Sleep Related Breathing Disorder (SRBD) types, Symptoms and Can sleep apnea kill you
Sleep-Related Breathing Disorders (SRBD) are a group of conditions characterized by abnormal breathing patterns during sleep, These disorders range from mild snoring to more severe conditions like obstructive sleep apnea (OSA), They can significantly impact sleep quality, daytime functioning, and overall health.
Sleep-Related Breathing Disorders
Sleep-related breathing disorders (SRBDs) include:
- Obstructive sleep apnea (OSA).
- Central sleep apnea and Cheyne-Stokes breathing (usually seen in patients with heart failure).
- Sleep hypoventilation syndrome.
Obstructive sleep apnea (OSA)
OSA is a highly prevalent disease characterized by recurring episodes of sleep-related collapse of the upper airway at the level of the pharynx, It is usually associated with loud snoring and increased daytime sleepiness.
The Main pathology in OSA hypopnea syndrome is obstruction of the upper airway which causes hypoxia (on the other hand COPD patients have obstruction of the lower airway). This is due to weakness of the dilator muscles of the neck that surrounds the upper airway and keeps it patent. If the dilator muscles become relaxed this causes the collapse of the airway either:
- Complete: Airflow reduced by more than 90% of baseline for more than 10s; obstructive if respiratory effort is present, central if no respiratory effort is present What is called Apnea.
- Partial: Airflow reduced by more than 30% of the baseline for more than 10s, in association with a 3% oxygen desaturation or arousal what’s called Hypopnea.
The small amount of air will try to overcome the resistance caused by the obstruction by increasing respiratory effort (and thus decreasing esophageal pressures) for 10 seconds or more leading to an arousal from sleep, but one that does not fulfill the criteria for a hypopnea or apnea, The gold standard for measuring RERAs is esophageal manometry which causes Respiratory Effort
To sum up, the events occurring to patients with OSA:
- Obstructive apnea.
- Obstructive hypopnea.
- PLAN.
- Snoring: due to vibration (air enters in narrow space) in the upper airway,
- Uvula thick and elongated (High-risk patients).
- Soft palate edematous and redundant (High-risk patients).
These 4 events may occur in the same patient or some of them.
Apnea hypopnea index (AHI); is the number of apneas and hypopneas per hour, A normal index is less than 5/ hour. Respiratory disturbance index (RDI); is the number of obstructive apneas, obstructive hypopneas, and respiratory effort-related arousals per hour of sleep, OSA is defined as either an RDI greater than 15 events per hour, or an RDI between 5 and 14 events per hour that are accompanied by daytime sleepiness, loud snoring, witnessed breathing interruptions, or awakenings due to gasping or choking.
Pathophysiology of OSA
- The pathogenesis of OSA involves both anatomic and neurologic components, The collapsing of the upper airway reduces its airway intraluminal diameter and O2 saturation decreases (hypoxia) at the time of apnea, respiration against a closed upper airway will activate the carotid receptors that cause Brady cardia, not tachycardia.
- During wakefulness, upper airway caliber is smaller in patients with sleep apnea compared with that in normal individuals, Individuals with OSA demonstrate an excess of upper airway soft tissue within the craniofacial structures that envelop the pharyngeal lumen.
- The respiratory effort to overcome the increased airway resistance, leading to the apneas and hypopneas that characterize OSA followed by a Microarousal transition of deep sleep to light sleep just for seconds) to restore the breathing.
- This leads to increasing sympathetic activity, increase the Heart rate and the Binod pressure at the termination of apnea.
- Fat deposition within the tongue is greater in apneic individuals compared with body mass index-matched normal subjects.
- Redistribution of extracellular fluid can occur during sleep and in the supine position, leading to significant increases in neck circumference and airway collapsibility, and a reduction in upper airway cross-sectional area.
- during the apnea, Bradycardia will occur but at the time of arousal, tachycardia will occur.
Epidemiology and risk factors:
- Age: The prevalence of OSA increases through mid-life, but plateaus after age 60-65 years.
- Gender: OSA is 2 to 3 times more prevalent in men than in women, Postmenopausal women are at a threefold risk for OSA compared with premenopausal women, likely related to lower levels of reproductive hormones.
- Obesity is the strongest risk factor for OSA. The prevalence of OSA progressively increases as the BMI and associated markers (e.g., waist-to-hip ratio) increase. Apple-shaped people are at higher risk than peer-shaped shaped they may develop Metabolic syndrome, DM, and OSA (but its absence can’t exclude OSA).
- Large neck circumference (collar size > 17 inches in males, > 16 inches in females).
- Family history.
- Specific genetic disorders (e.g., Down’s syndrome).
- Endocrine disorders: hypothyroidism and polycystic ovarian syndrome.
- Past stroke: may cause or result from OSA.
- Cardiovascular diseases: may be the cause of OSA or secondary to it.
- Crowded oropharyngeal airway: Upper airway and craniofacial anatomic features, such as macroglossia, overbite, narrow throat, enlargement of the soft palate, tonsillar and adenoidal hypertrophy, an elongated or enlarged uvula, a high arched or narrow palate, nasal abnormalities (e.g., septa I deviation or polyps), retrognathia, and micrognathia, all increase the risk for OSA.
Symptoms
- Snoring and daytime sleepiness are the most common presenting complaints of OSA, Daytime sleepiness is a common feature of OSA. However, it may go unnoticed, or its significance may be underestimated because of its insidious onset and chronicity, The patient may not describe the symptom as sleepiness, but may use other terms, such as fatigue. Careful questioning of the patient typically reveals a pattern of feeling sleepy or falling asleep in boring, passive, or monotonous situations. Moreover, it is the bed partner who frequently motivates the patient’s first visit to the clinician, complaining about intolerable snoring, snorts, and disconcerting apneas.
- Loud snoring: Most patients with OSA first come to the attention of a clinician due to a complaint about snoring.
- Resuscitative snorts (periods of silence terminated by loud snoring) during sleep.
- Witnessed apneas by bed partner.
- Restless sleep.
- Awakening with a sensation of choking, gasping, or smothering. Nocturnal choking or gasping is the most suggestive individual finding for OSA.
- Non-refreshing sleep and morning headache.
- Awakening with a dry mouth or sore throat due to mouth breathing.
- Nocturia: During apnea, the dilator muscles close the airway, but the respiratory muscles are activated so this increases the negative intrathoracic pressure >> increase venous return >> dilatation of the right atrium will increase ANP (Atrial Natriuretic Peptide) causes diuresis and nocturia.
- Symptoms attributable to disrupted sleep (e.g., excessive daytime sleepiness, fatigue, depression, irritability, inattention, morning headaches, poor neurocognitive performance (poor concentration, impaired memory, or concentration), erectile dysfunction, and motor vehicle accidents (due to sleeping while driving).
- All patients being evaluated for known or suspected OSA should be asked about recent motor vehicle crashes or near misses attributable to sleepiness. Motor vehicle crashes are two to three times more common among patients with OSA than without OSA. Treatment with continuous positive airway pressure (CPAP) reduces self-reported crashes.
- Insomnia: a small portion of patients with OSA complain of insomnia rather than daytime sleepiness because they are unable to maintain sleep.
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