Diapozitiv 1

Report
SLEEP-DISORDERED
BREATHING
Jasmina Gabrijelčič, MD
Golnik Hospital, Clinical
department for pneumology
and allergic diseases
HISTORY


C. Dickens: The Posthumous Papers of
the Pickwick Club; Joe, the fat boy
1965, Gastaut et al (Etude polygraphique des
manifestations episodique-hypnique et respiratoirsdiurnes et nocturnes, du syndrome de Pickwick)


1969- first tracheostomy performed
1980- first use of CPAP



Apnea: cessation of airflow > 10 sec in adults and
> 8 sec in children.
Hypopnea: partial (30- 50%) reduction of airflow,
or less- if desaturation (<90%) or arousal (EEG) is
observed, lasting
> 10 s
RERA: episodes of decreased inspiratory airflow and
increased respiratory effort, which culminate in an
EEG arousal, and do not meet the definition of either
apnea/hypopnea
MIXED APNEA

Initial absence of both airflow and
ventilatory effort, followed by evidence
of a return of effort but a continued
lack of airflow
RDI-respiratory
disturbance index
Combined total number of apneas,
hypopneas, respiratory effort-related
arousals occuring per hour of sleep
OSA-obstructive sleep
apnea



Mild OSA: 5-15 RDI/h of sleep
Moderate OSA: 15-30 RDI/h of sleep
Severe OSA: > 30 RDI/h sleep
Increasing upper airway resistance
CONTINUUM: FROM
SYMPTOMS TO DISEASE:




SNORING
UPPER AIRWAY RESISTANCE
SYNDROME (UARS)
OBSTRUCTIVE SLEEP APNEA
OBSTRUCTIVE SLEEP
APNEA/HYPOPNEA SYNDROME
DEFINITION

Repetitive episodes of upper airway
obstruction that occur during sleep,
usually associated with a reduction in
blood oxygen saturation and associated
features of daytime sleepiness and
snoring.
CLINICAL PRESENTATION
COMMON REASONS FOR REFERRAL:
– Excessive daytime sleepiness
– Loud snoring and/or apnea observed by
bed partner
LESS COMMON REASONS FOR REFERRAL:
–
–
–
–
–
–
Nocturnal/early morning headaches
Enuresis
Gastroesophageal reflux
Impotence
“seizures” at night
Psychiatric disorders
PREVALENCE
Estimated to be minimaly 2% in general
population (4% in men); higher in
elderly.
RISK FACTORS

OBESITY- especially central type;
if BMI > 29, then OSA 9-12 times more likely.
– NECK CIRCUMFERENCE






MALE GENDER- androgenic patterns of body fat
distribution favor fat deposition in the neck area;
ACROMEGALY
HYPOTHYROIDISM
STRUCTURAL CRANIOFACIAL ABNORMALITIES
CONGESTIVE HEART FAILURE (cause or
consequence?)
ALCOHOL AND DRUGS
PATHOPHYSIOLOGY
Recurrent closure of the pharyngeal airway during sleep
(velopharynx in 80%).
Increased collapsibilty can be due to:
LOCAL INFLUENCES:
 Decreased muscle activity during sleep,
 Local pharyngeal sensory neuropathy due to snoring
vibration trauma,
 Elevated positive surrounding pressure,
 Special anatomical abnormalities.
CENTRAL INFLUENCES:
 Reduced ventilatory motor output
IMAGING
DIAGNOSIS
GOLD STANDARD: In-laboratory
Polysomnography (PSG), including:
 measurement of airflow (nasal and oral
prongs),
 measurement of respiratory effort
(impedance, inductive pletysmography),
 oximetry,
 EEG,
 EOG,
 EMG (chin),
 ECG,
 snoring (microphones).
EXAMPLE OF A PSG
CONSEQUENCES OF OSA
REPETITIVE INTERMITTENT HYPOXIA
CONSEQUENCES OF OSA





Mood, neurocongnitive and behavioral
effects
Systemic hypertension
Ischemic heart disease and
arrhythmias
Cerebrovascular disease
Pulmonary artery hypertension
CORRELATION: OSA and
POLYMETABOLIC SYNDROME?
Signs of increased atherosclerosis in OSA


Measurements of structural/functional
changes: pulse wave velocity (PWV), intima
media thickness (IMT)
Measurements of increased oxidative stress,
increased inflammation, vascular smooth
cell activation (VEGF), platelet activation…
OSA is an independent risk factor for
atherosclerosis progression
CONSEQUENCES OF OSA


4 times increased risk of systemic
hypertension
2 times increased risk of myocardial
infarction and stroke
MANAGEMENT




Sleep hygiene, including weight
reduction
Oral (dental) appliances
Positive pressure therapy- CPAP
Surgical management
MANAGEMENT-mechanisms



Raising pharyngeal pressure above
Pclose (CPAP)
Changing the tube law of the passive
pharynx (oral appliances)
Increasing pharyngeal muscle tone
(avoidance of alcohol, hypnotics)
ORAL APPLIANCES
CHIN STRAP
 MANDIBULAR REPOSITIONING
APPLIANCES
 TONGUE REPOSITIONING
APPLIANCES
INDICATED IN SNORING/MILD OSA OR
IN MODERATE OSA WHEN OTHER
THERAPIES FAILED

SURGICAL MANAGEMENT




UVULOPALATOPHARYNGOPLASTY (UPPP)
MAXILLOMANDIBULAR ADVANCEMENT
TRACHEOSTOMY
PARTIAL OSTEOTOMY (MANDIBLE,
MAXILLA)
ONLY IN SELECTED PATIENTS OR WHEN
CPAP THERAPY FAILED
Continuous positive
airway pressure-CPAP



System consists of a blower unit that
generates and directs airflow
downstream to the patient and of a
mask (nasal, combined, oral).
Fixed pressure CPAP, AutosetCPAP, Cflex CPAP, BiPAP
First line therapy for moderate/heavy
OSA.

CPAP therapy was shown to be
effective in reversing all
structural/inflammation abnormalities
in OSA patients
CPAP
OSA
OSA + CPAP
CPAP
0 cm H2O
15 cm H2O
Example:before CPAP
Example: with CPAP
RISK FACTORS

OBESITY- especially central type;
if BMI > 29, then OSA 9-12 times more likely.
– NECK CIRCUMFERENCE






MALE GENDER- androgenic patterns of body fat
distribution favor fat deposition in the neck area;
ACROMEGALY
HYPOTHYROIDISM
STRUCTURAL CRANIOFACIAL ABNORMALITIES
CONGESTIVE HEART FAILURE (cause or
consequence?)
ALCOHOL AND DRUGS
2 TYPES OF OSA
PATIENTS?
PATHOPHYSIOLOGY
Recurrent closure of the pharyngeal airway during sleep
(velopharynx in 80%).
Increased collapsibilty can be due to:
LOCAL INFLUENCES:
 Decreased muscle activity during sleep,
 Local pharyngeal sensory neuropathy due to snoring
vibration trauma,
 Elevated positive surrounding pressure,
 Special anatomical abnormalities.
CENTRAL INFLUENCES:
 Reduced ventilatory motor output
IMAGING
DIAGNOSIS
GOLD STANDARD: In-laboratory
Polysomnography (PSG), including:
 measurement of airflow (nasal and oral
prongs),
 measurement of respiratory effort
(impedance, inductive pletysmography),
 oximetry,
 EEG,
 EOG,
 EMG (chin),
 ECG,
 snoring (microphones).

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