Obstructive Sleep Apnea

00:00 Welcome back.

00:02 Today we're going to discuss obstructive sleep apnea.

00:04 Obstructive sleep apnea, or OSA, is defined as recurrent upper airway obstruction during sleep that leads to chronic hypoxia and, over time, secondary pulmonary hypertension.

00:15 Keep that triad in mind.

00:17 Repeated obstruction, oxygen dropping, pressure building in the pulmonary circulation.

00:22 Let's set the stage with the broader classification of sleep-related breathing disorders so you know where OSA sits.

00:29 Sleep apnea, in general, means repeated cessation of breathing for more than 10 seconds during sleep and reflects a transient decrease in respiratory drive.

00:38 Within that, obstructive sleep apnea specifically results from soft tissues obstructing the airway, producing hypoventilation during sleep.

00:46 Central sleep apnea, or CSA, is different.

00:50 Here the problem is airflow limitation and or a ventilation abnormality driven by the central nervous system.

00:56 It can present with either hyperventilation or hypoventilation.

01:01 Mixed sleep apnea is, as the name implies, a combination of both obstructive and central components.

01:08 Finally, obesity hypoventilation syndrome, OHS, is a distinct entity in which excess adipose tissue in obese individuals leads to hypoventilation even while awake.

01:21 This is also known as Pickwickian syndrome.

01:24 All right, let's move into the epidemiology.

01:27 Incidence is high, about 20% to 30% in men and 10% to 15% in women.

01:33 Prevalence goes up as people age and tends to plateau after the seventh decade of life.

01:38 There are notable demographic differences.

01:40 African Americans are more likely to develop OSA regardless of age or body mass index.

01:45 Speaking of body habitus, obesity is a major driver.

01:48 A BMI of 30 or higher strongly correlates with obstructive sleep apnea.

01:53 Let's now talk about specific risk factors.

01:56 Craniofacial abnormalities such as microkinathia, kretrokinathia, macroglossia can all narrow the airway.

02:04 Advanced age, especially greater than 65 years, increases risk.

02:09 Alcohol or sedative use before sleep relaxes airway musculature and further promotes obstruction.

02:16 Endocrine and metabolic contributors matter too.

02:20 Acromegaly, which reflects excess growth hormone, and hypothyroidism, with its overall slowed metabolism, both increase risk.

02:29 Finally, any cause of poor muscle tone, including neuromuscular disease or brain injury, can compromise airway patency during sleep.

02:37 Let's switch gears and dig into pathophysiology, starting with what happens at sleep initiation.

02:43 As you fall asleep, there can be a reduced wakefulness drive to breathe.

02:49 There's also reduced motor output to the respiratory muscles.

02:52 As tone falls, the upper airway lumen is diminished.

02:56 That reduction in caliber raises upper airway resistance.

03:00 Now let's follow the apneic and hypopneic episodes that characterize OSA.

03:04 The airway progressively narrows.

03:06 Air flow drops.

03:08 Carbon dioxide accumulates, producing hypercapnia.

03:11 In response, the body ramps up respiratory effort, trying to overcome the obstruction.

03:16 What follows is a sympathetic surge.

03:19 The stress of struggling to breathe triggers tachycardia.

03:23 Blood pressure rises, so you see hypertension during these events.

03:27 And then come the pulmonary consequences.

03:30 Reduced air flow over and over again contributes to pulmonary hypertension by driving increased airway tone.

03:36 That happens because the lung tends to divert blood away from areas of hypoventilation by narrowing the vessels that lead into that.

03:47 It just doesn't make physiologic sense to perfuse an area of the lung if there's no oxygen in it.

03:53 Now, if the whole lung is hypoventilated because of upper airway obstruction, the entire pulmonary arterial supply can experience increased vascular narrowing, which obviously then causes pulmonary hypertension.

04:06 If this process continues, unchecked, strain on the right side of the heart can progress to core pulmonality.

04:12 To visualize the whole thing, think about the pathological cycle of obstructive sleep apnea.

04:18 Sleep onset often starts with snoring.

04:21 The airway collapses.

04:22 Breathing stops.

04:23 The body arouses just enough to reopen things, and the cycle repeats.

04:28 Let's now discuss the clinical manifestations.

04:31 A key practical point is that patients frequently are unaware of their own nighttime symptoms.

04:37 It's often a spouse or sleep partner who brings the problem to medical attention.

04:41 Staying with the sleep-related symptoms, patients may show nocturnal restlessness, and they can report vivid, strange, or even threatening dreams.

04:50 Sleep is often fragmented with interrupted sleep and frequent awakenings.

04:55 Bed partners may notice snoring, choking, or gasping episodes while the patient is asleep.

05:01 Nocturia, getting up at night to urinate, is also common.

05:05 Let's transition to cognitive and mood changes.

05:08 You may see a diminished ability to concentrate.

05:11 Broader cognitive deficits can develop.

05:14 Irritability and other mood changes frequently accompany chronic sleep disruption.

05:19 Now the physical and daytime symptoms.

05:22 Morning headaches are classic.

05:24 Daytime sleepiness, sometimes profound, is another hallmark that can impair work, school, and driving safety.

05:29 Before we leave manifestations, remember the long-term pathophysiologic changes.

05:34 Chronic disease progression can yield pulmonary hypertension and eventually right heart failure, core pulmonality.

05:41 Let's move on to diagnosis.

05:44 A simple and widely used screening tool is the Stop-Bang Questionnaire.

05:49 Ask, do you snore loudly? Are you tired during the day? Has anyone observed you stop breathing during sleep? Do you have high blood pressure? Is your BMI greater than 35 kilograms per meter squared? Are you age 50 years or older? What is your neck size? Greater than 17 inches in men or greater than 16 inches in women counts as positive.

06:11 And finally, gender.

06:12 Male sex adds risk.

06:14 Tallying these gives you a quick risk stratification before definitive testing.

06:19 Definitive diagnosis relies on polysomnography, the full overnight sleep study, which remains the gold standard diagnostic test for obstructive sleep apnea.

06:28 All right, let's wrap up with management.

06:30 First, weight loss is foundational and can significantly improve airway mechanics.

06:35 Avoidance is also therapy.

06:38 Cessation of sedatives and alcohol before sleep can reduce airway collapse.

06:42 Mechanical support options include oral appliances or splints worn during sleep that help prevent airway obstruction.

06:49 Positive airway pressure devices, most commonly continuous positive airway pressure or CPAP, provide pneumatic splinting of the airway and are a mainstay of treatment.

07:01 There are also implantable approaches such as hypoglossal nerve stimulation that move the tongue forward when apnea is detected, helping maintain patency.

07:11 And when conservative and device-based measures are insufficient or anatomy demands it, surgical interventions are considered.

07:17 And with that, we've covered obstructive sleep apnea.

07:19 Thanks for watching.