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Readings Flashcards

1
Q

In what year was OSA first described in the medical literature?

A

1965

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2
Q

What features regarding jaw movement make an oral appliance less likely to cause adverse events and increase patient compliance?

A

Allows vertical opening.

Allows lateral movement.

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3
Q

In what two ways do oral appliances maintain patency of the airway?

A

By increasing its dimensions and decreasing its collapsibility.

(Chest 2007;132;693-699)

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4
Q

How do oral appliances (physically) enlarge the airway and/or reduce its collapsibility?

A

This is mediated by anatomical changes that occur by advancement of the tongue and jaw. The activation of upper airway neuromuscular reflexes may also be relevant. These changes are not uniformly seen in all patients and this may explain differences in treatment outcomes. (Chest 2007;132;693-699)

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5
Q

What is a “complete response” and a “partial response” in treatment of OSA?

A

Complete: AHI 49%, but final AHI >5.

Chest 2007;132;693-699

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6
Q

According to a 2007 Chest article, what percentage of OSA patients can expect a clinically important response to OA therapy?

A

About 2/3 - 35% to 40% complete response, 25% partial response, which leaves 35% to 40% failures. (Chest 2007;132;693-699)

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7
Q

How does OA therapy compare to CPAP in terms of PSG, AHI, subjective and objective measures of sleepiness, and compliance?

A

PSG & AHI: OA is less
S/O sleepiness: Equal
Compliance: higher
(Chest 2007;132;693-699)

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8
Q

Why is higher compliance relevant even when the treatment is less effective?

A

The extent to which a treatment alleviates a health risk associated with a disease in clinical practice is a function of its efficacy and treatment adherence. The greater acceptance by patients of OA could result in greater treatment adherence and provide equivalent clinical effectiveness. (Chest 2007;132;693-699)

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9
Q

What was the 1 year treatment adherence rate of OA therapy compared to that of CPAP as reported in a 2007 Chest article?

A

77% OA (6.8 hours per night) vs. 46% CPAP (>4 hrs/night for 70% of nights). (Chest 2007;132;693-699)

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10
Q

Does OA therapy reduce BP levels in OSA patients?

A

Yes, early indications are that OA therapy may have a positive impact (2-4 mm Hg at 1- and 3-month checks in 2 studies). (Chest 2007;132;693-699)

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11
Q

OA vs. CPAP: Improvement of snoring

A

Moderate benefit vs. large benefit. (Chest 2007;132;693-699)

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12
Q

Comparison of OA to CPAP: improvement in AHI

A

OA: Moderate benefit CPAP: Large benefit

Chest 2007;132;693-699

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13
Q

Compare benefit of CPAP to OA: SpO2

A

OA: Mod CPAP: Large

Chest 2007;132;693-699

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14
Q

Compare benefit of OA to CPAP: sleep fragmentation

A

OA: mod CPAP: large

Chest 2007;132;693-699

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15
Q

Compare OA to CPAP: sleep architecture

A

OA: small CPAP: mod

Chest 2007;132;693-699

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16
Q

Compare OA to CPAP: S/O measures of daytime sleepiness

A

OA: mod CPAP: mod

Chest 2007;132;693-699

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17
Q

Compare OA and CPAP: reduction in BP

A

OA: mod CPAP: mod

Chest 2007;132;693-699

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18
Q

Compare benefits of OA to CPAP: neuropsychological function

A

OA: small CPAP: small

Chest 2007;132;693-699

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19
Q

Compare benefits of OA and CPAP: quality of life

A

OA: small CPAP: small

Chest 2007;132;693-699

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20
Q

Compare benefits of OA and CPAP: reduction in motor vehicle accident risk

A

OA: unknown CPAP: small

Chest 2007;132;693-699

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21
Q

What are the demographic, anthropomorphic, and physiologic predictors of a favorable response to OA therapy?

A

Remember, it is not currently possible to identify with certainty which patients will respond in clinical practice. Female, lower age, lower BMI, lower neck circumference, lower baseline AHI, supine-dependent OSA, primary oropharyngeal collapse during sleep.(Chest 2007;132;693-699)

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22
Q

What are the cephalometric predictors of a favorable response to OA therapy?

A

Remember, it is not currently possible to identify with certainty which patients will respond in clinical practice. Shorter soft palate, larger retropalatal airway space, decreased distance between hyoid and mandibular plane, narrower angle from sella to nasion to supramentale point, wider angle from the sella to the nasion to the subspinale point. (Chest 2007;132;693-699)

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23
Q

What are the upper airway predictors of a favorable response to OA therapy?

A

Remember, it is not currently possible to identify with certainty which patients will respond in clinical practice. Airway patency on MRI during Muller maneuver following mandibular advancement, improvement in airway patency with mandibular advancement during drug-induced “sleep” nasopharyngoscopy. (Chest 2007;132;693-699)

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24
Q

What are the key short-term adverse effects reported with OA therapy?

A

Excessive salivation, mouth dryness, tooth pain, gum irritation, headaches, TMJ discomfort.

These tend to be self-limiting but must be addressed early to increase the likelihood of treatment adherence. (Chest 2007;132;693-699)

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25
Q

What long-term adverse effects of OA therapy have been reported? What is the clinical significance of these effects?

A

Reduction of overjet, increase in facial height, increase in degree of mouth opening, changes in inclination of incisors, increase in mandibular plane angle.

The clinical significance remains uncertain. (Chest 2007;132;693-699)

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26
Q

What is the relationship between long-term adverse effects and the amount of time of OA therapy?

A

The long-term effects continue to increase with the increasing length of treatment (as shown in a 7.5-year study), suggesting that these changes continue to progress with time. (Chest 2007;132;693-699)

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27
Q

What predictors of long-term adverse effects of OA therapy have been identified?

A

A smaller change in overjet was more common in patients with a baseline overbite of >3mm, overjet of <3mm, and those who used a soft elastomeric device rather than a hard acrylic device. (Chest 2007;132;693-699)

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28
Q

How much time without breath must occur for an episode to be classified as apnea?

A

10 seconds or longer. (http://content.onlinejacc.org/cgi/content/full/52/8/686)

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29
Q

Oxyhemoglobin desaturations of what % have been associated with CV disease independently of confounding covariates?

A

Greater than or equal to 4%.

http://content.onlinejacc.org/cgi/content/full/52/8/686

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30
Q

How large of a reduction in airflow is necessary for an event to be classified as hypopnea?

A

A reduction of >50%, usually in association with a reduction of oxyhemoglobin saturation.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

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31
Q

Define hypercapnia.

A

High levels of CO2.

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32
Q

Which portion of the airway is most often associated with OSA?

A

The portion from the posterior nasal septum to the epiglottis.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

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33
Q

What physiologic characteristics lend to a smaller airway?

A

Large tonsils/adenoids, obesity, and small build (bone and soft tissue structures).

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

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34
Q

People with a smaller airway are more susceptible to OSA. What is one reason that has to do with reflex-driven muscle activation?

A

Negative pressure can cause collapse in a small airway. Mechanoreceptors activate the laryngeal muscles to become more tonic when the person is awake. If a person is dependent upon this reflex to maintain the patency of the airway, their airway may be vulnerable to collapse during sleep.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

35
Q

What is the accepted estimate of the prevalence of OSA?

A

1 in 5 adults has at least mild, and 1in 15 has moderate or severe.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

36
Q

What percentage of people with OSA have been diagnosed?

A

The estimate is fewer than 15% (>85% have not been diagnosed).

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

37
Q

How much more likely are males to have OSA compared to females?

A

Twice as likely.

http://content.onlinejacc.org/cgi/content/full/52/8/686

38
Q

In the general population, how much more likely are obese people to have OSA?

A

Four times more likely.

http://content.onlinejacc.org/cgi/content/full/52/8/686

39
Q

What is the reality of OSA in the general population when considered in light of the “Pickwickian” stereotype (morbidly obese, male, middle-aged, sleepy).

A

OSA is slightly more common in males and obese people, but is not rare in females or in nonobese persons and is more common in older people than the middle-aged. Furthermore, excessive daytime sleepiness and OSA are not strongly correlated in general population studies.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

40
Q

Among cardiovascular patients, what are the correlations between obesity, age, gender, presentation of sleepiness, and OSA?

A

Obesity: The only correlate in males (age not correlated).
Gender: similar odds ratio (OR) of male:female as in non-CV populations (about 2, or twice as likely).
Age: the only correlate in females (obesity not correlated).
Sleepiness: may not manifest in heart failure patients.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

41
Q

T or F: It is difficult to identify a causal role of OSA in DMII, CV disease, stroke, and hypertension even though it is well-established that the prevalence of these conditions is higher in OSA patients.

A

True.

http://content.onlinejacc.org/cgi/content/full/52/8/686

42
Q

What was the cause of most deaths in untreated OSA patients in one study which compared tracheotomy to no treatment (pre-CPAP)?

A

Cardiovascular. The treated individuals had higher BMI, higher AHI (69 vs. 43), yet more of the untreated individuals died. Most died of CV disease.

43
Q

What did an 11-year followup of patients in San Diego find in regards to mortality rate and cause of death in OSA patients vs. non-OSA patients?

A

That the mortality rate for CV disease was higher in OSA patients (35% for AHI<15, 56% for higher AHI).

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

44
Q

In the Nurses Health Study, snoring (as a marker of OSA) was found to be a predictor of what 3 diseases? What other sign was found to be a predictor of these 3 diseases?

A

Hypertension, DMII, CV disease.

Sign: short sleep duration.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

45
Q

Do both kinds of SA occur more commonly in patients with heart failure? Do they contribute to disease progression?

A

Yes.

They may.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

46
Q

Which four CV conditions are potentially specific indications for apnea evaluation?

A

Hypertension, especially resistant hypertension (requires 3 or more medications, 83% of these patients has OSA); atrial fibrillation; nocturnal angina; heart failure.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

47
Q

What is the relationship between age and the degree of deleterious CV consequences in OSA patients?

A

Younger people with OSA may be more likely to have hypertension, atrial fibrillation, and greater all-cause mortality.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

48
Q

How low can SpO2 go in severe OSA patients?

A

<60%.

http://content.onlinejacc.org/cgi/content/full/52/8/686

49
Q

How high can blood pressure go by the end of an apneic episode?

A

As high as 240/130. This occurs at a time of hypoxemia, hypercapnia, and adrenergic activation.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

50
Q

What are the sympathetic nervous system effects of OSA?

A

SNS activity persists even into daytime normoxic wakefulness. The SNS becomes activated in the peripheral vasculature (increased BP). Faster heart rate during resting wakefulness, suggesting increased cardiac sympathetic drive.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

51
Q

What effect does 100% oxygen have on the OSA patient?

A

Administration of 100% oxygen during wakefulness significantly lowers sympathetic activity, BP, and cardiac rate in OSA patients.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

52
Q

What is the relationship between cardiovascular variability and OSA?

A

Resting awake OSA patients have lower cardiac variability (associated with poorer outcomes; precursor to development of future hypertension) and higher BP variability (increased risk of end organ damage in hypertensive patients).

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

53
Q

What is endothelin and how does it pertain to OSA?

A

Endothelin is a vasoactive substance that is released during hypoxia and can persist for hours. It has been shown to raise BP in OSA patients. Endothelin levels decreased after four hours of CPAP.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

54
Q

T or F: OSA has been implicated as an important mechanism for triggering systemic inflammation (CRP, ILl-6, etc.).

A

True.

http://content.onlinejacc.org/cgi/content/full/52/8/686

55
Q

What percentage of OSA patients are hypertensive? What percentage of hypertensive patients have OSA?

A

50%.

30% (estimate, most are undiagnosed).

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

56
Q

What is unique about the 24-hour pattern of BP in OSA patients?

A

They have an attenuated nocturnal BP decline (non-dippers), which has been correlated with a higher all-cause mortality rate.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

57
Q

What are the immediate effects of apnea on BP, and how is that different in times of sleep-deprivation?

A

Acute increase in BP (about 20 mmHg in dog studies) that persists for several hours and is exacerbated in times of sleep-deprivation. This has been shown to be mediated by the SNS. Sleep interruption (via auditory stimulus) did not result in increased BP. 1-3 month apneic simulation resulted in daytime hypertension.

(http: //content.onlinejacc.org/cgi/content/full/52/8/686)
(http: //content.onlinejacc.org/cgi/content/full/52/8/686)

58
Q

What is the relationship between pregnancy and severity of OSA?

A

Third trimester, airway is smaller. Snoring increases. Resolves with parturition. OSA has been implicated in pregnancy-related hypertension.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

59
Q

Which hormone has been implicated in higher rates of resistant hypertension among OSA patients?

A

Increased aldosterone.

http://content.onlinejacc.org/cgi/content/full/52/8/686

60
Q

What are the effects, if any, of OSA treatment on BP?

A

The effects are moderate and variable: more severe OSA, more difficult to control hypertension, and more compliant patients may have more substantial BP reduction with treatment.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

61
Q

Is there any evidence that antihypertensive drugs affect OSA?

A

No, there is not.

http://content.onlinejacc.org/cgi/content/full/52/8/686

62
Q

Why might OSA be a causative factor in left ventricular systolic dysfunction?

A

Because higher BP is the most common risk factor for ventricular hypertrophy and failure. Nocturnal oxygen desaturation and nocturnal hypertension are both more strongly implicated than their diurnal counterparts in ventricular hypertrophy and failure.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

63
Q

Has it been established that OSA can cause heart failure?

A

No.

http://content.onlinejacc.org/cgi/content/full/52/8/686

64
Q

Can we conclusively say that OSA increases mortality in heart failure patients?

A

No. Studies so far are contradictory, although recent studies suggest an increased mortality rate.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

65
Q

Does treatment of OSA lead to a lower mortality rate in heart failure patients?

A

It may, but there are still no good studies (randomized clinical trials) on this.

(http://content.onlinejacc.org/cgi/content/full/52/8/686)

66
Q

What are the effects on OSA of treatment of heart failure?

A

Decreased intravascular volume and attenuated venous congestion resulting from heart failure treatment could potentially reduce OSA severity. However, there is no systematic evidence that specific drugs used to treat heart failure have any direct influence on the severity of OSA. (http://content.onlinejacc.org/cgi/content/full/52/8/686)

67
Q

Is the odds-to-risk ratio greater amongst OSA patients?

A

It is likely higher, but studies are conflicting - many are inferential. It appears that with increasing severity of OSA the OR increases. It does not appear that CSA has any influence on stroke risk.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

68
Q

How does a stroke impact the likelihood of OSA?

A

Patients after stroke have a high prevalence of OSA.

http://content.onlinejacc.org/cgi/content/full/52/8/686

69
Q

What are the effects of OSA on post-stroke patients?

A

Reduced motivation, cognitive capacity, higher risk of recurrent stroke and death, worse functional impairment, longer time in rehab and hospital.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

70
Q

What are the effects of stroke on SA?

A

Immediately after stroke, CSA dominates, then OSA is more prevalent. The prevalence is still high several months post-stroke, but not as high as immediately after.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

71
Q

What is the relationship between SA and arrhythmias?

A

They are more prevalent in OSA patients and increase with the number of apneic episodes and the severity of the related hypoxea.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

72
Q

What is the OR ratio of complex arrhythmias in patients with OSA?

A

2-4 fold higher risk.

http://content.onlinejacc.org/cgi/content/full/52/8/686

73
Q

What is the relationship between pacemakers and OSA?

A

59% of patients with pacemakers have sleep apnea syndrome - in patients with A/V block, the prevalence is 68%. The question is whether treatment of SA would have changed the need for pacing in some of these patients. In fact, the recommendation is that patients with pacemakers be systematically evaluated for SA because of its potential detrimental CV effects.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

74
Q

Is OSA a causative factor in atrial fibrillation?

A

It has not been definitively shown yet, but is hypothesized to be causative based on very strong evidence (higher OSA rates in afib pts compared to general CV pts, left atrial enlargement, etc.)
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

75
Q

Is OSA a causative factor in ventricular arrhythmias?

A

No conclusive evidence yet, but there is up to a 66% prevalence in SA pts compared to 0 to 12% in the general population. As is the case with most CV problems, they are manifest more at night and during apneic/hypopneic episodes than at other times in SA pts.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

76
Q

Bradyarrhythmias occur most often in which stage of sleep?

A

REM

http://content.onlinejacc.org/cgi/content/full/52/8/686

77
Q

After successful cardioversion in OSA afib pts, what is the risk of recurrence?

A

82% within one year, which is about double that of non-OSA pts.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

78
Q

Does treatment of OSA improve arrhythmias?

A

The evidence is inconclusive, but the answer is likely yes.

http://content.onlinejacc.org/cgi/content/full/52/8/686

79
Q

Can treatment of arrhythmias (pacing, etc.) effectively improve/treat OSA?

A

The evidence suggests that this is not the case.

80
Q

How much more prevalent is OSA in coronary artery disease pts than in the general population?

A

Double.

http://content.onlinejacc.org/cgi/content/full/52/8/686

81
Q

Why might OSA be a trigger for cardiac ischemia (CAD)?

A

Severe intermittent hypoxemia, acidosis, increased BP, and sympathetic vasoconstriction, in conjunction with simultaneous changes in intrathoracic and cardiac transmural pressures. In the longer term, the cardiac and vascular disease mechanisms described earlier, including endothelial dysfunction and systemic inflammation, may promote structural coronary artery damage.
(http://content.onlinejacc.org/cgi/content/full/52/8/686)

82
Q

Is there an association between OSA and CAD?

A

Multivariate analysis confirmed an independent association between OSA and subclinical coronary artery disease, as measurable by coronary artery calcification. It worsens as AHI worsens.

83
Q

Is there a relationship between OSA and sudden cardiac death?

A

in patients experiencing sudden cardiac death, those proven to be free of OSA have the greatest likelihood of death between 6 and 11 AM, the traditional window of cardiovascular vulnerability (271). In striking contrast, more than half of sudden cardiac deaths in patients with proven OSA occur during the sleeping hours, between 10 PM and 6 AM. Thus, OSA appears to affect the timing of sudden cardiac death; however, it is not yet known whether OSA increases the overall risk of sudden cardiac death.

Sleep Medicine (14 decks)

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