Ep 145: A 45-Year-Old Snorer
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This is Katarina Heidhausen, Executive Editor of Harrison's Principles of Internal Medicine. Harrison's Pod Class is brought to you by McGraw-Hill's Access Medicine, the online medical resource that delivers the latest content from the best minds in medicine. And now, on to the episode. Hi, everyone. Welcome back to Harrison's Pod Class. We're your co-hosts. I'm Dr. Kathy Handy. And I'm Dr. Charlie Wiener, and we're joining you from the Johns Hopkins School of Medicine. Today's episode is a 45-year-old snorer.

Kathy, today's patient is a 45-year-old man who's dragged into the clinic by his spouse because she's worried that he has sleep apnea after she saw a commercial on television. They've been married for 15 years and he's always snored some. Over the last six months, not only has his snoring gotten worse, but she thinks he stops breathing and then lets out a loud snort. Some nights, she has to go sleep in the kids' room because of the noise.

This doesn't sound like it's good for anyone. Can I have some more history about him? Sure. He's been very healthy his whole life and takes no medications. He works as a quality control officer at a manufacturing plant. About nine months ago, he was forced to work frequent late evenings and night shifts because the plant went to 24-hour operations. Since then, he's been exercising less frequently, eating irregularly, and he's gained 25 pounds and had to buy new clothes.

On review of systems, his only positive is that he's much more fatigued during the day. He often falls asleep at work and at home during quiet times. He denies dyspnea on exertion, wheezing, orthopnea, or PND. His physical examination is notable for normal vitals and a BMI of 31, and it was 25 a year ago. On oral examination, you notice that he has a shallow palate. On cardiac examination, he has a normal jugular venous pulse, normal lungs, and normal cardiac exam.

His only other abnormality is one plus pitting edema of the ankles. Okay, he's telling us a great story for sleep apnea. Remember, there are broadly two types of sleep disordered breathing, obstructive sleep apnea or OSA and central sleep apnea. How do you distinguish those two?

They're distinguished by apneas or hypopneas during sleep with physiologic consequences and are distinguished by OSA having apnea with ongoing or increasing inspiratory respiratory effort, whereas central sleep apnea is characterized by apnea with no evidence of inspiratory muscle effort.

These occur during sleep as the pharynx and hypopharynx have less neurologic tone and there is collapse during inspiration. The apnea or hypopnea is broken by an arousal and an effective breath, which often sounds like the loud snort. This patient sounds like he's having OSA, which is much more common than central sleep apnea. Yeah, we're going to talk about obstructive sleep apnea. Can you give me just a few words about central sleep apnea before we close that issue?

Sure. Central apnea in adults may occur alone or sometimes in combination with OSA. It can occur as a primary condition, as a response to high altitude, for example, or secondary to a medical condition, such as heart failure, medications like opioids, or even after a neurologic injury. Great. So let's get to the question. The question asks, based on this patient's presentation of suspected obstructive sleep apnea, all of the following statements are true except...

Option A is an overnight polysomnogram has the highest diagnostic sensitivity and specificity. Option B is continuous positive airway pressure or CPAP is the most efficacious therapy. Option C is his symptoms may improve with weight loss. Option D is he is at high risk of developing systemic hypertension. And option E is he likely has daytime hypercarbia. Okay, before we get into the options, let's review the criteria for diagnosing OSA.

It requires the patient to have one, either symptoms of nocturnal breathing disturbances, such as snoring or snorting or gasping or breathing pauses during sleep, or it can include daytime sleepiness or fatigue that occurs despite sufficient opportunity to sleep and is unexplained by other medical problems. The second thing is that you need to have five or more episodes of obstructive apnea or hypopnea per hour of sleep. This is called the apnea-hypopnea index or AHI.

The AHI is calculated as the number of episodes divided by the number of hours of sleep that are documented during a sleep study. So it sounds like our patient clearly meets the first criteria of symptoms. How do we define an apnea or a hypopnea? Each episode represents a reduction in breathing for at least 10 seconds and commonly results in at least a 3% drop in oxygen saturation or a brain cortical arousal from sleep.

OSA severity can be characterized by the frequency of breathing disturbances, the amount of oxyhemoglobin desaturation with respiratory events, the duration of apneas and hypopneas, the degree of sleep fragmentation, and the level of reported daytime sleepiness or functional impairment.

Okay, it sounds like our patient now needs a polysomnogram. Option A says overnight polysomnograms is the best test. Is that true? Yes, that is true. Since symptoms and signs do not accurately predict the severity of sleep-related breathing disturbances, specific diagnosis and categorization of OSA severity requires objective measurement of the breathing during sleep. The gold standard for diagnosis is an overnight polysomnogram, and that includes respiratory, cardiac, and EEG channels.

A negative in-laboratory polysomnogram usually rules out OSA. However, false negative studies can result from night-to-night variation in OSA severity, particularly if there was insufficient REM sleep or less supine sleep during testing than would be typical for the patient.

What about home sleep tests? They are increasing in use as they are more comfortable for the patient and generally less expensive. Home sleep tests that record only respiratory and cardiac channels are commonly used as a cost-effective means for diagnosing OSA. However, a home study may yield a false negative result if the sleep time is not accurately estimated or an individual is experiencing hypopneas with arousals rather than oxyhemoglobin desaturation.

So if there's a high prior probability of OSA and there's a negative home study, then that should be followed by a full polysomnogram. Okay. Options B and C both deal with therapy.

Yes, and again, both are true. But first, patients can be advised on how to try to improve sleep quality. So that's by improving sleep duration, regulate sleep schedules, encourage the patient to avoid sleeping in the supine position, treating nasal allergies, eliminating alcohol ingestion within three hours of bedtime, and minimizing the use of opiate medications.

Sedative hypnotic medications have inconsistent effects on OSA but should be avoided in most patients with moderate to severe OSA. And patients should be counseled to avoid drowsy driving. All good advice. And to the question, you said both treatment options were true. Weight gain is often associated with tipping a snorer into OSA, as is likely in our patient.

approximately 40 to 60 percent of cases of OSA are attributable to excess weight. Obesity predisposes to OSA through the narrowing effects of upper airway fat on the laryngeal lumen. Obese individuals are at a four-fold or greater risk of OSA than their normal weight counterparts. A 10 percent weight gain is associated with an over 30 percent increase in the apnea hypopnea index.

Even modest weight loss or weight gain can influence the risk and severity of OSA. It does improve after bariatric surgery. However, the absence of obesity does not exclude this diagnosis. And CPAP? CPAP is a standard medical therapy with the highest level of evidence for efficacy. So this gets delivered through a nasal or a nasal-oral mask. And CPAP works as a mechanical splint to hold the airway open. So that maintains the airway patency during sleep.

Rates of adherence to CPAP treatment are highly variable, though, and about 20 to 50% of patients don't tolerate it. Now, despite the limitations of CPAP, controlled studies have demonstrated its beneficial effect on alertness, mood, quality of life, work-related productivity, blood pressure, and even insulin sensitivity.

Uncontrolled studies also indicate a favorable effect on cardiovascular outcomes, cardiac ejection fraction, atrial fibrillation recurrence, and mortality risk. It really does work if the patient can tolerate it. There are some options for surgical, mechanical, or even neurostimulatory treatments for selected patients, but CPAP is still the most effective.

I think you gave away the answer to option D with your comments about CPAP. It sounds like patients with OSA are at risk for a number of cardiac and metabolic conditions. Yes, OSA is strongly associated with cardiac, cerebrovascular, and metabolic disorders, and with premature death. The likely mechanisms relate to the impact of sleep fragmentation, cortical arousal, and intermittent hypoxemia.

OSA-related respiratory events stimulate sympathetic overactivity, leading to acute blood pressure surges during sleep and nocturnal as well as daytime hypertension. OSA-related hypoxemia also stimulates release of acute phase proteins and reactive oxygen species that exacerbate insulin resistance and cause an augmented prothrombotic and proinflammatory state.

Inspiratory effort against an occluded airway causes large intrathoracic negative pressure swings, altered cardiac preload and afterload, and resulting in cardiac remodeling and reduced cardiac function. Hypoxemia and sympathetic-parasympathetic imbalance also may cause electrical remodeling of the heart and myocyte injury. Wow, that's a lot of bad effects due to this sleep-disordered breathing. Okay, so we know that options A through D are true. That means that option E is false. Yes.

Right. So most patients with mild to moderate obstructive sleep apnea will have a normal daytime PCO2. When they're awake, their respiratory drive is normal. There's a small subset of patients with OSA that progress to the obesity hypoventilation or Pickwickian syndrome, but that's small and typically associated with morbid obesity. The typical patient showing up with OSA and sleep clinic will have a normal daytime PCO2.

Great. To summarize, the teaching points of today's case is that obstructive sleep apnea, or OSA, is mediated by the loss of neurologic tone in the upper airway, provoking inspiratory effort against an occluded airway. OSA is best diagnosed with a polysomnogram. Treatment starts with lifestyle modification, trying to lose weight, but CPAP is the most effective therapy in most cases. The sequelae of obstructive sleep apnea involve multi-system diseases and therefore do mandate treatment.

And you can find this question and other questions like it in the Harrison's self-review book and online. And you can read more about this topic in the Harrison's chapter on sleep apnea. Visit the show notes for links to helpful resources, including related chapters and review questions from Harrison's, available exclusively on Access Medicine. If you enjoyed this episode, please leave us a review so we can reach more listeners just like you. Thanks so much for listening.