L65 Flashcards
Sleep apnea is a major risk factor for developing
HTN that don’t respond to meds
Obesity
Congestive heart
AFib // MI
Define sleep apnea // hypopnea syndrome
Repetitive episodes of decreased airflow that occur during sleep
Reduced O2 sats
Enhanced autonomic activity
Results in arousals w/ sleep fragmentation
What is the mallampati classification?
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
What are the 3 classifications of apnea events?
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
What is the body’s response during obstructive sleep apnea?
Brain stem sees lack of O2
Opens upper airway to remove the obstruction -> fire airway abductors (look at submentalis)
What is the characteristic EKG of central apnea?
HR slows until arousal happens
What change do you see to femoral artery pressure with repeated obstructive apneas?
Rise in femoral artery pressure
Indicates sympathetic response
How is severity of apnea determined?
Apnea index // respiratory disturbance index
Number of events in each hr
> 30 per 1 hr = severe
How does intermittent hypoxemia effect CV health
Leads to sympa stimulation
Might see O2 starvation -> oxidant stress -> release pro-inflam cytokines
How does large inspiratory decreases in pleural pressure effect CV health
- Increased venous return
- Septum shifts L
- RV dilates -> impaired LV ejection (decreased preload)
Net CO goes DOWN during big inspirations - decrease BP = pulsus paradoxus
How does EKG change during post-apnea arousal?
EKG goes to waking pattern
Why do sleep apnea pts have HTN?
Hypoxemia and arousals -> increase sympathetic tone
Impaired baroreceptor sensitivity
Net high BP
Explain how intermittent hypoxemia of apnea causes oxidant stress tissue damage.
Hypoxemia -> sympa Increased BP Parasympa stimulated -> reflex bradycardia Tissue hypoxia Oxidant stress in tissue
Why might apnea pts present with chest pain at night?
ST depression -> developing ischemia
What are 2 factors that increase your likelihood for apnea?
- Narrowed air passages: obesity or anatomic abnormalities
2. Loss of upper airway tone - REM sleep, suppressive drugs, alcohol, barbiturates
Which airway muscle protrudes the tongue
Genioglossus
Which airway muscle displaces hyoid arch anterior
Geniohyoid + sternohyoid
What is the air pressure in the airway during normal inhalation
Negative pressure to pull air in
What is pathophys of the airway for partial hypopnea/snoring
Loss of upper airway tone creases more negative pressures
Allows for easier collapse
What is the pathphys of the airway for complete apnea
Huge loss of airway tone leads to such negative pressure that the airway collapses
What happens to the airway during arousal
Actively open the airway by stimulating the muscles
Decrease the pressure in airway (less negative that the pressure that collapsed it)
Net inspiration
What is continuous positive airway pressure (CPAP)?
Most common apnea treatment - sleep machine!
Think as splint for upper airway
Administered via nasal or oro-nasal mask
What are the surgical options for apnea?
Uvulo-palato-pharyngo-plasty - aka cut out the uvula
Jaw advancement
Tracheostomy
What are other non-surg options for apnea
Mandibular repositioning - pulls jaw forward to keep mouth open
One way valves in nostrils - breathe out against resistor so pressure in pharynx goes up
