Module 2 Flashcards
Sleep apnea is defined as
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.
three patterns of apnea are
central, obstructive, and mixed
Central apnea occurs when
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
during obstructive sleep apnea (OSA),
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
Sleep hypopnea is
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.
apnea-hypopnea index (AHI) may be used to
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
respiratory disturbance index (RDI),
another commonly cited parameter, is defined as the AHI plus the average number of snoring-related arousals per hour.
A diagnosis of OSA is confirmed with AHI and RDI scores as follows:
*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.
Sleep-disordered breathing is an independent risk factor for the
development of hypertension and, subsequently, left ventricular dysfunction.
The patient with combined coronary artery disease (CAD) and OSA may have an increased cardiac risk because of
worsening of the relationship between myocardial oxygen demand and supply as a result of apnea-associated hypoxemia and activation of the autonomic nervous system
dysrhythmia associated with OSA
a. fib
treating OSA will improve effectiveness of a fib tx
OSA possible pulm side effect
cause mild pulmonary htn, often associated with right ventricular failure.
Unrecognized and untreated OSA is estimated to be ,
30% in the adult male population and to be 15% in the adult female population
OSA is most prevalent in
men older than age 50 and in postmenopausal women; in this latter group
why increase in OSA in men
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
Relatives of a person with sleep apnea have approximately
twice the normal risk of having sleep apnea
OSA aggravating factors (2)
obesity
etoh
best indicator of presence of sleep apnea
neck/collar size in men (larger than 17 in)
two states of sleep
REM
NREM
NREM 3 stages
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
Central apneas are more common in individuals who
live at high altitudes, where hypoxemia induces hyperventilation with associated alkalosis.
most important presenting symptom of sleep apnea
hypersomnolence- clear cut uncontrolled sleepiness
define hypersomnolence
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.
other sleep apnea symptoms
morning HA, falling asleep when performing purposeful activities, nocturnal restlessness, frequent urinations, choking, personality disturbance, sexual dysfunction
The snoring of OSA is
both loud (it can be heard in an adjacent room) and habitual (it occurs nightly).
OSA automobile accident rate
2-2.6x more
subjective assessments for OSA
Stanford sleepiness score (SSS)
epworth sleepiness scale (ESS)
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.
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.
The definitive test for sleep apnea is
an overnight polysomnogram
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.
general non med/sx tx OSA
avoid etoh, sedative, pain meds, hypnotics
weight loss, positional therapy
typical CPAP pressure
5-20 cm H20
OSA has been found to often co exist with
COPD
lung cancer accounts for ___% all cancer deaths
27%
1/4 of all lung CA pts
have no symptoms at diagnosis
have never smoked
4 types lung CA
- squamous cell
- small cell
- large cell
- adenocarcinoma
most prevalent carcinoma in both sexes
adenocarcinoma
early nonspecific lung CA symptoms
cough, fatigue
group with highest lung cA incidence
African American men
risk of lung CA increases with
duration of smoking
second leading cause of lung CA death
radon
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
squamous cell carcinoma
2nd most common
25-35%
bulky, invade cartilage, lymph nodes
adenocarcinoma
most common
35-45%
presents in periph portion of lungs
slower growing
mets: brain, liver, bone, adrenals
large cell carcinoma
least common-10%
large, periph, aggressive
1st degree relative with history of lung cancer increases risk by
2x
categories of lung CA symptoms
intrathoracic/local- regional
nonspecific systemic
symptoms from extrathoracic involvement
paraneoplastic syndromes
example of intrathoracic or local/regional symptoms of lung CA
cough, dyspnea, hemoptysis, wheeze
example of nonspecific systemic symptoms
weakness, fatigue, fever, anorexia
extrathoracic involvement symptoms
bone pain, headache, dizziness, lymphadenopathy
most frequent periph sign of lung CA
clubbing of fingers
example of paraneoplastic syndrome symptoms
cushing’s
gynecomastia
nephrotic syndrome
hypercoag
DIC
staging of lung CA
TNM
tumor (T0-T4)
lymph nodes (N0-N3)
mets (M0 or M1)
lung CA initial testing
CBC
CMP
EKG
AP/lat Chest XR
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
treatment that offers best cure for lung CA
resection
most common sx for lung CA
lobectomy
Neoadjuvant chemotherapy involves
giving antineoplastic drugs before surgery or radiation therapy.
Adjuvant chemotherapy involves
administering antineoplastic drugs after surgery or radiation therapy
indication for radiation in lung CA
inoperability
remission follow up lung ca
H and P every 3 months x2 years, Q6 months until year 5, then annually
atrial fib
one of most common arrhythmias
statis of blood in left atrium predisposes to emboli
CHADS score of ____ or greater, recommend oral anticoag
2
premature atrial contractions
no clinical significance
no correction needed unless underlying causes can be corrected
cause: caffeine, nicotine, etoh
CHADS score
all count for one point
Congestive heart failure
Hypertension (or txed htn)
Age >75 yrs
Diabetes
S Prior stroke or TIA
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
PVC
usually benign arrhythmias that does not require pharm intervention
first degree AV block
regular rhythm, only prolonged P-R interval (>0.2 seconds)
second degree AV block
Type I (Mobitz or Wenckebach)
Type II (Mobitz II)
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
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
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
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
a normal digitalis level should not be
the determining factor in assessing digitalis toxicity
most common heart diseases causes a fib
heart failure
htn
rheumatic heart dx
other causes of a fib
abrupt d/c of beta blockers
etoh ingestion (holiday heart)
hyperthyroidism
MI
cor pulmonale
The risk of stroke is increased in untreated atrial fibrillation after
48 to 72 hours
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.
standard of care after discovery of Mobitz type II
insertion of temporary pacemaker
“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
a fib clinical presentation- subjective
SOB, palpitations, angina, changing LOC, syncope
SVT clinical presentation subjective
dizziness, sob, chest pain, polyuria
VT subjective presentation
(non sustained) palpitations
(sustained) decreased levels of mentation, hypotension
dig toxicity subjective
anorexia, nausea, vomiting, changes in quality color vision, scotoma, headache, malaise, memory lapse
first degree heart block symptoms subjective
asymptomatic
3rd degree heart block symptoms subjective
symptomatic bradycardia, degree of symptoms based on origin of block
Mobitz type I block symptoms subjective
may/may not have symptoms of bradycardia, often becomes third degree
mobitz type ii symptoms subjective
severe bradycardia, change in loc, hypotension
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
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
SVT typical rate
150-250
mobitz I type heart rate
50-70
third degree typical rate
atrial: 60-100
ventricular: 25-60
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.
a fib tx initial
initial: control ventricular response, convert back to NSR with meds or cardioversion
meds: amiodarone, disopyramide
Before cardioversion, the patient should undergo
TEE to assess for the presence of mural thrombi.
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
rapid coag
achieved with iv heparin, start on warfarin that takes 5 days to achieve effect
The target INR in atrial fibrillation is
between 2 and 3
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
initial tx SVT
vagal maneuvers (coughing, lying on floor while elevating legs against wall, squatting), carotid massage
PSVT tx
, adenosine is the treatment of choice because it blocks electrical transmission through the AV node.
tx 1st degree heart block
none needed, asymptomatic
monitor for meds that prolong AV conduction
Mobitz type I tx
tx not needed unless symptoms
BB, CCB, dig
Eval for inferior wall MI
pacemaker
aortic stenosis usually not cause significant symptoms until
0.8 cm
normal is 3 cm
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)
aortic stenosis heard best
RICS in aortic valve
soft systolic ejection
mitral insufficiency
caused by degneration of mitral valve (rheum fever)
systolic
heard best: apex, radiates to axilla
mitral valve prolapse
most common valvular heart problem
predispose to thrombi
systolic
heard best at apex
benign systolic murmur
absence of cardiac pathology
heard in 80% of thin adults, children
heard at left sternal border
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.
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
Rheumatic heart disease is a result of rheumatic fever, an infection caused by
group A beta-hemolytic Streptococcus infection
Systolic murmurs are graded on a
1 to 6 scale, from barely audible to audible with the stethoscope held off the chest.
Diastolic murmurs are usually graded from
1 to 4 because these murmurs are not loud enough to reach grades 5 and 6.
The bell of the stethoscope is most helpful for auscultating
lower-pitched sounds
the diaphragm of stethoscope is best used for hearing
higher-pitched sounds
DI for murmur
Echo, EKG, Chest XR
MVP tx
lifestyle changes (lower HR, decrease stress, increase CO and blood volume)
surgery if severe
beta blockers
mitral stenosis tx
diuretics, sodium restriction
anticoag
surgery
mitral regurg
vasodilator
diltiazem, anticoag
aortic stenosis tx
aortic valve replacement
aortic regurg tx
dig, diuretics
arterial vasodilator
aortic valve replacement
PAD commonly manifests as
lower extremity claudication
claudication
cramping pain, triggered by exertion, relieved by rest
PAD is caused by
atherosclerosis, blood clots, trauma, spasms of smooth muscle in the arterial walls, and congenital structural defects in the arteries
PAD risk factors
male sex
smokers
obesity
coag abnormal
OCP
diabetes
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.
most common sites aneurysm
aorta
cerebral arteries
when raising legs, pt w/ PAD will have
pale, dusky red legs when dependent again
chronic venous insufficiency when legs raise
improved color
6 Ps of PAD
pain
pulselessness
pallor
paralysis
paresthesia
poikilothermia (coolness)
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.
ABI indicating moderate level of disease
0.6-0.9
severe ischemia ABI value
less than 0.5
PAD tx
lifestyle changes
walk 30 min 3-4x/week
keep legs dependent
avoid tight stockings
antiplatelet
tx claudication
cilostazol, causes vasodilation, inhibits plt aggregation
follow up PAD
every 3 months, unless ulcers, then weekly
Virchow’s triad—
venous stasis, endothelial injury, and hypercoagulable state
DVt primarily results as complication from
Virchow’s triad
increases risk for DVT
surgeries- ortho esp, hip or knee
risk of dvt with pregnancy increases
5x
Common causes of hypercoagulability are
estrogen use, pregnancy, and neoplasms
DVT subjective
pain in calf muscle, swelling, tenderness with massage
Homans’s sign
(pain on dorsiflexion of the foot) is now considered an unreliable diagnostic indicator, given its lack of specificity
well’s criteria
estimates probability of DVT
D-dimer with DVT
can r/o, but not diagnosis dvt
if intermediate/high probability of dvt order
compression ultrasound of femoral and popliteal
chronic venous insufficiency tx
light exercise, compression stockings, weight loss, elevation of legs
DVT tx
anticoag
traditionally admitted to hospital for tx
DVT follow up
hospitalized x1 week
anticoag x6 months if initial, 1 year if subsequent
