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14 Sleep-Disordered Breathing: AnExpanding Spectrum forthePulmonologist
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Sleep specialists agree the clinical treatment of CSA primarily focuses on management of the underlying primary disease process—usually Congestive Heart
Failure (CHF) but also underlying stroke, or opiate use, followed by the management of CSA-related symptoms, chiey the sleep impact.
Symptoms may also be attributed to complications of medications—for instance
diuretics causing nocturia and nighttime awakenings, or beta blockage causing
insomnia and nightmares—rather than considering a primary sleep disorder driving
the sleep fragmentation.
It is important to understand the complex pathophysiology underpinning central
sleep apnea syndrome though mechanisms remain incompletely understood. A signicant burden of data indicates that an exaggerated respiratory control response to
changes in the arterial tension of carbon dioxide (PaCO2) above and below a central
sleep apnea threshold is central to the pathogenesis of CSA syndrome.
We discussed normal ventilatory responses and sleep above. In the heart failure
patient signicant respiratory instability results from change in three driving forces:
hyperventilation; delayed circulation time; cerebrovascular reactivity. Normal
breathing is thus destabilized leading to respiratory instability and wide swings of
central sleep apneas and recovery hyperpneas. Both exert dramatic impact on sleep
architecture and result in a distinctive oscillation pattern in respiration described as
periodic breathing or Hunter–Cheyne–Stokes respiration.
Heart Failure patients chronically hyperventilate in wake and sleep thought to be
related to pulmonary congestion worsened in supine position when excessive uid
is displaced rostrally from the lower extremities to the thorax activating pulmonary
stretch receptors that stimulate ventilation raising respiratory rate. The underlying
cardiac dysfunction causes an exaggerated response to the prevailing lower PaCO2
(lowered by the increase in ventilation) and resets the apnea threshold driving central apneas which then eventually result in climbing PaCO2 levels and then triggers
an exaggerated respiratory drive to escalate ventilation and further lower the PaCO2
and the cycle of central apnea and hyperventilation begins once again. Matters are
worsened by the sluggish circulatory time in the heart failure patient delaying the
detection of circulating arterial blood gas tensions and leading to delayed intervention by the peripheral and central chemoreceptors.
Finally changes in the PaCO2 are critical to regulating cerebral blood ow otherwise known as cerebrovascular reactivity. In the heart failure patient’s brain, the
response to PaCO2 changes is also diminished compounding the respiratory instability further. Because of an impaired buffering mechanism to absorb excess hydrogen ions centrally, PaCO2 levels are more increased during hypercapnia and the
central respiratory control center cannot dampen ventilatory overshoots resulting in
severe hyperpnea or ventilatory undershoots leading to prolonged central apneas.
The respiratory oscillation of the CSA cycle is therefore destined to be perpetuated;
the patient permanently predisposed to have severe breathing instabilities during sleep.
As part of the respiratory control center seeking to control PaCO2 levels regulated, central respiratory control centers send signals to the diaphragm via the right
and left phrenic nerves each of which controls right and left hemidiaphragm
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Q. A. A. Ahmed
muscles. These signals control the contraction of the diaphragm, the largest and
primary inspiratory muscle of respiration engaged in the work of breathing.
Inspiratory muscle dysfunction is occurring during healthy ageing and this decline
in function is heightened in the heart failure population.
Inspiratory muscle dysfunction contributes to several aspects of both heart failure and pulmonary pathophysiology which includes a reduced ability to clear the
upper airway, a predisposition thus for pneumonia, reduced ability to sustain ventilation and gas exchange during exercise and thus reduced exercise tolerance, a propensity for alveolar hypoventilation due to shallow rapid breaths which again limits
ventilation and profound sympathetic nervous system activation which causes cardiac arrhythmias and tissue.
The neuromuscular integrity of the prime muscle of respiration—the diaphragm is the main determinant of the adequacy of respiration and being the prime muscle
for respiration during sleep its function becomes even more critical when accessory
muscles of respiration are quiescent, or in dream sleep, paralyzed. Changes with
both age and heart failure alter phrenic nerve function and neuromuscular junctions
consistent with neurodegeneration and denervation impacting the diaphragm as
well as intrinsic myocyte dysfunction including changes in contractile proteins,
accelerated muscle ber atrophy and changes in muscle ber distribution. Recent
investigations show that the heart failure patient may have intrinsically weakened
diaphragmatic muscles, and this may represent a marker for disease severity and
reduced exercise tolerance. We also see similar atrophy of the diaphragm in
advanced and chronic lung disease causing hyperination.
Many sleep specialists working in the pulmonary population do indeed recognize central sleep apnea syndrome [27] though I have found it depends very much
on the sophistication of the sleep center and the education of sleep technicians and
sleep physician scoring and interpreting sleep studies but assuming it is recognized
the treatments thus far have not been particularly satisfying for either the central
sleep apnea patient or the treating sleep specialist.
Limited indicated therapeutic options exist for patients with CSA, especially
patients with HF with all therapeutic options leading to most often only partial control of central sleep apnea events signicant challenges with compliance with an
array of positive airway pressure devices including CPAP, Bilevel PAP, and ASV
PAP devices—when they are not contraindicated by severity of lowered ejection
fraction below 45%. Often the heart failure patient identied to have central sleep
apnea syndrome has had numerous labor intensive and costly level I attended diagnostic polysomnography and numerous Level I attended in laboratory titration studies before treatment is commenced and numerous and protracted follow up
subsequently often without yielding end point measures of success in terms of normalization of respiratory indices or subjective improvement in quality of life.
Transvenous phrenic nerve stimulation (TPNS) is a unique physiological
approach to the treatment of CSA.The Remedē® System (ZOLL Respicardia, Inc.,
Minnetonka, MN, USA) [28] unilaterally stimulates one phrenic nerve to cause
hemi-diaphragmatic contraction resulting in diaphragmatic movement similar to
normal breathing, restoring inspiratory effort, terminating a central apnea and thus
14 Sleep-Disordered Breathing: AnExpanding Spectrum forthePulmonologist
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stabilizes the carbon dioxide level. Often with the stimulation of one hemidiaphragm by the Remedē® System (ZOLL Respicardia, Inc., Minnetonka, MN, USA)
the other hemidiaphragm becomes synchronously recruited into simultaneous contraction even though the phrenic nerve supply it is not stimulated by the device.
In this patient population namely their fatigue, daytime sleepiness, reduced daytime energy, nocturia, reduced exercise tolerance, isolation and social withdrawal
and interrupted sleep are the hallmarks of living with heart failure across disease
severity classication even when fully treated with tier one standard care in the rst
world (Figs.14.1, 14.2, and 14.3).
While focus on measured outcomes in the heart failure patient is commonly followed, ejection fraction, control of arrhythmias, end organ function and its correlates (kidney function, cerebral function), quality of life, and, specically, impacts
on sleep and related sleep dissatisfaction are all too often overlooked. This neglect
is often carried over into the sleep center where expertise in central sleep apnea is
often deeply lacking both in the recognition of the patient candidate and the disease
state but also the investigation, diagnosis, and treatment of this uniquely challenging sleep disorder patient population.
Today estimates project over 64.3 million people living with heart failure worldwide [29]. This number is growing amid younger age groups and there is a trend to
earlier recognition leading to increasing prevalence of HF with preserved EF.Also
worth noting is the devastating impact of the SARS COV-2 Covid 19 pandemic
which is already resulting in increased cardiovascular morbidity including heart
failure in survivors of the infection and the population at risk for CSAS in HF is
increasing and the imperative to better recognize CSAS.Without such tools, impairments to quality of life could remain unacknowledged.
Fig. 14.1 Nocturnal Polysomnography of an 81year old male with central sleep apnea syndrome
seen—central apnea events are marked in red. Notice related desaturations lag due to circulation time
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Fig. 14.2 Polysomnography of the same patient at 6 months following the Remede System
implanted, activated, and optimized at a stimulation rate set at 11 breaths per minute (0.18Hz).
Central Apnea Index improved from 53.8 events per hour to 0.3 events per hour. Notice resolved
desaturation
Q. A. A. Ahmed
Fig. 14.3 Chest X Ray of patient with implanted transvenous phrenic nerve stimulator with the
Zoll-Respicardia Remede System
TPNS therapy offers a chance to shed light on this much overlooked global
patient population bringing their sleep disorders into sharp focus for the rst time
and likely driving an entirely new patient population to formal sleep evaluation for
the rst time.
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14.14 Social Impacts ofSleep Loss
Sleep loss has been directly related to behavioral withdrawal, social isolation, and
feelings of loneliness. Independently, loneliness contributes to greater mortality and
loneliness is recognized to be a state distinct from either anxiety or mood disorders.
Patients living with chronic pulmonary disorders often have social withdrawal as a
function of their illness without the added impact of social isolation due to sleep
loss [30].
Much of the world has experienced the social isolation of lockdowns during this
global pandemic underlining our intense need for human connection. Investigations
into social isolation and sleep are revealing clearly identied but little-known phenomena including sleep loss as a “social repellant” driving interpersonal separation
of the sleep deprived patient from the social contact and vice versa. The asocial
impact of sleep loss has been shown to propagate in carefully conducted studies
looking at sleep deprivation, functional MRI data and human interaction. Those
encountering a sleep deprived individual even in brief 1-min interactions come
away feeling themselves lonelier and further averse to interacting with the sleep
deprived subject suggesting a social contagion of isolation due to sleep loss.
14.15 Sleep Disorders Beyond Breathing
In my practice I take great interest in examining the upper airway and try to teach
the patient and our fellows to take an interest in craniofacial development that may
have contributed to the diagnosis recognition of the craniofacial respiratory complex is imperative particularly when looking for obstructive sleep apnea in patients
of normal or below normal body mass and recognizing obstructive sleep apnea in
the pediatric population [31–34].
14.16 Conclusion
Sleep disorders in the pulmonary population are common. Pulmonologists need to
be well versed in the recognition of their diagnosis and treatment. Treatments are
advancing and involve positive airway pressure, oral appliance therapy, multimodal
surgical approaches on both the soft tissue and the craniofacial architecture, and
lately both upper airway and transvenous nerve stimulation depending on the nature
of the sleep-disordered breathing. Much more important is the role of the pulmonologist to empower both each patient and each referring physician and surgeon to
become an ambassador to the eld and a resource to the surrounding community
that more of humanity begins to learn that sleep is a biological necessity and that
disorders of sleep have wide-ranging impact on the health and well-being of the
wider population and entire societies.
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Take-Home Message
• Distinct clinical phenotypes of COPD inuence the likelihood of coexistent OSA.
• Overlap COPD patients with obstructive sleep apnea carry more signicant mor-
tality, and obstructive sleep apnea syndrome patients with coexistent COPD are
also at an increased risk of death.
• Interstitial lung disease (ILD) and Idiopathic pulmonary brosis should not be
overlooked in association with OSA in patients who do not improve enough with
CPAP therapy.
• The identication of central sleep apnea is crucial in patients with cardiac
disease.
Acknowledgment The authors acknowledge Dr. Robin Germany and Dr. Tim Meyer at
Zoll- Respicardia for permission in reproducing images of the Zoll-Respicardia REMEDE
system, digital clips of central sleep apnea syndrome, and expertise on central sleep apnea
syndrome.
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OSA inObstetrics andGynecology
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15
RenéDe León Salazar andCesarF.SaldañaSolorzano
15.1 Introduction
15.1.1 Definition andEpidemiology
Obstructive sleep apnea syndrome (OSAS) is a disease that constitutes a serious
public health problem, due to the consequences it has on the people who suffer from
it. The conditions that can occur are so varied and include, broadly speaking, the
physical, psychological, and socioeconomic aspects. According to different studies,
people who suffer from this syndrome have a higher risk of suffering trafc accidents, high blood pressure, problems with the perception of their quality of life, and
an increase in cardiovascular morbidity [1].
Obstructive sleep apnea (OSAS) is characterized by a repetitive collapse of the
upper airway during sleep, usually associated with oxygen desaturation and/or nocturnal awakenings. OSAS occurs in approximately 2% of women, and it is two to
ve times more prevalent in men. Hanser etal. have reported that the prevalence of
OSAS in women is 23.4%, while in men, it is 49.7% [2, 3].
This incidence has increased notable in recent years, in parallel with aging and
with the rise in obesity in the global population.
The symptoms commonly reported in women with OSAS are snoring (61%),
difculty falling asleep (32%), difculty staying asleep (19%), daytime sleepiness
(24%), sleep apnea observable (7%), body movements (60%), or restless legs syndrome (33%). It has been suggested that there may be a misdiagnosis or underdiagnosis of OSAS in women, since they tend not to report symptoms due to shame or
even because they report nonspecic symptoms of disorders of the breathing in
sleep, among which are: headache, fatigue, depression, anxiety, insomnia and
R. De León Salazar (*) · C. F. SaldañaSolorzano
OB/GYN, Monterrey, Nuevo León, México
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
P. M. Baptista et al. (eds.), Obstructive Sleep Apnea,
https://doi.org/10.1007/978-3-031-35225-6_15
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nocturnal awakenings [4–6]. The presentation of atypical symptoms leads to fewer
female patients being referred to sleep specialists, delaying diagnosis (and the registration of new cases).
R. De León Salazar and C. F. SaldañaSolorzano
15.1.2 Differences Between Men andWomen
There are differences between genders that affect the caliber of the airways, causing
recurrent pharyngeal obstruction during sleep. The pharynx is longer in man,
regardless of height. When the throat relaxes and collapses during sleep, the airways
close partially or totally restricting the passage of air to the lungs, producing microarousals due to lack of air, accompanied sometimes by a sensation of suffocation
such an interruption of air causing a decrease in oxygen.
Magnetic resonance imaging (MRI) has shown that the length of the airway,
tongue, soft palate, and total amount of tissue in the throat are less abundant in women.
Therefore, a longer pharynx in the man is more susceptible and tends to collapse [7].
15.1.3 Terminology
Obstructive apnea is dened as a decrease of more than 80% of the airow for 10s
(arrest of the respiratory signal) that can be of central or obstructive origin depending on diaphragmatic effort. A hypopnea is a decrease in airow of at least 30% for
10s, accompanied by a reduction in oxygen saturation of 4% or more. In the presence of thoracoabdominal effort, the apnea–hypopnea index (AHI) refers to the sum
of apnea and hypopnea events per hour of sleep. When this index is greater than ve
events per hour, the diagnosis of OSAS is made.
When the symptoms of daytime dysfunction or other neurological alterations are
directly attributed to sleep apneas/hypopneas, the obstructive sleep apnea is called
obstructive sleep apnea syndrome.
The respiratory disturbance index (RDI) is dened as the frequency of decrease
in saturation and/or nocturnal awakening per hour. The RDI can be mild when it is
5 to 15 events per hour; moderate when it is from 16 to 30 per hour and severe when
it is more than 30 events per hour.
For snoring, Lugaresi etal. [8, 9] proposed a three stages of snoring, which only
affects the companion.
• Stage 1: Snoring occupies long periods of sleep and daytime sleepiness.
• Stage 2: Snoring occupies long periods of sleep and daytime sleepiness and
poses problems.
• Stage 3: Snoring is associated with a severe picture of OSAS (obvious).
Women report more difculties sleeping; however, despite of recognizing such
alterations, many remain without a specic diagnosis. Currently, medicine focuses
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