Obstructive Sleep Apnea: our freshly baked bread and butter. (But OSA isn't delicious).

Even though OSA is one of the most common sleep problems we encounter, it takes up relatively quite a small amount of real estate in the ICSD-3.

Today let’s focus on what the manual has to say about OSA in adults.

What are the features of OSA?

A person with obstructive sleep apnea either fully stops breathing (apnea) due to a full obstruction, or has a partial obstruction (hypopnea) while they sleep.

That’s no good.

This leads to reduced blood oxygen saturation and/or brief arousals.

Oftentimes bed partners report snoring, and patients wake up feeling sleepy still.

How long do these events last?

Minimum of 10 seconds.

What stage of sleep are they most common in?

N1, N2, and REM. Especially REM. (Loss of muscle tone in REM makes you more predisposed to OSA during that time)

What can make OSA worse?

Weight gain, use of sedating medications prior to sleep, weight gain.

Does everyone with OSA report sleepiness?

No.

Whoa! What are other things people are concerned about then?

Insomnia, poor sleep quality.

Some people don’t have any complaints at all, but might have severe OSA in addition to symptoms like a-fib refractory to treatment (because of untreated OSA!).

Does severity of OSA correlate with symptoms of sleepiness?

No! AHI (apnea hypopnea index) does not correlate with degree of sleepiness.

What are associated features?

Stroke, A-fib, DM, Systemic HTN (independent risk factor!)

What are patients with severe OSA at risk for developing?

Pulmonary HTN, cor pulmonale. This happens more so in morbidly obese people or those with COPD.

Also can be associated with worsening of CHF.

Can make mood disorders, GERD and erectile dysfunction worse too. These are great incentives I've found to have people get their OSA treated if they are not sleepy.

Untreated OSA can exacerbate and/or induce nocturnal seizures.

That doesn’t sound nice at all.

Nope. It can make other sleep disorders worse too, such as parasomnias.

What is the diagnostic criteria?

This is dry, but we have to know it.

(A and B) or C satisfy the criteria:

A. The presence of one or more of the following:

1. The patient complains of sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms

2. The patient wakes with breath holding, gasping, or choking.

3. The bed partner or other observer reports habitual snoring, breathing interruptions, or both during the patient’s sleep.

4. The patient has been diagnosed with hypertension, a mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, or DM Type II

B. PSG or OCST (out of center sleep testing, e.g HSAT) demonstrates:

1. Five or more predominantly obstructive respiratory events (including RERAs) per hour

OR

C. PSG or OCST demonstrates:

1. >= 15 or more predominantly obstructive respiratory events (apneas, hypopneas, RERAs)/h of sleep on PSG or OCST

Who gets OSA?

Prevalence is 24% of Men and 9% of women, using an AHI >=5 criteria.

Prevalence increases with age.

Incidence increases in women after menopause.

More common in black people vs white people.

Prevalence accelerates between young adulthood and middle age, plateaus by age 65 years.

What can predispose or precipitate OSA?

Basically…weight gain. 60% of moderate to severe OSA is attributable to obesity.

People with normal BMI are more likely to have an anatomic upper airway obstruction (e.g. maxillomandibular malformation, high arched palate)

Instability in ventilator control (e.g. an exaggerated ventilatory response to a respiratory disturbance).

Menopause.

Nasal congestion, nasal restriction in general.

The apple doesn’t fall far from the tree, right?

First degree relatives are 2x more likely to have a relative with OSA.

Onset, Course, Complications

Severity typically gets worse over time as BMI increases. You can improve severity of OSA with weight loss.

Consequence of weight change are more evident in men than women. (Lucky!)

Complications: making all of the associated features worse that we just talked about.

How does OSA occur? Let’s talk about pathophysiology

OSA is multifactorial.

1) Upper airway anatomy

People commonly have reduced cross-sectional area of the upper airway…why? Bulk from excessive soft tissue from tongue, soft palate, lateral pharyngeal walls, craniofacial anatomy, or both.

When we breathe in, negative pressure get’s generated, leading to a tendency for the upper airway to collapse. The pharyngeal muscles and dilating muscles keep our airway open. They are less active with sleep onset.

This is not enough for people with OSA to keep their airway open. This is even more of an issue in phasic REM sleep when muscle tone is lower.

2) Decreased end-expiratory lung volume --> leads to decreased downward traction from tracheal tug

3) Falling ventilatory drive (associated with hypocapnia)

How do people start breathing again?

Events may or may terminate with an arousal.

Low PaO2 and High PaCO2 may increase muscle tone (“chemical stimuli”)

Upper airway mechanoreceptors may be stimulated

Change of sleep state may result in termination of respiratory event.

What causes the symptom of excessive daytime sleepiness?

Sleep fragmentation.

Note that mild hypercarbia can happen during respiratory events, especially during REM.

People with OSA have elevated inflammatory markers (due to repeated oxygen desaturation), and increased sympathetic nervous system activity. That’s what leads to all the sequelae we talked about.

Objective Findings

Scoring and sleep study findings will have its own dedicated post.

I think my patient has OSA, but what else could it be? Here’s a differential diagnosis.

We're getting to the end of the section. Whoohoo!

Isolated snoring. Hard to tell without getting a sleep study.

Central Sleep Apnea

Obesity hypoventilation syndrome. Here you’ll see daytime hypercapnia and excessive daytime sleepiness, but may not see other obstructive features like snoring.

Sleep-related hypoventilation. Can have excessive daytime sleepiness, will have hypoventilation during sleep, but not necessarily have OSA. You can have both diagnoses though (this is pretty common, and found while testing for OSA).

Other things that can make you sleepy… Like: insufficient sleep, idiopathic hypersomnia, narcolepsy.

Lastly…make sure the patient doesn’t have something else that can make it difficult to breath eat night like GERD, asthma, CHF etc.

There we have it. This is what the ICSD-3 has to say about adult OSA.

...Stay tuned for sleep study scoring and objective measurements of OSA.

...We'll talk about how to manage and treat it later too!

References:

1. American Academy of Sleep Medicine. International classification of sleep disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine, 2014.

2. Upper airway image accessed from: Blausen.com staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2).

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