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 respiratoirs diurnes 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

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, C flex 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).