AACN Advanced Critical Care Volume 27, Number 1, pp. 15-20 © 2016 AACN
Issues in
Advanced Practice
Valerie Sabol, RN, PhD, ACNP-BC, GNP-BC, CCNS, CCRN Department Editor
Diagnosing Sleep Apnea in Patients Hospitalized With Heart Failure: A Role for Advanced Practice Nurses Robin J. Trupp, RN, PhD, ACNP-BC, CHFN
H
eart failure is a chronic condition associated with high morbidity and mortality and a significant economic burden in the United States. As the most common admitting diagnosis in Medicare patients, the greatest portion of this economic burden stems from the care delivered during hospitalization.1 In 2013, the Centers for Medicare and Medicaid Services implemented a maximum 1% financial reimbursement penalty for acute care facilities with excessive readmission rates for heart failure, pneumonia, and acute myocardial infarction.2 Of importance, these penalties apply to all Medicare readmissions, not just the chronic conditions mentioned. Now in its third year with maximum penalties increased to 3% and expansion of the program to include chronic obstructive pulmonary disease and hip or knee replacements, a total of 2610 or 78% of all hospitals are being penalized for excessive readmissions, for an estimated total of $428 million.3 Consequently, to reduce readmission rates and associated health care costs, increased attention is being given to identifying and treating conditions that adversely affect heart failure. Yet, despite being the most common comorbid condition seen in heart failure,4 sleep apnea is not routinely considered as a contributor to acute exacerbations, leaving the condition largely undiagnosed. As a modifiable risk factor, recent studies have shown that the recognition and subsequent treatment of sleep apnea significantly reduces morbidity and mortality in patients hospitalized with heart failure.4,5 Thus hospitalization may present an opportune time to routinely screen, diagnose, and possibly initiate treatment in this high-risk population. Advanced practice nurses (APNs) are in prime positions to lead this charge. Sleep Apnea Sleep apnea is a term used to describe abnormalities in either the quantity or quality of respirations during sleep. Three main patterns of sleep apnea are recognized: central sleep apnea (CSA), where the patient does not breathe because of the periodic loss of the respiratory drive (includes Cheyne-Stokes respirations); obstructive sleep apnea (OSA), where the patient cannot breathe because of upper airway collapse and obstruction; and mixed sleep apnea, a combination of the two. Robin J. Trupp is Adjunct Assistant Professor, University of Illinois at Chicago, 845 S. Damen Avenue, Chicago, IL 60812 ([email protected]). The author served as a consultant to ResMed in 2015. DOI: http://dx.doi.org/10.4037/aacnacc2016815
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differential diagnosis, challenging clinical acumen. Reports of loud snoring and witnessed apneic events by family members serve as the universal clues for physicians, APNs, and other clinicians to consider sleep apnea, and these symptoms are likely to be evident during hospitalization. More commonly reported symptoms by patients are fatigue, daytime sleepiness, morning headaches, unrefreshed sleep, and frequent nocturnal awakenings. Rather than relying on patients or patients’ families to recognize and report symptoms, APNs are in a unique position to actively approach patients to determine which patients are at risk for sleep apnea. A number of screening tools have been developed to screen for sleep apnea, including the Berlin Questionnaire, Epworth Sleepiness Scale, and the Pittsburgh Sleep Quality Index. Unfortunately, none of these instruments has been validated in the heart failure population, making their usefulness for predicting sleep apnea in patients with heart failure unknown. Specific questions that would be most useful for identifying sleep apnea also have not been reported. Thus APNs are forced to ask nonspecific questions, such as Do you have any problems sleeping? or Are you tired during the day?, and must rely on other means to identify patients. In a large outpatient registry of more than 6800 stable patients with heart failure, left ventricular ejection fraction less than 25%, male sex, older age, increased body mass index (calculated as weight in kilograms divided by height in meters squared, ≥30), atrial fibrillation, and New York Heart Association class III/IV symptoms were clinical predictors of sleep apnea.15 These results suggest that the presence of 1 or more of these predictors should prompt clinicians to perform device-based screening for sleep apnea. More and more evidence supports the need for better diagnosis and implementation of treatment in patients hospitalized with acute heart failure. In a study that was the first of its kind, Khayat et al16 examined the impact of sleep apnea on heart failure readmissions and identified CSA as an independent risk factor for 6-month readmissions in patients hospitalized with decompensated heart failure, all of whom had an inpatient polysomnography sleep study completed during that index event. The effect size seen exceeded that of all known predictors of heart failure readmissions, including age, left ventricular
Sleep apnea is not a benign disorder that should be disregarded, because a number of profound and life-threatening consequences can occur if it is untreated. Consequences of sleep apnea range from decreased attention and focus, motor vehicle accidents, depression, glucose metabolism impairment, and a number of cardiovascular diseases, including hypertension, stroke, arrhythmias, heart failure, and sudden death.6 The evidence supporting these consequences is substantial, yet recognition and appreciation of sleep apnea by clinicians is poor, such that only a small portion of patients ultimately receive treatment. Significance of Sleep Apnea Whether obstructive, central, or a combination of the 2, sleep apnea is characterized by repetitive nightly recurrences of apnea and/or hypopnea (hypoventilation), followed by a recovery phase with hyperpnea (increased respiratory rate and effort). Patients experience a cyclic pattern of intermittent hypoxiareoxygenation, arousal (interruption of sleep lasting 3-15 seconds), increased inspiratory effort, and activation of the sympathetic nervous system throughout the night. In particular, the activation of the systemic nervous system is worrisome because it produces vasoconstriction and surges in blood pressure that have carryover effects into the following day.7 These physiological disturbances, which can occur 15 or more times per hour, are strikingly similar in both OSA and CSA and are associated with similar cardiovascular and immune system consequences, leading to the development and progression of a number of cardiovascular disorders, including hypertension, cardiac arrhythmias, and heart failure.6 Sleep apnea occurs in 65.7% of patients admitted for acute coronary syndromes,8 in at least 60% of stroke survivors,9 in 40% to 73% of individuals with atrial fibrillation,10 and in 47% to 76% of individuals with heart failure, whether due to heart failure with reduced ejection fraction (HFrEF) or to heart failure with preserved ejection fraction (HFpEF).11-13 In acute decompensated heart failure, 75% of hospitalized patients have been found to have sleep apnea.14 Just like heart failure, the incidence of sleep apnea increases with age and is associated with worse outcomes.11 Detection of Sleep Apnea Most signs and symptoms of sleep apnea are vague, nonspecific, and part of a large 16
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ejection fraction, cause of heart failure, and renal function. Another inpatient study17 of nearly 1100 patients with HFrEF revealed that both OSA and CSA were associated with increased mortality in 36 months of follow-up, even after adjustment for a number of covariates, including chronic kidney disease, age, sex, and serum level of sodium. In this same study,17 a new diagnosis of sleep apnea was also a novel independent predictor of heart failure readmissions. Researchers in other studies have reported reductions in emergency department visits and/or in all-cause hospital readmission rates in patients who had sleep apnea diagnosed as inpatients and then received treatment for sleep apnea before discharge.5,18 This growing body of evidence supporting the recognition, diagnosis, and treatment of sleep apnea during hospitalizations creates a prime opportunity for APNs to lead initiatives for improving clinical outcomes.
Figure 1: Image of in-hospital sleep study device. Reprinted with permission from ResMed (San Diego, California).
diagnosis, some patients may require a confirmatory outpatient polysomnography study. Treatment of Sleep Apnea Regardless of the type of sleep apnea, optimization of all indicated therapies for heart failure is critical for improved outcomes. This optimization includes using diuretics to manage fluid volume and symptoms, angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers to block the renin-angiotensin-aldosterone system, and b-blockers to diminish the effects of activation of the sympathetic nervous system.19 However, sleep apnea often persists despite optimized guideline-directed medical therapies, and it is not unreasonable to think that therapeutic efficacy may be mitigated by the nightly and repeated neurohormonal surges seen with sleep apnea. Therefore, results positive for sleep apnea warrant targeted treatment to reduce nocturnal respiratory disturbances in this at-risk group. Continuous positive airway pressure (CPAP) therapy is the most effective treatment for OSA. Acting as a pneumatic splint to maintain upper airway patency, CPAP delivers a single fixed pressure during inspiration and expiration. CPAP improves cardiac function,20,21 readmission rates, and clinical outcomes in patients with heart failure.4,5,18 Similar to CPAP, bilevel positive airway pressure (BiPAP) uses a higher inspiratory pressure to open the airway and a lower expiratory pressure. Rather than using a fixed pressure, autotitrating CPAP (autoPAP) devices use variable pressures to maintain airway patency and are
Inpatient Diagnosis of Sleep Apnea Although the “gold standard” for diagnosing sleep apnea remains overnight polysomnography performed in an outpatient sleep laboratory, a number of barriers exist for this standard, including out-of-pocket expenses, inconvenience, scheduling delays, and patients’ resistance. These barriers may be especially pertinent for patients recently discharged from the hospital. Fortunately, several devices are now available for the inpatient evaluation of sleep that have a greater than 90% positive predictive value for detecting sleep apnea.16 In-hospital device-based screening, also known as an unattended sleep study or home sleep testing, are simplified versions of polysomnography studies, using sensors that are applied at bedtime by the nurse to capture and measure respiratory effort, oxygenation, nasal airflow, and electrocardiographic data (Figure 1). Most facilities that use device-based screening conduct the studies after initial treatment for heart failure has been given and the patient is hemodynamically stable and off supplemental oxygen, usually on hospital day 3 or 4. Once the study is completed, the device data are downloaded and interpreted by a physician who is board certified in sleep medicine, who can bill for the technical component of the study. Depending on the insurance provider and the sleep disturbance 17
Issues in Advanced Practice
W W W .AACN ACCON LIN E .ORG
Implications for Advanced Practice Nurses The positive impact of nurse-directed teams on optimization of therapies and improving adherence has been well studied in heart failure and other chronic conditions.29-31 This same strategy is applicable to detecting and diagnosing sleep apnea in hospitalized patients with heart failure. Advanced practice nurses, as active members or leaders of interdisciplinary teams, can play major roles in changing existing clinical practice to begin inpatient device-based screenings. Rather than deferring the possibility of sleep apnea to primary care providers after discharge, the APN is in a position to lead an inpatient team approach for diagnosing and treating sleep apnea. This approach includes coordination of care and timely communication with outpatient providers, patients, and patients’ families for an effective transition. Figure 2 provides a proposed algorithm for detecting sleep apnea during hospitalization. Determining when the patient can be safely weaned from supplemental oxygen and is hemodynamically stable for device-based testing is within the scope of APN practice. If screening all inpatients with heart failure seems overwhelming, consider beginning with a group of patients, such as the “frequent flyers” who are readmitted quite often or those with 1 or more of the clinical predictors of sleep apnea (left ventricular ejection fraction < 25%, male sex, older age, increased body mass index [≥30], atrial fibrillation).15 Given the current state of affairs, it seems likely that any effort to recognize and treat sleep apnea would be a positive move. However, as with other changes in practice, ongoing data collection on readmission rates, polysomnography results, and other parameters is warranted. Given the particular hospital environment, it may be necessary to identify a sleep medicine specialist as an advocate for in-hospital device-based screening. This person may also be willing to interpret the data and facilitate outpatient polysomnography studies as necessary. Ongoing collaboration and communication with all community providers of outpatient care will be essential.
able to decrease that pressure if no abnormal respiratory events are detected. AutoPAP devices can also be programmed to CPAP and BiPAP modes as necessary. CSA is often a consequence, rather than the cause, of heart failure and is associated with worse outcomes.4,16 For patients with CSA, CPAP fails to improve mortality.22 Adaptive servoventilation, which provides ventilatory support, does improve cardiac function and prognosis23-25 and neurohormonal activation.26 Using a built-in servocontroller, adaptive servoventilation automatically adjusts pressure on a breath-by-breath basis to maintain a steady minute ventilation. However, a prospective trial in patients with HFrEF was recently halted because of increased relative cardiovascular mortality rate for those receiving adaptive servoventilation.27 Adherence to devices to treat sleep apnea is challenging and requires both commitment to and significant behavioral changes by the patient. However, as seen in other in-hospital initiated therapies,28 the hospital environment may provide the perfect “teachable moment” to educate the patient about sleep apnea, its consequences, and treatment and to emphasize the importance of adherence to device therapy. For patients who are unable or unwilling to have in-hospital screening, an outpatient polysomnography study as soon as possible after discharge is a reasonable option. In fact, if the patient is amenable, he or she could be discharged from the hospital and go directly to an outpatient sleep laboratory for testing. Ideally, the outpatient polysomnographic study would be done within 1 or 2 weeks of discharge, in order for any necessary treatment to be initiated and to prevent poor outcomes, such as a readmission. Information on how to schedule the polysomnography should be included on the discharge instructions and any communication to community providers. If the polysomnography is scheduled before discharge, the patient must have all necessary information on how to contact the sleep laboratory. Postdischarge calls to the patient should also emphasize and reinforce the importance of keeping the PSG appointment. Despite these efforts, it is an expectation that patients will cancel or fail to appear for the polysomnography. As always, appointments with the patient’s community provider(s) should be scheduled within 7 days of discharge.
Summary Identification and early treatment of sleep apnea in patients with heart failure is essential
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Patient admitted with decompensated heart failure (ejection fraction either reduced or preserved)
Hemodynamically stable? Off supplemental oxygen? Agrees to in-hospital sleep test?
Yes
Tests positive for sleep apnea on in-hospital device-based sleep test? Yes
No No
Schedule for outpatient polysomnography within 14 days of discharge
Optimize heart failure therapies Follow-up appointment within 7 days of discharge
Refer to sleep medicine department for treatment If sleep medicine department already on case, initiate treatment with positive airway pressure therapy
Figure 2: Algorithm for detecting sleep apnea in patients hospitalized for decompensated heart failure.
to reduce readmissions and avoid long-term complications from the disorder. Hospitalization appears to be an opportune time to identify sleep apnea, but clinicians must understand sleep apnea and the need for early intervention. Although the optimal strategy for accomplishing this has yet to be identified, concerted and consistent efforts to support early identification, diagnosis, and subsequent treatment of sleep apnea have the potential to significantly improve outcomes in this high-risk population. APNs are in prime positions to implement and lead this change in clinical practice, using in-hospital device-based screening with demonstrated high positive predictive value in detecting sleep apnea. We can—and should—do better! REFERENCES 1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360:1418-1428. 2. Center for Medicare and Medicaid Services. The 2,225 hospitals that will pay readmissions penalties next year. http://www.advisory.com/daily-briefing/2013/08/05/cms2225-hospitals-will-pay-readmissions-penalties-next-year. Published August 5, 2013. Accessed November 17, 2015. 3. Rau J. Medicare fines 2,610 hospitals in third round of readmission penalties. http://kaiserhealthnews.org/ news/medicare-readmissions-penalties-2015. Published October 2, 2014. Accessed November 17, 2015. 4. Khayat R, Jarjoura D, Porter K, et al. Sleep disordered breathing and post-discharge mortality in patients with acute heart failure. Eur Heart J. 2015;36(23):1463-1469. 5. Sharma S, Gupta A, Rubin S, et al. Treatment of sleep disordered breathing in patients admitted for decom pensated heart failure reduces 6 month hospital visits. J Am Coll Cardiol. 2015;65(10_S). 6. Somers VK, White DP, Amin R, et al. Sleep apnea and cardiovascular disease: an American Heart Association/ American College of Cardiology Foundation scientific statement from the American Heart Association Council for High Blood Pressure Research Professional
7. 8.
9. 10. 11. 12.
13. 14.
15.
16.
17. 18.
19.
19
Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing. J Am Coll Cardiol. 2008;52:686-717. Somers V. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest. 1995;96(4):1897-1904. Lee CH, Khoo SM, Tai BC, et al. Obstructive sleep apnea in patients admitted for acute myocardial infarction: prevalence, predictors, and effect on microvascular perfusion. Chest. 2009;35:488-495. Johnson KG, Johnson DC. Frequency of sleep apnea in stroke and TIA patients: a meta-analysis. J Clin Sleep Med. 2010;6:131-137. Jaffe LM, Kjekshus J, Gottlieb SS. Importance and management of chronic sleep apnoea in cardiology. Eur Heart J. 2013;34:809-815. Bitter T, Westerheide N, Faber L, et al. Adaptive servoventilation in diastolic heart failure and Cheyne-Stokes respiration. Eur Respir J. 2010;36:385-392. Vazir A, Hastings PC, Dayer M, et al. A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction. Eur J Heart Fail. 2007;9:243-250. Javaheri J. Sleep disorders in systolic heart failure: a prospective study of 100 male patients. Int J Cardiol. 2006;106:21-28. Khayat RN, Jarjoura D, Patt B, Yamokoski T, Abraham WT. In-hospital testing for sleep disordered breathing in hospitalized patients with decompensated heart failure: report of prevalence and patient characteristics. J Card Fail. 2009;9(15):739-746. Woehrle H, Arzt M, Oldenburg O, et al. Prevalence and predictors of sleep-disordered breathing in patients with stable chronic heart failure: final data of the SchlaHF Registry. J Am Coll Cardiol. 2015;65(10_S). Khayat R, Abraham WT, Brinkman V, Wannemacher J, Porter K, Jarjoura D. Central sleep apnea is a predictor of cardiac readmission in hospitalized patients with systolic heart failure. J Card Fail. 2012;18(7):534-540. Khayat R, Jarjoura D, Porter K, et al. Sleep disordered breathing and post-discharge mortality in patients with acute heart failure. Eur Heart J. 2015;36(23):1463-1469. Kauta SR, Keenan BT, Goldberg L, Schwab RJ. Diagnosis and treatment of sleep disordered breathing in hospitalized cardiac patients: a reduction in 30-day hospital readmission rates. J Clin Sleep Med. 2014; 10(10):1051-1059. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62:147-239.
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20. Mansfield DR, Gollogly NC, Kaye DM, Richardson M, Bergin P, Naughton MT. Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am J Respir Crit Care Med. 2004; 169:361-366. 21. Kaneko Y, Floras J, Phil D, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003;348(13):1233-1241. 22. Bradley T, Logan A, Kimoff R, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med. 2005;353:2025-2033. 23. Yoshihisa A, Suzuki S, Takeishi Y. Do adaptive servoventilation improve prognosis in heart failure patients? J Card Fail. 2014;20(10):S139. 24. Yoshihisa A, Shimizu T, Owada T, et al. Adaptive servo ventilation improves cardiac dysfunction and prognosis in chronic heart failure patients with Cheyne-Stokes respiration. Int Heart J. 2011;52(4):218-223. 25. Takama N, Kurabayashi M. Effect of adaptive servoventilation on 1-year prognosis in heart failure patients. Circ J. 2012;76(3):661-667.
26. Pepperell JC, Maskell NA, Jones DR, et al. A randomized controlled trial of adaptive ventilation for Cheyne-Stokes breathing in heart failure. Am J Respir Crit Care Med. 2003;168(9):1109-1114. 27. ResMed. http://www.resmed.com/content/dam/resmed /global/documents/serve-hf/Healthcare_Professionals _SERVE-HF_FAQs.pdf. Accessed November 17, 2015. 28. Fonarow GC. Importance of in-hospital initiation of evidence-based medical therapies for heart failure: taking advantage of the teachable moment. Congest Heart Fail. 2005;11(3):151-154. 29. Kutzleb J, Reiner D. The impact of nurse-directed patient education on quality of life and functional capacity in people with heart failure. J Am Acad Nurse Pract. 2006; 18(3):116-123. 30. Lowery J, Hopp F, Subramanian U, et al. Evaluation of a nurse practitioner disease management model for chronic heart failure: a multi-site implementation study. Congest Heart Fail. 2012:18(1):64-71. 31. Osevala ML. Advance-practice nursing in heart-failure management: an integrative review. J Cardiovasc Manage. 2005;16(3):19-23.
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Issues in
Advanced Practice
Valerie Sabol, RN, PhD, ACNP-BC, GNP-BC, CCNS, CCRN Department Editor
Diagnosing Sleep Apnea in Patients Hospitalized With Heart Failure: A Role for Advanced Practice Nurses Robin J. Trupp, RN, PhD, ACNP-BC, CHFN
H
eart failure is a chronic condition associated with high morbidity and mortality and a significant economic burden in the United States. As the most common admitting diagnosis in Medicare patients, the greatest portion of this economic burden stems from the care delivered during hospitalization.1 In 2013, the Centers for Medicare and Medicaid Services implemented a maximum 1% financial reimbursement penalty for acute care facilities with excessive readmission rates for heart failure, pneumonia, and acute myocardial infarction.2 Of importance, these penalties apply to all Medicare readmissions, not just the chronic conditions mentioned. Now in its third year with maximum penalties increased to 3% and expansion of the program to include chronic obstructive pulmonary disease and hip or knee replacements, a total of 2610 or 78% of all hospitals are being penalized for excessive readmissions, for an estimated total of $428 million.3 Consequently, to reduce readmission rates and associated health care costs, increased attention is being given to identifying and treating conditions that adversely affect heart failure. Yet, despite being the most common comorbid condition seen in heart failure,4 sleep apnea is not routinely considered as a contributor to acute exacerbations, leaving the condition largely undiagnosed. As a modifiable risk factor, recent studies have shown that the recognition and subsequent treatment of sleep apnea significantly reduces morbidity and mortality in patients hospitalized with heart failure.4,5 Thus hospitalization may present an opportune time to routinely screen, diagnose, and possibly initiate treatment in this high-risk population. Advanced practice nurses (APNs) are in prime positions to lead this charge. Sleep Apnea Sleep apnea is a term used to describe abnormalities in either the quantity or quality of respirations during sleep. Three main patterns of sleep apnea are recognized: central sleep apnea (CSA), where the patient does not breathe because of the periodic loss of the respiratory drive (includes Cheyne-Stokes respirations); obstructive sleep apnea (OSA), where the patient cannot breathe because of upper airway collapse and obstruction; and mixed sleep apnea, a combination of the two. Robin J. Trupp is Adjunct Assistant Professor, University of Illinois at Chicago, 845 S. Damen Avenue, Chicago, IL 60812 ([email protected]). The author served as a consultant to ResMed in 2015. DOI: http://dx.doi.org/10.4037/aacnacc2016815
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Issues in Advanced Practice
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differential diagnosis, challenging clinical acumen. Reports of loud snoring and witnessed apneic events by family members serve as the universal clues for physicians, APNs, and other clinicians to consider sleep apnea, and these symptoms are likely to be evident during hospitalization. More commonly reported symptoms by patients are fatigue, daytime sleepiness, morning headaches, unrefreshed sleep, and frequent nocturnal awakenings. Rather than relying on patients or patients’ families to recognize and report symptoms, APNs are in a unique position to actively approach patients to determine which patients are at risk for sleep apnea. A number of screening tools have been developed to screen for sleep apnea, including the Berlin Questionnaire, Epworth Sleepiness Scale, and the Pittsburgh Sleep Quality Index. Unfortunately, none of these instruments has been validated in the heart failure population, making their usefulness for predicting sleep apnea in patients with heart failure unknown. Specific questions that would be most useful for identifying sleep apnea also have not been reported. Thus APNs are forced to ask nonspecific questions, such as Do you have any problems sleeping? or Are you tired during the day?, and must rely on other means to identify patients. In a large outpatient registry of more than 6800 stable patients with heart failure, left ventricular ejection fraction less than 25%, male sex, older age, increased body mass index (calculated as weight in kilograms divided by height in meters squared, ≥30), atrial fibrillation, and New York Heart Association class III/IV symptoms were clinical predictors of sleep apnea.15 These results suggest that the presence of 1 or more of these predictors should prompt clinicians to perform device-based screening for sleep apnea. More and more evidence supports the need for better diagnosis and implementation of treatment in patients hospitalized with acute heart failure. In a study that was the first of its kind, Khayat et al16 examined the impact of sleep apnea on heart failure readmissions and identified CSA as an independent risk factor for 6-month readmissions in patients hospitalized with decompensated heart failure, all of whom had an inpatient polysomnography sleep study completed during that index event. The effect size seen exceeded that of all known predictors of heart failure readmissions, including age, left ventricular
Sleep apnea is not a benign disorder that should be disregarded, because a number of profound and life-threatening consequences can occur if it is untreated. Consequences of sleep apnea range from decreased attention and focus, motor vehicle accidents, depression, glucose metabolism impairment, and a number of cardiovascular diseases, including hypertension, stroke, arrhythmias, heart failure, and sudden death.6 The evidence supporting these consequences is substantial, yet recognition and appreciation of sleep apnea by clinicians is poor, such that only a small portion of patients ultimately receive treatment. Significance of Sleep Apnea Whether obstructive, central, or a combination of the 2, sleep apnea is characterized by repetitive nightly recurrences of apnea and/or hypopnea (hypoventilation), followed by a recovery phase with hyperpnea (increased respiratory rate and effort). Patients experience a cyclic pattern of intermittent hypoxiareoxygenation, arousal (interruption of sleep lasting 3-15 seconds), increased inspiratory effort, and activation of the sympathetic nervous system throughout the night. In particular, the activation of the systemic nervous system is worrisome because it produces vasoconstriction and surges in blood pressure that have carryover effects into the following day.7 These physiological disturbances, which can occur 15 or more times per hour, are strikingly similar in both OSA and CSA and are associated with similar cardiovascular and immune system consequences, leading to the development and progression of a number of cardiovascular disorders, including hypertension, cardiac arrhythmias, and heart failure.6 Sleep apnea occurs in 65.7% of patients admitted for acute coronary syndromes,8 in at least 60% of stroke survivors,9 in 40% to 73% of individuals with atrial fibrillation,10 and in 47% to 76% of individuals with heart failure, whether due to heart failure with reduced ejection fraction (HFrEF) or to heart failure with preserved ejection fraction (HFpEF).11-13 In acute decompensated heart failure, 75% of hospitalized patients have been found to have sleep apnea.14 Just like heart failure, the incidence of sleep apnea increases with age and is associated with worse outcomes.11 Detection of Sleep Apnea Most signs and symptoms of sleep apnea are vague, nonspecific, and part of a large 16
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ejection fraction, cause of heart failure, and renal function. Another inpatient study17 of nearly 1100 patients with HFrEF revealed that both OSA and CSA were associated with increased mortality in 36 months of follow-up, even after adjustment for a number of covariates, including chronic kidney disease, age, sex, and serum level of sodium. In this same study,17 a new diagnosis of sleep apnea was also a novel independent predictor of heart failure readmissions. Researchers in other studies have reported reductions in emergency department visits and/or in all-cause hospital readmission rates in patients who had sleep apnea diagnosed as inpatients and then received treatment for sleep apnea before discharge.5,18 This growing body of evidence supporting the recognition, diagnosis, and treatment of sleep apnea during hospitalizations creates a prime opportunity for APNs to lead initiatives for improving clinical outcomes.
Figure 1: Image of in-hospital sleep study device. Reprinted with permission from ResMed (San Diego, California).
diagnosis, some patients may require a confirmatory outpatient polysomnography study. Treatment of Sleep Apnea Regardless of the type of sleep apnea, optimization of all indicated therapies for heart failure is critical for improved outcomes. This optimization includes using diuretics to manage fluid volume and symptoms, angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers to block the renin-angiotensin-aldosterone system, and b-blockers to diminish the effects of activation of the sympathetic nervous system.19 However, sleep apnea often persists despite optimized guideline-directed medical therapies, and it is not unreasonable to think that therapeutic efficacy may be mitigated by the nightly and repeated neurohormonal surges seen with sleep apnea. Therefore, results positive for sleep apnea warrant targeted treatment to reduce nocturnal respiratory disturbances in this at-risk group. Continuous positive airway pressure (CPAP) therapy is the most effective treatment for OSA. Acting as a pneumatic splint to maintain upper airway patency, CPAP delivers a single fixed pressure during inspiration and expiration. CPAP improves cardiac function,20,21 readmission rates, and clinical outcomes in patients with heart failure.4,5,18 Similar to CPAP, bilevel positive airway pressure (BiPAP) uses a higher inspiratory pressure to open the airway and a lower expiratory pressure. Rather than using a fixed pressure, autotitrating CPAP (autoPAP) devices use variable pressures to maintain airway patency and are
Inpatient Diagnosis of Sleep Apnea Although the “gold standard” for diagnosing sleep apnea remains overnight polysomnography performed in an outpatient sleep laboratory, a number of barriers exist for this standard, including out-of-pocket expenses, inconvenience, scheduling delays, and patients’ resistance. These barriers may be especially pertinent for patients recently discharged from the hospital. Fortunately, several devices are now available for the inpatient evaluation of sleep that have a greater than 90% positive predictive value for detecting sleep apnea.16 In-hospital device-based screening, also known as an unattended sleep study or home sleep testing, are simplified versions of polysomnography studies, using sensors that are applied at bedtime by the nurse to capture and measure respiratory effort, oxygenation, nasal airflow, and electrocardiographic data (Figure 1). Most facilities that use device-based screening conduct the studies after initial treatment for heart failure has been given and the patient is hemodynamically stable and off supplemental oxygen, usually on hospital day 3 or 4. Once the study is completed, the device data are downloaded and interpreted by a physician who is board certified in sleep medicine, who can bill for the technical component of the study. Depending on the insurance provider and the sleep disturbance 17
Issues in Advanced Practice
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Implications for Advanced Practice Nurses The positive impact of nurse-directed teams on optimization of therapies and improving adherence has been well studied in heart failure and other chronic conditions.29-31 This same strategy is applicable to detecting and diagnosing sleep apnea in hospitalized patients with heart failure. Advanced practice nurses, as active members or leaders of interdisciplinary teams, can play major roles in changing existing clinical practice to begin inpatient device-based screenings. Rather than deferring the possibility of sleep apnea to primary care providers after discharge, the APN is in a position to lead an inpatient team approach for diagnosing and treating sleep apnea. This approach includes coordination of care and timely communication with outpatient providers, patients, and patients’ families for an effective transition. Figure 2 provides a proposed algorithm for detecting sleep apnea during hospitalization. Determining when the patient can be safely weaned from supplemental oxygen and is hemodynamically stable for device-based testing is within the scope of APN practice. If screening all inpatients with heart failure seems overwhelming, consider beginning with a group of patients, such as the “frequent flyers” who are readmitted quite often or those with 1 or more of the clinical predictors of sleep apnea (left ventricular ejection fraction < 25%, male sex, older age, increased body mass index [≥30], atrial fibrillation).15 Given the current state of affairs, it seems likely that any effort to recognize and treat sleep apnea would be a positive move. However, as with other changes in practice, ongoing data collection on readmission rates, polysomnography results, and other parameters is warranted. Given the particular hospital environment, it may be necessary to identify a sleep medicine specialist as an advocate for in-hospital device-based screening. This person may also be willing to interpret the data and facilitate outpatient polysomnography studies as necessary. Ongoing collaboration and communication with all community providers of outpatient care will be essential.
able to decrease that pressure if no abnormal respiratory events are detected. AutoPAP devices can also be programmed to CPAP and BiPAP modes as necessary. CSA is often a consequence, rather than the cause, of heart failure and is associated with worse outcomes.4,16 For patients with CSA, CPAP fails to improve mortality.22 Adaptive servoventilation, which provides ventilatory support, does improve cardiac function and prognosis23-25 and neurohormonal activation.26 Using a built-in servocontroller, adaptive servoventilation automatically adjusts pressure on a breath-by-breath basis to maintain a steady minute ventilation. However, a prospective trial in patients with HFrEF was recently halted because of increased relative cardiovascular mortality rate for those receiving adaptive servoventilation.27 Adherence to devices to treat sleep apnea is challenging and requires both commitment to and significant behavioral changes by the patient. However, as seen in other in-hospital initiated therapies,28 the hospital environment may provide the perfect “teachable moment” to educate the patient about sleep apnea, its consequences, and treatment and to emphasize the importance of adherence to device therapy. For patients who are unable or unwilling to have in-hospital screening, an outpatient polysomnography study as soon as possible after discharge is a reasonable option. In fact, if the patient is amenable, he or she could be discharged from the hospital and go directly to an outpatient sleep laboratory for testing. Ideally, the outpatient polysomnographic study would be done within 1 or 2 weeks of discharge, in order for any necessary treatment to be initiated and to prevent poor outcomes, such as a readmission. Information on how to schedule the polysomnography should be included on the discharge instructions and any communication to community providers. If the polysomnography is scheduled before discharge, the patient must have all necessary information on how to contact the sleep laboratory. Postdischarge calls to the patient should also emphasize and reinforce the importance of keeping the PSG appointment. Despite these efforts, it is an expectation that patients will cancel or fail to appear for the polysomnography. As always, appointments with the patient’s community provider(s) should be scheduled within 7 days of discharge.
Summary Identification and early treatment of sleep apnea in patients with heart failure is essential
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Patient admitted with decompensated heart failure (ejection fraction either reduced or preserved)
Hemodynamically stable? Off supplemental oxygen? Agrees to in-hospital sleep test?
Yes
Tests positive for sleep apnea on in-hospital device-based sleep test? Yes
No No
Schedule for outpatient polysomnography within 14 days of discharge
Optimize heart failure therapies Follow-up appointment within 7 days of discharge
Refer to sleep medicine department for treatment If sleep medicine department already on case, initiate treatment with positive airway pressure therapy
Figure 2: Algorithm for detecting sleep apnea in patients hospitalized for decompensated heart failure.
to reduce readmissions and avoid long-term complications from the disorder. Hospitalization appears to be an opportune time to identify sleep apnea, but clinicians must understand sleep apnea and the need for early intervention. Although the optimal strategy for accomplishing this has yet to be identified, concerted and consistent efforts to support early identification, diagnosis, and subsequent treatment of sleep apnea have the potential to significantly improve outcomes in this high-risk population. APNs are in prime positions to implement and lead this change in clinical practice, using in-hospital device-based screening with demonstrated high positive predictive value in detecting sleep apnea. We can—and should—do better! REFERENCES 1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360:1418-1428. 2. Center for Medicare and Medicaid Services. The 2,225 hospitals that will pay readmissions penalties next year. http://www.advisory.com/daily-briefing/2013/08/05/cms2225-hospitals-will-pay-readmissions-penalties-next-year. Published August 5, 2013. Accessed November 17, 2015. 3. Rau J. Medicare fines 2,610 hospitals in third round of readmission penalties. http://kaiserhealthnews.org/ news/medicare-readmissions-penalties-2015. Published October 2, 2014. Accessed November 17, 2015. 4. Khayat R, Jarjoura D, Porter K, et al. Sleep disordered breathing and post-discharge mortality in patients with acute heart failure. Eur Heart J. 2015;36(23):1463-1469. 5. Sharma S, Gupta A, Rubin S, et al. Treatment of sleep disordered breathing in patients admitted for decom pensated heart failure reduces 6 month hospital visits. J Am Coll Cardiol. 2015;65(10_S). 6. Somers VK, White DP, Amin R, et al. Sleep apnea and cardiovascular disease: an American Heart Association/ American College of Cardiology Foundation scientific statement from the American Heart Association Council for High Blood Pressure Research Professional
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