L65 Flashcards

1
Q

Sleep apnea is a major risk factor for developing

A

HTN that don’t respond to meds
Obesity
Congestive heart
AFib // MI

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2
Q

Define sleep apnea // hypopnea syndrome

A

Repetitive episodes of decreased airflow that occur during sleep
Reduced O2 sats
Enhanced autonomic activity
Results in arousals w/ sleep fragmentation

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3
Q

What is the mallampati classification?

A

Have pt open their mouth, lean forward, stick tongue out
Class 1 = wide open mouth
Class 2 = uvula at tongue base
Class 3 = uvula partially obscured by tongue
Class 4 = tongue completely obscures uvula

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4
Q

What are the 3 classifications of apnea events?

A

Obstructive = decrease or no airflow w/ chest wall movement (upper airway closed off)
Central = loss of effort to breathe, brain stem is not sending out breathing signals, no airflow or chest wall movement
Mixed - starts central ends up obstructive

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5
Q

What is the body’s response during obstructive sleep apnea?

A

Brain stem sees lack of O2

Opens upper airway to remove the obstruction -> fire airway abductors (look at submentalis)

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6
Q

What is the characteristic EKG of central apnea?

A

HR slows until arousal happens

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7
Q

What change do you see to femoral artery pressure with repeated obstructive apneas?

A

Rise in femoral artery pressure

Indicates sympathetic response

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8
Q

How is severity of apnea determined?

A

Apnea index // respiratory disturbance index
Number of events in each hr
> 30 per 1 hr = severe

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9
Q

How does intermittent hypoxemia effect CV health

A

Leads to sympa stimulation

Might see O2 starvation -> oxidant stress -> release pro-inflam cytokines

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10
Q

How does large inspiratory decreases in pleural pressure effect CV health

A
  1. Increased venous return
  2. Septum shifts L
  3. RV dilates -> impaired LV ejection (decreased preload)
    Net CO goes DOWN during big inspirations - decrease BP = pulsus paradoxus
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11
Q

How does EKG change during post-apnea arousal?

A

EKG goes to waking pattern

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12
Q

Why do sleep apnea pts have HTN?

A

Hypoxemia and arousals -> increase sympathetic tone
Impaired baroreceptor sensitivity
Net high BP

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13
Q

Explain how intermittent hypoxemia of apnea causes oxidant stress tissue damage.

A
Hypoxemia -> sympa
Increased BP
Parasympa stimulated -> reflex bradycardia
Tissue hypoxia 
Oxidant stress in tissue
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14
Q

Why might apnea pts present with chest pain at night?

A

ST depression -> developing ischemia

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15
Q

What are 2 factors that increase your likelihood for apnea?

A
  1. Narrowed air passages: obesity or anatomic abnormalities

2. Loss of upper airway tone - REM sleep, suppressive drugs, alcohol, barbiturates

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16
Q

Which airway muscle protrudes the tongue

A

Genioglossus

17
Q

Which airway muscle displaces hyoid arch anterior

A

Geniohyoid + sternohyoid

18
Q

What is the air pressure in the airway during normal inhalation

A

Negative pressure to pull air in

19
Q

What is pathophys of the airway for partial hypopnea/snoring

A

Loss of upper airway tone creases more negative pressures

Allows for easier collapse

20
Q

What is the pathphys of the airway for complete apnea

A

Huge loss of airway tone leads to such negative pressure that the airway collapses

21
Q

What happens to the airway during arousal

A

Actively open the airway by stimulating the muscles
Decrease the pressure in airway (less negative that the pressure that collapsed it)
Net inspiration

22
Q

What is continuous positive airway pressure (CPAP)?

A

Most common apnea treatment - sleep machine!
Think as splint for upper airway
Administered via nasal or oro-nasal mask

23
Q

What are the surgical options for apnea?

A

Uvulo-palato-pharyngo-plasty - aka cut out the uvula
Jaw advancement
Tracheostomy

24
Q

What are other non-surg options for apnea

A

Mandibular repositioning - pulls jaw forward to keep mouth open
One way valves in nostrils - breathe out against resistor so pressure in pharynx goes up

25
Q

What nerve would you stimulate to maintain tongue tone // stimulate abductors of the airway

A

Hypoglossal