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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 14 of 14. This is the beginning of the thread.
Posted by FredPotter on February 18, 2007, at 16:00:42
I wonder how many of us have this. I'm told I snore and stop breathing during the night. It's the most likely explanation for day-time sleepiness. If you've never had this it may sound unimportant, but it makes life desparately difficult. OSA is very common, particularly in people over 50, and is said to cause all sorts of things, eg depression. So my question is: is poor sleep, perhaps caused by OSA, the cause of some of our symptoms? Or is poor sleep the result of anxiety and depression? Maddeningly OSA seems to correlate strongly with insomnia
Fred
Posted by Larry Hoover on February 18, 2007, at 19:36:41
In reply to Obstructive Sleep Apnoea (OSA), posted by FredPotter on February 18, 2007, at 16:00:42
I would say that poor sleep is a cause of some of the symptoms, and could be a primary cause of depression. With OSA, you could be waking 50-150 times a night, but have no memory of those wakenings. You should get into a sleep clinic, where they'll monitor your sleep (called polysomnography). If you have OSA, and these wakenings, you'll likely get a positive airway pressure mask set-up. It keeps your airway from collapsing, and you don't have the apnea any more.
I think whoever told you about your apnea has done you a big favour.
Best,
Lar
Posted by FredPotter on February 18, 2007, at 21:42:25
In reply to Re: Obstructive Sleep Apnoea (OSA) » FredPotter, posted by Larry Hoover on February 18, 2007, at 19:36:41
Thanks Larry. I found out about obstructive sleep apnoea by searching the net I think. No doctor or psych has ever suggested it. Unfortunately there's a 2 year waiting list for sleeping tests in New Zealand. So I brought it up with my Doc who said apnea was a possibility and you can buy for about 85 American $ a plastic suction cap that fits over the tongue, so you go to sleep with your tongue stuck out. Terrible price. There are also compliance problems, like it gives me ulcers and soreness under the tongue and drops out while I'm asleep.
This device is called an AveoTSD and is developed in NZ, although I think it's about to hit the States.
Fred
Posted by Phillipa on February 18, 2007, at 21:48:07
In reply to Re: Obstructive Sleep Apnoea (OSA) » Larry Hoover, posted by FredPotter on February 18, 2007, at 21:42:25
I just know I could never sleep with a mask on my face. I don't snore maybe once in a while. And Fred come here or Europe for a real sleep test. Love Phillipa ps or go to Lar's
Posted by sdb on February 19, 2007, at 14:52:00
In reply to Obstructive Sleep Apnoea (OSA), posted by FredPotter on February 18, 2007, at 16:00:42
> I wonder how many of us have this. I'm told I snore and stop breathing during the night. It's the most likely explanation for day-time sleepiness. If you've never had this it may sound unimportant, but it makes life desparately difficult. OSA is very common, particularly in people over 50, and is said to cause all sorts of things, eg depression. So my question is: is poor sleep, perhaps caused by OSA, the cause of some of our symptoms? Or is poor sleep the result of anxiety and depression? Maddeningly OSA seems to correlate strongly with insomnia
> FredHi Fred,
If you think you have a OSAHS (HS = hypopnoe syndrom) I would discuss that with your doctor. If you awake during sleep and think that you have a fragmented sleep-awake rythm
these are symptoms for OSAHS. If your smoking or you're obese try to stop this. OSAHS can cause a cor pulmonale (right heart failure) and a circulus vitiosus which can be progressing a do harm to you. Of course there are treatments for that discuss that with your doc and google, collect information in the internet.http://www.healthcentral.com/common/includes/tip_sleep.html
sdb
Posted by sdb on February 19, 2007, at 15:05:10
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred, posted by sdb on February 19, 2007, at 14:52:00
> > I wonder how many of us have this. I'm told I snore and stop breathing during the night. It's the most likely explanation for day-time sleepiness. If you've never had this it may sound unimportant, but it makes life desparately difficult. OSA is very common, particularly in people over 50, and is said to cause all sorts of things, eg depression. So my question is: is poor sleep, perhaps caused by OSA, the cause of some of our symptoms? Or is poor sleep the result of anxiety and depression? Maddeningly OSA seems to correlate strongly with insomnia
> > Fred
>
> Hi Fred,
>
> If you think you have a OSAHS (HS = hypopnoe syndrom) I would discuss that with your doctor. If you awake during sleep and think that you have a fragmented sleep-awake rythm
> these are symptoms for OSAHS. If your smoking or you're obese try to stop this. OSAHS can cause a cor pulmonale (right heart failure) and a circulus vitiosus which can be progressing a do harm to you. Of course there are treatments for that discuss that with your doc and google, collect information in the internet.
>
> http://www.healthcentral.com/common/includes/tip_sleep.html
>
> sdbHere's some additional information (harrison's 16th)
247
Sleep Apnea
Eliot A. Phillipson
Sleep apnea is defined as an intermittent cessation of airflow at the nose and mouth during sleep. By convention, apneas of at least 10 s duration have been considered important, but in most patients the apneas are 20 to 30 s in duration and may be as long as 2 to 3 min. Sleep apnea syndrome refers to a clinical disorder that arises from recurrent apneas during sleep. The clinical importance of sleep apnea arises from the fact that it is one of the leading causes of excessive daytime sleepiness and contributes to important cardiovascular disorders. Indeed, epidemiologic studies have established a prevalence of clinically important sleep apnea of at least 2% in middle-aged women and 4% in middle-aged men.
Sleep apneas can be central or obstructive in type. In central sleep apnea (CSA) the neural drive to all the respiratory muscles is transiently abolished. In contrast, in obstructive sleep apnea (OSA) airflow ceases despite continuing respiratory drive because of occlusion of the oropharyngeal airway.
OBSTRUCTIVE SLEEP APNEA
PATHOGENESIS
The definitive event in OSA is occlusion of the upper airway usually at the level of the oropharynx. The resulting apnea leads to progressive asphyxia until there is a brief arousal from sleep, whereupon airway patency is restored and airflow resumes. The patient then returns to sleep, and the sequence of events is repeated, often up to 400 to 500 times per night, resulting in marked fragmentation of sleep.
The immediate factor leading to collapse of the upper airway in OSA is the generation of a critical subatmospheric pressure during inspiration that exceeds the ability of the airway dilator and abductor muscles to maintain airway stability. During wakefulness, upper airway muscle activity is greater than normal in patients with OSA, presumably to compensate for airway narrowing (see below) and a high upper airway resistance. Sleep plays a permissive but crucial role by reducing the activity of the muscles and their protective reflex response to subatmospheric airway pressures. Alcohol is frequently an important cofactor because of its depressant influence on the upper airway muscles and on the arousal response that terminates each apnea. In most patients the patency of the airway is also compromised structurally and is therefore predisposed to occlusion. In a minority of patients the structural compromise is due to obvious anatomic disturbances, such as adenotonsillar hypertrophy, retrognathia, and macroglossia. However, in the majority of patients the structural defect is simply a subtle reduction in airway size that can often be appreciated clinically as “pharyngeal crowding” and that can usually be demonstrated by imaging techniques. Obesity frequently contributes to the reduction in size of the upper airways, either by increasing fat deposition in the soft tissues of the pharynx or by compressing the pharynx by superficial fat masses in the neck. More sophisticated studies also demonstrate a high airway compliance—i.e., the airway is “floppy” and therefore prone to collapse.
PATHOPHYSIOLOGIC AND CLINICAL FEATURES
The narrowing of the upper airways during sleep, which predisposes to OSA, inevitably results in snoring. In most patients, snoring usually antedates the development of obstructive events by several years. However, the majority of snoring
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individuals do not have an OSA disorder, nor is there definitive evidence that snoring per se is associated with long-term health risks. Hence, in the absence of other symptoms, snoring alone does not warrant an investigation for OSA but does call for preventive counselling, particularly with regard to weight gain and alcohol consumption, and, when habitual, warrants conservative treatment similar to that for mild OSA (see below).
The recurrent episodes of nocturnal asphyxia and of arousal from sleep that characterize OSA lead to a series of secondary physiologic events, which in turn give rise in some patients to the clinical complications of the syndrome (Fig. 247-1). The most common manifestations are cognitive and behavioral disturbances that are thought to arise from the fragmentation of sleep and loss of slow-wave sleep induced by the recurrent arousal responses, and from nocturnal cerebral hypoxia. The most pervasive manifestation is excessive daytime sleepiness. Initially, daytime sleepiness manifests under passive conditions, such as reading or watching television; but as the disorder progresses, sleepiness encroaches into all daily activities and can become disabling and dangerous. Several studies have demonstrated two to seven times more motor vehicle accidents in patients with OSA compared with other drivers. Other related symptoms include intellectual impairment, memory loss, and personality disturbances.View Figure FIGURE 247-1 The primary sequence of events, physiologic responses, and clinical features of obstructive sleep apnea.
The other major manifestations of OSA are cardiorespiratory in nature and are thought to arise from the recurrent episodes of nocturnal asphyxia and of negative intrathoracic pressure, which increases left ventricular afterload (Fig. 247-1). Many patients demonstrate a cyclical slowing of the heart during the apneas to 30 to 50 beats per minute, followed by a tachycardia of 90 to 120 beats per minute during the ventilatory phase. A small number of patients develop severe bradycardia or dangerous tachyarrhythmias, leading to the notion that OSA may result in sudden death during sleep, but corroborative data are lacking. Unlike in healthy subjects, in patients with OSA systemic blood pressure fails to decrease during sleep. In fact, blood pressure typically rises abruptly at the termination of each obstructive event as a result of sympathetic nervous activation and reflex vasoconstriction. Furthermore, over 50% of patients with OSA have systemic hypertension. Several epidemiologic studies have implicated OSA as a risk factor for the development of systemic hypertension, and studies in an animal model demonstrate directly that OSA can cause sustained increases in daytime blood pressure. Emerging data also suggest that OSA can precipitate myocardial ischemia in patients with coronary artery disease and can adversely affect left ventricular function, both acutely and chronically, in patients with congestive heart failure. This complication is probably due to the combined effects of increased left ventricular afterload during each obstructive event, secondary to increased negative intrathoracic pressure (Fig. 247-1), recurrent nocturnal hypoxemia, and chronically elevated sympathoadrenal activity. Treatment of OSA in such patients often results in dramatic improvement in left ventricular function and in clinical cardiac status.
DIAGNOSIS
Although OSA occurs at any age, and is considerably more prevalent in women than was previously thought, the typical patient is a male aged 30 to 60 years who presents with a history of snoring, excessive daytime sleepiness, nocturnal choking or gasping, witnessed apneas during sleep, moderate obesity and large neck circumference, and often mild to moderate hypertension. In women with OSA, who are typically postmenopausal, the complaint of snoring is less frequent than in men, and daytime fatigue may be more common than outright sleepiness.
The definitive investigation for suspected OSA is polysomnography, a detailed overnight sleep study that includes recording of (1) electrographic variables (electroencephalogram, electrooculogram, and submental electromyogram) that permit the identification of sleep and its various stages, (2) ventilatory variables that permit the identification of apneas and their classification as central or obstructive, (3) arterial O2 saturation by ear or finger oximetry, and (4) heart rate. Continuous measurement of transcutaneous PCO2 (which reflects arterial PCO2) can also be very useful, particularly in patients with CSA. The key diagnostic finding in OSA is episodes of airflow cessation or reduction at the nose and mouth despite evidence of continuing respiratory effort. By the time most patients come to clinical attention they have at least 10 to 15 obstructive events per hour of sleep. Although controversial, recent data suggest that a high upper airway resistance during sleep (manifested by snoring) that is accompanied by recurrent arousals from sleep, even in the absence of apneas and hypopneas, can result in a clinically important sleep-related syndrome. Therefore, the absence of outright apneas and hypopneas in a symptomatic patient may not definitely exclude a sleep-related respiratory disorder.
Because polysomnography is a time-consuming and expensive test, there is considerable interest in the role of screening tests and of unattended home sleep-monitoring for the investigation of OSA. However, the predictive value of most screening tests is too low to be clinically definitive, and the role of unattended, simplified sleep studies in routine practice has yet to be established. Nevertheless, in patients with a high probability of OSA (based on a history of habitual snoring, nocturnal choking or gasping, witnessed apneas during sleep, and daytime sleepiness or fatigue), overnight recording of arterial O2 saturation by oximetry can be used to confirm the diagnosis and obviate the need for full polysomnography by demonstrating recurrent episodes of desaturation (at a rate of at least 10 to 15 events per hour). Negative results in such a patient do not exclude the diagnosis and mandate that the patient proceeds to polysomnography. In contrast, when the probability of OSA is low (only occasional snoring, no witnessed apneas, and no daytime sleepiness, fatigue, or other symptoms), the absence of nocturnal desaturation can be used to exclude OSA and obviate the need for full polysomnography. Based on these scenarios, it has been
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estimated that overnight oximetry can obviate the need for polysomnography in about one-third of clinic patients referred for consideration of OSA.
TREATMENT
Several approaches to treatment of OSA have been advocated, based on an understanding of the mechanisms involved ((Table 247-1). In establishing a treatment strategy, defining the severity of the disorder is essential, as indicated by the degree of clinical symptoms (particularly daytime sleepiness and fatigue) and the objective level of nocturnal respiratory and sleep disturbance. In severe OSA (significant daytime sleepiness or >30 obstructive events and arousals per hour of sleep), nasal continuous positive airway pressure (CPAP) is the treatment of choice. Nasal CPAP prevents upper airway occlusion by splinting the pharyngeal airway with a positive pressure delivered through a nasal mask. It is well tolerated and effective in >80% of patients, provided that they have received proper training. The established beneficial effects of CPAP include improvements in sleep quality, reduced daytime sleepiness and driving accidents, and decreased nocturnal hypertension. In patients with ischemic heart disease or congestive heart failure who also have OSA, nasal CPAP is the preferred treatment and the only one demonstrated to have a beneficial effect on cardiac status.
In patients with severe OSA who cannot tolerate nasal CPAP, upper airway surgery can be considered, with uvulopalatopharyngoplasty being the most commonly performed procedure. This operation is designed to increase the pharyngeal lumen by resecting redundant soft tissue. When applied to unselected patients with OSA, the response rate is <50%, but more discriminating selection of patients yields a higher rate of success. Other surgical approaches, including maxillofacial surgery, have variable results, but can be particularly effective in patients with craniofacial skeletal abnormalities.
In patients with mild to moderate OSA, nasal CPAP is superior to more conservative therapy but is often less well tolerated. Such patients can sometimes be managed effectively by modest weight reduction, avoidance of alcohol, improvement of nasal patency, cessation of smoking, and avoidance of sleeping in the supine posture. In addition, intraoral appliances, designed to modify the position of the mandible and tongue, can be effective and often better tolerated than nasal CPAP. Medications are generally ineffective in the management of OSA, except in patients with predominantly rapid eye movement (REM) sleep–related events in whom protriptyline or fluoxetine may be beneficial.
TABLE 247-1 Management of Obstructive Sleep Apnea (OSA)--------------------------------------------------------------------------------
Mechanism Mild to Moderate OSA Moderate to Severe OSA--------------------------------------------------------------------------------
↑ Upper airway muscle tone Avoidance of alcohol, sedatives —
↑ Upper airway lumen size Weight reduction
Avoidance of supine posture
Oral prosthesis Uvulopalatopharyngoplasty
↓ Upper airway subatmospheric pressure Improved nasal patency Nasal continuous positive airway pressure
Bypass occlusion Tracheostomy--------------------------------------------------------------------------------
Source: From Phillipson, with permission.
CENTRAL SLEEP APNEA
PATHOGENESIS
The definitive event in CSA is transient abolition of central drive to the ventilatory muscles. Several underlying mechanisms can result in CSA (Table 247-2). First are defects in the metabolic respiratory control system and respiratory neuromuscular apparatus. Such defects usually produce a chronic alveolar hypoventilation syndrome (in addition to CSA) that becomes more severe during sleep when the stimulatory effect of wakefulness on breathing is abolished. In contrast are CSA disorders that arise from transient instabilities in an otherwise intact respiratory control system. Common to all these disorders is a PCO2 level during sleep that falls transiently below the critical PCO2 required for respiratory rhythm generation. This type of instability is frequent at sleep onset, because the PCO2 level of wakefulness is generally lower than that required for rhythm generation in sleep; hence with loss of the stimulatory effect of wakefulness on breathing (referred to as the waking neural drive), an apnea develops at sleep onset until PCO2 rises to the critical level (Fig. 247-2). However, if the central nervous system state fluctuates at sleep onset between “asleep” and “awake,” a pattern of periodic breathing with central apneas or hypopneas develops as respiration follows the changes in state.
TABLE 247-2 Mechanisms Underlying Central Sleep Apnea--------------------------------------------------------------------------------
Underlying Mechanism Clinical Example--------------------------------------------------------------------------------
Defects in metabolic control system or respiratory muscles Primary and secondary central alveolar hypoventilation syndromes
Respiratory muscle weakness
Transient instabilities in central respiratory drive Sleep onset
Hyperventilation-induced hypocapnia
Idiopathic
Hypoxia (high altitude, pulmonary disease)
Cardiovascular disease, pulmonary congestion
Central nervous system disease
Prolonged circulation time--------------------------------------------------------------------------------
Source: From Phillipson, with permission.
View Figure FIGURE 247-2 Schematic diagram of the mechanisms underlying central sleep apnea at sleep onset. With loss of the waking neural drive to breathing, the arterial threshold PCO2 for rhythm generation increases above the PaCO2 present during wakefulness; ventilation (V) falls to zero and apnea ensues until PaCO2 rises above the threshold for rhythm generation during sleep. NREM, nonrapid eye movement. (From TD Bradley, EA Phillipson, Clin Chest Med 13:439, 1992.)
In most patients with CSA, the tendency to develop periodic breathing and central apneas during sleep is enhanced by some degree of chronic hyperventilation during wakefulness that drives the PCO2 level below the threshold required for rhythm generation during sleep.
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Such hyperventilation is frequently idiopathic in nature. Hypoxia, whether due to high altitude or to underlying cardiorespiratory disease, enhances the tendency to periodic breathing and CSA by a similar mechanism. Periodic breathing and CSA are also common in patients with congestive heart failure, in whom the periodic breathing is characterized by a classic crescendo-decrescendo pattern (Cheyne-Stokes respiration). Patients with heart failure and CSA have a higher left ventricular end-diastolic volume and filling pressure than do heart failure patients without CSA, suggesting that their hyperventilation results, at least in part, from pulmonary congestion and stimulation of pulmonary vagal receptors.
PATHOPHYSIOLOGIC AND CLINICAL FEATURES
In those patients whose CSA is a component of a chronic alveolar hypoventilation syndrome, daytime hypercapnia and hypoxemia are usually evident, and the clinical picture is dominated by a history of recurrent respiratory failure, polycythemia, pulmonary hypertension, and right-sided heart failure. Complaints of sleeping poorly, morning headache, and daytime fatigue and sleepiness are also prominent. In contrast, in patients whose CSA results from an instability in respiratory drive, the clinical picture is dominated by features related to sleep disturbance, including recurrent nocturnal awakenings, morning fatigue, and daytime sleepiness. In patients with congestive heart failure, CSA can be an important (and frequently overlooked) cause of daytime sleepiness and fatigue. In addition, studies indicate a higher mortality rate and higher rate of cardiac transplantation in congestive heart failure patients with CSA than in those without CSA, even when matched for functional class and left ventricular ejection fraction. This outcome probably relates to the fact that CSA can trigger sympathetic nervous activation in patients with heart failure and thereby exert a secondary deleterious effect on the underlying cardiac disorder.
DIAGNOSIS
Initially, many patients with CSA, particularly of the idiopathic type, are suspected clinically of having OSA because of a history of snoring, sleep disturbance, and daytime sleepiness. However, obesity and hypertension are less prominent in CSA than in OSA. Definitive diagnosis of CSA requires a polysomnographic study, with the key observation being recurrent apneas that are not accompanied by respiratory effort. Measurements of transcutaneous PCO2 are particularly useful in CSA. Those patients with a defect in respiratory control or neuromuscular function typically demonstrate an elevated PCO2 that tends to increase progressively during the night, particularly during REM sleep. In contrast, patients with instabilities in the respiratory control system typically demonstrate a mild degree of hypocapnia, which is an integral pathogenetic feature of their disorder (see above).
TREATMENT
The management of patients whose CSA is a component of an alveolar hypoventilation syndrome is essentially the same as management of the underlying hypoventilation disorder (Chap. 246). Management of patients whose CSA arises from an instability of respiratory drive is more problematic. Patients with hypoxemia usually respond favorably to nocturnal supplemental oxygen. For those with idiopathic CSA, respiratory stimulation with acetazolamide or central nervous system sedation with triazolam have been advocated, but results are variable and efficacy has not been established. Nasal CPAP (as for OSA) can be effective in idiopathic CSA, although definitive long-term trials are lacking and the treatment is less well tolerated than in patients with OSA. The mechanism by which CPAP abolishes central apneas may involve a small increase in PaCO2 as a result of the added expiratory mechanical load. In patients whose CSA is secondary to congestive heart failure, CPAP is particularly effective in improving sleep quality and daytime cardiac function. In fact, short-term randomized trials have demonstrated that CPAP has a beneficial effect on several surrogate markers of mortality in patients with congestive heart failure, including left ventricular ejection fraction, functional mitral regurgitation, and norepinephrine concentrations. Small, 5-year follow-up studies in such patients demonstrate that CPAP results in a decreased mortality rate. Larger randomized trials are currently in progress.
FURTHER READING
JAVAHERI S et al: Sleep apnea in 81 ambulatory male patients with stable heart failure. Circulation 97:2154, 1998Ovid Full TextBibliographic Links
KANEKO Y et al: Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med 348:1233, 2003Ovid Full TextBibliographic Links
MCNICHOLAS WT, Phillipson EA (eds): Breathing Disorders in Sleep. London, Saunders, 2002
PHILLIPS BG, Somers VK: Neural and humeral mechanisms mediating cardiovascular responses to obstructive sleep apnea. Resp Physiol 119:181, 2000Bibliographic Links
PHILLIPSON EA: Sleep disorders, in Textbook of Respiratory Medicine, 3d ed, JF Murray, JA Nadel (eds). Philadelphia, Saunders, 2000, pp 2153–2170
YOUNG T et al: Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med 157:1746, 1997Ovid Full TextBibliographic Links
BIBLIOGRAPHY
AMERICAN THORACIC SOCIETY: Indications and standards for use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndromes. Am J Respir Crit Care Med 150:1738, 1994Bibliographic Links
JAVAHERI S et al: Sleep apnea in 81 ambulatory male patients with stable heart failure. Circulation 97:2154, 1998Ovid Full TextBibliographic Links
KANEKO Y et al: Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med 348:1233, 2003Ovid Full TextBibliographic Links
MCNICHOLAS WT, PHILLIPSON EA (eds): Breathing Disorders in Sleep. London, Saunders, 2002
PHILLIPS BG, SOMERS VK: Neural and humeral mechanisms mediating cardiovascular responses to obstructive sleep apnea. Resp Physiol 119:181, 2000Bibliographic Links
Phillipson EA: Sleep disorders, in Textbook of Respiratory Medicine, 3d ed, JF Murray, JA Nadel (eds). Philadelphia, Saunders, 2000, pp 2153–2170
TERAN-SANTOS J et al: The association between sleep apnea and the risk of traffic accidents. N Engl J Med 340:847, 1999Ovid Full TextBibliographic Links
YOUNG T et al: Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med 157:1746, 1997
Posted by FredPotter on February 19, 2007, at 18:33:09
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred, posted by sdb on February 19, 2007, at 15:05:10
Thanks sdb for all the information. I'll report back when I've got used to this tongue device Fred
Posted by lcat10 on February 19, 2007, at 22:16:48
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred, posted by FredPotter on February 19, 2007, at 18:33:09
Fred; are you on the waiting list for a sleep study. This is awful that you have to wait two years. Can you go to Australia or elsewhere to have the test done??
I have obstructive sleep apnea and use the CPAP machine. It takes some getting used to, but once you are used to it, it is not that bad.
I had gained a lot of weight and had no energy. The sleep study showed I quit breathing a lot during the night; I forget how many times now. The CPAP machine works, and I was warned that I need to use it all the time.
I was told that over the years one's heart becomes damaged from the continual epidodes of stopping breathing. I was glad to learn I had not suffered any heart damage and have heard from my doctor that people die in their sleep eventually when the sleep apnea is really bad, and they do nothing about it. Usually this is older people like myself, in the 55+ range. I think I had it for at least five years and maybe longer before it was diagnosed in 2005.
Posted by FredPotter on February 19, 2007, at 22:28:19
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred » FredPotter, posted by lcat10 on February 19, 2007, at 22:16:48
Thanks for your info. I'm 60 so should die in my sleep any time now. Is it linked to incorrect breathing in waking life, like high chest breathing and a constant feeling of suffocation? I mean constantly having suffocating feelings throughout the night, even if not remembered, must leave its mark. I'm glad you're all sorted out and your heart is healthy
Fred
Posted by Larry Hoover on February 20, 2007, at 8:10:36
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred » lcat10, posted by FredPotter on February 19, 2007, at 22:28:19
> Thanks for your info. I'm 60 so should die in my sleep any time now. Is it linked to incorrect breathing in waking life, like high chest breathing and a constant feeling of suffocation?
No, Fred. Nothing like that. It's a mechanical problem caused by gravity and the natural sag of aging tissues. Genes might be a factor, as is body weight, but not necessarily. Gravity and aging. And don't worry about your age specifically. The adverse impact is progressive, so if you've been identified early, you'll not be dropping dead any time soon.
The CPAP machine simply inflates the sagging tissues like a balloon, preventing their collapse while lying down. I've never heard of the tongue splint thingy. Best of luck with it.
Lar
Posted by lcat10 on February 20, 2007, at 19:48:28
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred » lcat10, posted by FredPotter on February 19, 2007, at 22:28:19
Fred; no you are not too old; I am your age. It is not too late to do something about it. It does not have to do with what you think. Larry Hoover is correct. Besides, if I had never gotten the CPAP, likely it would have taken 10 years or more for damage to be noted. Get on the list to do a sleep study. It is not too late and won't be even two or three years from now. In the meantime, yes use the tongue thing they gave you.
Posted by yxibow on February 20, 2007, at 20:43:11
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred » FredPotter, posted by lcat10 on February 20, 2007, at 19:48:28
> Fred; no you are not too old; I am your age. It is not too late to do something about it. It does not have to do with what you think. Larry Hoover is correct. Besides, if I had never gotten the CPAP, likely it would have taken 10 years or more for damage to be noted. Get on the list to do a sleep study. It is not too late and won't be even two or three years from now. In the meantime, yes use the tongue thing they gave you.
I would agree with the CPAP -- it is the only major medically proven device for sleep apnea besides oral surgical intervention to remove tonsillar and uvular tissue which isn't done that much any more except for exceptional or ER cases (though my uvula does distend on bad nights at times -- partially obstructive sleep apnea sign.)
I need to have a sleep study done at some point, because I may have it as well. It is tied to my weight, which has increased because of past Remeron use and current Seroquel use, even with heavy excercise at the gym, which I get discouraged about at times. (I also need to stop raiding the cereal boxes in the morning -- but Seroquel makes them so inviting.)
Sleep study centres will vary on how they will allow psychotropic substances present. But I can't exist without my polypharmacy, including the sleep aids which at least give half-*ssed sleep for bad insomnia. Sometimes they may need to be persuaded or you may need to go shopping for another one if you need to stay on medication.
I wish you well-- Jay
Posted by lcat10 on February 20, 2007, at 21:13:43
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred » lcat10, posted by yxibow on February 20, 2007, at 20:43:11
Gosh Jay; some places won't allow the psychotropic meds to be present??? Odd. I had two different sleep studies done at the Univeristy of Chicago (sleep study lab) and was in a room by myself so any meds I had with me were fine. So, yes do the sleep study. The saving grace for me was they let me keep the TV on (after hours) as I convinced them I would fall asleep with the TV on. Nothing like a boring TV show to put me to sleep--standing up, sitting down, or lying down. I gained a lot of weight too, but it seems that sleep apnea also results in weight gain due to the lack of oxygen leading to feeling tired and leading to eating junk food with lots of carbs. So maybe if you did not have sleep apnea, you would not have gained so much weight on the med's. Who knows. Go for the sleep study.
Posted by FredPotter on February 20, 2007, at 21:38:46
In reply to Re: Obstructive Sleep Apnoea (OSA) }} Fred » yxibow, posted by lcat10 on February 20, 2007, at 21:13:43
Thanks for your input everybody. I read with interest that apnea can cause obesity, diabetes, depression, hypertension, erectile dysfunction etc etc. Like I say the waiting list for sleep studies is 2 years in New Zealand so I might record myself to give me some clues. I could put the recording on the Internet!
Meanwhile I'm trying to get used to having tongue lacerations and ulcers caused by the tongue device (sorry I mean my non-compliance (slight shifting of blame by manufacture))
Fred
This is the end of the thread.
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