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Flashcards in Sleep Disordered Breathing Deck (51)
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1
Q

What is the crux of the problem of obstructive sleep apnea?

A

The airway can be thought of as plumbing and while some portions are bound by bone, the nasopharynx and oropharynx are muscles so they can be collapsed which is the crux of the problem for obstructive sleep apnea.

2
Q

True or False: As you get older or gain weight, there is a narrowing of the upper airway (oropharynx)

A

True

3
Q

What’s going on here?

A

As you have a narrowing of your upper airway (shown as an increase supraglottic resistance), you have more electromyography activity (muscles increase tonic output to keep from collapsing)

4
Q

What happens to the upper airway in sitting vs. supine position? (particularly when sleeping)

A

When supine, everything in the front of our throat falls to the back. Particularly the tongue. This narrows the airway and increases resistance to airflow.

An infection may cause swelling and also cause narrowing of the airway. Or if you have alcohol before you sleep, your muscle tone will be decreased and this also narrows the airway.

5
Q

What is the effect of sleep on the upper airway?

A

A lot of protective mechanisms are lost.

Inspiratory premotor activation decreases, tonic premotor activation decreases, and reflex driven muscle activation is lost.

6
Q

What are Pcrit, PUS, PDS, zone 1, 2, and 3 for airway collapse?

A

Pcrit is the pressure of the collapsed part of the airway

PUS is the pressure upstream to the collapse

PDS is the pressure downstream to the collapse

Zone 1 is when Pcrit > PUS > PDS and the airway is completely occluded.

Zone 2 is when PUS > Pcrit > PDS . In Zone 2, the airway is narrowed but not collapsed. Pressure upstream is able to overcome the narrowing and this is the physics of snoring.

Zone 3 is when PUS > PDS > Pcrit and the airway is open

7
Q

What happens to PAO2 , PACO2, PaO2, and PaCO2 when there is airway collapse?

A

There is a loss of ventilation during airway collapse so

PAO2 and PaO2 go down, PACO2 and PaCO2 go up

8
Q

What is the upper airway recruitment threshold?

A

This is the threshold or magnitude of stimuli necessary (negative pressure, increased CO2, or decreased O2) required to elicit a response from upper airway dilator muscles to adequately overcome Pcrit

9
Q

What is the arousal threshold?

A

This is the magnitude of stimuli (negative pressure, increased CO2, or decreased O2) needed in order to trigger an arousal (waking up).

10
Q

What is loop gain?

A

Loop gain is the magnitude of ventilatory response to stimuli.

Once you arouse, you are in a deficit where your O2 is low and CO2 is high. You have to hyperventilate to correct this. Patients can have loop gain that doesn’t match the deficit (can either hyperventile or hypoventilate)

11
Q

What is the issue with patients with high upper airway recruitment threshold?

A

These patients have longer duration of obstructive events because it takes a greater stimuli for them to recruit their dilator muscles

12
Q

What is the issue with patients with low arousal threshold?

A

These patients have low threshold for arousal which causes them to wake frequently, hyperventilate frequently, which causes hypocapnia (low CO2), which can actually cause a decrease in upper airway muscle tone. A decrease in upper airway muscle tone will cause more obstruction in the oropharynx (upper airway). So, this leads to cyclic episodes of obstructive events.

13
Q

What is the issue with patients that have high loop gain?

A

These patients have a greater sensitivity to CO2 and O2 stimuli, so they hyperventilate which causes hypocapnia (low CO2) which causes decreased upper airway muscle tone which causes collapse of the oropharynx. Again, this leads to cyclic episodes of obstructive events.

14
Q

What is central sleep apnea/Cheyne-Strokes Respiration?

A

People with central sleep apnea/Cheyne-strokes respiration are overly sensitive to CO2 stimuli when sleeping which causes them to hyperventilate and overcompensate by blowing off too much CO2. This causes long periods of central apnea where the brain just thinks that it doesn’t have to breathe anymore because the CO2 was blown down so much.

This can be very disruptive and can lead to disruption of sleep and daytime symptoms.

15
Q
A

C. Pcrit > PUS > PDS

Zone 1

16
Q

For sleep disorder breathing, does collapse happen on inspiration or expiration?

A

Inspiration

17
Q

What is apnea? What are the 3 types?

A

Cessation of nasal and oral airflow for a duration of at least 10 seconds. There are 3 types of apnea: central, obstructive, and mixed.

Central - cessation or reduction of airflow that occurs in association with the abscence of ventilatory efforts

Obstructive - cessation or reduction of airflow that occurs despite the persistence of ventilatory efforts

Mixed - cessation or reduction of airflow with an initial central component and terminal obstructive component.

18
Q

What is hypopnea?

A

Reduction of airflow or amplitude of thoraco-abdominal movement by at least 30% from baseline for at least 10 seconds in duration and accompanied by oxyhemoglobin desaturation of 4% or more

19
Q

What are apnea index and apnea-hyopopnea index?

A

Apnea index is the number of apneas per hour of sleep time.

Apnea-hypopnea index (AHI) is the number of apneas plus hypopneas per hour of sleep time.

20
Q

True or False: We all snore occassionally

A

True

21
Q

For habitual snoring, do men or women snore more?

A

Men. (44% of men vs 28% of women)

22
Q

What is upper airway resistance syndrome?

A

It is a syndrome that about 9% of people have where the resistance to airflow leads to arousals. (Oxygen levels don’t fall and there is no collapse)

23
Q

Is obstructive, mixed, or central apnea most common?

A

Obstructive (85%)

Mixed (14%)

Central (1%)

24
Q

True or False: There is probably a higher prevalence of sleep apnea than we know about because of people who don’t present with symptoms

A

True

25
Q

What is cheyne-stokes breathing and what kind of people are more prone to this pattern of breathing?

A

Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing called an apnea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes. It is an oscillation of ventilation between apnea and hyperpnea with a crescendo-diminuendo pattern, and is associated with changing serum partial pressures of oxygen and carbon dioxide.

About 40-50% of patients with history of heart failure and 10% of patients with history of stroke have cheyne-stokes respiration.

26
Q

Sleep apnea morbidity and mortality is associated with increased risk of what?

A

Obesity

Cardiovascular disease (pulmonary HTN, CAD, HTN, HF, CVA, hyperlipidemia, diabetes mellitus/DM)

Motor Vehicle Crash

27
Q

When should you perform a sleep history? (3)

A
  1. High risk patient screening
  2. Routine health maintenance exam
  3. Patient reports symptoms
28
Q

Who should be a included in the high risk population screening for sleep studies?

A

Morbidly obese (BMI greater than 35)

CHF

Atrail fibrillation (in order to properly treat A. fib patients, you need to address their sleep apnea if they have it)

Treatment refractory hypertension

Type 2 diabetes

Nocturnal dysarhythmias

CVA

Pulmonary HTN

High-risk driving populations

Preoperative for bariatric surgery

29
Q

For routine health maintenance exams, what questions should be asked to investigate for sleep apnea? (5)

A

Is the patient obese?

Is the patient retrognathic? (overbite anatomy)

Does the patient complain of daytime sleepiness?

Does the patient snore?

Does the patient have hypertension?

30
Q

In what demographics is sleep apnea most prevalent in?

A

More commonly in males

Increased prevalence as people age up to 6th and 7th decades of life

Prevalence is greater in minority populations (asians can have sleep apnea at lower BMIs)

31
Q

What past medical history events increase chance of sleep apnea?

A

Chronic rhinitis

Acromegaly

Neuromuscular disorder

Amyloidosis

Upper airway anatomic abnormalities

Genetic syndromes (e.g. 80-90% of Down syndrome patients develop sleep apnea)

32
Q

True or False: family history of sleep apnea is irrelevant

A

False. If your parents have sleep apnea, you are more likely to have it too. You look like your parents on the outside, and you look like them on the inside too.

33
Q

What social history increases risk of sleep apnea?

A

Smoking (inflammation) and drinking (decreased muscle tone)

34
Q

What medications can cause someone to be more susceptible to sleep apnea?

A

Sedative-hypnotics and opioids. These put patients at high risk for both obstructive and central sleep apnea.

35
Q

What are the sleep apnea symptoms?

A

Excessive daytime sleepiness

Witnessed apneas

Snoring

gasping/choking at night

nonrefreshing sleep

memory loss

decreased concentration

decreased libido

irritability

decline in performance at work or school

nocturia (waking up to pee) or enuresis (inability to control urination)

  • attention deficit (in children)*
  • hyperactivity (in children)*
36
Q

What is the epworth sleepiness scale?

A

A questionairre asking about likelihood of falling asleep during normal activities

37
Q

What can be done on physical exam to examine the oropharynx?

A

Mallampati Classification system

This can help determine someone’s risk of sleep apnea

38
Q

How can neck circumference be used to assess sleep apnea?

A

If a man has a neck circumference greater than 17 inches or a woman has greater than 16 inches

39
Q

True or False: If a patient has sleep apnea symptoms, you should do a sleep test

A

True

40
Q

How are sleep studies done?

A

In-lab study

EEG - brain waves

EMG - muscle movement

Belts around stomach and chest to measure breath effort

ECG - heart

They are quite cumbersome and costly.

41
Q

What is a benefit of doing a split night study?

A

One part of the night is for diagnosis and another part of the night is therapeutic

42
Q

How are home sleep tests done?

A

They are diagnostic only and a patient is sent home with a belt to put around their chest, stomach, oxygen sensor for the finger and and oxygen tubing for the nose.

43
Q

Home sleep tests should not be done in what kind of patients?

A

Patients with cardiopulmonary comorbidities because of confounding. Home sleep test won’t be accurate enough.

44
Q

After a sleep study has been done, what is the AHI cutoff for doing treatment?

A

If AHI is greater than or equal to 5 and a patient has symptoms, they are treated for sleep apnea.

Or if a patient has AHI greater than 15 without symptoms, they are treated for sleep apnea.

The cutoffs are different for pediatrics.

45
Q
A

E. polysomnography

Polysomnography is a comprehensive recording of the biophysiological changes that occur during sleep.

46
Q

How do you treat obstructive sleep apnea?

A

General measures: sedative avoidance, smoking cessation, correction of precipitating conditions (e.g. hypothyroidism).

Weight reduction

Positional therapy (e.g. tennis-ball-sock in shirt for supine sleep apnea)

Oxygen therapy (particularly for central sleep apnea at altitude. takes away need to hyperventilate)

Pharmacotherapy

Positive airway pressure

Oral devices

Upper airway surgery

Nerve stimulation

47
Q

What is PAP therapy?

A

Positive airway pressure therapy.

This is the most effective and gold standard treatment for sleep apnea. It is a mechanical solution to a mechanical problem. Airway pressure keeps airways open in the PCrit

48
Q

What oral appliances are there to help with sleep apnea?

A

Tongue retainer and mandibular repositioner

49
Q

What are the surgical options for obstructive sleep apnea treatment?

A

Tracheostomy (for very severe sleep apnea)

This is a percutaneous tracheal opening distal to the pharynx that bypasses the area of upper airway obstruction.

This is indicated for patients with severe life-threatening OSA who are intolerant or unresponsive to other types of therapy

Maxillomandibular advancement

Advancement of both the maxilla and mandible. This enlarges the retrolingual and retropalatal airway. Positive response rates in up to 90% of cases but this procedure can cause regular pain so it’s not an operation that’s commonly recommended.

UvuloPalatoPharyngoPlasty (UPPP or UP3)

Excision of uvula, posterior portion of the soft palate, redundant pharyngeal tissue, tonsils, and tonsilar pillars. This is less effective than CPAP therapy and we hardly send patients for this operation anymore. The problem here is that the issue is usually with the tongue and not the soft palate.

Tonsillectomy and adenoidectomy

Removal of tonsils and adenoids. This may be effective in children with OSA due to adenotonsillar enlargement but this doesn’t really help adults. In adults, OSA is typically because a combination of issues including obesity and other things. In children, it’s typically more of an anatomical problem as children are less often morbidly obese with other OSA risk factors. That is why this is typically a solution for kids but not adults.

50
Q

How is nerve stimulation used to help with OSA?

A

Similar to a pacemaker, a device is implanted that has wires going to the intercostal muscles to sense respiratory effort and a wire that goes to the tongue which can cause the tongue to contract to keep the airway open. This is new and has a long way to go before it becomes common practice

51
Q
A

B. Tonsillectomy and adenoidectomy