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Sleep-Disordered Breathing in
Patients with Heart Failure: An Update
Nancy S. Redeker, Ph.D., R.N.
Professor & Associate Dean for Scholarly Affairs
Yale University School of Nursing
Introduction
Sleep-disordered breathing (SDB), including Cheyne-Stokes
Breathing-Central Sleep Apnea (CSB-CSA) and Obstructive
Sleep Apnea Hypopnea Syndrome (OSAHS), is common among
patients with heart failure (HF) and may occur in as many as
82% of patients.
1
These conditions may occur individually or in
combination and may result in exacerbation of cardiovascular
disease, increased mortality, consequences for daytime
functioning, and quality of life. The purpose of this article is to
discuss the epidemiology, pathophysiology, and consequences
of sleep-disordered breathing as relevant to HF and to review
the clinical management of heart failure patients who have
sleep-disordered breathing.
Cheyne-Stokes
Breathing-Central
Sleep Apnea
Cheyne-Stokes Breathing-Central Sleep Apnea (CSB-CSA) is a
condition associated with waxing and waning respiration
during sleep, with periods of central apnea, or cessation of
breathing. Periodic breathing is a term that denotes waxing and
waning patterns of tidal volume with hypopneas, rather than
apneas. Estimates of the prevalence of CSB-CSA among
patients with systolic HF have generally ranged from 27 to
63%.
1-5
However, more recently, Ferrier and colleagues
6
reported a rate of 15% in stable systolic HF patients managed
in a HF disease-management program. Redeker and
colleagues
7
found a rate of 9% in mixed systolic and diastolic
patients. Similarly, Rao et al.
8
found a rate of sleep-disordered
breathing of 27% in stable HF patients, but did not differentiate
between Cheyne-Stokes Breathing and obstructive apnea.
Variability in rates may be due to differences in demographic
characteristics (e.g., gender, age), the clinical characteristics of
the patients studied (e.g., ejection fraction and medications),
estimation of rates in patients referred to sleep clinics vs. the
general population of HF patients (referral bias) and sensors
and criteria used to evaluate sleep disordered breathing. Given
the fact that the studies showing reduced prevalence of CSB-
CSA are more recent, these differences may reflect changes in
treatment patterns favoring improvement.
Risk factors for CSB-CSA appear to be male gender,
hypocapnea, and atrial fibrillation,
2
but low ejection fraction has
also been implicated.
9
Differences in prevalence may also
reflect changes in treatment, as Cheyne-Stokes Breathing is
associated with changes in fluid congestion, and recent
evidence suggests that use of beta blockers may decrease
it.
1
0
These findings suggest that current evidence-based
approaches to managing HF may decrease rates of CSB-CSA,
although further research is needed to support this inference.
CSB-CSA may confer higher risk for ventricular tachycardia,
1
and some research has indicated that it contributed to
mortality, especially in men.
11-13
Others found no difference in
one or two-year survival
14
or at 52-month follow-up.
15
It is
possible that the higher levels of mortality associated with
CSA-CSB found in some studies may reflect the greater
association of poor cardiac status with CSB-CSA.
12
CSB-CSA is a respiratory abnormality that results from
increased ventricular filling pressure, pulmonary congestion,
and hyperventilation due to vagal stimulation of pulmonary
irritant receptors, and factors in HF pathophysiology.
Hyperventilation secondary to these abnormalities leads to
reductions in PaC0
2
, which, in turn, contribute to central
apneas due to the loss of the respiratory stimulus of C0
2
. Low
cardiac output and prolonged circulation time contribute to the
waxing-waning pattern of CSB-CSA. CSB-CSA results in
intermittent hypoxia, frequent arousals, sympathetic nervous
system activation, and surges in blood pressure and heart rate.
These cardiovascular alterations may, in turn, exacerbate the
pathophysiologic processes associated with HF.
16,17
The
cardiorespiratory changes result in frequent brief arousals
during lighter states of sleep that prevent its progression into
deeper stages.
Sleep deprivation resulting from CSB-CSA may have functional
and quality-of-life consequences, such as excessive daytime
sleepiness (EDS), poor cognitive function, disturbed mood,
poor functional performance and self-care deficits, although
research findings are somewhat conflicting.
1
8
Forty-four
percent of systolic HF patients had EDS, compared with 18% of
a comparison group who did not have HF.
19
In contrast, groups
of HF patients were no sleepier, as evaluated by self-report
than community residing adults, but were sleepier when
evaluated with objective tests.
20
Recent evidence suggests that
SDB did not confer additional risk of EDS in HF patients.
21, 22
HF
patients are at risk for poor cognitive function,
23
and sleep
deprivation may worsen it, yet cognitive function was not
associated with CSB-CSA.
24
Some researchers have found that
CSB-CSA was associated with poor New York Heart functional
classification, decreased six-minute walk test performance,
and other functional consequences,
5, 20, 25, 26
while others found
no associations of SDB with self-reported physical function,
21, 22
fatigue,
21
or the six-minute walk test.
27
Although the
relationships between SDB and symptom and functional
consequences are not clear-cut, there is sufficient evidence
suggesting that the potential functional and quality-of-life
consequences should be considered in clinical evaluation of HF
patients. Riegel and colleagues
28, 29
found that excessive
sleepiness in people with HF contributed to decrements in self-
care. Therefore, HF may have an impact on the self-care/self-
management of people with HF. These issues are discussed in
detail in a forthcoming paper.
18
Obstructive Apnea
Hypopnea Syndrome
(OSAHS)
OSAHS is a respiratory disturbance that results from repetitive
intermittent,partial or complete obstruction of the upper airway
during sleep. It is defined as upper airway instability that is
associated with snoring, reduction in airflow (hypopnea) or
complete cessation of airflow (apnea).
30
Like CSB-CSA, it is
associated with excessive daytime somnolence because of the
frequent brief arousals from sleep. These respiratory events
vary in frequency and may include a combination of events.
Nocturnal oxygen desaturation also frequently accompanies
the respiratory events. Persons with OSAHS may report
gasping or snorting during sleep, waking with a dry mouth
and/or headache. Bed partners may observe apneic events.
Epidemiological data suggest that OSAHS occurs in four
percent of the American middle-aged adult population.
31
However, it is believed that OSAHS is under-diagnosed.
Estimates of prevalence vary based on measurement and
cut-off scores on diagnostic criteria. Studies of HF patients
suggest that OSAHS occurs in 11-53% of systolic and mixed
groups of people with class II-IV HF.
1, 6, 32
OSAHS appears to be
the most prevalent form of sleep-disordered breathing among
diastolic HF patients, occurring in 55%,
33
although data are
sparse. Chan and colleagues
33
found that more severe sleep-
disordered breathing was associated with poor diastolic
function. Unlike CSB-CSA which is thought to be a
consequence of HF, OSAHS may be one of the pathways to HF
through its contributions to hypertension.
There is a growing body of epidemiological and clinical
research evidence for a link between OSAHS and hypertension,
cardiovascular morbidity and mortality. However, a causal
relationship has not yet been identified. Two large-scale studies
provide the most powerful epidemiological evidence to date for
the linkage between OSAHS and cardiovascular morbidity and
mortality. Researchers for the Wisconsin Sleep Cohort Study
34
found that there was a linear increase in blood pressure as the
apnea-hypopnea index (AHI – total number of apneas and
hypopneas/hour) increased in a sample of 1,060 employed
men and women between the ages of 30 and 60 years.
Longitudinal follow-up of 760 of these participants
demonstrated that there was a dose-response relationship
between sleep disordered breathing at baseline and the
development of hypertension four years later.
3
5
The Sleep Heart Health Study (SHHS) is a large multi-center
community-based, prospective study designed to evaluate the
link between OSAHS and cardiovascular morbidity and
mortality. Data obtained from
6, 132
middle-aged men and women
revealed that mean systolic and diastolic blood pressure and
prevalence of hypertension increased significantly at higher
levels of the apnea-hypopnea index. The odds ratio for
hypertension, comparing the highest AHI level (>30/hour),
compared with the lowest (< 1.5/hour) was 1.37 (confidence
interval = 1.03—1.83, p < .005). There was also a statistically
significant relationship between oxygen saturation of less than
90% and hypertension.
36
SHHS participants with higher levels
of the AHI were 2.38 times more likely to have HF than those
with the lowest AHI levels. Although AHI was also associated
with coronary disease, the likelihood of having HF was higher
at the highest levels of AHI.
37
Although these data are not
causal, they strongly implicate sleep-disordered breathing as a
pathway to HF.
The primary pathophysiological explanations for the link
between OSAHS and hypertension include hypoxemia,
increased respiratory effort, and cortical arousal associated
with respiratory events. Patients with OSAHS have higher levels
of sympathetic nervous system activation, as measured by
elevated circulating catecholamines and skeletal muscle
sympathetic nerve activity that may result from obstructive
respiratory events and cortical arousals. These changes may
lead to higher peripheral vascular tone and subsequent
hypertension.
There is evidence that CSB-CSA and OSAHS co-exist among HF
patients and the predominance of either condition may change
over the course of a night. Tkacova and colleagues
38
found
that obstructive apneic events decreased and central apneic
events increased among HF patients with both forms of
sleep-disordered breathing over the course of a night. These
changes appeared to correspond to cardiovascular
deterioration over the course of the night were associated with
increased circulation time and decreasing PC0
2
. The nature of
sleep-disordered breathing may also change between nights,
alternating between primarily obstructive and central apnea.
39
Co-occurrence of OSAHS and CSB-CSA is referred to as
complex sleep-disordered breathing and is associated with
highly unstable sleep and unmasking of CSA-CSB with
CPAP treatment.
40
Clinical Evaluation of
Sleep-Disordered
Breathing
Given the high prevalence of sleep-disordered breathing
among patients with HF, assessment of sleep and sleep
disorders and their consequences should be an important
component of routine clinical care. Non-specific signs and
symptoms associated with both CSB and OSAHS include
excessive daytime sleepiness, cognitive dysfunction, fatigue,
and disturbed mood. Since fatigue and activity intolerance
are almost universal experiences for patients with HF, it
is important to consider the potential contributions of
sleep-disordered breathing to these problems. Excessive
daytime sleepiness presents safety concerns, as it may have a
negative impact on reaction time, decision making, and safe
operation of machinery and motor vehicles. Therefore, patients
who are suspected of being excessively sleepy should be
cautioned about behaviors that may be a safety hazard.
Daytime performance usually improves with effective
treatment of sleep-disordered breathing.
Seventy percent of systolic and diastolic HF patients report
disturbed sleep.
1
9, 41
It is likely that a significant proportion of
this group may have sleep-disordered breathing, given that it is
associated with frequent, brief, nocturnal arousals. However,
disturbed sleep is also characteristic of insomnia, another
common sleep disorder. HF patients also report prolonged sleep
latency (difficult with falling asleep) and early morning
awakenings that may be more characteristic of insomnia.
Therefore, factors other than sleep-disordered breathing that
may contribute to these problems should be addressed. Some
of these may include medications (e.g., diuretics), nocturnal
pain or dyspnea, poor sleep habits that result in sleep
deprivation and environmental factors. Depression and/or
anxiety may also contribute to insomnia.
42
Periodic limb
movement disorder (PLMD) has also been found to be more
common in a small group of male HF patients compared to a
healthy comparison group, and may contribute to sleep
fragmentation,
43
and restless leg syndrome (RLS) is associated
with cardiovascular disease.
44
Therefore, the presence of RLS
periodic limb movements should also be considered.
Both CSB and OSAHS result in apneas during sleep that may be
observed by the bed partner. However, unlike CSB, OSAHS is
usually associated with loud snoring and may be associated
with choking, gagging, or snorting. In the absence of a bed partner,
however, the HF patient may not be aware of these events.
The likelihood of CSB-CSA is thought to be increased in the
presence of low ejection fraction, inadequate HF medication
management, and atrial fibrillation. Obesity, a large neck,
smoking, consumption of alcohol before bedtime, and use of
sedatives that reduce upper airway dilator muscle function
contribute to risk of snoring, apneas and hypopneas. Among HF
patients, obesity was associated with OSAHS in men, while
advanced age was associated with OSAHS in women.
2
Indications for referral of HF patients for specialized sleep
evaluations are the subject of ongoing discussion. However,
patients who snore and demonstrate excessive daytime
sleepiness, or have witnessed apneas should be referred for
polysomnographic evaluations. Those who complain of
frequent nocturnal arousals that are unexplained by
environmental factors, disturbed mood, or nocturnal discomfort
(e.g., pain or nocturia) are also candidates for evaluation in a
sleep laboratory setting. HF patients who have received optimal
medical management and are symptomatic and/or continue to
remodel should also be referred for sleep evaluation.
The gold standard for evaluation of sleep-disordered
breathing is nocturnal polysomnography (NPSG) conducted
in a sleep laboratory. Polysomnography consists of
electro-encephalography, chin electromyelography, and
electro-oculography to evaluate sleep duration, sleep latency,
and sleep stages. Central or obstructive apneas and hypopneas
are diagnosed through measurement of effort (chest and
abdominal expansion), air flow or pressure (thermistor or nasal
cannula), and oxygen saturation (pulse oximetry). Continuous
ECG is also obtained, thereby allowing evaluation of the
association of dysrhythmias with respiratory events. Other
physiological parameters can be measured, such as periodic
limb movements, depending on the purpose of the sleep
study. Excessive daytime sleepiness can be evaluated by
self-report, using such instruments as the Epworth Sleepiness
Scale or a Multiple Sleep Latency Test, an objective measure of
excessive daytime sleepiness.
A clinical PSG report includes information on the duration of
sleep, sleep stages, sleep latency (time from lights out until
sleep onset), and sometimes, an evaluation of the frequency of
brief nocturnal arousals. Essential to the diagnosis of sleep
disordered breathing is the AHI or Respiratory Index (RDI – sum
of the apneas and hypopneas/hour of sleep) and oxygen
saturation. Apneas and hypopneas will also be described as
central or obstructive, depending on their association with
respiratory effort (obstructive apneas are associated with
effort, central apneas and hypopneas are not. ).
There has been great interest in the application of home sleep
studies for the assessment of sleep-disordered breathing,
particularly in settings where PSG is not readily available. Such
monitors fall into the following classifications: 1) devices that
are capable of full portable PSG; 2) devices that permit
modified portable sleep apnea testing (at least 2 channels of
respiratory movement or respiratory movement and airflow,
heart rate or ECG, and oxygen saturation; and 3) devices that
obtain continuous recordings of oxygen saturation or airflow.
These devices may be used in an attended (laboratory) or
unattended (home) setting. An evidence-based review
concluded that their use is not recommended for patients with
HF at this time, as the validation studies have been conducted
primarily on patients without comorbid illness, and these
studies have focused primarily on screening for OSAHS and not
CSB-CSA.
45
Treatment of Sleep-
Disordered Breathing
There is no clear-cut indication for treatment of CSB-CSA, but
treatment should be considered when sleep is fragmented and
non-restorative, there are frequent nocturnal desaturations, or
the patient suffers from excessive daytime sleepiness.
Improvement of cardiac output through optimal medical
management appears to improve CSB. Although there have
been no long-term clinical trials, the application of nocturnal
oxygen has been shown in small studies to reduce nocturnal
periodic breathing. Nocturnal oxygen reduced apneas, periodic
breathing,
4
7
and frequency of oxygen desaturations during
sleep,
4
8
but it did not improve ventricular function or sleep
architecture.
47
Beta blocker drugs also reduce central apneas,
10, 49
but there is some evidence that their use may contribute
to nightmares.
50
Therefore, there may be some negative effects
on sleep.
There have been several recent reports of the promising effects
of Cardiac Resynchronization Therapy (CRT) on ejection
fraction, apnea hypopnea index, oxygen saturation and sleep
quality.
51-53
These effects are thought to be due to the effects of
CRT on circulation time. Therefore CRT may be beneficial in
some patients.
CPAP therapy reduces apneas and hypopneas and improves
nocturnal oxygen saturation and functional performance in
people with CSB-CSA.
54, 55
Its beneficial effects appear to occur
primarily through the improvement of periodic breathing. In a
randomized study of HF patients, with and without periodic
breathing, there were improvements in ejection fraction and
mortality only in those patients who had periodic breathing.
55
However, evidence obtained from the Canadian Positive Airway
Pressure (CANPAP) study,
56
a randomized clinical trial of the
effects of CPAP only on CSB-CSA, demonstrated that there was
no improvement in the treatment group at 18-month follow-up,
despite early trends toward improvement in the treatment
group. Therefore, use of a CPAP device is not currently
recommended for HF patients who have only CSB-CSA,
although these findings have generated a great deal of
controversy.
49, 57
One interesting outcome of the CANPAP trial
was the low accrual of patients, a factor that may be associated
with reduced levels of CSB-CSA with the advent of beta blocker
therapy. It is also important to note that the CANPAP findings
do not apply to HF patients who have OSAHS or complex sleep
disordered breathing, as these patients were not included in
the study.
Treatment of OSAHS is directed at reducing obesity, which is a
primary risk factor, and maintaining a patent airway during
sleep. Nasal Continuous Positive Airway Pressure (NCPAP)
serves as a splint that prevents the collapse and narrowing of
the airway throughout the night. CPAP improves apneas and
hypopneas in HF patients with OSAHS, but data on
cardiovascular outcomes are conflicting.
58
Reducing the use of
alcohol and sedating medications that reduce the function of
the upper airway dilator muscles is beneficial in improving
OSAHS, but little is known about the impact of these strategies
in HF patients. Patients whose OSAHS is more severe in the
supine position may benefit from sleeping in a lateral position.
Dental appliances that cause mandibular advancement and
tongue protrusion are successful about 50% of the time.
Surgical treatments such as laser-assisted uvulopalatoplasty
and reduction of the tongue volume are generally effective in
reducing snoring, but are not as effective as NCPAP or weight
loss in reducing obstructive events. For a detailed, but concise,
description of evaluation and management of the patient with
OSAHS refer to the article by Sanders and Redline.
59
Servo
ventilation is a new form of positive airway pressure therapy
that can be used for patients with periodic breathing or central
apnea. These new devices have been shown to significantly
improve central apnea and periodic breathing when compared
to CPAP, bi-level therapy or oxygen administration.
60, 61
Adherence to NCPAP is a significant concern, particularly since
nightly use for the duration of the sleep period is necessary for
a positive outcome. Patients may experience discomfort due to
the mask and have difficulty tolerating the nightly treatment.
Some patient education is usually provided in the sleep
laboratory at the time of the mask fitting and CPAP titration.
However, patient education and coaching should be continued
in the heart failure clinic. Ongoing evaluation of any problems,
misperceptions, and response to CPAP treatment is critical to
assuring a positive outcome. This may be especially relevant to
HF patients and their caregivers, who must incorporate the
OSAHS treatment into an already complex self-management
regimen. Outcomes assessment should include improvements
in daytime functioning, including mood, cognition, and
sleepiness, as well as self-reports of improved sleep. Despite
growth in knowledge about CPAP adherence over the past
several years, little is known about levels of adherence in these
patients or strategies to enhance it.
There has been exponential growth in the science and the
awareness of heart failure clinicians about the importance of
sleep and sleep disordered breathing over the past several
years. Clearly, evaluation and management of these conditions
needs to be a component of ongoing disease management for
heart failure patients.
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The American Association of Heart Failure Nurses (AAHFN) is pleased to provide you with the opportunity to earn one
free contact hour credit, sponsored by an educational grant from Respironics.
To receive the contact hour credit associated with this program, please follow these instructions:
• Read Sleep-Disordered Breathing in Patients with Heart Failure
• Log onto the American Association of Heart Failure Nurses website: www.aahfn.org
• Click on the Online CE button
• Click on the Post Test for Sleep-Disordered Breathing in Patients with Heart Failure
• Complete the Post Test
• Enter promotion code SDB08
If you successfully answer the questions, you will earn 1 contact hour credit.
You can print your Certificate of Completion immediately upon successful completion of the post test.
There is no charge for this course.
Earn a Free Contact Hour Credit
This program was sponsored by an educational grant
from Respironics, Inc.
Hoech KW 10/xx/08 MCI 4101921 PN 1034064
