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Sleep Medicine > Pathophysiology of OSA > Flashcards

Pathophysiology of OSA Flashcards

1
Q

Define apnea (medical definition).

A

Cessation of air flow for at least 10 seconds with continued chest and abdominal effort.

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2
Q

Medical definition of hypopnea.

A

Reduction in airflow for greater than 10 seconds with oxygen desaturation.

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3
Q

Six anatomical reason that OSA occurs (physiological/anatomical etiologies).

A

Tissue laxity
Redundant mucosa (both men and women: weight gain in neck is not visible until threshold is reached => double-chin, LATERALLY reduces airway)
Anatomic abnormalities
Decreased muscle tone (esp. of dilator muscles)
Airway collapse
Decreased airway patency (especially in nose-breathing - we are all obligate nose breathers)

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4
Q

What are four primary physiological effects of OSA?

A

Oxygen desaturation => endothelial dysfunction, impairment, damage
Arousal from sleep to wakefulness to restore muscle tone
Sleep fragmentation
Hypersomnolence

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5
Q

What are the four variables that most influence airway collapse?

A

Negative pressure on inspiration
Extralumenal positive pressure
Fat deposition
Small mandible

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6
Q

What are the two primary factors that promote airway patency?

A 
Phayrngeal dilator muscle contraction (genioglossus)
Lung volume (longitudinal traction): shorter airway, less traction (obese, viscera pushing against trachea) - longer airway, better maintenance of airway
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7
Q

Which upper airway sites contribute to OSA?

A

Nasal passages, soft palate, retrolingual tissues.

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8
Q

What is the Bernoulli principle?

A

A column of air/liquid flowing through a conduit produces a partial vacuum or negative pressure at the margins of the column. Increased flow (effort to breathe) increases the negative pressure (collapse of the airway).

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9
Q

What is the Venturi effect?

A

The Venturi effect describes the acceleration of flow as a current of air or liquid enters a narrowed passage (e.g. spray with garden hose by creating smaller lumen, shower, etc.).

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10
Q

What neck circumference is considered a risk factor for OSA?

A

17 inches in men, 16 in women.

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11
Q

Which type of thyroid disorder is a risk factor for OSA?

A

Hypothyroidism.

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12
Q

What is considered “abnormal” on Epworth scale?

A

5-10 is considered the cutoff. He uses 7 in his clinic.

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13
Q

Why does OSA tend to cause weight gain?

A

Too tired to exercise. Hyperglycemic (cortisol levels up, it is glucogenic, insulin resistance).

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14
Q

Why does the gastroesophageal reflex worsen in patients with OSA?

A

Increased pressure from trying to breathe harder forces the GE junction to open - add in the excess viscera of obesity and it’s even worse. Plus circadian rhythm increases stomach acid during sleep. Aspiration of acid is common in OSA patients (silent aspiration - they’re not aware of it) - worsens asthma, likely cause in idiopathic pulmonary fibrosis.

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15
Q

Why do OSA patients not retain CO2?

A

The CO2 levels take several minutes before hypercapnia results. In apnea, the episodes are not that long. CO2 is not much of an issue. The issue is hypoxemia.

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16
Q

Why does nocturia occur in OSA patients?

A

Water is pulled into the central circulation due to the pressures created from the labored breathing (decreased airway). Brain receives signal that there is too much volume in the blood (similar to CHF, pulmonary edema), sends PNP (a diuretic which also blocks antidiuretic hormone). Bladder fills up more.

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17
Q

What is the best predictor of OSA?

A

Obesity.
BMI > 40, 40% OSA
BMI > 50, 50% OSA

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18
Q

Neck circumference as a predictor of OSA.

A

> 17 inches men, >16 inches women.

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19
Q

How many channels are measured in polysomnography?

A

16-18 channels.

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20
Q

What does the PSG measure?

A 
EEG (brain waves)
EOG (eye movement)
EMG (muscle movement)
Nasal and oral airflow
Respiratory muscle effort and abdominal muscle effort
POX
ECG
EMG on legs
Sleep position
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21
Q

What is tonic REM?

A

REM with no muscle movement. Lower density of eye movement.

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22
Q

What is phasic REM?

A

It is off and on during REM. Muscles twitch, but body is paralyzed. Faster REM (increased density).

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23
Q

What happens to BP, heart rate, cardiac output, and peripheral resistance in NREM and tonic REM?

A

They all go down.

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24
Q

What happens to BP and heart rate in phasic REM?

A

They both go up.

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25
Q

What happens to cardiac output and peripheral resistance in phasic REM?

A

They both go down.

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26
Q

What is another way of looking at BP, heart rate, cardiac output, and peripheral resistance in NREM, tonic REM, and phasic REM?

A

They all go down in NREM and tonic REM. Peripheral resistance and cardiac output go down in phasic REM, but the heart rate and BP go up in phasic REM. So, PR and CO drop in ALL phases of sleep, but phasic REM increases the other measures of cardiac function.

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27
Q

How is stroke volume affected during NREM, tonic REM, and phasic REM?

A

There is no change to stroke volume in any of these phases of sleep.

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28
Q

Sleep and the heart: stage N1

A

Stable autonomic regulation
Marked sinus arrhythmia (correlated with breathing)
High baroreceptor gain (stability of BP and HR coordination)

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29
Q

Stage N2 sleep and the heart.

A

Bursts of sympathetic activity - K-complexes - results in transient increased HR and BP.

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30
Q

Stage N3 and heart.

A

Decline in muscle sympathetic activity.

Slow HR and low BP.

31
Q

Transition to REM and the heart.

A 
Bursts of vagal activity
Sinus arrest
Position change
Rapid fluctuation in HR and BP
Very hemodynamically unstable - high risk of CV events in at risk individuals
32
Q

REM and the heart

A

Increased sympathetic activity

Variability/instability of HR (irregular heart beat) and BP - high risk to at risk patients

33
Q

How does sleep affect BP in a healthy individual?

A

Decrease in BP of 10% (10-20 mmHG). Those who don’t are “non-dippers.”

34
Q

What are the risks for “non-dippers” (BP and sleep)?

A

Ventricular arrhythmias
Cardiac hypertrophy
Sudden cardiac death (in women)

35
Q

When looking at a sleep study, what is “paradox”?

A

It is asynchronous activity between the thoracic and abdominal musculature. During normal breathing, the abdominal and thoracic muscles work together to breathe. During hypoxic/apneic events, they become asynchronous as they strive to get air into the lungs.

36
Q

Pharyngeal collapse leads to sleep apnea which results in increased CO2 and decreased O2. This signals chemoreceptors in the brain. What do these chemoreceptors initiate?

A

Arousal and sympathetic nervous system activity (fight or flight).

37
Q

What is the effect of sleep apnea on oxygen levels to the myocardium?

A

The decreased oxygen to the myocardium occurs during a sympathetic event - the heart wants to pump more blood but doesn’t have the fuel to do so.

38
Q

What are the long-term dangers of low myocardial oxygen supplies during sympathetic events?

A 
Cardiac ischemia
Coronary artery disease (CAD)
Cardiac arrhythmias
Cardiac hypertrophy
CHF
Stroke volume goes down
39
Q

How does the sympathetic response affect the pulmonary system during an apneic event?

A

Hyperventilation/try to breathe harder (increased demand for oxygen) with reduced airway. Leads to vasoconstriction in the pulmonary vascular bed: Hypoxemia in the lungs leads to reduction in pulmonary bloodflow in order to maintain the relationship between cardiac output (Q) and ventilation (V) (VQ mismatch).

40
Q

What is the effect of pulmonary vasoconstriction?

A

Increased pulmonary vascular resistance leads to increased pressure in the pulmonary artery, which persists until the apneic episode stops.

41
Q

What happens to inspiratory pressure during an apneic/hypopneic episode?

A

The inspiratory pressure (Pit) initially drops. The body’s response is to increase inspiratory effort. This increases the myocardial O2 demand because the heart/muscles are doing more work. Again, more O2 needed in a setting of reduced O2 supply.

42
Q

What are the three broad categories of complications from OSA?

A

Cardiovascular, metabolic, and neurocognitive.

43
Q

What percentage of hypertensives have OSA?

A

30-35%

44
Q

What percentage of untreated OSA have hypertension?

A

40%

45
Q

What percentage of refractory (drug resistant) hypertension have OSA?

A

80%

46
Q

Does treatment of OSA improve hypertension?

A

Yes.

47
Q

What percentage of stable CHF patients have OSA?

A

Stable CHF: diagnosed but asymptomatic, ejection fraction (EF)20. 34%

48
Q

What percentage of symptomatic CHF patients have OSA?

A

75% of men with symptomatic CHF have OSA.

47% of women with symptomatic CHF have OSA.

49
Q

What percentage of CHF patients with pulmonary edema have OSA?

A

Pulmonary edema = emergency department with lungs full of liquid.
82% of these patients have OSA.

50
Q

What does the American College of Cardiology recommend with regards to OSA and CHF?

A

All patients with difficult to control CHF must go through a thorough sleep evaluation and, if needed, a sleep study.

51
Q

How is the prognosis of CHF affected by OSA?

A

OSA + CHF = worse prognosis.

52
Q

How does treatment of OSA affect CHF outcomes?

A

Treatment of OSA in CHF patients improves cardiac function, quality of life, and survival. This is one of very few examples of medical intervention increasing survival time (longevity) in humans.

53
Q

What are the 1- and 2-year mortality rates in CHF patients who have OSA?

A

1-year CHF/OSA mortality rate: 12%

2-year: 25%

54
Q

What are the qualities of the CHF in OSA/CHF non-survivors?

A

Higher NYHA class (more symptomatic)
More depressed EF
Larger atria (because of more blood volume/fluid in heart)
Larger left ventricle
Greater percentage of the night in periodic breathing (CSA) and OSA with a HIGHER AHI

55
Q

Which cardiac conditions have been shown to improve with successful treatment of OSA?

A 
CV disease
Hypertension
Coronary artery disease (CAD)
Cardiovascular events
In fact, in CAD and CV, the treated OSA have better outcomes than non-OSA controls with these diseases.
56
Q

What is the relationship between OSA and atrial fibrillation?

A

Incidence of afib is very significantly higher in OSA patients.
Incidence of AF in non-OSA patients: 32%
Incidence of AF in OSA patients: 49%
p=.0004

57
Q

What percentage of CAD patients have OSA?

A

30%

58
Q

What is the incidence rate of OSA in stroke patients?

A

The prevalence of AHI>10 in patients with ischemic or hemmorhagic stroke: 70.

59
Q

What are the effects of OSA on neurons?

A

Chronic OSA has been shown to cause destruction of neurons due to hypoxemia. Results in decreased intelligence/brain function.

60
Q

What is the relationship between OSA and stroke?

A

Bidirectional. “OSA is both a risk factor for and is common in patients with stroke, and may adversely impact both survival and prognosis.”

61
Q

What are the neurobehavioral effects of OSA?

A

Unable to sustain attention
Negative impacts on memory and executive function (decision-making)
Significantly impaired quality of life and social functioning
High prevalence of minor psychiatric morbidity (depression, bipolar, schizophrenia, generalized anxiety disorder)

62
Q

What is insulin resistance and why does it cause hyperglycemia?

A

Hyperglycemia results from insulin resistance, which is:
An impaired insulin secretory response to glucose
Decreased insulin effectiveness in stimulating glucose uptake by skeletal muscle and in restraining hepatic glucose production

63
Q

What is metabolic syndrome?

A 
All of these must be present:
Hyperinsulinemia
Glucose intolerance
Dyslipidemia (cholesterol & lipid disorders)
Central obesity
Hypertension
64
Q

What is the relationship between metabolic syndrome and CV disease?

A

Patients with metabolic syndrome are at significantly greater risk of developing CV diseases because each of the conditions of the syndrome is an independent risk factor of CV disease.

65
Q

What is the relationship between OSA and automobile and occupational accidents?

A

The rate of accidents goes up as AHI gets higher. This represents a public health issue.

66
Q

Hypertension and diabetes are both risk factors for which CV disease and how does OSA impact that condition?

A

Atherosclerosis. Both HTN and diabetes rates are higher among OSA patients. Therefore, OSA is a risk factor for atherosclerosis.

67
Q

According to a 20-year followup study published in JCSM 2014/04, what is the hazard ratio of all-cause mortality in patients with moderate/severe OSA?

A

4.2

EN

68
Q

According to a 20-year followup study published in JCSM 2014/04, what is the hazard ratio of cancer mortality?

A

3.4

EN

69
Q

According to a 20-year followup study published in JCSM 2014/04, what is the hazard ratio of stroke?

A

3.7

EN

70
Q

According to a 20-year followup study published in JCSM 2014/04, what is the hazard ratio of cancer incidents?

A

2.5

EN

71
Q

Why does the incidence of SDB increase with age?

A

Soft palate lengthens
Pharyngeal fat pads increase in size
Shape of bony structures around pharynx changes
Response of genioglossus to negative pressures decreases

72
Q

Is OSA pathological in the elderly?

A

Most studies show no increase in mortality in the older adult
Most studies show that elderly adults with SDB are: excessively sleepy, have decreased quality of life, decreased cognitive abilities, and greater risk of nocturia, hypertension, and CV disease (Sleep Med Rev 2007:11(2)).

73
Q

How does OSA impact the OR of cognitive impairment in the elderly?

A

AHI>15 OR 1.4, 95% CI 1.03-1.9

AHI≥30 OR 3.4, 95% CI 1.4-8.1

SaO2 nadir<80% OR 2.7 95%

Each standard deviation increase in AHI was associated with 70% greater odds of cognitive impairment. (Spira AP et al Sleep-disordered breathing and cognition in older women. J Am Geriatr Soc 2008;56:45-50.)

74
Q

Does treating apnea in the older adult lead to improvements?

A

Reduces or eliminates apneas and hypopneas
Improves sleep architecture
Is superior to placebo
Improves daytime sleepiness
Improves self-reported symptoms (snoring and gasping)
Improves motor speed and nonverbal learning and memory
Improves vascular resistance, platelet coagulability and other factors affecting cardiac function
Has a positive effect on nocturia, reducing the number of voids per night. (Weaver TE, Chasens ER. Continuous positive airway pressure treatment for sleep apnea in older adults. Sleep Med Rev 2007; 11(2))

Sleep Medicine (14 decks)

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