 seconds and alter the sleep cycle with a return to stage 1 NREM. Arousals are associated with abrupt increases in sympathetic and decreased parasympathetic activities, exceeding that seen during wakefulness. Compared to relaxed awakening, where increased sympathetic activity occurs without a withdrawal of parasympathetic activity, this difference may account for the dramatic changes in blood pressure and heart rate seen during arousals. 7,8 Since most time is spent in NREM stages, sleep should be a period of hemodynamic and cardiovascular tranquility; however sleep disorders disrupt this relaxed state. Sleep-Disordered Breathing Sleep-disordered breathing (SDB) describes a family of disorders characterized by abnormalities in either the respiratory pattern or the quantity of respirations during sleep. The estimated prevalence of significant SDB in the general population is 2% to 4%. 3 SDB has been strongly linked to cardiovascular diseases, especially early-onset coronary artery disease and hypertension Studies have also shown that SDB occurs frequently in HF and is associated with increased mortality. 3,10 15 Previous observations by Javaheri concluded that HF patients with depressed ejection fractions have a higher prevalence of SDB. 11 The prognosis for HF patients with SDB is worse than for those without, as these patients are more likely to experience arrhythmias, recalcitrant hypertension, clinical deterioration, and increased mortality rates 5,11 18 (Fig 1). Sleep-disordered breathing can be depicted as either those who cannot breathe or those who will not breathe. Obstructive sleep apnea (OSA) depicts the cannot-breathe patient whose pharyngeal airway is periodically collapsed or partially collapsed during sleep, triggering arousals to resume ventilation (Fig 2). Obstructive sleep apnea is the most common form of SDB and affects an estimated 15 million Americans, with prevalence rising as a consequence of increasing obesity. 19 The relationship between OSA and hypertension is well documented. 12,20 22 Central sleep apnea (CSA) and Cheyne-Stokes respirations (CSR) are also known as periodic breathing and occur in the will-not-breathe patient as a result of both an absence of airflow and inspiratory effort. In CSA the problem is neurologic, not physical, in nature as the message to breathe from the brainstem does not reach the diaphragm and no inspiratory effort is made (Fig 3). Cheyne-Stokes respiration is characterized by oscillation in the respiratory effort with a crescendo-decrescendo sequence separated by a central apnea. 23 To qualify an apneic episode as pathologic, the apnea must last at least 10 seconds. Central events occur most frequently after NREM sleep, particularly after arousals, and central sleep apnea is the main predictor of ventricular arrhythmias. 14,24 CSA-CSR is the most common form of SDB in HF and neurologic disorders. 23 Hypopnea is another term used in sleep medicine and is defined as a 50% reduction in airflow, a less than 50% reduction combined with a 3% decrease in pulse oximetry (SaO 2 ), or an arousal from sleep. The Apnea Hypopnea Index (AHI) is a measurement used to diagnose SDB and is computed by adding the total number of apneic or hypopneic events divided by the total hours of sleep. A normal AHI is less than 5 per hour. The threshold most commonly used to diagnose SDB is an AHI of greater than 15 events per hour, but this value may vary slightly from sleep laboratory to sleep laboratory. In patients with systolic left ventricular dysfunction, the AHI may be over 30 events per hour. 25 It should not be surprising that these patients complain of constant fatigue. The consequences of SDB on the cardiovascular system are many (Table 1). Falls in PaO 2 and rises in PaCO 2 decrease oxygen delivery throughout the body

3 Heart of Sleep S69 FIGURE 1. Relationship between heart failure and sleep-disordered breathing after an initial myocardial injury that results in decreased cardiac performance; neurohormonal systems are activated in order to increase cardiac output and renal perfusion. While initially compensatory, if untreated or undertreated with medications proven to stop the deleterious effects of constant neurohormonal effects (ACE inhibitors and beta blockers), the heart begins to enlarge and dilate (remodel), further decreasing cardiac output. Despite medications, sleep disorders also stimulate the neurohormonal systems through arousals, desaturations, and diminished rest to name a few, and thereby contribute to both HF disease progression and the incidence of arrhythmias. (Printed with permission from Nexan, Inc, Alpharetta, Ga.) and lead to organ dysfunction. This, in combination with the pulmonary vasoconstriction that occurs, leads to increased right ventricular afterload. As explained earlier, arousals cause surges in sympathetic activity leading to increased system vascular resistance and decreased myocardial oxygen delivery, causing angina, myocardial infarction, and arrhythmias. 26 In addition, sleep disorders decrease the efficiency of sleep, increasing stage 1 NREM sleep. As a result of increased early NREM time, sympathetic activity is further heightened, escalating the adverse consequences of increased left ventricular afterload, left ventricular hypertrophy, arrhythmias, and myocyte cell death. 27 In an already struggling left ventricle, these consequences lead to further deterioration in function and contribute significantly to the morbidity and mortality associated with HF. 4,5,19 Recognizing Patients With Sleep Disorders Most SDB cases go unrecognized by the medical community, creating a mismatch between disease prevalence and medical appreciation of its impact. One explanation for this lack of recognition is that common symptoms are nonspecific and are part of many acute and chronic illnesses. For example, sleepiness can be caused by any number of activities that reduce total sleep time (ie, off-shift work, household demands), medications, or reduced light exposure. Patients with HF typically have complaints of chronic fatigue, intermittent paroxysmal nocturnal dyspnea or orthopnea, somnolence, and disrupted sleep patterns. 12,18 These same symptoms are also seen in patients with SDB. Thus healthcare providers have a great challenge in distinguishing SDB as a possible contributor to the development of HF or as a consequence. Physical examination yields little information in predicting SDB, with the possible exception of uncontrollable hypertension. Weight alone is not a powerful predictor either, because of variations between body height and body size. Neck circumference has been implicated as a possible tool for identifying SDB, especially OSA, but the results remain controversial. However body mass index (BMI, kg/m 2 )

4 S70 Journal of Cardiovascular Nursing November/December 2004 FIGURE 2. Patient with obstructive sleep apnea abnormal sleep study. Note the episodes of minimal respiratory movement and fall in pulse oximetry into the upper 80%. As the patient experiences an arousal, there is increased respiratory movement with a subsequent rise in SpO 2. (Reprinted with permission from Nexan, Inc, Alpharetta, Ga.) has a powerful predictive ability in OSA and is easily measured within the clinical environment; 27 40% to 60% of patients treated for sleep apnea have an increased BMI. 19,27 A history of loud snoring, observed episodes of apnea, excessive daytime somnolence, nocturnal dyspnea, snoring, or restless sleep may be clues for SDB. The challenge lies in asking the right questions. The use of questionnaires to quantify self-perceptions about health and well-being in general or in specific diseases is increasing. General health status survey tools, such as the Short Form 36 Health Survey Questionnaire (SF-36) and Medical Outcomes Survey have been shown to correlate with sleep FIGURE 3. Patient with Cheyne-Stokes respirations abnormal sleep study. Note the oscillation pattern of Cheyne-Stokes respirations with hyperpneic phases followed by apneic phases. This is associated with a fall in oxygen saturations to 75% to 80% and mild changes in the heart rate. (Reprinted with permission from Nexan, Inc, Alpharetta, Ga.)

5 Heart of Sleep S71 TABLE 1 Outcomes in Sleep-Disordered Breathing Noncardiovascular Outcomes Cardiovascular Outcomes Poor sleep Nighttime arrhythmias Sleepiness Hypertension Cognitive impairment Coronary artery disease Motor vehicle accidents Pulmonary artery hypertension Decreased quality of life Cerebrovascular accident disorders. 28 In addition, specific tools such as the Epworth Sleepiness Scale have been developed to identify high-risk individuals. Hence these simple questionnaires may be utilized in the clinical environment to assist with patient identification. For example, patients with complaints of chronic fatigue, daytime somnolence, or snoring could be screened with one of these tools. In general, patients with HF should be considered for a sleep study if they experience continued hypertension despite treatment with 2 or more antihypertensive agents, have atrial fibrillation, have New York Heart Association (NYHA) functional class III IV symptoms despite optimal HF medications or have echocardiographic evidence of worsening left ventricular function despite optimal medications. 29 Worsening left ventricular dysfunction is best described as a falling ejection fraction or continued dilation of the left ventricle, as measured in the left ventricular end diastolic dimensions. As discussed above, obstructive sleep apnea patients tend to be heavier and be heavy snorers. OSA risk for men is associated with BMI greater than 30 kg/m 2 and advancing age. 14 For women, 14 increased risk develops several years after menopause or around age 60. Diabetics may also have a propensity for developing SDB, especially as a consequence of obesity and the metabolic syndrome. On the other hand, central sleep apnea patients tend to be 60 years old or more and have a history of atrial fibrillation. 14 Diagnosis and Treatment Optimization of HF medications should be the initial approach to treatment, since this alone may resolve or improve SDB. 30,31 By controlling volume, diuretics reduce filling pressures, venous pressures, and upperairway congestion as well as symptoms of paroxysmal nocturnal dyspnea and orthopnea. ACE inhibitors and beta blockers block the deleterious effects of the neurohormonal cascade seen in HF, and in doing so improve hemodynamics, including decreased filling pressures and increased ejection fraction and stroke volume. Beta blockers in particular oppose the effects of the sympathetic nervous system and decrease heart rate and blood pressure. ACE inhibitors and beta blockers have been shown to halt or reverse disease progression, reduce symptoms and improve quality of life, and reduce morbidity and mortality Their combined use has become the standard of care and is included in all guidelines and recommendations for the care and management of HF. 40,41 If medication optimization provides little or no improvement, referral to a sleep specialist for an overnight sleep study or polysomnography (PSG) is warranted. Before taking a PSG, the sleep specialist will obtain a complete history and perform a detailed physical examination, looking for malformations of the jaw or the oropharyngeal airway, or problems related to the thorax or chest wall expansion. If the history and examination confirm the likelihood of an SDB, a PSG is scheduled. Performed in a sleep laboratory, the PSG is a diagnostic test that collects multiple physiologic parameters during sleep. These parameters include electroencephalogram activity to determine the stage of sleep, electromyography of the jaw and calf to document muscle activity during sleep, and electrocardiograms to record heart rate and arrhythmias. Respiration is also evaluated by pulse oximetry for oxygen saturation, by evaluating respiratory effort with devices that determine chest and abdominal wall movements, and measuring airflow using a thermistor or thermocoupler. In order to most closely replicate normal sleep, the spouse may be encouraged to accompany the patient. Each sleep study is then thoroughly evaluated by the specialist, looking for apneas, hypopneas, arousals, restless limbs, desaturations, and arrhythmias. After reviewing all the data, an AHI is computed, and the patient is scored on the basis of this AHI. An AHI less than 5 events per hour is normal or not indicative of SDB, whereas 5 to 15 events per hour designates mild-moderate SDB. An AHI greater than 15 events demonstrates severe SDB requiring treatment; a second PSG is then scheduled in order to initiate and titrate the appropriate therapy and then evaluate its efficacy. For patients with mild-moderate SDB, strategies to reduce further risk include lifestyle modifications targeted at weight loss. Small reductions in weight can reduce obstructive events. Norman et al looked at the impact of exercise training in OSA and determined that exercise reduces AHI rates and BMI as aerobic capacity and quality of life increases. 42 Avoiding alcohol or sedatives prior to bedtime can be helpful to simply reduce the number and duration of apneic events. Merely changing sleeping positions, from supine to decubitus, may also be effective. While overnight sleep studies have been the gold standard to diagnose and then treat sleep disorders, 2-night studies create limitations from both the cost of the test and any delay associated with getting a

6 S72 Journal of Cardiovascular Nursing November/December 2004 FIGURE 4. Normal sleep study. Stable heart rate and rhythm, respiratory pattern and depth, and oxygen saturation via pulse oximetry. (Reprinted with permission from Nexan, Inc, Alpharetta, Ga.) PSG scheduled, performed, and interpreted (Fig 4). In order to improve efficiency, split-night studies are becoming more commonplace, and in part demanded by some third party payors In a split-night study, the first half is the diagnostic PSG, while the second half is used to implement and evaluate therapy. Split-night studies have not been shown to reduce either treatment acceptance or adherence. 43,44 In addition, several home testing devices to screen for SDB have been developed and approved by the Food and Drug Administration. 46 For example, the ClearPath system (Nexan, Inc, Alpharetta, Ga), is a multiparameter device applied in outpatient settings that collects and stores electrocardiogram (EKG) and respiratory data. 46 Core parameters collected include a 2-lead EKG, oxyhemoglobin saturation and desaturation, and thoracic impedance indicative of respiratory rate and depth. Able to collect and store data for 18 hours, ClearPath s data acquisition is activated before the patient leaves the clinic and continues until it is removed the next morning. The ClearPath system and its components are then returned to the clinic, either via mail or in person, for downloading and interpretation. If the results are indicative of SDB, the patient is referred for a splitnight study for confirmation and treatment. Continuous positive airway pressure (CPAP) is the treatment of choice for obstructive sleep apnea, and its effectiveness is well documented. 10,17,18,47,48 By increasing upper-airway pressure, CPAP acts as a pneumatic splint to prevent oropharyngeal collapse. The AHI has been shown to decrease significantly in patients treated with CPAP In addition, HF patients with Cheyne-Stokes respirations treated with CPAP had improvement in survival, increased left ventricular ejection fractions, and improvements in functional class. 49 However, CPAP is associated with variable adherence rates because of real or perceived difficulties related to its use. Nasal dryness and congestion, device interfaces, and troubles with CPAP titration are the most common side effects. Nasal side effects account for one third of CPAP discontinuation but may be alleviated through the use of humidification or use of face (oronasal) masks. 52 Just 4 hours of CPAP can provide benefit in sleepiness, snoring, quality of life, and cognitive function, with carryover effects for 3 to 4 hours. 53 Using CPAP for just half the night has advantages for the remainder of the night plus the next day. Consequently, strategies to improve adherence are critical. Because of perceived issues related to adherence, some healthcare providers may assume the patient will not tolerate CPAP and thus do not refer them for sleep studies. This is analogous to the belief that beta blockers will not be tolerated by HF patients and thus are not prescribed by many healthcare providers. However, randomized clinical trials have demonstrated no difference in tolerance between beta blockers and placebos, even in advanced HF. 35 An approach that has been proven to be effective in

7 Heart of Sleep S73 multiple studies is the impact of a nurse-directed team approach to optimize medications and improve adherence This same strategy is applicable for CPAP. Often a patient has a single interaction with a respiratory company that supplies the CPAP equipment and its operating instructions. Should there be difficulties related to nasal dryness, facial abrasions, etc, the patient is unsure of whom to call for assistance. While multiple studies have looked at variables that can affect adherence, such as depression, anxiety, and social support, the greatest observed variable seems to be initial problems encountered on the first night of treatment, which affects ensuing CPAP usage. 52,57 In a study by Hoy et al, an intensive educational program, including nursing support, significantly increased CPAP usage. 58 Implementing a nurse-directed approach to patient management could prove highly effective in improving adherence by centralizing communication and information. In addition, a proactive approach could be taken for routine surveillance of problems or questions, especially after treatment initiation. The ideal nurse would be knowledgeable not only on HF and SDB, but also on the different types of masks offered, airway pressure modalities available, and indications for heated versus unheated humidification. Such a program could dramatically affect CPAP adherence and ultimately patient outcomes. Javaheri has shown that central sleep apnea is the predominate sleep abnormality seen in HF patients and that the vast majority of these patients have central events. 59 Oxygen therapy for HF patients has shown a modest reduction for all events but showed a more dramatic reduction in central apneas. 50 Nocturnal oxygen also decreases arousals and episodes of desaturation. Thus, some investigators and clinicians use oxygen therapy as an alternative to CPAP for HF patients with central sleep apnea. 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