Upon successful completion of this course, you will be able to:
- Define OSA and describe its symptoms, causes, pathology, and treatments
- Discuss the interactions/relationships between COR PULMONALE & OSA
- Identify and discuss the wide variety of sleep disorders, including their symptoms, consequences, and treatments
- Explain what is meant by "insomnia" and discuss its prevalence and treatments
- Discuss the current status of sleep among people living in the United States
An Introduction to Obstructive Sleep Apnea
The following case history is an example of a healthcare worker's introduction to sleep medicine. The setting is a clinic. The patient is a 32-year-old make who appears fit and trim and quite healthy. He is accompanied by his wife, a young woman who despite looking fit, trim and healthy appears to be exhausted.
Caregiver: What brings you to the clinic?
Spouse: He snores and I cannot sleep
Caregiver: Are you tired during the day?
Patient: No
Spouse: Yes you are. You fall asleep every time you sit down.
Patient: That's just because I am working so much.
Caregiver: What time do you go to bed?
Patient: Usually around 10:00.
Caregiver: And what time do you get up?
Patient: 7:00.
Caregiver: Do you feel rested when you get up in the mornings?
Patient: Yes
Spouse: No you're not. You're grumpy and you have to drink 4-5 cups of coffee to get going.
Caregiver: Does your husband snore every night?
Spouse: Yes. From the moment he falls asleep to the moment the alarm goes off. And it is so loud you can hear it throughout the whole house.
Caregiver: Do you notice that he stops breathing at night?
Spouse: Yes and then I lie there and worry when he will start. Often I have to kick him to get him breathing.
Caregiver: Do you two like movies?
Spouse: Yes, but I won't go to the theater with him anymore, because as soon as the lights go out he falls asleep and begins to snore.
An examination was performed and then a sleep test ordered. The couple returned after the sleep test, which showed moderate obstructive sleep apnea with an apnea hypopnea index of 30.
Caregiver: You have obstructive sleep apnea.
Spouse: I told you so I thought it was something like this
Patient: What does that mean?
The caregiver explained the diagnosis, and the resultant problem of hypertension, heart attack and stroke.
Patient: Well, what can we do about this?
Caregiver: You need to be treated with nasal CPAP.
Patient: What is that?
The caregiver explained and the patient hardly listened.
Patient: How about an operation?
Caregiver: No, you need to be treated with CPAP.
Patient: I am not wearing a machine.
Spouse: What happens if he doesn't treat this?
Caregiver: He may die prematurely
Patient: I will think about it, but I don't think this is necessary. We can go now honey.
Two weeks later, the couple returned. Serious family discussion had obviously ensued.Patient: I've decided to try CPAP
Caregiver: This is a good decision
The patient was referred for a CPAP titration and trial. He returned with his wife one month later.Caregiver: How are things going?
Patient: I can't believe it. I feel like a new person. I get up refreshed and never fall asleep at work. My morning headaches are gone, I don't get up to pee 3 times a night.
Spouse: Better yet, I can sleep. He doesn't snore, we can go to the movies and we are making love like we did before we got married.
And so began the caregiver's introduction to sleep medicine
Cardiovascular Associations of OSA
So, you've gotten a preliminary introduction to Obstructive Sleep Apnea and have gotten an idea about the typical people that OSA affects. In the following section, we will discuss the various pathological cardiovascular processes caused by and associated with OSA. The goal is to get through this section without entering into sleep. Hopefully you find the entertainment verging on tasteful and the information poignant.
The story on hypertension (HTN) and OSA is complicated namely because one must consider the effects of OSA on blood pressure during sleep and wakefulness.
Normal sleep should cause a drop in arterial pressure by way of an increase in parasympathetic mediated vasodilatation and a decrease in cardiac output (see Figure 1.1). This phenomenon is termed "dipping", and is completely normal. Conversely, it is well-documented that apneic episodes and the resulting oxyhemoglobin desaturation seen in OSA cause elevated blood pressure during sleep (see Figure 1.2).
This is a no-brainer-hold a pillow over your bed partner's mouth while they sleep and watch their pressures soar through the roof! (Disclaimer: Actually, do not try this at home!) The mechanism is felt to be hypoxemia-induced activation of the sympathetic nervous system causing catecholamine release. OSA patients who experience elevated nocturnal pressures are termed "non-dippers". This is an abnormal physiologic state, which, over the long-term, can lead to significant morbidity. While the association between OSA and diurnal hypertension is difficult to prove because of confounding factors, the data supporting the association are quite convincing.
Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea.
Figure 1: Blood Pressure Response to Sleep:1.1: Normal physiologic "dipper" response-blood pressure decreases during sleep.
1.2: Abnormal "nondipping"response characteristic in OSA patients. Note that blood pressure remains at or above diurnal values.
Approximately half of all OSA patients have hypertension. When multivariate analysis and linear multivariate regression techniques were applied to evaluate contributions to the formation of daytime hypertension, OSA was found to be an independent risk factor in both men and women. The effect appears to be most profound in younger patients of normal weight.
Several different studies have corroborated that OSA is an independent risk factor for persistent diurnal HTN. Since the association between OSA and hypertension has such profound repercussions for the health of your future patients, it cannot be emphasized enough. It is well documented that treatment of OSA with continuous positive airway pressure (CPAP) can improve patients' diurnal and nocturnal HTN.
Additionally, compared with controls, OSA patients have higher plasma and urine levels of catecholamines and more plasma thromboxane than plasma prostacyclin. With treatment of OSA, norepinepherine and thromboxane levels fall favoring relative vasodilatation. All these data support the strong association between OSA and the development of both diurnal and nocturnal HTN.
Now we get to the meat and potatoes of OSA, and how it can kill. There are innumerable studies in both humans and animals about the effects of ventilation and sleep state on cardiac rhythm. To better understand this process let's look at a typical day in your life as a healthcare giver. By examining the response of your autonomic physiology to both stress, sleep, and stressful sleep, we will elucidate the main dysrhythmias linked to OSA. These include the vagally mediated bradycardias that occur during apnea onset, and the sympathetically mediated ventricular arrhythmias that occur upon arousal from apneic episodes. Using our understanding of the autonomic nervous system, the manner in which obstructive sleep apnea causes cardiovascular morbidity and mortality will become clear.
A day in the life of YOU is fairly stressful. It consists of taking ceu courses, being pimped by attending department meetings, checking in on I.C.U. patients, and making sure you get something to eat. During your typical day, the sympathetic nervous system and its catecholamines facilitate cardiovascular responses to stressful stimuli. For example, when your department manager asked you to recite the calculated creatinine clearance formula in front of everyone this morning, your heart beat faster (very fast) and your arterial pressure rose (very high). You may even have experienced a premature ventricular complex or two as the extra load of catecholamines that was released into your serum came into contact with your myocardium. As your autonomic system faultlessly prepared you to flee from this stressful situation, you stoically remained, and blubbered some excuse about how your parakeet came down with pneumonia. Consequently, you spent all last night in the vet ER so you did not have time to brush up on that formula you were supposed to be ready to recite today. As the last words of your response emerged from you lips, it was clear to everyone within earshot, including yourself, that your prospect for moving up the ladder in the department had just vanished.
Unfortunately for you, but fortunately for us, your degrading and stressful experience has demonstrated some important points: 1) Meetings can be difficult with taskmasters who have been well trained in the Art of Humiliation and 2) the autonomic nervous system greatly influences the entire cardiovascular system including blood pressure and cardiac rhythm. It is through the interaction between the autonomic nervous system and the cardiovascular system during sleep that dysrhythmias occur in OSA.
Ashamed and forlorn, you dash off to the library to look up that silly formula and thereby attempt to salvage your day. You find the proper book, settle down in a comfortable chair and prepare to learn about renal physiology. At the exact moment that the book is cracked, however, you begin to enter the first stages of NREM sleep.
It is now, that the Autonomic Balance of Power shifts-Sympathetica, God of War and Destruction, and His catechol army retreat for cover in your nerve terminals as Parasympathetica, Goddess of Rest and Relaxation reigns supreme over your bodily functions through her multiheaded warrior, The Vagus. Well, you get the idea!
From a cardiovascular standpoint, the net result of NREM sleep is a slowing of your heart rate and a decrease in your arterial pressure. Normal NREM sleep produces fewer ventricular arrhythmias than any other period because of the change in your autonomic tone. Catecholamines are arrhythmogenic. When Sympathetica and His army are ruling over your bodily functions, one would expect you to have arrhythmias from the effects of catechol surges on your heart. This is exactly what we saw when you blew your honors grade in Medicine. When catecholamine input is withdrawn, however, as in NREM sleep, the vagus and the inherent cardiac pacemaker deliver a slow, steady and predictable heart rate.
Let's get back to you, asleep in the library, in order to see when obstructive apneas occur and how they result in arrhythmias. Through all the stages of NREM sleep you go, the frequency of your brain waves slowing and gaining more amplitude. You have an occasional K-complex and sleep spindle register as you pass through NREM stage 2, then you transition into NREM stage 3 and 4--you are now in slow wave sleep. From here, you quietly await your inevitable entry into REM sleep. As your brain waves 12 become less synchronized and your eyes begin to samba under your lids, all your skeletal muscles to lose their tonic input from your brain and become flaccid. Somewhere in your head you hear, "Ladies and Gentlemen, on behalf of the captain and Wing and a Prayer Airlines, Welcome to Dream Land!" You have entered REM sleep-the sleep stage where obstructive apneas are most prevalent.
As you begin a dream sequence that includes you and a special someone sharing a vegan picnic meal in a secluded mustard field, you are completely unaware that an obstructive apnea is about to transform this romantic Hollywood scene into a real-life nightmare. Within moments of entering REM sleep, your head falls backwards, fully extended, and all of your pharyngeal dilator muscles lose their tonic input. Your abnormal head position causes your airway anatomy to resemble that of an OSA patient. Combined, your newly acquired abnormal airway anatomy and the loss of pharyngeal muscular tone cause your airway to obstruct. My friend, you have now entered the obstructive sleep apnea zone!
As the apnea continues, your dream content changes. Your special friend morphs into your angry Renal Attending! He begins to grab tofu sandwiches and shove them down your throat, yelling, "Let's see how your kidneys handle this protein load!" While you feel as if there is tofu stuck in your throat rendering you unable to breathe, in reality, your own airway anatomy is causing obstruction. In response to your loss of ventilation, parasympathetic tone mediates a mammalian diving reflex-like response. Your heart rate slows to decrease myocardial oxygen demand, and you wait to see what the oxygen drought will bring.
During an obstructive apnea, vagally mediated arrhythmias are quite common, including bradycardias, sinus pauses, and second-degree AV blocks. These are the first type of arrhythmias seen in OSA. As apnea persists, metabolic requirements sap your precious oxygen stores causing oxyhemoglobin saturation to fall and carbon dioxide levels to rise. Consequently, the chemoreceptors in your carotid bodies begin firing like mad telling your respiratory center, "Scotty, we need more…power". They respond in their Scottish affect, "Captain, we're giving her all she's got!" Like Kirk at the helm, you're helplessly trusting that the diaphragm will generate enough force to overcome the glottic obstruction.
Although the exact mechanism has not been identified, something magical occurs at this crucial juncture that keeps you from asphyxiating to death. Many feel that the increased neurogenic activity that is flogging your respiratory drive centers combines with the falling oxygen tension in your blood to activate your Reticular Activating System (RAS). The RAS responds to this suffocation by arousing you from REM sleep, allowing restoration of muscle tone to the pharyngeal dilators, and activating your sympathetic nervous system. The result is resolution of the obstruction, and resumption of ventilation.
Obstructive apneas cause abrupt changes in autonomic tone. At apnea onset, parasympathetic tone predominates. Towards the end of an apnea, however, increasing inspiratory efforts and decreasing oxygen saturation cause arousal from sleep and a surge in sympathetic tone. Of all the arrhythmias in OSA, the most common is the bradytachyarrhythmia. It results directly from the myocardial response to changes in autonomic tone. It is characterized by an increase in parasympathetic tone at apnea onset causing bradycardia immediately followed by a sympathetic surge causing tachycardia at apnea termination. This arrhythmia is present in over 75% of patients with OSA.
Oxyhemoglobin desaturation and increased circulating catecholamines cause the third type of arrhythmias seen in OSA. If we were to do a systems' check at the end of an apneic episode, we would find:
1) Oxyhemoglobin saturation is low and barely able to meet myocardial metabolic requirements.
2) A surge of arrhythmogenic catecholamines has been released into the blood stream and will increase myocardial oxygen requirements when it contacts the myocardium.
3) Afterload is maximized as a result of the sympathetic surge.
4) There is a respiratory acidosis.
All these factors-low oxygen supply, high myocardial oxygen demand, acidosis, and arrhythmogenic catecholamines-converge at apnea termination to create the optimal setting for all sorts of interesting ventricular arrhythmias (ectopic focuses, tachycardia, bigeminy). These are seen particularly in patients with underlying cardiovascular disease. In OSA patients without overt coronary disease, apneic episodes resulting in oxyhemoglobin saturation levels below 60% are associated with ventricular arrhythmias. In patients who have severe coronary disease or pre-existing conduction abnormalities, however, apneas causing oxyhemoglobin saturations below even 80% can trigger ventricular arrhythmias. These ventricular dysrhythmias can progress to fatal arrhythmias and ultimately death in all OSA patients.
Now that we are aware of the main types of arrhythmias characteristic for OSA patients-bradyarrhythmias, bradytachyarrhythmias, and tachyarrhythmias-the question arises: what can be done about these potentially fatal rhythms? Multiple studies have demonstrated that apnea-induced arrhythmias resolve with effective treatment of OSA! Preventing apneic episodes subsequently prevents autonomic instability and low oxygen saturations-the basic ingredients that cause the characteristic arrhythmias in OSA. In fact, effective OSA treatment prevents most of the other significant pathological processes associated with OSA. These treatments will be discussed in later in this course.
If you understood the cardiac arrhythmia section, the rest of the pathological processes associated with OSA will be a cakewalk. The pathophysiology is the same; it is simply applied differently. The key to understanding the cardiovascular effects of OSA lies in understanding apnea-induced arousals. We discussed the abrupt shift in the autonomic tone that occurs when apneas cause arousal from REM sleep. The resulting sympathetic surges cause increased myocardial oxygen demands by increasing the major determinants of MVO2 (isotropy, chronotropy, and afterload). OSA causes myocardial ischemia by way of a simple supply and demand problem.
When a sympathetic surge causes all the determinants of MVO2 to increase, and the supply of oxygen is limited by an apnea, the result is ischemia! The principle is the same in a person who has arteriosclerotic coronaries; any increase in myocardial oxygen demand is met with ischemic pains because of limited oxygen supply! One Koehler study found that 83% of nocturnal ischemic events occurred during apneic episodes in REM sleep characterized by persistent oxyhemoglobin desaturation. Moreover, there is a strong association between apneic indices and myocardial infarction. In a retrospective analysis of patients who suffered myocardial infarction, Hung et al. found that an apnea index of greater than 5.3 was independently predictive of having myocardial infarction (the statistically significant odds ratio approached 23!). While there might be chicken and egg uncertainty with this association, logically it makes sense that apneas would predispose to myocardial infarctions for the aforementioned reasons. However, for completeness sake and to add some complexity to the issue, congestive heart failure caused by a myocardial infarction could cause a crescendo-decrescendo Cheyne-Stokes breathing pattern that would create apneic episodes that were not present before the infarction. However, it seems that the majority of post-infarction patients with significant apnea indices had their infarction as a result of their apneas, and not the other way around. Then again, it seems that there was a reptile egg and some Darwinism that created the chicken, so take this view with a proverbial grain of salt.
We must also consider the possibility that OSA may cause other pathophysiologic states that predispose to infarction such as increased coagulability. Recently, a well-designed study found that OSA patients had higher blood viscosities and fibrinogen levels compared with controls. Another study found that effective CPAP treatment caused fibrinogen levels to normalize. Increased blood viscosity and serum fibrinogen levels could potentially lead to increased coagulability, which could further predispose to myocardial infarction. Regardless, of the exact mechanism, the association between OSA and myocardial infarctions cannot be ignored!
As for sudden cardiac deaths, we look to the Scandinavians and their amazing database to find that snoring is an independent risk factor for sudden nocturnal cardiac deaths. While this finding only implicates OSA in sudden death, when we amass our understanding of OSA and its effects on the autonomic nervous system, the associations with myocardial dysrhythmias, ischemic events, and infarctions it seems perfectly logical that OSA should be a risk factor for sudden nocturnal cardiac death!
We've discussed the implications of OSA on the heart specifically on the increased risks of dysrhythmias, ischemia, infarction and sudden cardiac death. Well, I saved this one for last and gave it a special section because it is especially interesting. Heart failure and OSA should be enough to send shivers down your spine. Not only does the pathophysiologic mechanism challenge us to widen our perspectives about the severity of the morbidity of sleeping disorders, but also there is a Chagas-esque exoticness associated with OSA causing heart failure. Ask yourself how many VA patients with CHF you've seen whose failure resulted from ischemia or valvular disease?
These mechanisms for inducing CHF are so banal-like Big Macs, Toyota Tercels or Wal-Mart-sure, they do the job, but when you've experienced one, you've seen them all. It would be so much more refreshing to work with a patient whose CHF resulted from OSA. This would be like traveling across India on the Orient Express to bathe in the Ganges River or indulging in a Fruit du Mer Risotto infused with white truffle oil and century-old balsamic vinaigrette. You get the point. Hopefully, after perusing this section you will begin to realize that even with the relatively large incidence of OSA causing CHF, this knockout combination maintains a je ne sais quoi quality that memorializes them in our hearts and memories.
Cor pulmonale is heart failure caused by a primary lung pathology. The pathogenesis includes an increase in pulmonary vascular pressure causing right heart hypertrophy and subsequent right heart failure. Right heart failure subsequently leads to left heart failure. Often, the inciting mechanism that causes this chain of events is hypoxia leading to vasoconstriction of the pulmonary vascular tree, OSA plays a role in the development of heart failure via three main mechanisms. The result is an incidence of right heart failure in OSA patients of about 10%. The first mechanism deals with the altered chemoreceptor mediated ventilatory response in some OSA patients. Blunted responses to hypoxia and pH changes lead to the development of hypoventilation in the OSA patient. A decreased ventilatory drive combined with frequent nocturnal apneic episodes leads to persistent nocturnal hypoxemia.
Hypoxic pulmonary vasoconstriction results in an effort to minimize V/Q mismatching. The right heart consequently has to push against elevated pulmonary vascular pressures, which over time leads to hypertrophy then to failure. These two effects of OSA-global hypoventilation and frequent nocturnal apneas-are the main mechanisms for de novo development of heart failure. OSA, however, also exacerbates existing heart failure through elevated arterial pressures (resulting from apnea induced sympathetic activation) causing increased myocardial oxygen demand. This increased work on the left ventricle causes hypertrophy and predisposes to ischemia. This chain of events has been implicated in worsening the LV function of patients with both OSA and CHF. To complicate this issue, however, most CHF patients have a form of sleep-disordered breathing that is felt to be caused by LV failure leading to pulmonary congestion.15 The resulting Cheyne-Stokes breathing also contributes to worsening heart failure. As one would guess, treatment of CHF patients with nocturnal CPAP has been shown to improve function and heart failure.
While the incidence of stroke occurring in OSA patients is about 7%, the relationship has not been formally studied with prospective double-blinded studies. Despite this, the preponderance of evidence points towards OSA predisposing to cerebral infarction. As seen in cardiac infarction and sudden cardiac death, many investigators have determined that snoring is an independent risk factor for developing stroke. This association becomes even stronger when hypertension and snoring co-exist. While we already know that apneas lead to nocturnal hypertension through a shift in the autonomic nervous system, studies have also demonstrated that intracerebral pressures increase in relation to apnea duration and oxygen desaturation. Doppler studies have demonstrated a watershed distribution hypoperfusion in the brains of OSA patients. Impairment in cerebral vascular auto regulation in OSA patients has also been demonstrated.
So, I present to you a recipe that is guaranteed to knock off the hemispheres of your dinner guests! Mix intermittent bursts of hypertension with cerebral vessels that are unable to properly buffer significant pressure changes, fold in a background of watershed hypoperfusion, add a dash of increased blood viscosity and a pinch of potentially increased coagulability, place in a cranium whose pressure is set to rise with apneic episodes and you have a fabulous recipe for cerebral infarction that can be served either hot or cold at your local nursing homes! I challenge you to think of what type of visual aid would best demonstrate this recipe for disaster to your patients. Perhaps in the spirit of the anti-drug campaign, we should start a "This is your brain on OSA" campaign. Instead of a fried egg, we could show a head CT demonstrating an enormous watershed or hemorrhagic infarct. Combine this with a correspondingly graphic clinical example: Left ventricular volume in patients with heart failure and Cheyne-Stokes respiration during sleep. and perhaps this would finally achieve the shock value needed to wake people up to the dangers involved in OSA, no pun intended!
Treatment Principles for OSA
While there exist innumerable interventions of varying efficacies for treating OSA, most are variations of a limited number of central themes. By understanding a few principles about the pathogenesis of OSA, the logic behind existing treatment paradigms will become apparent. Subsequently, a discussion about treatment options will be very easy to understand! In this short section, we will encounter three main principles about the pathogenesis of OSA.
Principle 1: What causes OSA?
At the most basic level, OSA is caused by a mechanical obstruction occurring somewhere in the upper airway that makes a person unable to breathe during sleep despite ventilatory efforts. The obstruction is in the upper respiratory tract and may involve the nose, pharynx or larynx. The most common obstructions involve the uvula/soft palate and base of the tongue. While the site of the obstruction is unimportant, the effects are devastating, as we've seen in the complications section. In addition to anatomy, we must also infer that there is some neurological predilection to developing this obstruction. When sleep occurs, the neurologically mediated tonic input to the pharyngeal dilator muscles decreases. For some individuals, this results in a smaller pharyngeal diameter but no sleep-disordered breathing. For OSA patients, however, this withdrawal of muscle tonicity results in partial airway obstruction. Anatomy and/or neurogenic regulation of pharyngeal relaxation, therefore, differ between OSA patients and non-sufferers!
Principle 2: Where do the obstructions occur and why?
Most suffers of OSA obstruct at any of three anatomical locations (Figure 2). The most common site is at the level of the pharynx. Repetitive blunt trauma of the soft palate during snoring causes tissue edema. Pharyngeal obstruction is caused by the edematous soft palate collapsing onto the posterior pharyngeal wall. Certain neurological or anatomical contributions will make obstruction at the pharynx worse. These include: reduced tonic input to the pharyngeal dilator muscles, large tonsils, or redundant soft tissue in the pharynx. All will decrease the patency of the upper airway. The second most common site for obstruction is at the level of the tongue base. While there is an enormous variation in tongue sizes, large tongues nestled within small pharynxes is a guaranteed way to achieve horrible, suffocating, near death OSA. A third site of obstruction is in the nose. A nose should consist of two large boreholes that lead to the nasopharynx. The nasal passages may become obstructed because of a deviated septum, dust mites, mold or other allergens causing mucosal inflammation, nasal polyps or other obstructing anatomy.
Figure 2: Sites of Obstruction in OSA: oropharynx (tongue base), soft palate/tonsils, and nasal passage (in ascending order of arrows)
Regardless of the cause or location of the airway obstructions, the net effect is the same-increased resistance causing reduced airflow. Think of the river and the dam analogy-place a dam in a river and you get less flow downstream. Because all three of these anatomical sites are located in series, their resistance is additive. Consequently, a few mild obstructive lesions in the upper airway can generate enormous resistance.
Another major contribution to airway obstruction is the large negative intra-thoracic pressure generated by the contraction of the diaphragm. This diaphragmatic action creates a vacuum in the airway that pulls both air and anatomy inward. The result is a narrowing of the upper airway. Because OSA patients have increased airway resistance, their diaphragms must generate large negative intra-thoracic pressures in order to achieve effective ventilation. Such a large negative force causes a greater inward force on the pharyngeal anatomy. In this way, increased airway resistance in OSA patients creates a spiraling effect where adaptive responses result in a worsening of the pathologic mechanism.
Principle 3: Who gets these obstructions?
Some wrongly believe that semi-starved, runway-models are immune from developing OSA. Some may also think that OSA is a disease only for the "big boned" of the world. Well, the truth is anyone can get OSA! OSA is caused by a combination of poorly designed anatomy and probably an abnormal withdrawal of muscle tone in the pharynx during sleep. Certainly, obesity plays a role in worsening the severity of OSA.
By mass effect, obesity contributes to upper airway compression and to decreased lung volumes. While the mechanism of how airway compression exacerbates OSA should be self-evident, the role of lung volume in the pathogenesis of OSA is less apparent. Underinflated lungs do not contain the oxygen reserved needed to buffer against oxygen desaturation during apneic episodes. Thus in obese individuals with OSA, airway compression and small lung volumes result in more frequent and severe oxygen desaturations, nocturnal arousals and sympathetic surges. While an increased BMI will inevitably make OSA more severe, under no circumstances do all obese individuals have OSA. Conversely, obesity is not a pre-requisite for developing OSA. Put another way, Ali McBeal might have OSA, and the late, great Chris Farley may not have had OSA! OSA also progresses with age. Those who snore in their 20s and 30s obstruct in their 40s. This is clearly a progressive illness.
Treatments for OSA
Treating OSA can be fun and rewarding since there are so many radically different approaches that can positively affect the lives of OSA patients. These range from non-invasive therapies like CPAP, weight loss, dental prostheses, pharmacotherapy, and improved sleep positioning to surgical therapies aimed at correcting the anatomical abnormalities that cause OSA.
By far, the most successful and least invasive treatment for OSA is CPAP (continuous positive airway pressure). The use of CPAP in OSA has been studied extensively since its introduction by Professor Colin Sullivan in 1981. The results are remarkable! CPAP normalizes sleep architecture; it eliminates daytime sleepiness, nocturnal obstructive apneas, nocturnal desaturations, and nocturnal arrhythmias; it decreases nocturnal and daytime blood pressures, and improves mortality within the OSA cohort. When used on a regular basis, CPAP reverses or eliminates all the pathology that is associated with OSA!
The concept behind CPAP is relatively simple: air pressure is employed to splint open the airway. In fact, the CPAP machine has been likened to a Hoover vacuum cleaner running in reverse! While present day machines are much more advanced than the old Hoover vacuum cleaners, the concept of using pressurized air to splint open an airway remains the same. Modern day CPAP machines have clean tubing, filtered air, comfortable masks, quiet motors and titratable pressure that is delivered during both inspiration and exhalation. Typically, CPAP inspiratory pressures (5-15 cm water) are larger than exhalation pressures (5-10cm water) since the negative pressure generated during an inspiration provides additional inward force that further collapses an already compromised airway.
One of the biggest problems with CPAP has nothing to do with the efficacy of therapy itself, but rather with the compliance of patients.
Patients on CPAP are non-compliant because either they are unable to tolerate the feeling of high pressures (12-15cm water) in their airways, or their mask causes irritation, most commonly on their nasal bridge. In addition to these impediments, some patients with inadequate support from their bed partners will not remain compliant . Over the years, multiple advancements have been made in the design and technology of CPAP. Patients who once could not tolerate high airway pressures in conventional machines are now able to use CPAP regularly because of the auto-titrating machines. These CPAP machines auto-titrate the pressures delivered to the patient on a breath-to-breath basis so that the minimum amount of pressure needed to keep the airway patent is used. This modification combined with newer, more comfortable masks will have a dramatic impact on CPAP compliance rates.
While using CPAP on a regular basis is not easy, with improved product designs, patient education and an excellent social support network, CPAP therapy can prove to be a painless experience that can confer amazing benefits to affected patients.
So, when you're with newly diagnosed OSA complaining to your father about how hard it is to use the new CPAP machines, be prepared for the "When I was Your Age" monologue. He will remind you that he not only walked to work in three feet of snow, uphill in both directions, but also, his CPAP machine was a Rube Goldberg gas-powered model, made from duct tape and garden hose that delivered only a single pre-set 22 pressure.
While he is probably indulging the truth, the fact remains that a diagnosis of OSA requiring regular CPAP therapy is no longer as difficult as it may have once been! While CPAP is a fantastic treatment for OSA, some people simply cannot tolerate it. Additionally, other people have isolated, localized anatomical sites that account for their OSA. In these cases, surgical intervention is an appropriate treatment. While there are many surgical procedures aimed at helping OSA, they generally fall into two categories based on severity of the intervention. I like to think of them as Minor League surgery and Major League surgery.
Just as there are many minor league baseball players of varying skill levels, so are there many surgeries of varying efficacies aimed at treating OSA. These procedures generally consist of a surgeon tinkering with the anatomy of the nose and pharynx in an effort to relieve sites of localized obstruction. Minor League procedures generally do not result in profound anatomical alterations, but rather, simply modify or resect excess/obstructing tissue! Surgery is tailored to the individual's obstructing anatomy.
Commonly recommended operations include septoplasty, turbinate reduction, tonsillectomy, soft palate excision (this is called uvulopalatal pharyngoplasty or UP3), tongue reduction and tongue advancement. While these procedures generally help OSA patients with localized anatomical defects, they are temporizing interventions only because most Minor League surgeries, except the UP3, do not have long-term outcome studies supporting their use as a definitive cure for OSA. Another reason these surgeries are felt to be temporizing measures only deals with the mechanics of the repairs. Over time, the anatomical correction gained from most of these surgeries reverts due to the power of times and tissue plasticity.
If the Minor League interventions fail to alleviate OSA symptoms or a patient has particularly advanced OSA, Western Medicine has devised two Major League curative interventions. The first is the maxillomandibular advancement (MMA) or the jaw thrust. The aim of this surgery is to turn back the clock on Darwinian evolution by taking a Homo sapiens' face and remodeling it into that of a chimpanzee's.
Although this may sound like the procedure Michael Jackson underwent, I assure you the result is more characteristic of a Jay Leno profile. Through this process of breaking the upper and lower jaws, advancing them anteriorly 12mm, then fixating them with hardware, the tongue and palate are pulled away from the pharynx so that it no longer obstructs the sleeping airway. The result is a Neanderthal circa the Paleolithic Age minus the pronounced brow, dragging knuckles and the "Me Tarzan, you Jane." mentality. Long-term follow up studies on the patients that undergo this surgery suggest that significant SDB is cured in 90 percent of the cases and the appearance changes are fine. Unfortunately, the surgery requires 3 months of interdental fixation and has a 1 percent risk of serious complications.
The second Major League operation for OSA is a tracheostomy. As we discussed above, OSA is caused by bad anatomy of the upper airway. If that anatomy is bypassed with a large hole in the trachea, OSA ceases to exist! Unfortunately, because purulent pulmonary secretions dripping from a hole in your throat are not socially acceptable in western society, tracheostomy is typically reserved for severe cases of OSA. Perhaps a fitting social intervention for ex-OSA patient's who undergo these curative procedures would be a match making singles service. Typical personal want-ads might read: "DWM with strong jaw seeking D/SWF with drippy neck for friendship and possibly more, purulence OK" or "Tarzan seeking Jane to swing in trees and share bananas. Must be non-snorer."
Aside from CPAP and surgical interventions, the single most beneficial treatment for OSA is weight loss. Patients with OSA who lose a fraction of their weight can significantly improve their apnea indexes. Furthermore, obese patient with OSA who lose most of their extra weight can potentially cure their OSA. This is impressive and seemingly simple, but extremely difficult in reality! The typical OSA patient is not a model of health fitness. Many are obese, and some morbidly obese with associated co-morbidities- osteoarthritis of the hips and knees, impaired pulmonary function with dyspnea on exertion, and cardiac and peripheral vascular disease manifesting as angina, claudication, and possibly syncope/dizziness with exertion. Add excessive daytime fatigue to this picture of jumbled pathology and see how many of these individuals want to go for a run around the lake every morning to lose weight?
To make this concept more experiential, try this exercise next time you are on overnight call. Take a large backpack and fill it with 100 pounds of sand. Put it on-this is your new body habitus. Go about your day of rounding on patients, climbing stairs, sitting down, standing up, walking, you get the point. Continue this activity throughout the day, into the night (make sure you don't sleep or neglect your on-call cross cover duties!), and then into the next day. Just for kicks, stay up an additional night (now 48 hours straight without sleep). When the next morning rolls around see how much you feel like engaging in some brisk exercise followed by a rewarding breakfast of wheat grass juice and non-fat bran muffins.
For all you who may think that you are up for the challenge, try to consider yourself with advanced osteoarthritis in your knees and crushing angina. After this visualization, losing weight becomes less of a priority. By this point, most would opt for some good tasting French fries, a comfortable couch, and a funny Seinfeld episode over a run around the lake. Welcome to the world of OSA patients!
Having completed that exercise in experiential education, I think we can all agree that getting patients with OSA to lose weight is an enormous feat. In fact, the only way that obese OSA patient's can stand a chance at losing weight is if their OSA is properly treated with an effective intervention. By eliminating their incredible fatigue with CPAP, they have one less obstacle to overcome in their quest for a normal body habitus! For those who are able to reach their lean fighting weight, they will reap the rewards of an improved self-image, a decrease in the morbidity associated with obesity, and perhaps a future without OSA.
The remaining treatments for OSA vary in their efficacies, and for completeness I will mention each briefly. There exist numerous dental prosthetics on the market that fall into two categories. The first pulls the tongue forward which prevents it from falling back and blocking the airway. The second repositions the mandible anteriorly by moving the mandible and associated structures. These devices can often be adjusted until just the correct amount of movement has been achieved to prevent airway obstruction. These devices are discussed more thoroughly (and quite comically) in the case studies. The bottom line is that some practitioners swear by the use of oral appliances, while others scoff at them.
If they work for your patients they can be an effective and preferable option to surgery. There is also pharmacotherapy. Progestational agents like Medroxyprogesterone acetate (MPA) accentuate the hypercapnic chemoreceptor reflex. While these agents increase respiration in hypoventilatory patients during the day, they have little if any effect on apneic episodes during sleep. Additionally, there are proponents of tricyclic antidepressant (TCA's) use for treating OSA. Here, the aim is to capitalize off the side effect profile of TCA's-a diminution of REM sleep. Since REM is the part of sleep in which most apneas occur, the theory is to reduce apneas by eliminating REM. While this therapy does reduce total number of apneas during a night, patients still have abnormally high apnea indices. While TCA's may not be an effective treatment for OSA, at least the patients taking them will not be so depressed about their dysfunctional sleep!
Finally, there is always the tennis ball sewn in the back of the shirt trick. This intervention aims to keep snorers off their backs so gravity does not pull their tongues and palates into their pharynxes! While this intervention may work for some cases of positional snoring, or positional OSA, patients who snore or stop breathing in other positions will continue to obstruct.
Sleep-Disordered Breathing Grab Bag
By this time, you may be confused about the distinction between obstructive sleep apnea and sleep-disordered breathing, since they seem to describe overlapping phenomena. Sleep-disordered breathing, however, refers to the entire spectrum of breathing disorders that cause problems with sleep. Thus, obstructive sleep apnea is a subset of sleep-disordered breathing. Pathological states included in this subset are: snoring, upper airway resistance syndrome, obstructive sleep apnea, heart failure, stroke, and hypercapnic COPD. While snoring, upper airway resistance syndrome and obstructive sleep apnea are discussed separately for simplicity, these particular conditions probably represent a continuum of common pathophysiology. This section will impart pearls of information in a grab bag fashion. Hopefully these quips will round out your understanding of sleep-disordered breathing and OSA.
Snoring causes a significant disruption to bedroom harmony and is associated with the development of hypertension. Several publications have demonstrated that snoring without concurrent OSA is an independent risk factor for the development of hypertension.
The key to the management of snoring is to determine whether OSA co-exists. A multi-channel home sleep test can accomplish this. For patients with a normal apnea-hypopnea index (AHI) whose snoring causes significant disruption in the bedroom, options exist. The most successful treatment is likely to be weight loss. Nasal CPAP is also very effective in the treatment of snoring, but because most snorers do not have sleep apnea, the benefit derived from CPAP therapy is often insufficient to motivate patient compliance. In cases where CPAP is not an
option, the Otolaryngology community has proposed numerous surgical therapies for the treatment of snoring.
UARS:
Upper airway resistance syndrome is a fascinating illness. Patients with UARS present with symptoms of daytime sleepiness, fatigue and depression, but sleep testing fails to document an impressively elevated AHI. Only in-hospital polysomnographic studies with pharyngeal balloon measurements will demonstrate an increase in pharyngeal pressure associated with EEG arousals. These patients respond well to treatment with nasal CPAP. Because of its immediate response to CPAP treatment, a significant number of sleep physicians consider UARS a form of obstructive sleep apnea.
OSA:
Obstructive sleep apnea has been discussed sufficiently. The extensive morbidity and mortality caused by OSA, however, should beg the question what evolutionary advantage is gained by this disease. My advisor, Dr Davidson, has proposed an interesting anatomical evolutionary theory on why humans are the only mammals aside from English Bulldogs to have developed OSA. It is his belief that OSA is a recent illness that results from the anatomical changes that facilitated speech.
In order to speak, the distance from the lips to pharynx and pharynx to vocal cords must be equidistant and the pharynx must be a narrow, collapsible, compliant tube. To achieve the first of these changes, the larynx descended. Man is the only mammal with the larynx descended beneath the level of the soft palate. The tongue base followed the descent of the larynx resulting in its current position partially in the oropharynx. To shorten the lip to pharynx distance, the maxilla and mandible retruded. This was achieved in part by a shortening of the sphenoid bone and in part by a decrease in the length of the maxilla and mandible. These changes caused the tongue to lapse further into the oropharynx.
To create a narrow and compliant pharynx, the anterior and posterior boarders approached one another. The foramen magnum rotated anteriorly causing the spine to push the pharynx anteriorly and the midface was repositioned posteriorly causing the pharynx to be pushed towards the spine. The anatomical changes that have facilitated speech-laryngeal descent, posterior retraction of the midface, an oropharyngeal tongue base, and a narrow and floppy pharynx-have predisposed man to the development of obstructive sleep apnea. In considering the evolutionary process, one may ask why natural selection did not weed out individuals with OSA. I will remind you that only recently has man's life expectancy exceeded 30-40 years. Obstructive sleep apnea occurs more frequently when people are 40 - 50 and older, a time when most have passed their procreative period and are no longer subject to the normal selection forces seen in evolution.
Sleep-Disordered Breathing and Gender
Gender based differences in the manifestations of sleep-disordered breathing can often confuse the diagnosis and thereby delay treatment. Because sleep-disordered breathing was thought to be primarily a male disorder, the symptoms in women are often overlooked or misinterpreted. Men tend to present with snoring, apneic episodes and daytime sleepiness. When evaluated with sleep testing, most will demonstrate an elevated AHI. Women are less likely to report snoring, and their daytime sleepiness is often assumed to be depression. Their symptoms may often be more vague and generalized. Consequently, sleep-disordered breathing in women is commonly mistaken for depression and subsequently under-diagnosed.
Heart Failure and Sleep-Disordered Breathing:
There are millions suffering from varying degrees of heart failure. Some snore, some exhibit Cheyne-Stokes breathing and most have abnormal sleep studies. Nonetheless, congestive heart failure is improved with nasal CPAP. For mild heart failure, the standard nasal CPAP with an autotitrating device is remarkably therapeutic. For those with Grade III and IV heart failure, particularly those with Cheyne-Stokes breathing, more sophisticated CPAP paradigms are required for effective treatment.
Stroke and Sleep-Disordered Breathing
Two-thirds of the patients who have suffered stroke will exhibit obstructive sleep apnea and other abnormalities of sleep. While nasal CPAP compliance in this patient population requires hard work and lots of emotional support, those who are able to comply will demonstrate significant improvement in their sleep function and their quality of life.
Hypercapnic COPD
Patients with hypercapnic COPD can be preemptively treated with nasal or full mask bi-level PAP treatment. (COPD is virtually never treated with nasal CPAP because of lung involvement and the need for ventilation as well as upper airway stabilization). This diminishes CO2 accumulation during sleep, improves pulmonary function and improves general well being.
Sleep-Disordered Breathing Associations
There are a myriad of medical conditions associated with sleep-disordered breathing, including nocturia, nighttime epilepsy and nighttime arrhythmia requiring a pacemaker. A number of patients with ocular abnormalities, particularly nighttime retinal hemorrhages, also have sleep-disordered breathing. All of these conditions will respond to nasal CPAP.
Central Sleep Apnea
Central Sleep Apnea (CSA) is a condition characterized by apneas in the absence of ventilatory effort. Conditions that cause CSA include any neurological or muscular disorders that affect the respiratory control center, the innervation of the diaphragm, or the muscles of respiration. These would include encephalitis, cerebral infarct, tumor, old polio, amyotrophic lateral sclerosis, quadriplegia, muscular dystrophy, and kyphoscoliosis respectively. CSA is also seen in cases of heart failure, manifesting as Cheyne-Stokes respiration. Depending on the severity of ventilatory impairment and the stability of neurological impairment (progressive vs. non-progressive disease), treatments for CSA include use drugs to stimulate the respiratory center, periodic non-invasive ventilation with bi-level positive airway pressure, electrical diaphragmatic pacing and, in severe cases, continuous ventilatory support.
Sleep-Disordered Breathing in Children
Thus far, I have not mentioned pediatric obstructive sleep apnea. This condition is generally a consequence of enlarged adenoids and palatine tonsils. It is reported that 10 percent of children snore and 2 percent have documentable obstructive sleep apnea. A tonsillectomy and adenoidectomy procedure will usually cure kids of pediatric OSA and thereby cause dramatic improvements in daytime behavior and school performance.
Sleep-Disordered Breathing in the Elderly
The prevalence of sleep disordered breathing in the elderly (24%) is substantially higher than in younger adults. Although BMI is still the best predictor of the presence of sleep disordered breathing, obesity is less of an issue in the elderly. The slender, older man or woman who snores and is excessively sleepy may still need an evaluation for OSA. In addition, many of the symptoms of sleep-disordered breathing may mistakenly be thought of as part of normal aging, for example, difficulty sustaining attention, slowed response time, difficulty with memory, and decreased performance. These symptoms may all be misinterpreted as dementia.
As sleep-disordered breathing began to be recognized as a medical condition, in-hospital polysomnography was the tool of choice for reaching a diagnosis. The gold standard involves monitoring multiple physiologic functions during sleep in a hospital sleep laboratory. For all practical purposes, every physiologic function barring one's bowel activity is "watched over" in this test. Information is gathered about heart rate, heart rhythm, blood pressure, blood oxygen saturation, muscle activity, brain wave activity, eye movement, airflow, and chest wall movement during every moment of sleep.
With experience, economic restrictions and a limited number of individuals capable of performing in-hospital polysomnography, however, the portable home sleep test has become a viable alternative to diagnosing sleep disorders. Home sleep tests vary with respect to the amount of data they collect. The comprehensiveness ranges from recording only a single variable (airflow, oximetry etc.), termed level IV testing, to recording all the variables entailed in standard polysomnography, termed level II testing. As one would expect, the more variables recorded, the more sensitive and specific the test becomes. Currently, the minimum requirements needed for a home sleep test to be an effective diagnostic test are a separate measures of respiration, a measure of heart rate, and an oxygen saturation. This degree of testing, termed level III testing, has proven specific and sensitive in screening sleep disorders.
Additionally, because the home sleep test occurs in the patient's own bedroom instead of the hospital laboratory, it is better accepted, less expensive and may document sleep patterns that are more characteristic of a patient's normal sleep. By monitoring the nocturnal physiological function, sleep testing has become the tool diagnose SDB.
The key to deducing the diagnosis of OSA via a home sleep test is through use of the respiratory channel. Information for this channel is obtained via very sensitive detectors of airflow that are placed beneath the nose and in front of the mouth. Information from these sensors forms the basis for diagnosing OSA. Apneas are defined as a ninety percent or greater decrease in airflow for ten or more seconds. Hypopneas are defined as a fifty to ninety percent decrease in ventilation for ten or more. The apnea index (AI) is reported as the number of apneas per hour of sleep. The same is true for the hypopnea index (HI). The apneas and the hypopneas are added to form the Apnea Hypopnea Index (AHI), also called the respiratory distress index (RDI). This is reported as the number of apneas plus hypopneas per hour of sleep. In home sleep tests which have no measure of sleep/wake, the AI and the AHI are approximated from the time spent in bed. As we will see in the following cases, the information from the multi-channel home sleep test imparts objective data about sleep parameters that allow a practitioner to individually tailor treatment.
Figure 1 is a normal sleep study while Figure 2 is an abnormal sleep study. As you compare the two, the differences should become obvious. The normal study has a minimum amount of ink while the abnormal study has tons of ink. If you could simply weigh the ink here, you would know the severity of the sleep-disordered breathing.
From AutoSet Portable II Plus (ResMed, San Diego)
Looking at the specific channels, the first is pulse oximetry. A person in normal sleep maintains a normal blood oxygen level. You can see that the normal study oximetry shows essentially 99% saturation throughout the night. The abnormal study shows repeated desaturations. Note that these come in bursts or periods of deep sleep. Oxygen desaturations are unhealthy and are associated with cardiovascular stress. The more severe the sleep-disordered breathing, the more severe one typically sees the oxygen desaturations.
The next channel reports the flow volume of nasal ventilation. In the normal individual, nasal ventilation is smooth and of low amplitude. In obstructive sleep apnea, it is erratic and of greater amplitude. People who stop breathing take larger breaths upon arousal.
From AutoSet Portable II Plus (ResMed, San Diego)
Ventilation that is erratic in rhythm and large in amplitude implies a more severe case of sleep-disordered breathing.
The next channel shows a recording of snoring. While the only silent sleepers are those in the morgue, the majority of people do make some noise during nighttime breathing. This is reflected in the normal study. Conversely, those with sleep-disordered breathing may make a substantial amount of noise. The abnormal sleep study depicts a patient who snores like a freight train. The units are arbitrary, but for definition's sake, one unit is 75 decibels at a distance of 10 centimeters from the mouth. The next channel shows the individual apneas and their duration, measured in seconds.
The next channel is a histogram of cumulative apneas and hypopneas per hour. The data at the bottom, are the critical aspects of the sleep evaluation. They include age, gender, apnea index (AI), apnea hypopnea index (AHI) and the lowest oxygen desaturation (LSAT). While most sleep recording machines display more data than we have included, this additional information tends to confuse the novice, and is consequently omitted. For completeness, however, chest movement and abdominal movement may be part of the data to differentiate obstructive from central sleep apnea. Information about leg movements and body position, namely prone, supine and right or left lateral can be included.
Electrocardiogram and EEG (polysomnography only) can also be included in the data (the latter is used to determine sleep stage and sleep architecture). For home sleep tests that do not use an EEG, the sleep/wake cycle can be approximated with actigraphy-the charting of movements during sleep. Using an accelerometer the size of a wristwatch, movement during sleep can be determined. When the patient is sleeping, movement will be at a minimum, and conversely at a maximum when the patient is awake.
To reinforce the key features of sleep-disordered breathing, we present several cases.
CASE ONE
The first case is a 23-year-old second year medical student who presented by himself stating that he was snoring and chronically tired. His girlfriend suggested that he may have sleep apnea and in any case, his snoring was so bad that she could no longer sleep near him. He studied every night until midnight. On Monday, Wednesday and Friday he arose at 6:00 AM. On Tuesday, Thursday and Saturday he arose at 7:00 AM. On Sunday, he arose at 8:00 AM. He was sleepy and often fell asleep during class.
Examination
On examination, the patient appeared to be a normal 23-year-old male with height and weight of 5'7", 170 lbs. and a BMI of 24. ENT exam showed a mildly deviated septum. He had undergone tonsillectomy as a child. His pharynx appeared normal. Trans-nasal endoscopy showed normal anatomy of the pharynx, nose and larynx. An overnight sleep study was performed and the results are shown.
Questions
1. What is your interpretation of the sleep study?
2. What are the causes of this man's snoring?
3. What are the causes of this man's sleepiness?
4. What treatment recommendations do you suggest?
Answers
1. You may recognize this sleep study, as it is identical to that in Figure 1, a normal sleep study.
2. Snoring is caused in most cases by a vibration of the uvula. Air rushing by this restricted portion of the airway causes the uvula to vibrate, making the snoring sound. In some cases, the posterior tongue will contribute to the sound, but as uvulectomy resolves snoring in 90% of patients, it is presumed that the uvula is the primary site of snoring. In this case, the sleep study shows a silent snoring channel, and yet the bed partner who did not accompany the patient stated that he snored and disrupted her sleep. This presentation is not the usual, but is certainly seen. Everyone makes some breathing related noise during sleep. In some cases, when the bed partner is an extremely light sleeper, virtually any movement or noise can disrupt their sleep. This problem can be exacerbated by a deteriorating relationship. It is important to note that a complaint of SDB should always be taken seriously and properly evaluated by a sleep test, just as was done in this case. One should only rule out the existence of SDB after thorough sleep testing has been done.
On further questioning, the medical student revealed that his relationship had been strained. His partner was under a great deal of stress and had been blaming him for causing many of the stressors that their relationship was experiencing.
3. The amount of sleep that people need is genetically programmed. When this amount of sleep is not fulfilled, sleep debt begins to accrue. It is said that the only debt in the United States that exceeds the national financial debt is the national sleep debt. Indeed, we each carry our own sleep debt. On Mondays, Wednesdays and Fridays, this patient accumulated two hours of sleep debt. On Tuesdays, Thursdays and Saturdays, he accumulated one hour of sleep debt. This is a nine-hour sleep debt per week. Carried on week after week, this debt accumulation resulted in a very tired medical student. From the perspective of efficiency and success in medical school, this patient would have done better going to bed at 11:00 PM on a regular basis, and permitting himself to sleep in on Saturday or Sunday morning to make up for the week's sleep loss.
Excessive daytime sleepiness, which can be a result of medication, sleep deprivation, obstructive sleep apnea and many other etiologies, makes one prone to accidents. Compared to properly rested individuals, tired people have 7 times the incidence of motor vehicle accidents. Additionally, they are non-productive and are often involved in failing relationships. The medical student's sleepiness may have contributed to the stress in his relationship, resulting in his partner's complaint that he made too much noise at night. The diagnosis should point to the obvious treatments. The responsibility for change lies with the student.
CASE TWO
The next case is a 48-year-old businessman who presented to the University Sleep Clinic for an evaluation for sleep apnea. His wife accompanied him and provided much of the history. He is a hard- working, successful professional who has snored for most of his adult life. The wife reports that his snoring has become increasingly louder over time. Also, over the past several years, his wife noted an increase in the frequency and duration of apneic episodes. Despite up to 10-12 hours of sleep per night, the patient remains sleepy during the day. He falls asleep in meetings and spends his weekends at home napping. Needless to say, his problem is beginning to impair his professional and marriage life.
Examination
On examination, he was 6'1", 230 lbs. with a BMI of 30. His upper respiratory exam showed a reasonably patent nasal cavity. On oral exam, he had a Mallampati class 4 upper airway, and his tonsils were 2+. His uvula was long and edematous and his tongue appeared to fill his entire mouth.
On trans-nasal fiber optic exam, the soft palate was indeed retro-displaced. The base of tongue was positioned posteriorly. His vallecula was occupied by his tongue. This caused posterior displacement of his epiglottis. The distance from the epiglottis to the pharynx, the posterior air space, was only millimeters wide. Based on the symptoms of snoring, apneic episodes, and excessive daytime sleepiness, a multi-channel home sleep study was ordered. The results are shown.
Questions
1. What is your diagnosis?
2. What is the relationship of BMI to AHI?
3. What is a mallampati examination?
4. What is the treatment recommendation for this gentleman?
5. How does obstructive sleep apnea get this bad prior to diagnosis?
Answers
1. The patient has an AHI of 50, indicating severe obstructive sleep apnea. Most consider an AHI less than 5 as normal, while an AHI of 5 to 15 is considered mild OSA, 15 to 30 is moderate and greater than 30 is severe.22 Using this criteria, up to 24% of adult males and 9% of adult females would have an abnormal AHI. Currently, there is not sufficient medical evidence to support the treatment of mild forms of OSA. There is concern, however, that early intervention in OSA will significantly reduce morbidity and mortality just as we have found in dealing with hypertension, diabetes and lipid abnormalities. This patient, therefore, has severe OSA as supported by the AHI, the LSAT and his symptoms.
2. The relationship between BMI and AHI is an interesting one. Certainly, obesity makes OSA worse. It exacerbates existing airway obstructions via mass effects and causes more severe desaturations during apneic episodes as a result of smaller residual lung capacities. It is important to realize, however, that obesity does not cause OSA. Poor upper airway anatomy and neurologically mediated hyper-relaxation of the pharyngeal dilator muscles are the causes of OSA. With that said, however, weight loss is an important treatment intervention for OSA. Most OSA patients who are able to lose even minimal weight can gain improvement in symptoms. Those who are able to achieve their ideal weight can oftentimes cure themselves of OSA.
3. Mallampati was an anesthesiologist in Canada who was interested in finding criteria that would predict a difficult intubation. Mallampati developed a system in which he examined the relationship of the tongue to the uvula and soft palate in the relaxed, gently opened mouth. Mallampati class 1 means the entire uvula and tonsillar fossae are visible, Mallampati 2 means the tip of the uvula and/or part of the tonsils are obscured by the tongue, Mallampati 3 means the entire uvula is obscured, and Mallampati 4 means all of the soft palate is obscured. Mallampati scores of 3-4 are associated with difficult intubation and they are commonly seen in patients with obstructive sleep apnea. An awake physical examination may not predict obstructive sleep apnea, since there is a significant difference in the airway during sleep and while awake. There is, however, a sense that a smaller airway, a thicker neck and visible airway obstructions including a deviated septum, large tonsils, a long edematous uvula, posterior tongue displacement and narrow posterior air spaces are all consistent with the diagnosis of sleep apnea.
4. The treatment of choice is nasal CPAP. If this fails, the patient may be considered a candidate for surgical treatment. Interventions such as septoplasty, tonsillectomy, tongue base suspension and uvulopalatopharyngoplasty (UP3) are an option for CPAP failure in mild cases of SDB or in patients with obvious anatomical obstructions such as nasal polyps or very big tonsils. Patients with moderate and severe obstructive sleep apnea, however, typically require either a tracheostomy or a maxillomandibular advancement.
The temporizing surgical treatments such as septoplasty, tonsillectomy and uvulopalatopharyngoplasty (UP3), even when combined with a tongue suspension procedure, will often not relieve the obstruction sufficiently to cure moderate or severe SDB. Maxillomandibular advancement (MMA) and tracheostomy are the only surgical interventions that are able to provide total cures for OSA. While MMA has a 90% cure rate, it is considered a rather rigorous undertaking. It has a 1% incidence of significant morbidity including infection, slippage, malocclusion and pain. For those who require it, it is available, but it is not to be taken lightly. For most patients, a conventional tracheostomy is not an attractive option. There are however, tracheal buttons that connect the trachea with the anterior neck and sit flush with the neck skin. The tube is capped during the day and is only opened at night. For many with advanced sleep apnea who cannot tolerate CPAP, this is the technique of choice.
5. The medical profession is still learning about sleep medicine, and many medical schools have not yet included it as part of their regular curriculum. Hence, my interest in writing this primer. The majority of physicians faced with a sleepy patient will simply advise them to get more rest. If the patient appears overweight, they will advise them to lose weight. Rarely will they take a sleep history. It is only recently that the primary care physicians are thinking about referring for sleep evaluation and treatment.
CASE THREE
Case three is a 30-year-old orthodontist who was accompanied by his wife. He described himself as a very loud snorer. Before his examination, he and his wife had vacationed with another couple in a motor home. After two days, the other couple had to leave because of his snoring. When questioned about apneic episodes, his wife thought that they occurred sometimes. When questioned about his sleep behavior, the patient reported going to bed between 9:00 and 10:00 PM and awaking between 6:00 and 7:00 AM, with headaches. He reported difficulty arising in the morning, but denied any overt symptoms of daytime sleepiness.
Examination
The patient was an average, healthy 30-year-old male in good physical shape. Height was 5'11". Weight was 185 lbs. BMI was 26. ENT exam showed no significant obstructive abnormalities. The nose appeared patent. The tonsils were resected when he was a child. Mallampati was 3. The uvula was edematous, but not elongated. At fiber optic exam, the vallecula was obscured by tongue base, but the posterior space was not otherwise compromised. A multi-channel home sleep study was recommended. The results are shown.
Questions
1. What is the diagnosis?
2. What is the recommended treatment?
3. What is the role of dental orthotics in the management of sleep apnea?
4. What is the importance of spousal support in CPAP compliance?
Answers
1. The diagnosis is moderate obstructive sleep apnea with an AHI of 22. The AHI is not terribly high, but the patient is impressively symptomatic. He sleeps 10 hours per night on average. He wakes up unrefreshed. His morning headaches are considered a result of 45 carbon dioxide retention causing cerebral vasodilatation. The LSAT of 82 for a 30 year old with an AHI of 22 is concerning.
2. Nasal CPAP. While there is interest on the part of the surgeons to treat patients with a low AHI, nasal CPAP is still the first line of treatment. Only those who fail CPAP should be considered for surgery. In addition, surgical results do not appear to be long-lived. This man is 30. We know from the previous case that sleep apnea progresses. This man will clearly develop worsening obstructive sleep apnea as he ages, and while it may be possible to improve his situation in the short term with surgical therapies, over the long-term, nasal CPAP is inevitable.
3. When CPAP was recommended to the patient, he inquired about the use a dental device. Dental devices have been recommended as a therapy for snoring and sleep apnea. Proponents of dental devices say that by opening the mouth and thrusting the mandible several millimeters anteriorly, they can reduce snoring and decrease obstructive sleep apnea. Assuming these reports are valid, this is accomplished at significant cost. The pressure that these devices put on the teeth causes them to move, similar to the effects of orthodontic braces. They also distort the normal anatomy of the temporomandibular joint and thereby create problems. It is hard to imagine that this form of therapy for 50 to 70 years would be acceptable. One can imagine a scenario where chronic use of the device would slowly push the mandibular teeth forward to the point where first the incisors, then the canines, then the premolars and finally the molars would protrude out the front of the mandible. The result would be an unhappy patient with an edentulous mandible, severe TMJ, severe obstructive sleep apnea, and a horribly unsightly smile. Because of the need for long-term therapy, this patient was counseled against the use of dental devices.
The most important variables that determine compliance rates are the time that patients spend with their treating health care team and the energy provided by their spouse. Life long CPAP compliance is difficult to achieve for both technical and emotional reasons. Patients can experience nasal obstruction and mouth leaks, so it is important that a skilled professional be available to counsel and assist patients. If the spouse is unsupportive, or if using CPAP interrupts the patient's sexual relationship, the patient will probably become non-compliant. Conversely, if the spouse attends the diagnostic and the treatment sessions and is supportive about the patient wearing the CPAP, the patient will most likely wear the CPAP and derive significant benefit. In successful cases, the patients will become accustomed to using the machine and will even travel with the CPAP. Only on rare occasions, such as during an illness, will they not use the machine.
CASE FOUR
Case four is a 12-year-old boy who presented with loud snoring. His mother noted witnessed apneic episodes. When she discussed this with her pediatrician, she was advised to consult with a specialist. Neither he nor his mother noted any other sleep symptoms.
Examination
On examination, the patient was a thin 12-year-old male, 54 inches, and 99.5 pounds with a BMI of 24. On examination, the patient had a normal nose. He had 3.5+ tonsils and no other obvious abnormality. The patient was recommended for an overnight sleep study. The results are shown.
Questions
1. What is the diagnosis?
2. What is the recommended treatment?
3. What is the role of obstructive sleep apnea in enuresis?
4. What is the recommended treatment for pediatric snoring?
Answers
1. The diagnosis is obstructive sleep apnea. An AHI of 14 is abnormal for anyone and it is certainly abnormal for a child. As children do not breathe as deeply, snoring may not be detected as easily. Any elevation of AHI over 5 in a child who snores and has large tonsils should be taken seriously.
2. Pediatric sleep apnea is different from adult sleep apnea. The anatomic abnormalities are different. Generally speaking, 90% of pediatric apnea is effectively treated with tonsillectomy and adenoidectomy. In this case, because of the very large tonsils, the T&A is recommended.
Tonsils are typically graded on a scale of 0 to 4:
0 reveals no tonsil
1+ shows tonsils that come to the tonsillar fossae, but do not protrude into the pharynx 2+ shows tonsils that protrude into the pharynx 3+ shows tonsils that protrude at least 50% of the distance to the midline of the pharynx 4+ shows tonsils that touch in the midline.
This patient had 3.5+, meaning he had very large tonsils that were not quite touching.
The patient did undergo T&A. Postoperatively, the patient made an uneventful recovery and underwent a follow up sleep test six weeks later. The results showed an AHI of 1. The mother stated that the snoring and apneic episodes disappeared the night of the surgery.
3. When asked about changes in behavior, the patient's mother reported that he was more relaxed and seemed to be doing better in school. She also noted that before surgery, her son had wet the bed every night, and after the surgery, he had not wet the bed once. In fact, enuresis in children is frequently caused by snoring and sleep apnea, and is mostly corrected by T&A. In adults, this is seen as nocturia. Most adults assume this is secondary to prostatic hypertrophy because it usually occurs at the time that prostate problems arise and it occurs slowly. However, some of the nocturia may not be due to BPH and may be due to SDB. It certainly is a pleasant benefit of successful sleep disordered breathing treatment.
4. As 10% of children snore and 2% have sleep apnea, one may wonder how many of these children would benefit from T&A. Given what we know about the negative effects of sleep deprivation on well being, attention and learning, it seems fitting that the 2% with sleep apnea should definitely undergo T&A. Management of the remaining 8% who do not have sleep apnea is less clear. Meaningful prospective studies have yet to address this issue. Additionally, no one has addressed the interconnectedness of pediatric and adult sleep apnea. For instance, does treatment of pediatric sleep apnea affect the development of adult sleep apnea? Like many sleep specialists, Dr. Davidson's impression is that pediatric sleep apnea is a different anatomic illness than adult sleep apnea. Thus, the management of pediatric sleep disordered breathing should not have any effect on the subsequent development of the disease in adulthood.
CASE FIVE
Case five is a 50-year-old woman, five years post-menopausal, who was self-referred for snoring because her husband had refused to sleep in the same bedroom. She was unaware of apneic episodes. She denied excessive daytime sleepiness.
Examination
On physical examination, she had a height of 5'5", a weight of 158 lbs. and a BMI of 27. ENT exam showed a patent nose. Mallampati was 2. Tonsils were 2+. On fiber optic exam, the pharynx seemed somewhat narrowed, but obvious obstruction was not evident. A multi-channel home sleep test was recommended. The sleep study is shown.
Questions
1. What is the diagnosis?
2. What is the treatment?
3. What are the symptoms of sleep apnea in women?
4. What is upper airway resistance syndrome?
Answers
1. The patient has an AHI of 5. Based on AHI alone, the diagnosis is mild obstructive sleep apnea.
2. Her treatment is nasal CPAP, which tends to be extremely effective. Treatment paradigms are no different for women than they are for men.
3. Symptoms of obstructive sleep apnea in women are often different from those in men. As seen in the previous cases, men often report snoring, apneic episodes and excessive daytime sleepiness. Women, on the other hand, seem to report loss of energy, loss of consortium, fatigue and even depression. These conditions are commonly diagnosed as hypothyroidism, depression etc. Treatment with CPAP will often reverse these subjective symptoms, so it is clear that they can be caused by sleep apnea. The vague, more generalized symptoms of OSA in women make deducing a diagnosis more difficult. Additionally, while one may not be inclined to treat a male with an AHI of 5, a woman with any of the above symptoms and an AHI of 5 probably warrants treatment.
4. Upper airway resistance syndrome (UARS) is a condition in which apneas and hypopneas are not prevalent despite the presence of elevated esophageal pressures during nocturnal respiration. An increased pressure in the esophagus implies elevated resistance in the airway. If one measures the nocturnal EEG in these patients, one finds that arousals occur during periods of elevated esophageal pressures. This condition has been called upper airway resistance syndrome. It is an indication for treatment with CPAP. UARS is effectively treated this way. Like most in his field, Dr. Davidson believes that the diagnosis of UARS can be deduced from a mild elevation in AHI, the patient's symptoms, and specialized metrics on the sleep test (degree of flattening, for example). If the diagnosis of UARS is suspect, a trial of nasal CPAP is warranted. If the symptoms improve, the diagnosis is confirmed. If CPAP does not provide improvement, the diagnosis is probably not UARS. Many believe that there is a continuum in the development of obstructive sleep apnea, beginning with snoring, progressing to upper airway resistance syndrome and then progressing to moderate and ultimately severe obstructive sleep apnea. It is unclear if this evolution in sleep-disordered breathing is true.
Sleep Disorders and Anesthesia
|
Sleep disorders and their consequences are found in all realms of medicine-from insomniacs seeking treatment in the outpatient clinics to OSA patients experiencing nocturnal arrhythmias during an ICU admission. Given the prevalence of patients with sleep disorders, as a physician-to-be, it is vital that you know how to properly take care of these individuals. The impetus for creating a section on sleep and anesthesia was not to advertise the greatness of the field into which I am entering, but rather to raise awareness of how you can get into trouble when caring for patients who have sleep disorders. More than any other specialist, the anesthesiologist must have a keen understanding of the anatomy and pathophysiology of patients with sleep disorders. This is especially true for OSA patients.
Anesthesia removes a person's ability to maintain their vital functions and reflexes. Through the use of narcotics and fluorinated inhalation agents, autonomic reflexes are blunted, patients become unresponsive, airways obstruct and ventilatory control becomes reflexive. The result is cardiovascular instability, partial or complete airway obstruction, and dampened ventilatory drive. The use of paralytics only compounds these problems by causing complete relaxation of the pharyngeal muscles and atonicity of the diaphragm. The result is a floppy unprotected airway and no independent ventilation. The anesthesiologist is trained to induce an adequately deep plane of anesthesia (induction), support the vital systems while a patient is anesthetized (maintenance) and to wake the patient up at an appropriate time (emergence). It is during both induction and emergence that problems arise with patients who have OSA.
During the induction phase of anesthesia, the airway must be secured for ventilation. Practically, this becomes an enormous problem in patients with OSA. As we previously mentioned, the Mallampati classification for difficult intubations tend to correlate well with prevalence of OSA. In other words, OSA patients tend to be difficult intubations because of their bad upper airway anatomy-short fat necks with limited extension, edematous pharyngeal tissue, and large obstructing tongues. All of these factors impair an anesthesiologist's ability to achieve an endotracheal intubation via standard laryngoscopy techniques. Moreover, to aggravate this scenario, most difficult intubations are also difficult or impossible to manually ventilate. Therefore, if an OSA patient undergoes induction and the anesthesiologist happened to not clue into the airway exam or the history of OSA, they might find themselves in a predicament where they are unable to ventilate their patient. Unless a surgical airway is achieved hastily, the patient will die from asphyxiation. To prevent such a scenario, OSA patients with significant anatomical obstruction should undergo awake intubations facilitated by fiber optic visualization.
The key idea to remember here is that OSA patients will need special handling during induction. During emergence, the bad anatomy and the altered physiology of OSA patients combine with residual anesthetic agents to create the potential for a lethal situation. While a patient who has just emerged from anesthesia may appear awake, often this is illusory. Recently emerged patients still have a considerable amount of anesthetic and paralytic agents in their systems. The effect is the s | 
