Sleep Related Breathing Disorders

Date: 
Thursday, November 29, 2018

Sleep Related Breathing Disorders
Shahira Loza
Director of The Cairo Center For Sleep Disorders
President of The Egyptian Scientific Society of Sleep Medicine & Research
Board Member of The World Association of Sleep Medicine
Sleep related breathing disorders are a spectrum of respiratory disturbances occurring during sleep . In the International Classification of Sleep Disorders ICSD 3rd edition, they comprise Obstructive Sleep Apnea disorders, Central Apnea Syndromes, Sleep Related Hypoventilation disorders, Sleep Related Hypoxemia disorders and Snoring. The awareness of breathing disturbances during sleep has increased in recent years mostly due to the significant advances in diagnosis and treatment .
1- Obstructive Sleep Apnea Disorders
OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) upper airway obstruction occurring during sleep. These events result in drop of blood oxygen saturation and drop in heart rate and are terminated by brief arousals. Apneic and hypopneic events last a minimum of 10 seconds and they can occur in any stage of sleep Non Rem N1, N2 , N3 and Rem Sleep. Events are usually longer with more severe decrease in oxygen saturation when they occur during Rem sleep and when the individual is sleeping supine. Oxygen saturation usually returns to baseline values following resumption of normal breathing provided there is no underlying pulmonary pathology.
The estimate of the prevalence of clinically significant of OSA in developed countries is about 5%. The Wisconsin Sleep Cohort Study of 3513 subjects aged 30-60 years found that 4% of men and 2 % of women had OSA defined as apnea hypopnea index ( AHI) of greater than 5, associated with daytime sleepiness.
Polysomnography of OSA patient
Obesity: Considered the most important risk factor, about 40% of those with a BMI of 40% and 50% of those with a BMI of 50 have significant OSA. Neck size of 43 cm in men and 40 cm in women is considered highly predictive of risk of OSA .
Age: Prevalence of OSA increases with age.
Sex: Before the age of 50, men are twice as likely as women to have OSA , this gap decreases after menopause. Women appear to have a greater age related risk and an increase in the prevalence of apnea after menopause.
Family history; studies have shown a higher prevalence among offspring of family members with OSA compared with general population.
Endocrine: Hypothyroidism is more prevalent in individuals with OSA . it was found that 1.4 and 4 % of those diagnosed with OSA have hypothyroidism.
Behavioral Factors: are also risk factors for the development and increased severity of OSA. Smoking which causes irritation, edema and mucus production all contributing to upper airway obstruction. Alcohol and sedative medications lead to upper airway muscle relaxation.
Syndromes affecting airway caliber: In syndromes such as Pierre Robin, Prader -Willi and Down syndromes, OSA is strongly suspected.
Diagnosis:
Diagnosis of OSA is made through an overnight Polysomnography (PSG) study aided by tests and questionaires. PSG provides data which includes air flow, respiratory rate, cardiac rate, snoring , movement, snoring and position during sleep. Diagnostic criteria : A PSG demonstrating 5 or more obstructive respiratory events + symptoms and signs.
Patients may complain of nighttime symptoms such as snoring, snorting, witnessed respiratory pauses, insomnia, enuresis or nocturia , heart burn and daytime symptoms such as , excessive daytime sleepiness, morning headaches, cognitive deficits, personality changes and erectile dysfunction.
Signs of OSA include Obesity, Hypertension, uncontrolled diabetes, cardiac arrhythmia, nasal obstruction, crowded oropharynx and retrognathia.
The consequences of OSA vary with the severity. Changes include episodic hypercapnia, hypoxia
negative intrathoracic pressure, increase in pulmonary and systemic pressure, cyclic slowing then increase in heart rate and surges of sympathetic tone at event termination.
Medical complications include Cardiovascular complications such as hypertension, arrhythmia, CVD, CHF. Metabolic complications as diabetes and obesity are a major cofounding factor, both are worsened with increase BMI, but studies have shown that obese and non obese patients have abnormal glucose metabolism related to OSA. Patients may experience other complications such as Erectile disfunction, Neuro cognitive disorders and Cerebrovascular disease.
Treatment:
Choice of treatment of OSA depends on OSA severity, symptoms, co morbid medical conditions, patients preference and economic factors. Types of treatment include behavioral, medical, surgical treatment and Continuous Positive Airway Pressure
According to severity:
Snoring / mild OSA ——— Positional therapy
(nonsupine position)
———Treatment of nasal congestion
———-Weight loss
———-Oral appliance
———-Surgery
Moderate OSA ————-PAP treatment
————-Oral appliance
————-Surgery
————Weight loss/ positional therapy
( adjunctive)
Severe OSA ————PAP treatment
Positive Airway Pressure Therapy for OSA
PAP therapy remains the treatment of choice for most patients with Sleep Related Breathing Disorders, specially when predominantly obstructive..
PAP devices function to pneumatically splint the airway
Components of devices are Flow generator, Patient interface, Tubing connecting the two and a Heated humidifier which reduces discomfort.
The interface is the mask the patient wears. A typical PAP mask is lightweight, it’s edges surrounded by a softer hypoallergenic material to create a seal. Masks include a vent that allows CO2 to escape. Types of inter faces include Nasal masks, Nasal- Oral, Oral , Nasal pillows or a combination. They come in various sizes and are held in place by straps, clips or velcro.
There are several Positive Airway Pressure modalities:
• Continuous Positive Airway Pressure CPAP
• Bilevel Continuous Positive Airway Pressure BiPAP
• Auto titrating Positive Airway Pressure APAP
• Adaptive Servoventilation ASV and Non Invasive Positive Pressure Ventilation , for patients with predominately central and mixed episodes.
There are several ways to determine the Optimal Positive Airway Pressure:
1. Traditional approach : titration in lab during an attendee full night Polysomnography study.
2. Split Night titration : initial diagnostic portion of the study followed by PAP titration.
3. Auto titration : only in selected patients, they should have no lung disease, no heart diseases, no CSA or other forms of hypoventilation.
Outcome studies of PAP therapy report beneficiary effects on Sleep Quality, Alertness, Blood pressure control, heart function and mortality rate.
PAP related quality of life improvement , mood and neurocognitive functions benefits and reduced care

utilization.
Adverse effects of therapy, although rare , the most common is difficulty or inability to tolerate the mask and the machine . Complaints include : nocturnal awakenings, nasal problems (dryness- congestion ), gastric distention , mask may cause skin irritation, it s leakage can cause ocular irritation. These factors are addressed through PAP therapy education programs which reportedly improve CPAP utilization. Good mask fitting, the use of humidification and Psychotherapy to deal with anxiety claustrophobia all increase a patient’s adherence to PAP use.
2- Central Sleep Apnea Syndromes
Central apnea in adults is a cessation in airflow of 10 seconds or longer associated with an absence of respiratory effort.
Patients with Central Sleep Apnea are less than 5-15% of patients with sleep apnea evaluated in most sleep centers. The increase in number of patients with central sleep apnea is due first to an increased recognition of sleep disordered breathing in congestive heart failure CHF and a substantial number of patients with systolic heart failure have Cheyne- Stokes breathing central sleep apnea ( CSB- CSA). Second to the more aggressive use of opiates to control pain. Some patients may develop central apnea when exposed to PAP treatment. Thus sleep centers can expect to see more patients with Central Sleep Apnea.
Classification of CSA Syndromes:
. Hypocapnic ( normal or low PCO2 )
These patients have normal or low Pa CO2 during wakefulness, during sleep these patients do not develop hypercapnia.
- Primary CSA,
- Cheyne-Stokes breathing pattern
- High altitude periodic breathing
- Complex sleep apnea ( treatment emergent )
. Hypercapnic ( normal or high PCO2)
In contrast patients with CSA due to drug or substance and primary sleep apnea of infancy have normal or increased daytime PaCO2 and may develop or have worsening hypercapnia during sleep
1- Won’t breathe
A- Central hypoventilation
- Congenital and idiopathic central hypoventilation syndromes.
- Brain tumors , cerebrovascular disease.
- Structural brain disorders- Chiari’s syndrome
- Apnea of infancy
B- Medication induced CSA ( narcotics / opiates )
- Central sleep apnea with normal or increased daytime PCO2
- Complex sleep apnea , treatment emergent .
C- Obesity hypoventilation hypoventilation syndrome.
2- Can’t breathe
A- Restrictive thoracic cage disorders
B- Neuromuscular disorders
- Motor neuron disease ( poliomyelitis)
- Neuropathy
- Neuromuscular junction disorders (myasthenia gravis)
- Myopathy ( muscular dystrophy )
3- Sleep Related Hypoventilation Syndromes
1- Sleep Related Non obstructive Alveolar Hypoventilation idiopathic due to abnormal ventilatory control.
2- Congenital Central Alveolar Hypoventilation Syndrome.
3- Sleep Related Hypoventilation due to Medical Condition
* Due to lower airways obstruction( COPD, bronchiectasis - cystic fibrosis).
* Due to pulmonary parenchymal or vascular disorders ( pulmonary fibrosis - interstitial lung disease)
* Due to abnormality of the chest wall or neuro muscular disorders ( kyphoscoliosis , amyotrophic lateral sclerosis ALS, Obesity hypoventilation Syndrome )