| |
AccessPharmacy's Quick Test lets you test your pharmacologic knowledge and anonymously compare your results to those of your peers. Sign up for our free AccessPharmacy e-newsletter and twice a month Quick Test will appear in your email inbox. Quick Test is developed by Terry L. Schwinghammer, PharmD, AccessPharmacy's Editor-in-Chief, from the site's online resources. Your results will be ranked against those of your peers.
|
|
Quick Test posted on 10.31.11:
| Sleep Apnea and its Treatment
| SLEEP APNEA
Approximately 15 million Americans have sleep-disordered breathing. The prevalence of sleep apnea in the U.S. adult population is 4% in males and 2% in females. It appears to be more common in African Americans and less common in Asian populations. Sleep apnea also occurs in children and adolescents. It is characterized by repetitive episodes of cessation of breathing during sleep followed by blood oxygen desaturation and brief arousal from sleep to restart breathing. As a result, individuals with sleep apnea experience fragmented sleep, poor sleep architecture, and periods of apnea and hypopnea. Polysomnography (PSG) is used to diagnose and quantify sleep apnea as central, obstructive, or mixed. Central sleep apnea (CSA) involves impairment of the respiratory drive, whereas obstructive sleep apnea (OSA) is caused by upper airway collapse and obstruction. Patients with mixed sleep apnea experience both central and obstructive sleep apnea. Severity of sleep apnea is determined by the number of apnea (total cessation of airflow) and hypopnea (partial airway closure with blood oxygen desaturation) episodes documented by PSG, and is expressed by calculating the respiratory disturbance index (RDI). Mild sleep apneics have an RDI of between 5 and 15 episodes per hour, moderate 15 to 30, whereas individuals with severe OSA can exhibit more than 30 episodes per hour.
Sleep apnea can affect behavior, cognitive abilities, and systemic disease. Neurocognitive sequelae are important factors in motor vehicle accidents, loss of work-related productivity, and personality changes. Alleviation of sleep disordered breathing can have a beneficial impact on both cardiovascular and neurobehavioral conditions.
| OBSTRUCTIVE SLEEP APNEA
OSA is characterized by partial or complete closure of the upper airway, posterior from the nasal septum to the epiglottis, during inspiration. The reason for the loss of upper airway patency is not fully understood and is likely caused by several competing factors. Anatomical factors including neck obesity, narrow airway, and fixed upper airway lesions (e.g., polyps, enlarged tonsils) can narrow the upper airway. Intraluminal negative pressure generated during each inspiration also promotes collapse of the upper airway that competes with dilating forces, primarily the pharyngeal dilator muscle. Acromegaly, amyloidosis, and hypothyroidism as well as neurologic conditions that impair upper airway muscle tone may cause OSA. The hallmarks of OSA are witnessed apneas, gasping, or both. Other recognized signs, symptoms, and considerations of sleep apnea include obesity, snoring, hypertension, daytime sleepiness, and family history.
OSA is increasingly linked to cardiovascular and cerebrovascular morbidity and mortality, independent of other risk factors. Individuals with OSA are at risk for developing hypertension, and when hypertension is present, it is often resistant to drug therapy. Alleviation of sleep disordered breathing (with nasal continuous positive airway pressure) can improve blood pressure and attenuate some of the potential hemodynamic and neurohumoral responses that may link OSA to systemic disease.
| TREATMENT: OBSTRUCTIVE SLEEP APNEA
In the absence of an underlying cause (e.g., hypothyroidism, acromegaly), alleviation of sleep disordered breathing is the primary goal of treatment. Nonpharmacologic measures are the treatments of choice. There is no drug therapy for OSA. However, medications that worsen sleep should be avoided. Practice parameters for the treatment of OSA have been published by the American Academy of Sleep Medicine.
| Nonpharmacologic Therapy
Positive Airway Pressure
Nasal positive airway pressure (PAP) during sleep is the standard treatment for most patients with OSA. PAP produces a positive pressure column in the upper airway using room air to maintain patency. A flexible tube connects the PAP machine to a mask that covers the nose.
PAP delivery may be continuous (CPAP) or bilevel, providing a reduced applied pressure during expiration. During PSG, the pressure setting is increased (up to 20 cm H2O) until sleep-disordered breathing is eliminated. Barriers to PAP adherence, such as ill-fitted mask and nasal dryness, can be managed. PAP nonadherence for one night results in a complete reversal of the gains made in daytime alertness. In the clinical setting, poor PAP adherence may impact blood pressure control and management in patients with OSA and hypertension.
| Weight Reduction
Obesity can worsen sleep apnea, and weight management should be implemented for all overweight patients with OSA. OSA can itself predispose to weight gain and in obese patients with mild OSA weight loss alone can be effective. Individuals who are morbidly obese and have severe OSA can undergo gastric stapling for weight loss.
| Surgery
Surgical therapy (uvulopalatopharyngoplasty) opens the upper airway by removing the tonsils, trimming and reorienting the posterior and anterior tonsillar pillars, and removing the uvula and posterior portion of the palate. This is not a first-line option because it is invasive. In very severe cases tracheostomy can be necessary. This procedure can be indicated for select individuals that are morbidly obese, have severe facial skeletal deformity, experience severe drops in oxygen saturation (e.g., less than 70%), or have significant cardiac arrhythmias associated with their OSA.
| Other Therapies
For individuals that experience OSA only during certain sleep positions (e.g., on their back), positional therapies can be effective alone but are usually used in conjunction with PAP therapy. Oral appliances can be used to advance the lower jawbone and to keep the tongue forward to enlarge the upper airway. These therapies should be considered when PAP therapy cannot be tolerated.
| Pharmacologic Therapy
The most important pharmacologic intervention is the avoidance of all CNS depressants (e.g., alcohol, hypnotics) and drugs that promote weight gain. Weight gain worsens OSA. CNS depressant use is potentially lethal as it reduces the brain's reflex ability to cause a mini-arousal and resume breathing. In addition, certain CNS depressants can relax airway muscles, promoting upper airway collapse. Medications that can cause rhinopharyngeal inflammation and cough as a side effect of therapy (i.e., ACE inhibitor) may also worsen sleep-disordered breathing.
There is no drug therapy for OSA. In clinical trials, serotonergic agents (e.g., fluoxetine, paroxetine), tricyclic antidepressants (TCAs) (i.e., imipramine, protriptyline), respiratory stimulants (aminophylline and theophylline), medroxyprogesterone, and clonidine do not clinically improve severity of OSA. The effects of antihypertensive agents on sleep apnea are inconsistent and are likely not clinically significant.
Modafinil (Provigil) is a wake-promoting medication and is FDA approved to improve wakefulness in patients who have residual daytime sleepiness while treated with PAP. Initiation of wake-promoting medications should only be attempted in patients who are using optimal PAP therapy to alleviate sleep-disordered breathing and are free of cardiovascular disease. In patients with concurrent rhinitis, nasal steroids are recommended for use along with PAP therapy.
| Evaluation of Therapeutic Outcomes
Individuals with sleep apnea should be evaluated after 1 to 3 months of treatment for improvement in alertness and daytime symptoms (improvement in memory and decreased irritability) and weight reduction. Individuals experiencing symptoms (e.g., daytime sleepiness, snoring, loss of blood pressure control) despite PAP therapy should have PSG repeated. Symptoms can recur if patients gain weight, requiring a higher pressure setting. Conversely, PAP pressure settings can be decreased if weight loss is achieved. Patient adherence to PAP therapy can be monitored by assessing the built-in compliance meter that measures the hours used at effective pressure.
| CENTRAL SLEEP APNEA
CSA causes fragmented sleep and consequent daytime somnolence. However, unlike OSA, arousals from sleep are not required to initiate airflow. During PSG, there is an absence of airflow out of the mouth and nose with no activation of the inspiratory muscles. The prevalence of CSA is not well established and is less than OSA. CSA can be idiopathic but more commonly is caused by underlying autonomic nervous system lesions (e.g., cervical cordotomy), neurologic diseases (e.g., poliomyelitis, encephalitis, and myasthenia gravis), high altitudes, and congestive heart failure. For these reasons, potential underlying causes for CSA should be evaluated and treated. For example, worsening CSA in heart failure patients can signal the need to optimize heart failure therapies.
A few medications have been studied in the setting of high altitude, heart failure, and idiopathic CSA, including acetazolamide, which induces a metabolic acidosis that stimulates respiratory drive, and theophylline, which improves severity of CSA but has no effect on clinical variables. PAP therapy with or without supplemental oxygen also improves CSA. However, due to the lack of randomized trials there is no consensus on if and how CSA should be routinely managed, particularly in the setting of heart failure.
|
| | | About AccessPharmacy | Core Curriculum | Subscription Information | Advisory Board | Contact Us | Help | Privacy Notice | Terms of Use | Notice | Additional Credits and Copyright Information
 
Copyright © 2011 The McGraw-Hill Companies, Inc. All rights reserved. Any use is subject to the Terms of Use and Notice. For further information about this newsletter, contact onlinecustomer_service@mcgraw-hill.com.
You have received this message because you opted-in to receive information and special offers from McGraw-Hill Professional. We hope you enjoyed receiving this message. However, if you would like to unsubscribe from receiving emails from McGraw-Hill Professional, please follow this link.
UNSUBSCRIBE
If you would like to update your preferences, please visit: http://www.mhprofessional.com/account/?mode=interest&action=unsub&e=ignoble.experiment@arconati.us .
You can also write to us at: Privacy Officer, McGraw-Hill Professional, 1221 Avenue of Americas, 46th Floor, 10020. View our Corporate Privacy Policy at http://www.mcgraw-hill.com/privacy.html. To learn more about how McGraw-Hill Professional applies this Policy, you can contact privacy@mhedu.com. Copyright © 2011, The McGraw-Hill Companies, Inc. |  |
