SLEEP RELATED

BREATHING DISORDERS

PRESENTER:
Dr. MUSSA SWEYA
SUPERVISOR:
Dr. G. SHAYO
DEFINITION
• The term breathing-related sleep disorder refers to a spectrum of
breathing anomalies ranging from chronic or habitual snoring to frank
obstructive sleep apnea (OSA)
OR, in some cases, obesity hypoventilation syndrome (OHS)

• Sleep apnea is the intermittent cessation of airflow at the nose and

mouth during sleep

• Apneas of at least 10 s duration are important but in most cases the

apneas last 20-30 s and can last as long as 2-3 min
TYPES OF SLEEP RELATED BREATHING DISORDERS

• Obstructive sleep apnea

• Central sleep apnea

• Obesity Hypoventilation syndrome

ETIOLOGY
• Complex interactions among the central and peripheral nervous
systems, upper airway musculature, and neurotransmitters may result
in partial or complete collapse of a portion or portions of the upper
airway

• Data suggest that the primary defect is an anatomically small or

collapsible pharyngeal airway in combination with a sleep-related fall
in upper airway muscular tone
CONTRIBUTING FACTORS
These factors may contribute, alone or in combination, to the presence and
severity of this disorder
 airway anatomy (eg, adenotonsillar hypertrophy),
 nasal obstruction,
 presence and distribution of body fat,
 and muscle tone
Patients with neuromuscular disease have additional risk factors that may predispose them
to sleep-disordered breathing
 central nervous system (CNS) involvement,
 chest wall deformity with restrictive lung disease,
 diaphragmatic weakness,
 increased upper airway resistance,
 and impaired respiratory chemosensitivity.
EPIDEMIOLOGY
• According to estimates, at least 2–4% of the adult population experience
breathing-related sleep disorders

• Elderly population show significantly higher rates of sleep-disordered breathing,

28–67% in men and 20-54% in females

• OSA may affect as many as 30% of adults and is more common in men than
women
• The prevalence of OSA was 11.5% in Dar es Salaam (Shayo et al. 2015)

• No sex difference exists before puberty, and after menopause

Obstructive sleep apnea
• Obstructive sleep apnea (OSA) is a disorder that is characterized by
obstructive apneas, hypopneas, and/or respiratory effort-related
arousals caused by repetitive collapse of the upper airway during sleep

• OSA is the most common sleep-related breathing disorder

• The prevalence appears to be increasing and may relate to the

increasing rates of obesity or increased detection rates of OSA
Pathophysiology of OSA
• Occlusion of the oropharyngeal airway results in progressive asphyxia
until there is a brief arousal from sleep, whereupon airway patency is
restored and airflow resumes

• The patient then returns to sleep and the process is repeated over the
night
• Sleep becomes fragmented
Pathophysiology of OSA
• The immediate factor leading to collapse of the upper airway is
generation of sub-atmospheric pressure during inspiration and which
exceeds ability of airway dilator and abductor muscles to maintain
airway stability

• During wakefulness upper airway muscle activity is greater than

normal to compensate for airway narrowing and high airway
resistance
 OSA RISK FACTORS
Older age Prevalence of OSA increases from young adulthood through the sixth to seventh
decade, then appears to plateau
Male sex OSA is approximately two to three times more common in males than females
the risk appears to be similar once females are peri- and postmenopausal
Obesity a 10% increase in weight was associated with a six-fold increase in risk of OSA
The majority of individuals with obesity hypoventilation syndrome (OHS) have
OSA (90%)
Craniofacial and upper airway Craniofacial or upper airway abnormalities increase the likelihood of having OSA
abnormalities e.g. abnormal maxillary or short mandibular size, a wide craniofacial base, and
tonsillar and adenoid hypertrophy
Smoking Smoking may increase the risk of or worsen OSA. In one study, current smokers
were nearly three times more likely to have OSA than past or never smokers
Family history of snoring or there may also be a genetic predisposition to OSA through factors such as
OSA craniofacial structure,
40% of the variances AHI has genetic basis
Medical Conditions a/w OSA
CLINICAL FEATURES
DIAGNOSTIC EVALUATION
• OSA is not a clinical diagnosis and objective testing must be
performed for the diagnosis
• Diagnostic testing for OSA should be performed on patients with;
Excessive daytime sleepiness (EDS) on most days
• and the presence of at least two of the following clinical features of
OSA:
habitual loud snoring,
witnessed apnea or gasping or choking during sleep, and
diagnosed systemic hypertension
EVALUATION TOOL PARAMETERS
• None of these tools have been shown to be superior to a history and
physical examination

• Proven to be useful in outpatient setting

• Examples;
STOP-Bang questionnaire
Epworth Sleepiness Scale (ESS)
STOP-Bang questionnaire
DIAGNOSTIC TESTS
DIAGNOSIS
By PSG; The diagnosis of OSA is confirmed if either of the two criteria below is
present:
1. 5 or more predominantly obstructive respiratory events per hour of sleep in a
patient with one or more of the following:
 Sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms
 Waking up with breath holding, gasping, or choking
 Habitual snoring, breathing interruptions, or both noted by a bed partner or other
observer
 Hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke
congestive heart failure, atrial fibrillation, or type 2 diabetes mellitus
2. 15 or more predominantly obstructive respiratory events (apneas, hypopneas) per
hour of sleep regardless of the presence of associated symptoms or comorbidities
DISEASE SEVERITY
TREATMENT
• The goals of OSA therapy are to resolve signs and symptoms of OSA,
improve sleep quality, and normalize the apnea-hypopnea index and
oxyhemoglobin saturation levels

• The approach should be that of a chronic disease that requires long-

term, multidisciplinary management

• Common to all guidelines is the recommendation that, in addition to

reviewing the behavioral modifications, all patients diagnosed with
OSA should be offered positive airway pressure (PAP) as initial
therapy
EDUCATION AND BEHAVIOUR
Patient education:
• The patient should be educated about the risk factors, natural history, and
consequences of OSA

• Importantly, all patients should be warned about the increased risk of motor
vehicle crashes associated with untreated OSA and the potential consequences of
driving or operating other dangerous equipment while sleepy

• Patients should be counselled that they should always inform their medical
providers that they have sleep
• apnea, especially if they are to have surgery or start opiate medications
EDUCATION AND BEHAVIOUR
• Weight loss and exercise: for overweight and obese patients. Rarely leads to
complete remission but a/w improvement in quality of life ( decrease AHI,
daytime sleepiness, blood pressure)
• Sleep position: During the diagnostic sleep study, some patients will be observed
to have OSA that develops or worsens during sleep in the supine position.
Sleeping in a non-supine position (eg, lateral recumbent) may correct or improve
OSA in such patients and should be encouraged
• Alcohol avoidance: All patients with untreated OSA should avoid alcohol prior to
sleep, because it can depress the central nervous system, exacerbate OSA, worsen
sleepiness, and promote weight gain
• Concomitant medications: Any clinician who prescribes medication for the
patient should be informed that the patient has OSA. particular, benzodiazepines
should be avoided in untreated patients
POSITIVE AIRWAY PRESSURE THERAPY
• Positive airway pressure (PAP) therapy is the mainstay of therapy for
adults with OSA

• The mechanism of continuous PAP (CPAP) involves maintenance of a

positive pharyngeal transmural pressure so that the intraluminal
pressure exceeds the surrounding pressure

• CPAP also stabilizes the upper airway through increased end-

expiratory lung volume. As a result, respiratory events due to upper
airway collapse (eg, apneas, hypopneas) are prevented
POSITIVE AIRWAY PRESSURE THERAPY
Other treatment modalities
Oral appliance Surgical Management
• Mandibular advancement device
• Tongue retaining device
MORBIDITY AND MORTALITY
• Obesity, advanced age, and snoring have been found to be important
factors in the progression of sleep-disordered breathing

• OSA-related death is rare, a few patients with very severe OSA have
died in their sleep soon after being diagnosed with the disease

• Morbidity with OSA falls into 2 major categories: (1) neuropsychiatric

or social and (2) cardiovascular.
MORBIDITY AND MORTALITY
Neuropsychiatric or psychosocial Cardiovascular
excessive daytime sleepiness, • Untreated OSA may be
poor concentration and associated with hypertension and
memory, congestive heart failure
decreased performance,
irritability,
depression, and • Systemic hypertension occurs
disturbed social relationships. in 45-90% of patients with OSA.

• significantly increased risk of

motor vehicle accidents (7 fold)
OBESITY HYPOVENTILATION SYNDROME
• Obesity hypoventilation syndrome (OHS) is defined as the presence of
awake alveolar hypoventilation in an obese individual which cannot
be attributed to other conditions associated with alveolar
hypoventilation

• OHS is associated with increased cardiovascular morbidity and

mortality.

• Consequently, early detection and treatment are crucial to minimize

these adverse effects
 DEFINITION AND STAGING
• OHS is defined by raised awake arterial pressure of carbon dioxide (PaCO2 )
levels in patients with obesity in whom alternative causes hypercapnia and
hypoventilation have been excluded
• European Respiratory Society taskforce has proposed a staging schema for
hypoventilation in patients with obesity (ie, body mass index [BMI] >30 kg/m )

STAGE DEFINITION
0 Patients with OSA and no hypercapnia
I Obesity associated sleep hypoventilation but normal awake PaCO2 and serum HCO3 <27mmol/L

II Obesity associated sleep hypoventilation but normal awake PaCO2 and serum HCO3 >27mmol/L

III Obesity Hypoventilation Syndrome (OHS) patients with or without concurrent OSA
IV OHS patients with or without concurrent OSA with significant cardiometabolic comorbidities
RISK FACTORS
• The major risk factor for OHS is obesity (body mass index [BMI] >30
kg/m )

• Other risk factors may include:

Significant increase in waist:hip ratio (i.e, central obesity)
Reduced lung function due to obesity
Reduced inspiratory muscle strength
Severe obstructive sleep apnea (OSA; eg, apnea hypopnea index
>30 events per hour)
CLINICAL MANIFESTATIONS
• The clinical manifestations of OHS are nonspecific and reflect the
manifestations of obesity

• Symptoms and physical findings of OSA include daytime hypersomnolence,

loud snoring, choking during sleep, resuscitative snorting, fatigue, impaired
concentration and memory, a small oropharynx, and a thick neck

• Many patients with OHS present late in the course of their disease and have
manifestations of end-stage disease including:
Severe hypoxemic hypercapnic respiratory failure
Right heart failure from pulmonary hypertension
LABORATORY TESTS
• Elevated serum bicarbonate (>27 mEq/L): clue that the patient is
chronically hypercapnic, non-specific however

• Hypercapnia (arterial pressure of carbon dioxide [PaCO2 ] >45 mmHg):

Consistent with the phenomenon of hypoventilation

• Hypoxemia (PaO <70 mmHg)

• Polycythemia: Polycythemia due to recurrent hypoventilation- or OSA-

associated hypoxemia is uncommon but may be present as a late manifestation
DIAGNOSIS
• OHS is a diagnosis of exclusion that can be made when the following
criteria are met:

Obesity (body mass index [BMI] >30 kg/m2)

Awake alveolar hypoventilation as indicated by a partial arterial
pressure of carbon dioxide >45 mmHg
Alternative causes hypercapnia and hypoventilation have been
excluded
TREATMENT
• The most effective treatment is weight loss,

• but it is often possible to relieve the symptoms by nocturnal

ventilation with positive airway pressure(CPAP)
CENTRAL SLEEP APNEA
• Central apnea occurs when both airflow and ventilatory effort are absent
for at least 10 seconds or more

• It can result from a failure of the ventilatory drive (idiopathic form) or

may be due to secondary causes such as CHF or neurologic disorder

• The idiopathic form is less common than secondary causes

• Central apneas can also occur during sleep-onset in otherwise healthy

individuals and during sleep at high altitude
Pathophysiology of CSA
• During the waking state respiration is controlled by three
processes,
Metabolic (automatic)
Wake-related drive to breathe and
Behavioral (voluntary) systems.

• During NREM sleep;

The wake-related drive to breathe and behavioral control systems are
abolished and,
Respiration is controlled entirely by the metabolic control system,
Primarily by the hypercapnic ventilatory drive and to a lesser degree
by the hypoxic ventilatory drive
Pathophysiology of CSA
A PaCO2 above the apneic threshold stimulates ventilation,
whereas a PaCO2 below this threshold leads to a central apnea that
continues until PaCO2 increases and once again exceeds the apneic
threshold

Metabolic system Consists of chemoreceptors for hypoxia (carotid

body) and hypercapnia (carotid body and medulla) as well as brainstem
systems that regulate ventilation to maintain stable levels of pH, PaO2
and PaCO2
RISK FACTORS FOR CSA

• Sleep disturbance: Increased frequency of sleep-wake transitions

• Gender: Men are more likely to have central apneas due to a higher
hypocapnia-apneic threshold during NREM sleep

• The lower apneic threshold in women than in men could be mediated

by both female and male hormones
RISK FACTORS FOR CSA
• Age: Central apneas are more common in older adults due to the
increased prevalence of underlying medical disorders (eg, CHF),
neurologic disorders, or greater sleep disturbance and awakenings

• Altitude: Central apneas can develop acutely following ascent to high

altitudes

• Heart failure Stroke, hypothyroidism , acromegaly , renal failure ,

methadone etc
RISK FACTORS FOR CSA
TREATMENT
• Supplimental oxygen and positive airway pressure are the mainstay of
treatment
1-Central apnea due to hyperventilation
• CPAP – Continuous positive airway pressure
• BIPAP - Bilevel positive airway pressure with a set backup respiratory rate
2-Central apnea due to hypoventilation
• NIPPV – Nasal intermittent positive pressure ventilation
THANK YOU