Module 2 Flashcards

1
Q

Sleep apnea is defined as

A

a temporary pause in breathing during sleep that lasts at least 10 seconds. For a confirmed diagnosis, this should occur a minimum of five times an hour.

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2
Q

three patterns of apnea are

A

central, obstructive, and mixed

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3
Q

Central apnea occurs when

A

both airflow and respiratory efforts are absent. Central apneas are a result of an absence of neural output from the brainstem’s respiratory control center, which leads to a lack of inspiratory effort. The respiratory center in the brain fails to respond to elevated carbon dioxide concentrations

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4
Q

during obstructive sleep apnea (OSA),

A

respiratory efforts persist although airflow is absent at the nose and mouth. Airflow obstruction occurs when the tongue and the soft palate fall backward and partially or completely obstruct the pharynx

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5
Q

Sleep hypopnea is

A

a period of hypoventilation, or decreased airflow, defined as a 50% reduction in thoracoabdominal movements, with a 4% decrease in oxygen saturation lasting at least 10 seconds during sleep.

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6
Q

apnea-hypopnea index (AHI) may be used to

A

define and quantify the severity of OSA. The AHI is obtained by dividing the total number of events (the number of apnea episodes plus the number of hypopnea episodes) throughout the entire night by the total sleep time in hours

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7
Q

respiratory disturbance index (RDI),

A

another commonly cited parameter, is defined as the AHI plus the average number of snoring-related arousals per hour.

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8
Q

A diagnosis of OSA is confirmed with AHI and RDI scores as follows:

A

*AHI or RDI greater than or equal to 5 and less than 14 if comorbid factors such as excessive daytime sleepiness, hypertension, stroke, or heart failure are present, or

*AHI or RDI greater than or equal to 15 in the absence of comorbid factors.

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9
Q

Sleep-disordered breathing is an independent risk factor for the

A

development of hypertension and, subsequently, left ventricular dysfunction.

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10
Q

The patient with combined coronary artery disease (CAD) and OSA may have an increased cardiac risk because of

A

worsening of the relationship between myocardial oxygen demand and supply as a result of apnea-associated hypoxemia and activation of the autonomic nervous system

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11
Q

dysrhythmia associated with OSA

A

a. fib
treating OSA will improve effectiveness of a fib tx

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12
Q

OSA possible pulm side effect

A

cause mild pulmonary htn, often associated with right ventricular failure.

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13
Q

Unrecognized and untreated OSA is estimated to be ,

A

30% in the adult male population and to be 15% in the adult female population

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14
Q

OSA is most prevalent in

A

men older than age 50 and in postmenopausal women; in this latter group

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15
Q

why increase in OSA in men

A

men usually have a significantly higher pharyngeal and supraglottic resistance than women, which makes them more susceptible to pharyngeal collapse and OSA and may contribute to the male predominance of the syndrome

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16
Q

Relatives of a person with sleep apnea have approximately

A

twice the normal risk of having sleep apnea

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17
Q

OSA aggravating factors (2)

A

obesity
etoh

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18
Q

best indicator of presence of sleep apnea

A

neck/collar size in men (larger than 17 in)

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19
Q

two states of sleep

A

REM
NREM

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20
Q

NREM 3 stages

A

stage I- slow eye movement, precede sleep onset
stage II- sleep spindles, slow eye movement
stage III- low frequency high amp delta waves no slow eye movement

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21
Q

Central apneas are more common in individuals who

A

live at high altitudes, where hypoxemia induces hyperventilation with associated alkalosis.

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22
Q

most important presenting symptom of sleep apnea

A

hypersomnolence- clear cut uncontrolled sleepiness

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23
Q

define hypersomnolence

A

it is clear-cut, uncontrollable sleepiness. It develops over a long period and is first experienced by a patient as sleep onset when attention is not demanded (e.g., when watching television, sitting in a college lecture, or waiting at a traffic light). Eventually, situations requiring more attention are affected, such as long-distance driving or quiet conversation.

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24
Q

other sleep apnea symptoms

A

morning HA, falling asleep when performing purposeful activities, nocturnal restlessness, frequent urinations, choking, personality disturbance, sexual dysfunction

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25
The snoring of OSA is
both loud (it can be heard in an adjacent room) and habitual (it occurs nightly).
26
OSA automobile accident rate
2-2.6x more
27
subjective assessments for OSA
Stanford sleepiness score (SSS) epworth sleepiness scale (ESS)
28
stanford sleepiness score
SSS is used to record the degree of sleepiness experienced by a patient at a given time and does not necessarily relate to his or her overall propensity to fall asleep. It is an introspective measure of sleepiness where the patient rates his or her alertness on a 7-point scale at different times during the day. If the score falls below a 3 when he or she should be feeling alert, a serious sleep deficit exists.
29
epworth sleepiness scale
ESS measures sleepiness as a reflection of a patient’s tendency to fall asleep during eight specific nonstimulating situations. Each situation is scored from 0 to 3. A total score of 10 is considered abnormal.
30
The definitive test for sleep apnea is
an overnight polysomnogram
31
MSLT test
day after polysomnogram no antidepressants x2 weeks the patient is instructed to take five 20-minute naps 2 hours apart. Healthy subjects have a sleep latency of greater than 7 minutes in the MSLT. A test is considered consistent with excessive daytime sleepiness if sleep onset occurs within 7 minutes. The presence of two sleep-onset REM episodes in the appropriate clinical setting is diagnostic of narcolepsy.
32
general non med/sx tx OSA
avoid etoh, sedative, pain meds, hypnotics weight loss, positional therapy
33
typical CPAP pressure
5-20 cm H20
34
OSA has been found to often co exist with
COPD
35
lung cancer accounts for ___% all cancer deaths
27%
36
1/4 of all lung CA pts
have no symptoms at diagnosis have never smoked
37
4 types lung CA
1. squamous cell 2. small cell 3. large cell 4. adenocarcinoma
38
most prevalent carcinoma in both sexes
adenocarcinoma
39
early nonspecific lung CA symptoms
cough, fatigue
40
group with highest lung cA incidence
African American men
41
risk of lung CA increases with
duration of smoking
42
second leading cause of lung CA death
radon
43
small cell lung cancer
15% whitish gray growth around main bronchus results from smoking more often than NSCLC grows more rapidly, mets earlier more responsive to chemo
44
squamous cell carcinoma
2nd most common 25-35% bulky, invade cartilage, lymph nodes
45
adenocarcinoma
most common 35-45% presents in periph portion of lungs slower growing mets: brain, liver, bone, adrenals
46
large cell carcinoma
least common-10% large, periph, aggressive
47
1st degree relative with history of lung cancer increases risk by
2x
48
categories of lung CA symptoms
intrathoracic/local- regional nonspecific systemic symptoms from extrathoracic involvement paraneoplastic syndromes
49
example of intrathoracic or local/regional symptoms of lung CA
cough, dyspnea, hemoptysis, wheeze
50
example of nonspecific systemic symptoms
weakness, fatigue, fever, anorexia
51
extrathoracic involvement symptoms
bone pain, headache, dizziness, lymphadenopathy
52
most frequent periph sign of lung CA
clubbing of fingers
53
example of paraneoplastic syndrome symptoms
cushing's gynecomastia nephrotic syndrome hypercoag DIC
54
staging of lung CA
TNM tumor (T0-T4) lymph nodes (N0-N3) mets (M0 or M1)
55
lung CA initial testing
CBC CMP EKG AP/lat Chest XR
56
USPSTF screening for lung CA
low dose CT Chest in adults 55-80 who have 30 pack year smoking history and currently smoke or quite within the past 15 years
57
treatment that offers best cure for lung CA
resection
58
most common sx for lung CA
lobectomy
59
Neoadjuvant chemotherapy involves
giving antineoplastic drugs before surgery or radiation therapy.
60
Adjuvant chemotherapy involves
administering antineoplastic drugs after surgery or radiation therapy
61
indication for radiation in lung CA
inoperability
62
remission follow up lung ca
H and P every 3 months x2 years, Q6 months until year 5, then annually
63
atrial fib
one of most common arrhythmias statis of blood in left atrium predisposes to emboli
64
CHADS score of ____ or greater, recommend oral anticoag
2
65
premature atrial contractions
no clinical significance no correction needed unless underlying causes can be corrected cause: caffeine, nicotine, etoh
66
CHADS score
all count for one point Congestive heart failure Hypertension (or txed htn) Age >75 yrs Diabetes S Prior stroke or TIA
67
difference between atrial tachycardia and atrial flutter
both present with more than one observable P wave before QRS Atrial tach- p wave rate of 140-250/min atrial flutter rate- pwave of 250-250/min
68
PVC
usually benign arrhythmias that does not require pharm intervention
69
first degree AV block
regular rhythm, only prolonged P-R interval (>0.2 seconds)
70
second degree AV block
Type I (Mobitz or Wenckebach) Type II (Mobitz II)
71
Second degree av block type I
Mobitz I or Wenckebach occurs with AV nodal area with progressive lengthening of PR interval until QRS complex dropped can become 3rd degree
72
second degree AV block type II
Mobitz II occurs within/below bundle of His normal or lengthened PR interval and periodic drop of QRS complex
73
3rd degree heart block
when atria beat regularly, at normal rate, but no excitation transmitted from atria to ventricles **fatal** QRS and p wave are no in relation to each other at all
74
Those arrhythmias most commonly seen in digitalis toxicity are
atrial tachycardia with AV nodal block, accelerated junctional rhythms, atrial fibrillation with a slow or regular ventricular response, second-degree heart block—Mobitz type I (Wenckebach), and ventricular dysrhythmias
75
a normal digitalis level should not be
the determining factor in assessing digitalis toxicity
76
most common heart diseases causes a fib
heart failure htn rheumatic heart dx
77
other causes of a fib
abrupt d/c of beta blockers etoh ingestion (holiday heart) hyperthyroidism MI cor pulmonale
78
The risk of stroke is increased in untreated atrial fibrillation after
48 to 72 hours
79
A transient second-degree AV heart block type I may be associated with
an acute inferior MI. It may also be associated with heart failure or digitalis toxicity.
80
standard of care after discovery of Mobitz type II
insertion of temporary pacemaker
81
“preexcitation syndrome.
bundle of Kent accessory tract, which is seen in individuals with Wolff-Parkinson-White (WPW) syndrome. Because conduction down this bypass pathway directly transmits a depolarizing impulse to the ventricles faster than impulses sent down the AV node
82
a fib clinical presentation- subjective
SOB, palpitations, angina, changing LOC, syncope
83
SVT clinical presentation subjective
dizziness, sob, chest pain, polyuria
84
VT subjective presentation
(non sustained) palpitations (sustained) decreased levels of mentation, hypotension
85
dig toxicity subjective
anorexia, nausea, vomiting, changes in quality color vision, scotoma, headache, malaise, memory lapse
86
first degree heart block symptoms subjective
asymptomatic
87
3rd degree heart block symptoms subjective
symptomatic bradycardia, degree of symptoms based on origin of block
88
Mobitz type I block symptoms subjective
may/may not have symptoms of bradycardia, often becomes third degree
89
mobitz type ii symptoms subjective
severe bradycardia, change in loc, hypotension
90
a fib objective symptoms
irregularly irregular heart beat (100-180 beats/min). New onset of activity intolerance ** sometimes stroke is first symptom b/c of traveling emboli
91
PSVT objective
“frog sign” because the rapid, regular expansion of the neck veins resembles the puffing motion of a frog, which may be noted by the patient’s family members
92
SVT typical rate
150-250
93
mobitz I type heart rate
50-70
94
third degree typical rate
atrial: 60-100 ventricular: 25-60
95
Tilt-table testing (autonomic testing) is useful in patients with
arrhythmias when syncope may be due to a vasovagal response. The patient is tilted to approximately 70 degrees in conjunction with isoproterenol infusion. Syncope due to bradycardia and/or hypotension will occur in about one-third of patients with recurrent syncope.
96
a fib tx initial
initial: control ventricular response, convert back to NSR with meds or cardioversion meds: amiodarone, disopyramide
97
Before cardioversion, the patient should undergo
TEE to assess for the presence of mural thrombi.
98
Anticoagulation therapy should be initiated in all patients who
remain in atrial fibrillation for longer than 48 hours or who experience atrial fibrillation of unknown duration
99
rapid coag
achieved with iv heparin, start on warfarin that takes 5 days to achieve effect
100
The target INR in atrial fibrillation is
between 2 and 3
101
Watchman device
for pt with nonvalvular a fib close left atrial appendage of heart, reduces risk of stroke warfarin x6 weeks, then plavix x4 months, then d/c
102
initial tx SVT
vagal maneuvers (coughing, lying on floor while elevating legs against wall, squatting), carotid massage
103
PSVT tx
, adenosine is the treatment of choice because it blocks electrical transmission through the AV node.
104
tx 1st degree heart block
none needed, asymptomatic monitor for meds that prolong AV conduction
105
Mobitz type I tx
tx not needed unless symptoms BB, CCB, dig Eval for inferior wall MI pacemaker
106
aortic stenosis usually not cause significant symptoms until
0.8 cm normal is 3 cm
107
aortic stenosis
long symptom free period, rapid clinical deterioration (dyspnea, syncope, chest pain, heart failure) look for narrow pulse pressure 50/50 murmur (in 50% of pt older than 50 yrs)
108
aortic stenosis heard best
RICS in aortic valve soft systolic ejection
109
mitral insufficiency
caused by degneration of mitral valve (rheum fever) systolic heard best: apex, radiates to axilla
110
mitral valve prolapse
most common valvular heart problem predispose to thrombi systolic heard best at apex
111
benign systolic murmur
absence of cardiac pathology heard in 80% of thin adults, children heard at left sternal border
112
hemic murmur is
heard in hyperkinetic or high-volume states such as anemia, fever, or in response to exercise. The murmur has a crescendo–decrescendo pattern and is harsh; both heart sounds are preserved. Because there is no cardiac pathology associated with this condition, it resolves when the underlying high-flow state normalizes.
113
Bacterial endocarditis is most often due to
septicemia caused by Staphylococcus aureus or Streptococcus viridans (alpha-hemolytic) infection increased risk with IV drug users, indwelling IV catheters
114
Rheumatic heart disease is a result of rheumatic fever, an infection caused by
group A beta-hemolytic Streptococcus infection
115
Systolic murmurs are graded on a
1 to 6 scale, from barely audible to audible with the stethoscope held off the chest.
116
Diastolic murmurs are usually graded from
1 to 4 because these murmurs are not loud enough to reach grades 5 and 6.
117
The bell of the stethoscope is most helpful for auscultating
lower-pitched sounds
118
the diaphragm of stethoscope is best used for hearing
higher-pitched sounds
119
DI for murmur
Echo, EKG, Chest XR
120
MVP tx
lifestyle changes (lower HR, decrease stress, increase CO and blood volume) surgery if severe beta blockers
121
mitral stenosis tx
diuretics, sodium restriction anticoag surgery
122
mitral regurg
vasodilator diltiazem, anticoag
123
aortic stenosis tx
aortic valve replacement
124
aortic regurg tx
dig, diuretics arterial vasodilator aortic valve replacement
125
PAD commonly manifests as
lower extremity claudication
126
claudication
cramping pain, triggered by exertion, relieved by rest
127
PAD is caused by
atherosclerosis, blood clots, trauma, spasms of smooth muscle in the arterial walls, and congenital structural defects in the arteries
128
PAD risk factors
male sex smokers obesity coag abnormal OCP diabetes
129
clinical manifestations of PAD are
extremity pain (claudication), weak pulse, pallor, paresthesias, and palpable coolness of the lower extremity. Long-standing PAD causes muscle atrophy, diminished hair growth, and discolored, hardened toenails of the extremity.
130
most common sites aneurysm
aorta cerebral arteries
131
when raising legs, pt w/ PAD will have
pale, dusky red legs when dependent again
132
chronic venous insufficiency when legs raise
improved color
133
6 Ps of PAD
pain pulselessness pallor paralysis paresthesia poikilothermia (coolness)
134
If arterial insufficiency is suspected and the pulses are absent
, a Doppler ultrasound flow study should be performed, which can quantify the degree of the ischemia.
135
ABI indicating moderate level of disease
0.6-0.9
136
severe ischemia ABI value
less than 0.5
137
PAD tx
lifestyle changes walk 30 min 3-4x/week keep legs dependent avoid tight stockings antiplatelet
138
tx claudication
cilostazol, causes vasodilation, inhibits plt aggregation
139
follow up PAD
every 3 months, unless ulcers, then weekly
140
Virchow’s triad—
venous stasis, endothelial injury, and hypercoagulable state
141
DVt primarily results as complication from
Virchow's triad
142
increases risk for DVT
surgeries- ortho esp, hip or knee
143
risk of dvt with pregnancy increases
5x
144
Common causes of hypercoagulability are
estrogen use, pregnancy, and neoplasms
145
DVT subjective
pain in calf muscle, swelling, tenderness with massage
146
Homans’s sign
(pain on dorsiflexion of the foot) is now considered an unreliable diagnostic indicator, given its lack of specificity
147
well's criteria
estimates probability of DVT
148
D-dimer with DVT
can r/o, but not diagnosis dvt
149
if intermediate/high probability of dvt order
compression ultrasound of femoral and popliteal
150
chronic venous insufficiency tx
light exercise, compression stockings, weight loss, elevation of legs
151
DVT tx
anticoag traditionally admitted to hospital for tx
152
DVT follow up
hospitalized x1 week anticoag x6 months if initial, 1 year if subsequent