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14 Sleep-Disordered Breathing: AnExpanding Spectrum forthePulmonologist
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physiologic responses to the disease including alveolar hypoventilation which is
negatively impacted by sleep in COPD resulting in worsening hypoxemia, reduced
functional residual capacity, increased airway resistance and worsening VQ mismatch. Sleep also results in respiratory muscle hypotonia which gets worse in REM
sleep. There is additionally a reduced respiratory drive during sleep and the upper
airway is narrowed in sleep, all of which promotes negative impact on various
aspects of respiration resulting in hypoxemia and the COPD patient’s respiratory
mechanics and ventilatory control are also disturbed during sleep due to several
factors.
COPD patients are often hypoxemic during wakefulness, and the resting oxygen
saturation levels tend to reside on the steeper portion of the oxygen–hemoglobin
dissociation curve—during sleep, there will have disproportionately greater falls in
oxygen saturation related to respiratory events in the major sleep episode. These
patients desaturate dramatically, as we measured them in polysomnography.
Additionally, they experience further VQ mismatch and reduced functional residual
capacity because of emphysema (absolute loss of alveolar units available for gas
exchange) and because of hyperination of the lungs and subsequent attening of
the diaphragm and that further worsens nocturnal hypoxemia in COPD.
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14.7 Exaggerated Physiologic Hypoventilation
DuetoCentral Respiratory Effects
In normal health the respiratory control system consists of a matrix of central and
peripheral chemoreceptors and central nervous system respiratory rhythm generators interacting continuously in relation to the lung dynamics, chest wall expansion
and arterial gas content to maintain tightly controlled oxygen and carbon dioxide
tightly regulated between a narrow window. The system maintains a negative feedback loop. In wakefulness, normal breathing is impacted by both metabolic and
behavioral stimuli. For instance, exercise-induced metabolic acidosis or diureticinduced metabolic alkalosis alter paCO2 due to altered CO2 production and drive
changes in respiratory rate, tidal volume, and (combined) the work of breathing.
These changes in respiratory rate and effort are in response to feedback from peripheral and central chemoreceptors. Behaviors—stress—which can cause involuntary
breath holding, speech, swallowing (all of which cause voluntary pauses in respiration) also modify respiration.
Sleep eliminates behavioral stimuli, leaving only metabolic stimuli to exert inuence. Thresholds for control of respiration change from waking to sleeping state,
and in fact, in normal healthy individuals with normal sleep parameters, ventilation
become less rigorously controlled, tolerating a physiologic state of relative hypercapnia—in other words, the respiratory control responses to paCO2 during healthy
sleep are blunted to avoid excessive respiratory drive causing EEG arousals and
eventually awakening from sleep.
Also during healthy sleep, in normal individuals, PCO2 becomes the only stimulus driving respiration during sleep—an increase of PCO2 driving respiration, a
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decrease suppressing respiration. If PaCO2 falls below a tightly regulated apneic
threshold, respiration ceases entirely, and a central sleep apnea event prevails continuing until only a sufcient rise in PaCO2 triggers a respiratory effort and resumes
respiration.
COPD patients experience ventilatory control much like other normal individuals and we will return to this in the discussion on central sleep apnea syndrome.
During all stages of sleep the respiratory center signals respiratory drive and
response to chemical, i.e., chemoreceptor inputs which are blunted during sleep and
respiratory muscle responses to the drivers for respiration are also reduced, particularly during REM sleep, exacting a marked impact on COPD patients who may be
reliant on accessory muscles for respiration [11].
During REM sleep healthy individuals experience marked alveolar hypoventilation and ventilation maybe 40% lower than during wakefulness because of reduction in tidal volume and increase in upper airway resistance and reduced inspiratory
drive centers so normal individuals will experience a fall in arterial oxygen saturation during REM sleep. In normal individuals this does not cause physiologic distress. The COPD patient will also experience these changes, but the physiologic
hypoventilation is worsened, resulting in profound hypoxemia and patients—especially if they have respiratory insufciency which is marked—have increased physiologic dead space, worsening of the alveolar hypoventilation with lower-than-normal
tidal volumes during sleep—a perfect storm. The COPD patient therefore is already
very vulnerable during sleep and vulnerable to a rise in CO2 and falls in oxygen
before any comorbid obstructive sleep apnea syndrome is considered.
Additionally, these patients experience much more light sleep stage N1 and light
sleep stage N2, much more stage shifting—meaning that the sleep is markedly less
consolidated than normal, and they tend to have more nocturnal awakenings and
greater sleep fragmentation. If they do have comorbid obstructive sleep apnea syndrome it will be markedly worse during REM sleep, and therefore, the REM sleep
also tends to be fractured interrupted and decient.
Q. A. A. Ahmed
14.8 Altered Airway Resistance andRespiratory
Muscle Contractility
In normal sleep, upper airway resistance is increased compared to during wakefulness. This is related to the loss of muscle tone in the upper pharyngeal muscles and
changes in the ventilator responses to hypoxemia and hypercapnia and probably
contributes to hypoventilation. These changes also occur in COPD patients but the
compensatory dilatory response of supraglottic airways which results in increases in
CO2 tension is signicantly lower. COPD patients who lack the ability to respond
properly to the lowering of the upper airway resistance that can make nighttime or
sleep-related hypercapnia and hypoxemia worse are more compromised in sleep
and will experience more work of breathing and more sleep-disordered breathing.
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Additionally, because of circadian changes in airway dimensions which are normal,
bronchoconstriction can become more exaggerated in the COPD patient, further
worsening airway resistance in the lower areas of the tracheobronchial tree.
Clinically signicant bronchospasm ensues.
The sleeping state is also associated with hypertonia of skeletal muscle including
the tongue, the pharynx, the larynx, and the intercostal muscles. There is a change
in the relative contribution of the thoracic cage and the abdominal compartment to
breathing and during REM sleep where we see muscle atonia in all striated muscle
there is marked loss of tonic activity in the intercostal muscles which are imperative
in the COPD patient dependent on accessory musculature for work of breathing.
This loss of muscle tone is related to a supraspinal inhibition of gammon motor
neurons and also some alpha motor neurons and additionally some presynaptic inhibition of afferent terminals from muscle spindles. Contrast this with the diaphragm
that is driven almost entirely by alpha motoneurons and has many fewer spindles,
and the intercostal muscles have little tonic or postural activity and thus escape the
reduction of this kind of drive during REM sleep which is fortunate, allowing the
primary muscle of respiration to continue functioning during the most perilous
stage of sleep.
As the COPD patient enters REM sleep and loses or has a reduced accessory
respiratory muscle activity, hypoventilation which is normal in healthy sleep,
becomes markedly worse and especially so in the COPD patient who is very reliant
on accessory muscle activity to maintain ventilation. This patient will develop CO2
elevation, i.e., ventilatory failure during sleep.
In the advanced COPD patient with a diaphragm stretched related to lung hyperination, the diaphragm is less efcient at contracting and that will make the thoracic cage more reliant on accessory muscle contribution to breathing. Advanced
COPD is associated with sarcopenia, skeletal muscle atrophy and dysfunction worsening the contribution of accessory muscles. Sleeping in the supine position or
semirecumbent position further worsens diaphragmatic efciency because abdominal contents counteract diaphragmatic contraction and with all of the muscles of
respiration quiescent during REM sleep except the primary muscle of respiration
the diaphragm that becomes so compromising to the COPD patient, we can expect
to see paradoxical breathing and further hypoventilation. The COPD patient with
advanced disease thus sleeps very poorly and will demonstrate profound sleep
maintenance insomnia and daytime sleepiness.
If we now consider respiratory mechanics during sleep and COPD, as COPD
progresses in severity, the mismatch between VQ relationships also worsens—the
result of progressive airow limitation and escalating emphysematous destruction
of the pulmonary vascular bed which limits to the ability for gas exchange. A small
but signicant reduction in functional residual capacity also occurs during sleep
related to the reduction in tonic muscle activity we described above and increase in
airway resistance will make the VQ relationships worse in dependent lung zones
while the patient is lying down, when small airways will become further closed and
worsen gas exchange and ventilation relationships even more.
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Q. A. A. Ahmed
14.9 Sleep intheCOPD Patient
Sleep quality is frequently impaired in these patients and contributes signicantly to
reports of daytime fatigue daytime sleepiness and reduction in quality of life is been
reported by these patients when surveyed. Most COPD patients report disturbed
sleep and report their COPD symptoms also disturbing their sleep. COPD patients
report insomnia sleep onset insomnia, sleep maintenance insomnia nonrestorative
sleep and increased reliance on hypnotic medications that themselves can sometimes suppress respiration. These patients been found to be sleepier than average in
the daytime and furthermore the pulmonary symptoms in the form of nocturnal
cough, nocturnal wheezing, also contribute to sleep fragmentation and sleep maintenance insomnia. As COPD becomes more severe sleep complaints escalate and
will have profound pathophysiologic effects.
These patients tend to have very fragmented interrupted sleep with frequent
arousals and awakenings reduced stage III sleep and reduced REM sleep. It has
been reported that there is an association between degree of hyperination and
reduction in sleep efciency in patients with overlap syndrome independent of any
coexisting obstructive sleep apnea or disease severity of any coexisting obstructive
sleep apnea.
Quality of sleep in the COPD patients is not improved by adding supplemental
oxygen and it is believed that higher levels of hypercarbia during sleep, i.e., nocturnal
hypercapnia related to the alveolar hypoventilation that gets worse in these patients
during sleep is a much stronger stimulant in provoking EEG arousals and awakenings.
Also, because of the increased work of breathing related to the disadvantageous
mechanics of the chest during sleep in the COPD patient, results in stimulation of
mechanoreceptors in the chest wall and lower airways also fragmenting sleep.
This patient is often on medications including bronchodilators and medications
like theophylline that can cause tachycardia and insomnia themselves. Cigarette
smoke exposure results in EEG arousal in the active smoker COPD patient and even
in those exposed to passive smoke including newborns were exposed to passive
cigarette smoke develop insomnia. If the COPD patient has discontinued smoking,
withdrawal from nicotine can also result in frequent EEG arousals, predominance of
stage I sleep and a sensation of nonrestorative sleep.
Even though COPD is so well known, well recognized, readily diagnosed and has
many treatment strategies, most pulmonologist are not considering the impact of sleep
on the COPD patient and the impact of COPD on the sleep of the patient nor other
considering comorbid obstructive sleep apnea in these patients. This is where pulmonologists with sleep medicine expertise can have an enormous impact [12].
14.10 Sleep inPulmonary Overlap Syndromes (OVS)
Over 30years ago, recognizing patients who have both had COPD and obstructive
sleep apnea syndrome, David Flenley coined the term Overlap Syndrome. The term
“pulmonary overlap syndrome” was rst used in reference to only patients with
comorbid COPD and obstructive sleep apnea syndrome, though now the denition
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is extended to patients with comorbid obstructive sleep apnea syndrome and other
chronic lung diseases including interstitial lung disease. A distinct denition
remains lacking and the patient population with OVS remains diverse encompassing both chronic lung disease and obstructive sleep apnea syndrome of any severity,
both of which span a broad spectrum. The current denitions of obstructive sleep
apnea syndrome may be insufciently rigorous for assessing obstructive sleep
apnea in the setting of chronic hypoxemic lung disease particularly as obstructive
sleep apnea syndrome is dened by specic desaturation criteria and distinguishing
hypoxemia due to chronic lung disease from concurrent sleep-disordered breathing
event may be difcult [13].
Basic interactions between COPD and OSAS are not completely understood
including, for example, the full spectrum of effects of COPD on upper airway
collapsibility.
Even so, the commonest diseases presenting in the ofce of the pulmonologist
will be COPD, asthma, and obstructive sleep apnea syndrome and many of these
patients will have coexisting disease.
Nocturnal hypoxemia is one of the most distinctive and important abnormalities
measured in both COPD and obstructive sleep apnea syndrome. The overlap syndrome patient will have marked worsening of nocturnal hypoxemia than patients
who have either one or other of the disease alone. It is the nocturnal hypoxemia that
drives sympathetic nervous system activation which is the pathognomonic hallmark
of sleep-disordered breathing and drives systemic and pulmonary increases in blood
pressure, drives arrhythmias, and increases reactive oxygen species production and
many other negative sequelae.
One of the profound frustrations of the sleep specialist is trying to quantify disease severity using the apnea-hypopnea index which would not necessarily account
for the severity of desaturations seen in these patients even if events are rare.
Fortunately investigators are searching for other surrogates to compensate for the
known pitfalls of the AHI but until then we must consider the entire clinical picture.
In patients with the overlap syndrome AHI use is a surrogate for obstructive sleep
apnea syndrome severity seems to play a small role in the development of pulmonary hypertension compared to the extent of the severity of the COPD.Daytime
hypoxemia hypercarbia and reduction in obstructive lung function will be more
likely to be predictors of right heart failure and severity of AHI) This also related to
the failure of AHI to distinguish longer duration events from shorter duration events,
to provide equal weighting to apneas and hypopneas—probably not physiologically
equivalent, and failure to distinguish hypoxic from nonhypoxic events.
While management of obstructive sleep apnea syndrome is recognized and discussed elsewhere in this book it is imperative to raise awareness of sleep-disordered
breathing in these pulmonary patients who are already so compromised in pulmonary function. Overlap COPD patients who have obstructive sleep apnea carry
greater mortality and obstructive sleep apnea syndrome patients who had coexistent
COPD were also at an increased risk of death. Even when adjusting for disease
severity of COPD presence of obstructive sleep apnea increases risk of death. Data
showed that treatment with continuous positive airway pressure in this patient population reduces the added mortality risk and confers a survival benet.
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It is very important to diagnose obstructive sleep apnea in this compromised
patient population with irreversibly progressive disease who are living with an
entirely treatable sleep disorder. Treating the sleep disorder could have a signicant
impact on the overall survival and quality of life.
While optimization of the underlying lung disease is the rst step in treating
these patients, rapid diagnosis and an implemented management plan for underlying obstructive sleep apnea discovered in this patient is paramount.
Oxygen therapy may be indicated in these profoundly hypoxemic patients, but
care must be taken that correction of hypoxemia does not worsen hypercarbia—in
some patients, the primary respiratory drive may in fact depend on hypoxemia,
removed by supplemental oxygen. This means that supplemental oxygen should be
carefully adjusted with the lowest amount of supplemental oxygen needed to avoid
CO2 narcosis and our preference in our practice is to always achieve airway patency
with positive airway pressure in the sleep center in the obstructive sleep apnea syndrome patient before resorting to supplemental oxygen if possible. We also recommend optimization of body mass and positional therapy in addition [14].
Careful review of the patient’s pharmacologic therapy of COPD should be considered to minimize the effect of steroids and bronchodilators and nebulizers on
promoting insomnia including timing of these agents where possible away from
bedtime and to optimize control of the obstructive lung disease to minimize interference with sleep.
Certainly, these patients will often request medications to promote sleep and
there may be a role for benzodiazepine and nonbenzodiazepine hypnotics which
facilitate sleep onset short sleep latency improve sleep efciency reduced EEG
arousal capability and may provide some benet, but I would be very reluctant to
commence these until any sleep-disordered breathing has been fully treated with
positive airway pressure and even then for as limited a dose and duration as possible. These patients may benet from cognitive behavioral therapy for insomnia
while they are awaiting to adjust to positive airway pressure for obstructive sleep
apnea syndrome before considering any pharmacotherapy. For the more severe
COPD patients, benzodiazepine and nonbenzodiazepine hypnotics may be out of
the question because of the degree of respiratory depression they may produce [15].
While there are separate indications for noninvasive positive pressure ventilation
in the patient with COPD and marked respiratory insufciency in our practice, we
are very aggressive with treating even mild sleep-disordered breathing with positive
airway pressure or mandibular advancement therapy because of the benets of treating obstructive sleep apnea in this patient population.
Also it has been shown that there are improvements in long-term nocturnal noninvasive positive pressure ventilation in COPD patients with hypercapnia respiratory failure including improvements in respiratory muscle strength and endurance,
sleep quality, daytime oxygen and nighttime oxygen levels and daytime PCO2 and
PCO2 levels at nighttime and these improvements are more marked with noninvasive positive pressure ventilation and now with supplemental oxygen probably
because of a resetting and resting of chronically fatigued respiratory muscles that
may rejuvenate and perform better in the daytime and reversal of micro atelectasis
14 Sleep-Disordered Breathing: AnExpanding Spectrum forthePulmonologist
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by lung expansion, positive pressure ventilation and of course maintaining airway
patency during sleep which also reduces work of breathing.
For this reason overlap syndrome patients benet from nocturnal positive airway
pressure and distinctions must be made as to what is best for the patient based on the
coexisting sleep-disordered breathing, whether they need CPAP or bilevel positive
airway pressure and still may still need some supplemental oxygen in addition after
which hypnotics may also be required in low dose.
Bilevel positive airway pressure may have a particular role to allow reduction in
expiratory pressures and make positive air pressure more comfortable in this patient
population. Therapeutic goals for these patients are undened. Most practitioners
seek to eliminate sleep-disordered breathing both by objective criteria as well as by
patient-dened outcomes of sleep satisfaction and improved quality of life much the
same as we seek in other patient populations [16].
While patients with severe COPD may benet from treatment with bilevel positive airway pressure due to improvement in nocturnal ventilation, for other patients
conventional treatment with CPAP maybe adequate. Nonetheless despite these
unknowns, it is important to recognize patterns of sleep and sleep disorders in this
patient population which will be readily encountered in any sleep disorders medicine practice due to the widespread prevalence of both obstructive sleep apnea and
COPD [17].
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14.11 Sleep andInterstitial Lung Disease
Interstitial lung disease (ILD) includes a diverse array of lung disorders characterized by restrictive lung physiology. ILDs include idiopathic pulmonary brosis sarcoidosis autoimmune-related pulmonary disorders such as systemic sclerosis and
hypersensitivity pneumonitis or restrictive lung disease following drug exposure
such as amiodarone. Sleep has been most widely examined among these conditions
in the setting of idiopathic pulmonary brosis (IPF) [18].
14.12 Sleep andIPF (Idiopathic Pulmonary Fibrosis)
IPF is, by denition, without known cause, characterized by a chronic and unremitting course with episodes of relapses—acute exacerbations and associated acute
decline in lung function interspersed with periods of stability. It is the most common
cause of Usual Interstitial Pneumonitis. Prognosis tends to be very poor, and physicians typically have focused on ameliorating only the most disabling symptoms.
Histologically these patients are dened by ndings of usual interstitial pneumonitis (UIP). Unlike COPD, IPF is relatively uncommon, rendering investigation of
sleep and sleep disorders more difcult but recently there is an interest in examining
sleep as a potential for modifying disease outcomes [19].
Patients with IPF report impaired sleep quality, excessive daytime sleepiness,
increased sleep maintenance insomnia, reduced sleep efciency, reduced total sleep
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time and reduced REM sleep percentages. Worsening of hypoxemia is seen during
sleep especially during REM sleep and there is evidence of an increased prevalence
of obstructive sleep apnea syndrome in these patients. Sleep-disordered breathing is
found to be extremely prevalent in the IPF patient population—reports range from
more than two thirds of all patients to over 90% of patients studied.
Treatment of obstructive sleep apnea syndrome can certainly improve quality of
life and perhaps disease outcome.
Nocturnal cough maybe a prime contributor to sleep disruption as well as the
impact of medications including corticosteroids which are well known to cause
insomnia. Comorbid depression and other affective disorders are commonly seen in
the IPF patient which further impacts sleep and increases likelihood of insomnia.
Medications used to treat these comorbid affective disorders may further impact
daytime function and increase daytime sleepiness.
Patients are noted to have nocturnal tachypnea in IPF compared to normal controls. Nocturnal desaturations during sleep can be more severe than the desaturations seen during exercise suggesting that sleep is a major stressor to the IPF patient.
If challenged with obstructive sleep apnea syndrome in addition, sleep in the IPF
patient can become severely disrupted.
Treatment goals remain the same as treatment of other patients with obstructive
sleep apnea and improving sleep quality in these patients offers a chance to reduce
morbidity for patients with a poor long-term prognosis and escalating short term
morbidities.
Q. A. A. Ahmed
14.13 Critically Important thePulmonologist Does Not
Overlook Central Sleep Apnea Syndrome
Because of the societies where we practice in the developed world, our patients are
very likely to have comorbid non communicable diseases in the setting of sleep
disorders presenting to the pulmonologist sleep specialist.
Seventy percent of all cardiac patients will have a form of sleep-disordered
breathing [20]. Increasingly we recognize the impact of sleep-disordered breathing
on diseases our cardiology colleagues treat, including arrhythmias, coronary artery
disease myocardial infarction and congestive heart failure. There is growing awareness of the sleep-disordered breathing in the congestive heart failure patient who
remains unrecognized in the pulmonologist ofce even though they frequently
come in for dyspnea, snoring and disrupted sleep. Among these patients, the central
sleep apnea patient is the least recognized most often misdiagnosed and mistreated
by sleep specialists.
Though the New England Journal editorialized [21] over 15years ago that sleep
medicine represented the “new cardiovascular frontier,” recognition of sleepdisordered breathing in the cardiac patient remains lacking—patients often presenting to the sleep specialist years or decades after established heart disease and
irreversible loss of cardiac function all too often caused in part by the detrimental
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pathophysiology of decades of increased sympathetic nervous system tone caused
by repetitive desaturations and reoxygenation during sleep which results in pro
inammatory stressors, arrhythmias, cardiovascular remodeling and long term morbidities. As their pulmonologists we can have an enormous impact on their cardiovascular outcomes.
Despite the high prevalence of chronic congestive heart failure patients with central sleep apnea syndromes, these patients in particular remain an under recognized,
neglected patient population in terms of their sleep disorders, sleep dissatisfaction
and the impact of their sleep on their global function.
A separate entity, central sleep apnea syndrome, is both highly prevalent and
much neglected in the congestive heart failure patient. The heart failure patient may
often demonstrate, obstructive sleep apnea syndrome with or without central sleep
apnea syndrome in the setting of additional sleep-disordered breathing phenomena
including Periodic Breathing also known as Hunter–Cheyne–Stokes respiration
(CSR) [22] describing crescendo decrescendo changes in tidal volume is highly
prevalent in patients with heart failure. Generally speaking, individual heart failure
patients may demonstrate predominantly either obstructive sleep apnea syndrome
or central sleep apnea syndrome, but it is not uncommon for the two forms to coexist. These patients are among the most complex sleep-disordered patients a sleep
specialist will encounter. They are also the most difcult to treat which may be
partly why they are less often successfully managed and remain poorly understood.
The identication of central sleep apnea is very important in patients with cardiac disease. Central sleep apnea can only be diagnosed on polysomnography by a
sleep disorders specialist familiar with the distinctive events dened as absence of
airow in the setting of absent respiratory effort seen on chest and abdominal leads.
Usually left as an exception instead of a rule, it has been a diagnosis typically made
it is so pronounced it cannot be ignored. However, with new therapies which either
can only treat central sleep apnea (phrenic nerve stimulation) or cannot treat CSA at
all (hypoglossal neurostimulation and dental appliances), clarifying when each
form of sleep-disordered breathing—separating obstructive sleep apnea from central sleep apnea—has now become crucial.
While AHI has been shown to be very reproducible between technicians at 88%
[23], even central and obstructive apneas can be misclassied with central apneas
misclassied 52% of the time. If the effort belts are not appropriately tightened,
events may appear central when they are in fact obstructive in nature. Conversely, in
severe heart failure, central apneas may look obstructive due to “cardiac noise” on
the thoracic belt which may mimic respiratory effort. By increasing the amplitude
of the channel, it becomes clear that the rate is much faster than a breath and the
event can still be considered a central apnea.
Even more difcult than central apneas is the controversial area of central hypopnea classication. Whether 3% or 4% desaturation cutoff is used, distinguishing
central apneas versus central hypopneas remains difcult [24]. Until now all hypopneas in my sleep center had been automatically classied as obstructive. I am now
teaching my sleep center the distinctions. The gold standard is to place an
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esophageal probe to determine negative inspiratory esophageal pressure changes
measured in mmHg, but this is not practical in the clinical setting and used only in
the research setting.
Currently, there are at least two different ways to classify obstructive versus central hypopneas [24], and the agreement with gold-standard studies is under 70% for
both methods. The answer to this variability may come from a standardized approach
in augmenting scoring. Articial intelligence may be able to complement scoring of
events with consistency, even though it is doubtful that the time would come when
studies could be scored without oversight by technologists and clinicians skilled in
sleep medicine [25].
Nonetheless, once the sleep specialist begins to become committed to evaluating
sleep-disordered breathing in the cardiac population, central sleep apnea will inevitably present. Between 25% and 40% of patients with chronic HF have central sleep
apnea (CSA) [26]. Moreover, although CSA syndrome is more common in patients
with HF and reduced ejection fraction. CSA is also diagnosed in patients with HF
and preserved ejection fraction. Patients with HF and CSA experience poor quality
of life due to an array of troublesome symptoms including but not limited to sleep
onset insomnia—often caused by sleep onset central apnea—sleep maintenance
insomnia, nonrestorative sleep, nocturia which disrupts sleep, nocturnal enuresis
particularly related to diuretic medication and tremendous daytime impact of the
severe sleep fragmentation resulting from all the above.
These patients develop erratic sleep–wake patterns, profound daytime hypersomnolence, circadian rhythm disorders related to the impaired sleep hygiene from
daytime sleepiness, additional insomnia resulting from daytime napping. Their
sleep remains non refreshing so despite the daytime naps patients report sleep dissatisfaction, unremitting fatigue reduced energy and signicant social isolation
leading to depression.
Nocturnal sleep disruption can be so signicant to become a precipitant for institutionalization due to the severe burden of the sleep disorder falling on the primary
caregiver. The fragmented sleep drives increased sympathetic nervous system tone
which spills over into wakefulness and leads to increased arrhythmias, cardiovascular morbidity including poorly controlled hypertension, ischemic events including
unstable angina, worsening of congestive heart failure and eventually paroxysmal
nocturnal dyspnea, nocturnal angina, and impaired cognitive function. These symptoms adversely impact quality of life, patient outcomes, and portend a poor
prognosis.
While objective measures of an improved apnea hypopnea index, respiratory
distress index or improved central sleep apnea index dene outcomes and guide
conventional treatment with CPAP, BiLevel PAP, or Adaptive ServoVentilation
modes of PAP, truly successful management of sleep disorders focuses greatly on
resolution of the daytime or waking impact of the underlying sleep disorder and
restoration of function in activities of daily living as assessed by the patients subjective measures of sleepiness, sleep quality and functional quality of life. Resolution
of insomnia is also critical to patient sleep satisfaction and well-being and additionally has a major impact on the primary caregiver.
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