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Sleep Apnea: The Noisy Killer Ahmed Syed Ali, M.D., and John E. Morley, M.D. Dr. Ali is a visiting scientist in the Division of Geriatric Medicine at Saint Louis University Health Science Center. Peto: "Falstaff is fast asleep behind the arris and snorting like a horse."Like snoring, sleep apnea is much older than Shakespeare, but only recently has it been understood as something different from ordinary snoring, and as a potentially deadly disease. Depending on its severity and its cause, sleep apnea is associated with a variety of heart and breathing problems, including heart arrhythmias, high blood pressure, hardening of the arteries, even heart failure and death. It is a peculiarity of this noisy disease that it announces itself to everyone within earshot -- except its victims. The medical definition of sleep apnea is a temporary stoppage of breathing during sleep, occurring at least 30 times during the night. The stoppage must be longer than the usual interval between breaths while asleep. Ten seconds is normal for adults. There are three basic kinds of sleep apnea: the pure central type (CSA), which is caused by problems with the lungs or the breathing mechanism itself; the obstructive type (OSA), in which an obstruction interferes with normal airflow; and mixed sleep apnea (MSA), which combines features of both. Because the vast majority of cases are obstructive, when people discuss sleep apnea, most of the time they are referring to OSA. Sleep apnea is an extremely common condition in older persons, occurring in at least 50% of persons over 60 years.1 For comparison, sleep apnea occurs in only 6% of middle aged women and 9% of middle aged men. The History of Sleep Apnea Both central and obstructive apnea had been observed by doctors as early as 1877. Later, researchers Osler and Burwell2 named the combination of obesity; hypersomnolence, or excessive sleepiness; and inadequate airflow to the lungs during sleep as "Pickwickian Syndrome," after a loud-snoring character from Charles Dickens' novel, Pickwick Papers. In 1965, a team led by a Doctor Gastaut3 simultaneously recorded sleep and breathing patterns in a patient with Pickwickian Syndrome and found distinct patterns corresponding to all three types of apneas. In 1969, doctors began to treat OSA by tracheostomy. This operation involved bypassing the upper airway and mouth by cutting an opening in the trachea and inserting a breathing tube. Since then, researchers have learned a great deal more about sleep apnea, in particular how to identify the many different parts of the mouth and upper airway that may be involved in the condition. This better understanding has led to many new treatments. The Three Types of Sleep Apnea Central Sleep Apnea (CSA) In CSA, respiratory muscle activity simply stops for periods of time. Pure CSA is uncommon; it occurs as a result of lung problems or in people with a brain stem lesion. So-called "Cheyne-Strokes respiration" is a form of central sleep apnea found in patients with congestive heart failure, stroke, or kidney disease. The exact cause of CSA is often unknown, but recent findings suggest that enhanced sensitivity to carbon dioxide might play a pivotal role.4 Mixed Sleep Apnea (MSA) In MSA the breathing mechanism stops for a time. When it resumes, it is obstructed as in OSA. Obstructive Sleep Apnea (OSA) In OSA, the lungs operate normally, but airflow is blocked because the upper airway becomes temporarily narrowed or closed. The site of obstruction may be anywhere from the nose to the glottis. Most frequently, the primary obstruction occurs in the nasopharynx, at the level of the soft palate. Unlike CSA and MSA, OSA is fairly widespread.5 In the US, more than three million men and one and a half million women suffer from OSA, as defined by an Apnea Index of five or more, plus daytime sleepiness. The Apnea Index equals the average number of apnea episodes per hour of sleep. How Obstructive Sleep Apnea Occurs Most people with OSA have a smaller than normal pharynx, or a pharynx that is abnormally collapsible. Normally, our pharynxes are capable of collapsing or changing shape to some degree; otherwise we would not be able to speak or swallow. When the pharynx serves as a conduit of airflow, however, it must be able to resist collapse in order to remain open. These various functions are regulated by a group of muscles that alter the shape or narrow the pharynx for swallowing or talking, but hold it open when we inhale. Even in normal people who do not suffer from OSA, sleep interferes with this regulating mechanism. It does this by6 relaxing the upper airway muscles and dulling the reflexes that prevent the pharynx from collapsing. Partial collapse results in snoring and, in some cases, prolonged hypoventilation, or insufficient air flow to the lungs. Complete closure results in apnea. The body's usual response to apnea is to wake itself enough that the muscles in the pharynx can act to clear the obstruction. These repeated or partial wakings interfere with normal sleep patterns and leave sufferers sleepy during the day. Health Problems Caused by Sleep Apnea Sleep Apnea can lead to heart arrhythmias, particularly bradycardia, or a slowing down of the heartbeat. It can also cause atrio-ventricular block, or interference with the electrical impulses that regulate the heartbeat. On top of that, once airflow is reestablished, sufferers can experience tachycardia, or speeding up of the heartbeat; or rapid, irregular twitching of the heart muscles. Other bad effects of sleep apnea include severe hypoxia, or lowered levels of oxygen in the bloodstream; congestive heart failure; pulmonary hypertension, or high blood pressure in the lungs; and hypertension, or high blood pressure. Studies show that sleep apnea sufferers are at increased risk for early death, though not necessarily during sleep. Studies of people in nursing homes have found that, for some reason, women with sleep apnea are especially prone to premature death. Also associated with sleep apnea are accelerated atherosclerosis, or hardening of the arteries, and myocardial infarction, or lack of blood supply to part of the heart.7 Are You at Risk for OSA? You are more likely to come down with OSA if you are over 50 years of age or have any of the following risk factors:
Because they are asleep when they experience the most obvious symptoms, many sufferers are completely unaware that they have sleep apnea at all. It is usually a tired and annoyed bed partner who urges a sleep apnea sufferer to see the doctor. The typical sleep apnea sufferer has OSA. He is a hypertensive, obese, middle-aged or older man with a large neck (collar size of 17.5 or greater) and an abnormally "crowded" upper airway. He may also have some or all of the following symptoms:
If enough of these symptoms are present or there is some other reason to suspect sleep apnea, the doctor will run tests that include a screen for hypothyroidism, arterial blood gases to detect hypoxemia, an EKG to detect arrhythmia or complete heart block, heart x-ray, and hemoglobin analysis. Even after testing, sleep apnea can be difficult to diagnose.8,9,10 For this reason, doctors have come up with something called the "Sleep Apnea Clinical Score." A patient with a score of 10 or lower has a very low probability of having sleep apnea and does not need further evaluation. A patient with a score of 15 or higher has a high probability of having sleep apnea and should be tested further. Those with scores between 10 and 15 should be given a home apnea test. Devices such as the Sleep Apnea Clinical Score are helpful in making a diagnosis, but they are not an exact science. For example, it is probably a good idea for anyone with otherwise unexplained excessive daytime sleepiness to see a doctor for evaluation; and a sleepy, loud snorer who appears to experience apneas should be examined during sleep, even in the absence of risk factors such as, say, a large neck. The best way to examine a suspected OSA sufferer during sleep is with a test called polysomnography. This test monitors a variety of physiological factors during sleep, including heart rate, breathing, and the level of oxygen saturation in the blood. A complete work-up for OSA also includes otolaryngological examination, electroencephalography, electroocculography, electromyography, electrocardiography, oximetry, and measurement of respiratory effort and airflow. Non-Surgical Treatments for OSA Behavioral treatments for the disease include:
Orthodontic devices (which hold the lower jaw forward) and tongue retaining appliances (which hold the tongue forward) are helpful for some sufferers, especially those with mild or so-called "positional" apnea. In 1981, sleep apnea was reported to be cured by utilizing a vacuum-cleaner blower motor which blew air through silastic tubing into the nose.11 This is called nasal continuous positive airway pressure, or CPAP. CPAP has been a major advance in mechanical treatment and has largely replaced tracheostomy. A major drawback of CPAP is that it is uncomfortable and that it must be used all night, every night. Because of this, only 75% of OSA sufferers continue to use nasal CPAP for more than one year. Surgical Treatments for OSA The standard surgical treatments for OSA are: Uvulopalatopharyngoplasty -- cutting off of some pharyngeal soft tissue and amputation of approximately 15 mm of the free edge of the soft palate and uvula -- can be helpful for some OSA sufferers. Only half of all operations, however, are successful. Tonsillectomies (removal of the tonsils), with or without adenoidectomy (removal of the adenoids), and nasal septoplasty (alteration or removal of parts of the septum, or nasal wall) are commonly used to relieve upper airway obstruction. Tracheostomy, the original surgical treatment for OSA, has numerous adverse effects, including causing difficulty with speech and problems with infection. Today, this procedure is reserved for patients with life-threatening arrhythmias or other severe disability, who have failed to respond to less radical treatments. There is also a number of newly-developed, advanced surgical techniques that have been developed for OSA. These are highly technical and should be discussed with a specialist. They include:
Sleep apnea is a common problem, particularly for the elderly. Fortunately, it is also a treatable condition and one that is much better understood and better treated with each passing year. If ignored, sleep apnea can have serious health consequences. Anyone who has several of the risk factors or who is experiencing any of the symptoms of sleep apnea should be evaluated by a doctor.
References 1. Janssen JP, Pache JC, Nuod LP. Physiological changes in respiratory function associated with aging. Eur Respir J 13:197-205, 1999. return 2. Stoohs R, Guilleminault C: Cardiovascular changes associated with the obstructive sleep apnea syndrom. J Appl Physio 72:582-589, 1992. return 3. Gastaut, H, Tassarini, CA, Duron, B. Ploygraphic study of the episodic diurnal and nocturnal (hypnic and respitory) manifestation of the Pickwick syndrom. Brain Res 1965;2:167. return 4. Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Eng J Med 341: 949-54, 1999. return 5. Pack, AI. Obstructive sleep apnea. Advances in Internal Medicine. 1994;39:517. return 6. Mezzanotte, WS, Tangel, DJ, White, DP. Walking genioglossal EMG in sleep apnea patients vesus normal controls (a neuromuscular compensatory mechanism). J clin Invest 1992;89:1571. return 7. Ohga, Eijiro, Takahide Nagase, Tetsuji Tomita, Shinji Teramoto, Takeshi Matsuse, Hirrofumi, and Yasuyoshi Ouchi. Increased levels of circulating ICAM-1, VCAM-1, and L-selectin in obstructive sleep apnea syndrom. J. Appl. Physio. 87(1):10-14, 1999. return 8. Viner, S, Szalai, JP. Hoffstien, V. Are history and physical examination good screening test for sleep apnea? Annals of Internal Medicine 1991;115:356. return 9. Crocker, BD, Olson, LG, Saunders, NA, et al. Estimation of the probability of disturbed breathing during sleep before a sleep study. Am Rev Respir Dis 1990;142:14. return 10. Flemons, WW, Whitelaw, WA, Brant, R, Remmers, JE. Likehood ratios for a sleep apnea clinical prediction rule. Am J Respir Crit Care Med 1994;150:1279. return 11. Sullivan CE, Issa FG, Berthon-Jones M, et al: Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares. Lancet 1:862-865, 1981. return 12. David W. Eisele, MD: Phillip L. Smith, MD: Daniel S. Alam: Alan R. Schwartz, MD. Direct hypoglossal nerve stimulation in obstructive sleep apnea. Arch Otolaryngo Head Neck Surg. 1997;57-61. return 13. Chabolle F, Wagner I, Blumen MB, Sequert C, Fleury B, De Dieuleveult T. Tongue base reduction with hyepiglottoplasty: a treatment for sever obstructive sleep apnea. Laryngoscope. 109(8):1273-80, 1999 Aug. return |
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