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Sleep apnea
- 1.
- 2. • Sleep apneais defined as the cessation of airflow at the nose andvmouth lasting at least 10 seconds. • Sleep apnea is quantified using polysomnography (PSG) and is classified into two major categories: • obstructive and central. • Central sleep apnea involves impairment of the respiratory drive, while obstructive sleep apnea is caused by intermittent upper airway obstruction.
- 3. • Some patientswill experience both central and obstructive sleep apnea. • Patients with this sleep disorder have a high risk of morbidity and mortality
- 4. • Sleep apneais very common. Approximately 9% of females and 24% of males experience sleep apnea. • Sleep apnea is two to three times more common in men, and it is more common in middle-aged men than in younger men. • As many as 80% of middle-aged men snore, and 25% of heavy snorers have sleep apnea. • Sleep apnea may be less prevalent in elderly patients, and it is theorized that this may be evidenced by sleep apnea’s effect on mortality
- 5. OBSTRUCTIVE SLEEP APNEA • Obstructive sleep apnea (OSA) is a potentially life-threatening condition characterized by snoring. • At one end of the spectrum are those individuals who snore intermittently with little sleep disruption, and at the other end are patients who snore heavily and have severe gas exchange disturbances and respiratory failure, causing them to gasp for air. • These episodes are repeated as often as 600 times per night.
- 6. • As aresult of these frequent arousals, hypoxia and sleep fragmentation occur. • Hypoxia may lead to daytime sleepiness, impaired attention and memory, and personality changes. • Individuals with sleep apnea are usually not aware of the snoring or respiratory pauses, and symptoms are most frequently reported by their bed partner.
- 7. • OSA iscaused by occlusion of the upper airway due to factors such as obesity, and fixed upper airway lesions such as polyps, as well as enlarged tonsils or adenoids or the tongue. • It can also be caused by acromegaly, amyloidosis, and hypothyroidism, as well as neurological conditions that impair upper airway muscle tone. • Medical complications include arrhythmias, hypertension, cor pulmonale, and sudden death.
- 8. • Treatment ofOSA must be individualized and depends on the severity of the disordered breathing and the amount of sleep disruption. • Patients with severe apnea (>20 episodes per hour on PSG and excessive daytime somnolence) and those with moderate apneas (5 to 20 episodes per hour on PSG and excessive daytime somnolence or other daytime symptoms) have shown significant improvement and reduction in mortality with treatment. • Nonpharmacologic measures are the treatments of choice.
- 9. • Weight lossmay eliminate the apnea and reduce daytime hypersomnia; however, improvement is only limited. • Treatment of underlying causes of obstruction (e.g., tonsillectomy, nasal septal repair, and nonsedating antihistamines for allergic rhinitis) may eliminate apneas during sleep. • In patients with mild apnea and snoring with no daytime symptomatology, management may include avoidance of a supine sleep position.
- 10. • Continuous positiveairway pressure (CPAP) during sleep is the standard treatment for most patients with OSA. • CPAP acts as a splint to maintain the patency of the oropharynx during respiration. • Compliance is variable, ranging from 25% to 70%, and is the major limitationof this treatment. • One night of noncompliance results in a complete reversal of the gains made in daytime alertness
- 11. • The mostimportant pharmacologic intervention is the avoidance of all CNS depressants (e.g., alcohol, anxiolytics, hypnotics, narcotics, and zolpidem). • Preliminary studies suggest that zaleplon does not interfere with respiratory function. • CNS depressant use is potentially lethal since it inhibits the brain’s reflex ability to cause a mini-arousal and resume breathing
- 12. • Medication therapyshould be reserved for patients with mild OSA and those who are treatment resistant. • Protriptyline in doses of 10 to 30 mg daily reduces the frequency of apneas and increases oxygen saturation.
- 13. • The mechanismof action may be related to a decrease in REM sleep, the sleep stage in which most apneas occur. • Imipramine was found to exert similar effects to protriptyline in two uncontrolled studies. • Fluoxetine and paroxetine have shown results similar to those of protriptyline, with fewer adverse effects.
- 14. • The SSRIsmay be preferable to tricyclic antidepressants due to their similar efficacy but fewer adverse effects. • Medroxyprogesterone (MPG) has proved disappointing in OSA, showing no results in curing nighttime apnea. • In contrast, MPG does appear to have a beneficial effect in daytime hypercapnia. • At present the only role for MPG is in OSA patients with awake respiratory failure or noncompliance with CPAP.
- 15. • Theophylline isa respiratory stimulant that has been frequently used in patients with OSA. • Studies with theophylline have shown questionable efficacy. • Some studies have shown a reduction in obstructive events, but an increase in the number of arousals, increasing daytime sleepiness. • Mixed reviews have also been found for antihypertensive agents.
- 16. • Studies haveevaluated the effects of angiotensin-converting enzyme inhibitors, calcium channel blockers, metoprolol, and clonidine, showing reduction in the frequency of apnea. • Studies have also shown that antihypertensives can increase OSA. • Thus the efficacy of these agents is unclear.
- 17. CENTRAL SLEEP APNEA • Central sleep apnea (CSA) is a form of apnea in which breathing effort is not detected, in contrast to obstructive apnea, in which attempts at breathing are vigorous. • CSA makes up only 10% of all apneas. Hypercapnic patients usually present with a morning headache and daytime somnolence, while nonhypercapnic patients complain of insomnia and nocturnal awakenings with shortness of breath or gasping.
- 18. • Although themajority of cases are idiopathic, identifiable causes are nasal obstruction, autonomic nervous system lesions (e.g., cervical cordotomy), neurological diseases (e.g., poliomyelitis, encephalitis, and myasthenia gravis), and congestive heart failure.
- 19. • The primarytreatment approach for CSAis supplemental oxygen and CPAP. • Pharmacologic treatments include acetazolamide, theophylline, and MPG. • Acetazolamide induces a metabolic acidosis that stimulates respiratory drive. • Long-term studies have shown a 70% reduction in CSA with acetazolamide, and no effect on obstructed breathing events.
- 20. • It hasbeen suggested that acetazolamide induces a resetting of the CO2 response threshold. • Clinical use is limited because of adverse effects such as electrolyte changes, paresthesias, and precipitation of calcium phosphate salts in alkaline urine. • Theophylline may have some efficacy in CSA related to congestive heart failure.
- 21. • In onetrial there was a 60% reduction in central apneas per hour of sleep compared with 20% with placebo,29 but further study is needed. • In nonhypercapnic CSA patients, treatment may consist of benzodiazepines (triazolam or temazepam) to reduce arousals, and acetazolamide, CPAP, and oxygen to stabilize breathing patterns