Sindromul de Apnee Nocturnă

Sindromul de apnee
nocturnă
Apnea =no airflow for ≥10 seconds
Hypopnea= reduction in airflow by at least 30%
from baseline for ≥10 seconds accompanied by
oxygen desaturation ≥3% or arousal from sleep
Sleep apnea =presence of at least five episodes

per hour of apnea and/or hypopnea
Obstructive sleep apnea/hypopnea syndrome (OSAHS) is
caused by upper airway closure during inspiration,
punctuated by brief arousals that terminate apneic
episodes.
Central sleep apnea (CSA) is characterized by
respiratory pauses during sleep related to absence of
respiratory effort
Snoring =vibration of respiratory structures and

the resulting sound due to obstructed air
movement during breathing while sleeping. I
OBSTRUCTIVE SLEEP
APNEA/HYPOPNEA SYNDROME
-DIAGNOSIS
(1)either symptoms of nocturnal breathing disturbances (snoring,
snorting, gasping, or breathing pauses during sleep) or daytime
sleepiness or fatigue that occurs despite sufficient opportunities
to sleep and is unexplained by other medical problems; and
(2) 5 or more episodes of obstructive apnea or hypopnea per hour
of sleep (the apnea-hypopnea index [AHI], calculated as the
number of episodes divided by the number of hours of sleep)
documented during a sleep study.
or
In the absence of symptoms
if AHI is >15 episodes/h.
Airway collapse in OSAHS
“suctioning” force= negative intraluminal pharyngeal
pressure.
airway patency is dependent on the stabilizing
influence of the pharyngeal dilator muscles.
reduction in neuromuscular output results in

transient episodes of pharyngeal collapse
The episodes of collapse are terminated when

ventilatory reflexes are activated and cause
arousal, thus stimulating an increase in
neuromuscular activity and opening of the airway.
severe during REM (rapid eye movement) sleep,

when neuromuscular output to the skeletal
muscles is particularly low, and in the supine
position due to gravitational forces
Risk factors for OSAHS
A.Major Risk factors :1.obesity and 2.male sex.
B.Additional risk factors :

-mandibular retrognathia and micrognathia,
-a positive family history of OSAHS,
-genetic syndromes that reduce upper airway patency
(e.g., Down syndrome, Treacher-Collins syndrome),
-adenotonsillar hypertrophy (especially in children),
-menopause (in women),
-and various endocrine syndromes (e.g., acromegaly,
hypothyroidism).
Obesity Predisposes to Obstructive Sleep Apnea
enlargement of soft tissue

structures within and
surrounding the airway
excess of fat deposition
under the mandible and in
the tongue, soft palate, and
uvul
Lung volumes are markedly reduced

by a combination of increased
abdominal fat mass and recumbent
posture
obesity-related leptin resistance ( neuroanatomic interactions for stable

breathing)
SYNDROME Z =OSA + METABOLIC SYNDROME

2.MALE GENDER
1.android patterns of obesity (resulting in upper-airway

and abdominal fat deposition)
2.and relatively greater pharyngeal length, which

exacerbates collapsibility.
Premenopausal women are relatively

protected from OSAHS by the influence of sex
hormones on ventilatory drive.
Pathophysiology
-sleep fragmentation
-cortical arousal
-impact of intermittent hypoxemia on vascular, cardiac,
metabolic, and neurologic functions.
-OSAHS-related respiratory events stimulate sympathetic
overactivity
-High level of acute phase proteins and oxigen reactive
species
-Insuline resistance and lipolysis
-Prothrombotic and proinflamatory state
-Cardiac remodeling because of augmented negative
intrathoracic pressure and modified
cardiac preload and postload.
sequence of events in obstructive sleep apnea syndrome
Pulm Med. 2013; 2013: 521087.

OSAHS severity
-frequency of breathing disturbances (AHI),

-the amount of oxyhemoglobin
desaturation with respiratory events,
-the duration of apneas and hypopneas,
-the degree of sleep fragmentation,
-and the level of daytime sleepiness or
functional impairment.
SYMPTOMS AND HISTORY
Nocturnal symptoms
sleep history -assistance from a bed partner or household member
Snoring =vibration of respiratory structures and the resulting sound due

to obstructed air movement during breathing while sleeping
Gasping/Snorting=termination of individual apneas with abrupr airway
opening
Awakening/sleep disruption
Nocturia
Daytime symptoms –excessive sleepiness

-dry mouth
-heartburn
-diaphoresis of chest and neck
-morning headaches
-trouble concentrating
-irritability/mood disturbances
PHYSICAL FINDINGS
Comorbid conditions/etiologic factors
hypertension and regional (central) obesity,
Heart failure signs; left or right side
Cor pulmonale signs; OSAHS alone is not thoght to cause cor pulmonale
nasal cavity :polyps,

septal deviation,
other signs of obstruction
oropharynx small orifice with crowding due to an enlarged tongue,

a low-lying soft palate with a bulky uvula,
large tonsils,
high-arched palate,
micro/retrognathia
LABORATORY FINDINGS ;
1.Diagnostic Tests
The gold standard for diagnosis of OSAHS is an overnight polysomnogram (PSG)
false-negative studies:
can result if the study did not collect representative information on the patient’s usual
sleep, particularly if there was insufficient REM sleep or inadequate supine sleep during
testing.
physiological information collected
measurement of breathing (changes in airflow, respiratory excursion),

oxigenation(hemoglobin oxygen saturation),
body position,
and cardiac rhythm.
home sleep studies measure:
sleep continuity
sleep stages (by electroencephalography, chin
electromyography, electro- oculography, and actigraphy),
limb movements (by leg sensors),
snoring intensity.
Other tests
-cephalometric radiography,
-MRI, CT,
- fiberoptic endoscopy,
-Cardiac testing :impaired systolic or diastolic ventricular
function / abnormal cardiac structure.
- Overnight blood pressure =“non-dipping” pattern
Obstructive Sleep Apnea/Hypopnea Syndrome
(OSAHS): Quantification and Severity Scale
• Apnea-hypopnea index (AHI)a: Number of apneas plus hypopneas per hour of
sleep
• Respiratory disturbance index (RDI): Number of apneas plus hypopneas plus

RERAs per hour of sleep
• Mild OSAHS: AHI of 5–14 events/h
• Moderate OSAHS: AHI of 15–29 events/h
• Severe OSAHS: AHI of ≥30 events/h

Respiratory Event Definitions
• Respiratory effort-related arousal (RERA):
Partial obstruction that does not meet the criteria for
hypopnea but provides evidence of increasing inspiratory
effort (usually through pleural pressure monitoring)
punctuated by an arousal
• Flow-limited breath:
A partially obstructed breath, typically within a hypopnea or
RERA, identified by a flattened or “scooped-out” inspiratory
flow shape
The inspiratory flow
pattern in a patent
airway is rounded
and peaks in the
middle
30s of no
airflow
Central apnea in a patient with Cheyne-
Stokes respiration
Hypopnea.
Partial obstruction
of the pharyngeal
airway can limit
ventilation
Respiratory
effort-related
arousal (RERA)
sleep study
AHI and the profile of oxygen saturation over the night (mean, nadir, time at low levels).
the respiratory disturbance index,
includes the number of respiratory effort-related arousals in addition to the number
of apneas plus hypopneas.
sleep latency (time from “lights off” to first sleep onset),
sleep efficiency (percentage of time asleep relative to time in bed),
arousal index (number of cortical arousals per hour of sleep),
time in each sleep stage
periodic limb movement index.
OSAHS severity can be further characterized according to the degree of sleep
fragmentation associated with respiratory disturbances.
the frequency of cortical micro-arousals or awakenings per sleep hour (arousal index),
reduction in sleep continuity (low sleep efficiency),
reduction of time in deeper stages of sleep (stage N3 and REM sleep),
and increases in light sleep (stage N1).
The detection of autonomic arousals :
surges in blood pressure, changes in heart rate, and abnormalities in cardiac
rhythm, also provides relevant information on OSAHS severity.
OSAHS severity:
-the degree of sleep fragmentation associated with respiratory
disturbances.
-the frequency of cortical micro-arousals or awakenings per

sleep hour (arousal index)
- reduction in sleep continuity (low sleep efficiency)
- reduction of time in deeper stages of sleep (stage N3 and

REM sleep)
and increases in light sleep (stage N1)
-The detection of autonomic arousals :

- surges in blood pressure,
-changes in heart rate
-Arterial blood gas measurements made during wakefulness are
usually normal.
- Waking hypoxemia or hypercarbia: coexisting cardiopulmonary
hypoventilation
syndrome
-severe nocturnal hypoxemia :elevated hemoglobin values.
-A multiple sleep latency test or a maintenance of wakefulness test

can be useful in quantifying sleepiness and helping to distinguish
OSAHS from narcolepsy
OBStRUCtIVE SLEEP APNEA AND tyPE 2 DIABEtES
regular snoring and OSA are independently
associated with alterations in glucose
metabolism.
intermittent hypoxia and sleep fragmentation
OSA might induce insulin resistance and

increase the risk of developing type 2
diabetes
OSA patients with AN suffer from the

most profound oxygen desaturations
during sleep
CPAP has an impact on diabetic

metabolism in terms of a better glucose
control in both groups.
Mechanism of obstructive sleep apnea
and non-alcoholic fatty liver disease.
:Obstructive sleep apnea syndrome and metabolic syndrome
Pulm Med. 2013; 2013: 521087.

TREATMENT
-lifestyle
-comorbidities
-Reduce Weight
-optimize sleep duration (7–9 h);
-regulate sleep schedules (with similar bedtimes and
wake times across the week);
-encourage the patient to avoid sleeping in the
supine position;
- treat nasal allergies;
-increase physical activity;
-eliminate alcohol ingestion (which impairs
pharyngeal muscle activity) within 3 h of bedtime;
minimize use of sedating medications.
-Patients should be counseled to avoid drowsy driving

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Sindromul de apnee

Sleep apnea =presence of at least five episodes

Snoring =vibration of respiratory structures and

reduction in neuromuscular output results in

The episodes of collapse are terminated when

severe during REM (rapid eye movement) sleep,

B.Additional risk factors :

enlargement of soft tissue

Lung volumes are markedly reduced

obesity-related leptin resistance ( neuroanatomic interactions for stable

SYNDROME Z =OSA + METABOLIC SYNDROME

1.android patterns of obesity (resulting in upper-airway

2.and relatively greater pharyngeal length, which

Premenopausal women are relatively

Pulm Med. 2013; 2013: 521087.

-frequency of breathing disturbances (AHI),

Snoring =vibration of respiratory structures and the resulting sound due

Daytime symptoms –excessive sleepiness

nasal cavity :polyps,

oropharynx small orifice with crowding due to an enlarged tongue,

physiological information collected

measurement of breathing (changes in airflow, respiratory excursion),

• Respiratory disturbance index (RDI): Number of apneas plus hypopneas plus

• Mild OSAHS: AHI of 5–14 events/h

• Moderate OSAHS: AHI of 15–29 events/h

• Severe OSAHS: AHI of ≥30 events/h

-the frequency of cortical micro-arousals or awakenings per

- reduction in sleep continuity (low sleep efficiency)

- reduction of time in deeper stages of sleep (stage N3 and

and increases in light sleep (stage N1)

-The detection of autonomic arousals :

- Waking hypoxemia or hypercarbia: coexisting cardiopulmonary

-A multiple sleep latency test or a maintenance of wakefulness test

intermittent hypoxia and sleep fragmentation

OSA might induce insulin resistance and

OSA patients with AN suffer from the

CPAP has an impact on diabetic

Pulm Med. 2013; 2013: 521087.

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