obstructive pulmonary disease
characterized by increased resistance airflow as a result of airway obstruction or narrowing
types of obstructive pulmonary diseases
asthma
copd
cystic fibrosis
bronchiectasis
copd
obstructive pulmonary disease with progressive limitation in airflow that is not reversible
preventable if treater early
chronic bronchitis
presence of cough and sputum production for at least 3 months in each of 2 consecutive years
emphysema
destruction of alveoli and is a pathologic term that explains only one of several structural abnormalities in copd
copd pathophysiology
loss of elastic recoil
obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm
air goes in easily but remains in the lungs (causing increased co2)
bronchioles collapse
result of chronic inflammation
risk factors for copd
cigarette smoking
occupational chemicals and dust
air pollution
severe reoccurring infections
genetics
aging
asthma
male
geriatric changes (copd)
gradual loss of elastic recoil of the lung with stiffening of the chest wall
gas exchange
clinical manifestations of copd
chest breathing (use of accessory and intercostal muscles)
wheezing or chest tightness
underweight
chronic fatigue
coughing so severe is fractures ribs
physical examination findings of copd
barrel chest
wheezes
decreased breath sounds
tripod position
pursed lip breathing
prolonged expiratory phase
cyanosis
right sided heart failure
copd diagnosis determined by
pulmonary function test (measures the amount of air you can inhale and exhale and whether your lungs deliver enough oxygen to your blood)
lower FEV1 indicates
a sicker patient
diagnostic studies for copd
chest x ray
echocardiogram
sputum for culture and sensitivity
abg
copd heart manifestations
hypertrophy of right side of heart as a result of pulmonary hypertension
copd heart symptoms
dyspnea (lung crackles)
distended neck veins
hepatomegaly
peripheral edema
weight gain
treatment for copd exacerbations
short acting bronchodilators (beta 2 agonists) and muscarinic antagonist
oral systemic corticosteroids
antibiotics
supplemental oxygen therapy
diuretics
humidification
has drying effect on mucosa
supplied by nebulizers, vapotherm, and bubble-through humidifiers
bullectomy
large air sacs that form from destroyed alveoli that are removed to improve lung function
tracheostomy
surgically created stoma used to
establish a patient airway
bypass airway obstruction
facilitate secretion removal
permit long-term mechanical ventilation
facilitate weaning from mechanical ventilation
advantages of tracheostomy
easier to keep clean
better oral and bronchial hygiene
patient comfort increased
less risk of long-term damage to vocal cords
speaking valves
thin diaphragm that opens on inspiration and closes on expiration
air flows over vocal cords during exhalation
must be deflated o use cuffless tube
removal of tracheostomy
patient must be hemodynamically stable
stable intact respiratory drive
can adequately exchange air and expectorate
monitor site for bleeding
splint stoma with fingers when coughing, swallowing, or speaking
risk factors for pneumonia
advanced age
immunocompromised
underlying lung disease
immobility
altered consciousness
smoking
endotracheal intubation
community acquired pneumonia (cap)
infection occurs in community or within 2 days of hospitalization
hospital acquired pneumonia (nosocomial)
infection occurs 48 hours after hospitalization (5-10 cases per 1000 hospital admissions)
risk increased by intubation and mechanical ventilation
aspiration
materials from mouth or stomach enter the lungs
health care associated pneumonia
hospitalized in acute care hospital for 2 or more days within 90 days of infection
usually in long-term facilities
received iv antibiotics, chemo, or wound care within 30 days of infection
ventilator associated pneumonia (vap)
airway infection that must have developed more than 48 hours after a patient is intubated
leading cause of death of hospital acquired infections
interventions for vap
elevation of head of bed
sedation vacations
peptic ulcer prophylaxis
deep venous thrombosis prophylaxis
oral care
aspiration of pneumonia
entry of substances from the mouth or stoma into the trachea and lower airway
associated with loss of consciousness and tube feeding
pneumoccal pneumonia manifestations
upper respiratory infection
cough
dyspnea
fever
chills
malaise
pleuritic chest pain
mycoplasma pneumonia
younger people
working/living in crowded areas
headache
chills
fever
chest pain
sore throat
dry cough
hospital acquired pneumonia manifestations
fever
chills
productive cough
leukocytosis
looks sick
assessment of pneumonia
oxygenation
increased respiratory rate and fever
rhonchi/crackles and bronchial breath sounds
tactile fremitus
dullness to percussion
skin warm and dry
flushed and diaphoresis
community acquired pneumonia (cap) treatment
penicillins
cephalosporins
macrolides
fluroquinolins
start within 4-8 hours
antivirals supportive care
hospital acquired pneumonia (hap)
ciprofloxacin
piperacillin
latent tb
granuloma intact
bacteria dormant
no further progression of active disease
active tb
compromised or inadequate immune system response
granuloma ulcerates
cheesy material into bronchi
bacili airborne
inflammatory response
bronchopneumonia
symptoms of tb
bad cough lasting 3 weeks or longer
chest pain
coughing up blood or sputum
weakness and fatigue
weight loss
no appetite
chills
fever
sweating at night
medical treatment for tb
inh
rifampin
pyrzinamide
ethambutol
nursing management for tb
promote airway clearance
promote adherence to treatment regimen
promote activity and adequate hydration
cardiac output
the amount of blood pumped by the heart per minute
stroke volume x heart rate
systemic vascular resistance
the amount of force exerted on the circulating blood by the vasculature of the body
determined by length and diameter of blood vessels and viscosity of blood within vessels
hypertensive emergency
occurs over hours to days
bp greater than 220/140 with target organ disease
hypertensive urgency
occurs over days to weeks
bp greater than 180/110 with no clinical evidence of target organ disease
complications of hypertensive crisis
hypertensive encephalopathy (headache, seizures, n and v, and confusion)
renal insufficiency
cardiac decompensation (mi, hf, and pulmonary edema)
aortic dissection
mean arterial pressure equation
map = (co x svr) + cvp (central venous pressure)
treatment for hypertensive crisis
iv titrated to map
monitor cardiac and renal function
neurologic checks
determine cause
education to avoid future crisis
cardiac assessment for hypertensive crisis
assess for murmurs and gallops
assess for heart failure
lung assessment for hypertensive crisis
assess for evidence of pulmonary edema (wheezing and rales)
abdominal assessment of hypertensive crisis
assess for bruits (renal artery stenosis)
abdominal aortic aneurysm
auscultate for murmur (aortic dissection)
extremities assessment of hypertensive crisis
assess pulses (if different may suggest aortic dissection)
diagnostic testing for hypertensive crisis
chest x ray
chest computed tomography
transthoracic echocardiogram (distinguishes diastolic dysfunction, transient systolic dysfunction, and mitral regurgitation)
treatment for hypertensive urgency
oral administration of meds (nicardipine, captopril, and labetatol)
normalize blood pressure gradually for 24-48 hours
observe patient for several hours prior to discharge
nicardipine dosing
20-40 mg orally every 8 hours
captopril dosing
25 mg orally ever 8-12 hours
labetatol dosing
initial dose 200 mg orally then additional 200-400 mg dose after 6-12 hours
treatment for hypertensive emergency
admit patient to icu for iv medications and management of end-organ dysfunction
lower bp 10-15% over the first hour
nicardipine iv dosing
initial infusion 5 mg/hour increasing 2.5 mg/hour every 5 minutes to a max of 15 mg/hour
sodium nitroprusside iv dosing
0.3-0.5 mcg/kg/minute increase by 0.5 mcg/kg/minute every few minutes to a maximum dose of 10 mcg/mg/minute
labetatol iv dosing
10-20 mg iv followed by bolus doses of 20-80 mg at 10 minute intervals until target bp reached at 300 mg cumulative dose
esmolol iv dosing
initial loading dose 500 mcg/kg/minute over 1 minute then 50-100 mcg/kg/minute to max dose of 300 mcg/kg/minute
peripheral vascular disease
inadequate return of venous blood from the legs to the heart caused by damage to the valves allowing blood to leak backwards
peripheral arterial disease
progressive narrowing of arteries typically in pelvis and legs
leading cause of pad
atherosclerosis
risk factors for pvd and pad
family hx of premature mi or stroke
older than 50
overweight or obese
inactive lifestyle
smoking
diabetes
hypertension
high ldl and triglycerides
causes of pad
arteriosclerosis
blood clot
diabetes (higher blood sugar = more damage to vessels)
inflammation of arteries (autoimmune)
infection
structural defects
injury
clinical manifestations of pad
claudication
buttock pain
numbness/tingling of leg and foot
changes in skin color
changes in skin temp
sores that do not heal
uncontrolled hypertension
renal insufficiency/failure
thin shiny skin
hair loss on lower legs
pallor of foot w elevation
diminish
complications of pad
atrophy of skin and underlying muscles
delayed healing
wound infection
tissue necrosis
arterial ulcers
how pad is diagnosed
ankle brachial plexus
ultrasound doppler test
angiogram
treatment of pad
angioplasty and stents (invasive)
atherectomy (invasive)
peripheral artery bypass surgery
medications for pad
ramipril (ace inhibitor)
aspirin (antiplatelet agent)
clopidogril (plavix)
medications for intermittent claudication (symptom of pad)
cilostazol (inhibits platelet aggregation and vasodilates)
pentoxifylline (lowers blood viscosity and increases rbc flexibility)
nursing interventions for pad
assess pulses
temp
color
cap refill
hair distribution
open areas
movement
and pain assessment
nursing education for pad
exercise improves oxygen extraction in legs and skeletal metabolism
walking is the most effective exercise
pvd risk factors
dvt
varicose veins or family hx of varicose veins
obesity
pregnancy
inactivity
smoking
extended periods of sitting or standing
female
over 50
symptoms of pvd
swelling in lower legs and ankles
aching or tiredness in the legs
new varicose veins
leathery looking skin on legs
flaking or itching skin
stasis ulcers
diagnosis of pvd
vascular ultrasound
nursing education for pvd
avoid sitting or standing for long periods of time
exercise regularly
lose weight if overweight
elevate legs
wear compression stockings
good skin care
treatment of pvd
sclerotherapy
ligation and stripping
ambulatory phlebectomy
vein bypass
heart failure
complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill and eject blood
heart failure results in
ventricular dysfunction
decreased cardiac output
decreased tissue perfusion
fluid retention
preload
volume in ventricles awaiting delivery
afterload
pressure in aorta to overcome
myocardial contractility
intrinsic ability to shorten and develop muscle tension
renin angiotensin aldosterone system responds to
decreased co2
decreased renal blood flow
increased renin from kidneys
aldosterone is for
sodium retention
adh
secreted by posterior pituitary and increases water absorption with increases in blood volume
sympathetic nervous system involvement in hf
increases catecholamines (increases epinephrine and norepinephrine leading to vasoconstriction)
leads to increased bp, afterload, and hr
ventricular remodeling
process of changing shape and mass of ventricles
ventricular dilation
enlargement of chambers
muscle fibers stretch to increase contractility
ventricular hypertrophy
increase in cardiac wall thickness
initially serves to increase contractility
decrease inside volume
systolic hf
ef less than 40%
diastolic hf
ef greater than 50%
hf causes
left ventricular dysfunction
uncontrolled htn
volume overload due to excess dietary sodium, excess dietary fluid, and hepatic dysfunction
renal insufficiency (fluid retention)
high output state
hormonal disturbances
medication related
substance abuse
infe
left sided hf symptoms
dyspnea
orthopnea
cough (dry hacking)
s3 heart sounds
pulmonary edema (crackles)
fatigue/weakness
right sided hf symptoms
increased weight gain
jvd
edema
fatigue/weakness
hypertension
hepatomegaly
labs to monitor with hf
bnp
troponin
cbc
cmp
coagulation panel
management of hf
loop diuretics
oxygen
vasodilators
inotropic support
iv morphine
bipap/vent
digoxin
ace inhibitors (for hf treatment)
captopril
enalapril
lisinopril
ramipril
ace inhibitors (for hf treatment) function
reduction in mortality
improvement in exercise tolerance
improves symptom control
ace inhibitors (for hf treatment) adrs
hypotension
hyperkalemia
cough
taste disturbance
angio 2 receptor blockes (hf)
losarten
valsarten
used in patients who are ace 1 intolerance
can be added to beta blockers, digoxin, and diuretics
beta blockers (hf) cardioselective
metoprolol
bisoprolol
beta blockers (hf) nonselective
cardvedilol
start with hemodynamically stable patient with no fluid retention
watch for hyperglycemia
symptoms may worsen in 3-6 months
nursing assessments for patients with hf
daily weights
i&o's
fluid restriction
labs (creatinine and electrolytes)
ef
diet
atherosclerosis
begins as soft deposits of fat that harden with age
major cause of cad
c-reactive protein
nonspecific marker of inflammation
elevated in patients with cad
chronic exposure associated with unstable plaques and oxidation of ldl cholesterol
collateral circulation
arterial anastomoses within the coronary circulation
increased with chronic ischemia
nonmodifiable risk factors for cad
age
gender
ethnicity
family hx
genetic predisposition
modifiable risk factors for cad
elevated serum lipids (cholesterol, triglycerides, hdl, and ldl)
hypertension
tobacco use and second hand smoke exposure
physical inactivity
obesity
diabetes
metabolic syndrome
psychologic states
homocysteine level
substance abuse
statin (treatment for cad)
inhibit cholesterol synthesis decreasing ldl and increasing hdl
must monitor for liver damage and myopathy
niacin (treatment for cad)
lowers ldl and triglyceride by inhibiting synthesis
increases hdl
flushing, pruritis, GI side effects and orthostatic hypotension are all side effects
fibric acid derivatives (lopid)
decrease triglycerides and increase hdl
has GI side effects
bile acid sequestrants (welchol)
increase conversion of cholesterol to bile acids
GI side effects and can bind with other drugs
ezetimibe (zetia)
decrease absorption of dietary and biliary cholesterol
modifications for physical activity for older adults
longer warm up
longer periods of low level activity
longer rest periods
avoid extremes of temperature
30 minutes most days minimum
cad angina
reversible ischemia
occurs when arteries are blocked 75% or more
hypoxic within 10 seconds of occlusion
viable for 20 minutes
clinical manifestations of cad angina
pressure/ache
squeezing, heavy, choking, or suffocating sensation
indigestion or burning
various locations
clinical manifestations of cad chronic stable angina
intermittent chest pain that occurs over long period with the same pattern of onset duration and intensity of symptoms
5-15 minute duration
ST segment depression
control w drugs
silent ischemia
ischemia that occurs in the absence of any subjective symptoms
associated with diabetic neuropathy
confirmed by ECG changes
nocturnal angina
occurs only at night but not necessarily during sleep
angina decubitus
chest pain that occurs only while lying down
relieved by standing or sitting
prinzmetal's (variant) angina
occurs at rest usually in response to spasm of major coronary artery
seen in patients with a history of migraine headaches and Raynaud's
spasm may occur in the absence of cad
microvascular angina
chest pain occurs in the absence of significant coronary atherosclerosis or coronary spasm
myocardial ischemia associated with abnormalities of the coronary microcirculation
affects small distal coronary arteries
short acting nitrates
dilate peripheral and coronary blood vessels
give sublingually tablet or by spray
if no relief in 5 minutes call ems
can use prophylactically
long acting nitrates
reduce angina incidence
side effect are headache and orthostatic hypotension
can be given orally, nitroglycerin ointment, or transdermal release
collaborate care for chronic stable angina
angiotensin converting enzyme inhibitors
beta adrenergic blockers
calcium channel blockers
sodium current inhibitor (ranexa)
diagnostics for chronic stable angina
chest x ray
labs
12 lead ekg
calcium score screening heart screen
echocardiogram
exercise stress test
pharmacologic nuclear imaging
automaticity
ability to initiate an impulse
excitability
ability to respond to an impulse
conductivity
ability to transmit an impulse
contractibility
ability to response with pumping action
how does the cardiac cell work?
cardiac cells contract (depolarization) and depolarization spreads through gap junctions
cardiac conduction system
refers to system of electrical signaling that instructs these muscle cells to contract
three ion channels of the cardiac action potential
fast sodium channels
slow calcium channels
potassium channels
depolarization
contraction of the heart
causes membrane to become permeable to sodium and potassium (sodium flows in potassium flows out)
positive electrical potential outside the cells
SYSTOLE
repolarization
resting state of the heart
sodium channels close and potassium flows outside cells until the end
outside of cell returns to negative electrical potential
DIASTOLE
sa node
sets up pace of the heart
inherent rate of 60-100
junctional fibers
designed to carry action potential rather slowly so that atria to contract and force blood into the ventricles
av node
relays impulses from sa node to ventricles
located in wall between right atrium and right ventricle
inherent rate 40-60
av bundle
group of fast conducting fibers carry the av node activity to the intraventricular septum really quickly
inherent rate 20-40
purkinje fibers
fibers that run along the outer edge of ventricles
map of electrical impulse in heart
sa node
atrial syncytium
junctional fibers
sa node
av bundle
bundle branches
pukinje fibers
ventricular syncytium
sns influence
supplies atria and ventricles
epinephrine is the mediator
increases rate of sa node, av node, excitability, and force of contractility
pns (vagus nerve) influence
affects primarily atria
acetylcholine is mediator
decreases sa node, rate of av conduction, and excitability
ekg
measures the direction of electrical impulses from cardiac cells
as electrical current travels toward negative pole
wave form deflects downward from isoelectric line
as electrical current travels toward positive electrode
wave form deflects upward from isoelectric line
proper skin prep before placing electrodes
soap and water NO ALCOHOL
get rid of excess body hair
ekg paper 5 large boxes is
1 second
ekg paper 15 large boxes
3 seconds
calculating heart rate rule of 10
regular or irregular rhythm
count number of r waves in 6 second strip x 10 = hr
p wave
atrial depolarization
qrs complex
ventricular depolarization
t wave
ventricular repolarization
u wave
final phase of repolarization
normal pr interval
0.12-0.20 seconds
normal qrs complex interval
0.04-0.12
normal qt interval
less than 0.4 seconds
can be affected by age and gender
also affect my medications (zofran and anesthetics) and electrolyte imbalances (magnesium and potassium)
ekg paper small boxes
0.04 second
ekg paper large boxes
0.20 second
sinus rhythm
rate 60-100 bpm
regular rhythm
p waves = 1 to each qrs complex
qrs = all the same (less than 0.12)
normal!
sinus bradycardia
hr less than 60 bpm
regular rhythm
p waves = 1 to each qrs complex all the same shape and size
qrs all the same (less than 0.12)
may impact cardiac output
normal in conditioned athlete
treatment based off symptoms in cardiac patients
can be caused by vaso
sinus tachycardia
hr 101-150
regular rhythm
p waves = 1 to each qrs; same shape and size
qrs all the same (less than 0.12)
decreased ventricular and coronary artery filling time
may cause cardiac ischemia
may lead to increased OR decreased bp
caused by sympathetic stimulat
sinus pause
irregular during pause
underlying sinus rhythm
sudden decrease in rate (may cause syncope or dizziness)
no p wave or qrs complex during pause or arrest
diseased sa node, vagal stimulation, mi
treatment depends on length of pause (atropine and pacer at the
types of atrial dysrhythmias
pac
psvt
a flutter
a fib
premature atrial contraction (pac)
early beat in normal rhythm
p wave early and differs in size and shape from other p waves
normal qrs
may have short pause after pac
may arise from bigeminal, trigeminal, or couplets
precursor of afib
can signal hf, pericarditis, hormones, caffeine, electr
supraventricular tachycardia
a rapid tachyarrhythmia that originates above the ventricle (also called PSVT paroxysmal supraventricular tachycardia)
svt causes
heart failure
thyroid disease
heart disease
chronic lung disease
smoking
too much alcohol
too much caffeine
drug use
asthma meds and certain otc meds
surgery
pregnancy
atrial flutter
sawtooth pattern
rapid atrial rate (250-350)
abnormal electrical circuit in the atria
ventricular rhythm usually regular
s/s of decreased cardiac output
shortness or breath
tiredness
chest pain
fluttering heartbeat
lightheadedness
fainting
swelling in you
causes of atrial flutter
age
high blood pressure
diabetes
coronary artery disease
heart failure
congenital heart disease
past heart surgery
obesity
alcohol consumption
lung disease
overactive thyroid
sleep apnea
over exercising
family history
atrial fibrillation (afib)
disorganized ineffective quivering of the atria
no p waves
ventricular rate is totally irregular and varied
no pri
uncontrolled a fib = greater than 100 ventricular bpm
controlled a fib = less than 100 ventricular bpm
apical/radial pulse deficit
causes of afib
heart valve disorders
cardiomyopathy
mi
copd/lung diseases
chf
pericarditis
sick sinus functioning
congenital heart disease
overactive thyroid
high bp
previous heart surgery
stress due to surgery, pneumonia, or other illness
sleep apnea
bradycardia treatment
observe for symptoms
if symptomatic atropine 0.5 mg-1 mg iv pacemaker on standby
tachycardia treatment
treat cause (rhythm can be compensatory)
beta blockers or calcium channel blockers
holter monitor
small wearable device that keeps track of heart rhythm
can detect irregularities of rhythm that ekg cannot
implantable loop recorder
type of heart-monitoring device that records heart rhythm continuously for up to 3 years
records electrical signals of your heart and allows remote monitoring by small device inserted beneath the skin
treatment of svt
vagal maneuvers
adenosine
synchronized cardioversion if severe symptoms
cardizem (1 choice of calcium channel blockers)
beta blockers
digoxin (will not lower bp)
cardioversion
synchronous defibrillation with less use of energy
patient is usually awake and hemodynamically unstable
painful! medicate before
treatment of afib
want to reset rhythm
electric cardioversion
pharmacological cardioversion (calcium channel blockers, amiodarone, digoxin)
ablation
anti-coagulation
left atrial appendage closure (watchman device)
warfarin (coumadin)
blocks liver from using vitamin K to make clotting factors (vitamin K is antidote)
5-7 days to be effective
international normalized ratio (INR)
tests how much time it takes for a patient's blood to clot
range is 2-3
avoid foods with high vitamin K
non vitamin k oral anticoagulants
pradaxa (dabigatran) thrombin inhibitor
xarelto (rivaroxaban)
eliquis (apixaban)
causes of premature ventricular contarctions
caffeine
alcohol
nicotine
epinephrine
electrolyte imbalance
hypoxia fever
exercise
emotional stress
mi
hf
cardiomyopathy
cad
mvp
treating the cause of pvc
assess patient (hemodynamically stable)
electrolyte therapy
oxygen therapy
further diagnostics
cardiomyopathy
condition which makes it harder for heart to pump and supply blood to the other parts of the body
dilated cardiomyopathy
pumping dysfunction (mostly l ventricle) chamber enlargement
typically presents between 30-60 y/o
most common in african american males
third leading cause of heart failure
most common form of cardiomyopathy
ischemic dilated cardiomyopathy
coronary artery disease
myocardial infarction
non-ischemic dilated cardiomyopathy
familial (genetics) Duchenne muscular dystrophy
structural heart (valves, pressure or volume overload, l to r shunt)
alcohol
drugs (chemo, cocaine, toxins ex) co2, lead, mercury)
endocrine
immune (autoimmune, hypersensitivity, transplant rejection, infect
cardiomyopathy evaluation
echocardiogram
ekg
stress test or coronary angiography
lab tests (genetic mutation)
cardiac biopsy
troponin and bnp
treatment of dilated cardiomyopathy
ace inhibitors/arbs
beta blockers
treat underlying cause
implantable cardioverter defibrillator
LVAD (does not have a pulse)
hypertrophic cardiomyopathy
commonly inherited cv disease
largely caused by gene mutations
complication include syncope, hf, and sudden death
signs and symptoms of hypertrophic cardiomyopathy
may be asymptomatic
chest pain
dyspnea
syncope
palpitations
systolic murmur
treatment of hypertrophic cardiomyopathy
no intensive sports (low intensity workouts)
beta blockers
verapamil (ca channel blocker)
diltiazem (for those intolerant to verapamil)
implantable cardioverter devices
permanent pacemakers
septal ablation
heart transplant
restrictive cardiomyopathy
heart muscle characterized by impaired ventricular filling with typically preserved systolic function and normal or mildly increased ventricular wall thickness
causes of restrictive cardiomyopathy
amyloidosis
cardiac sarcoidosis
hemosiderosis
management of restrictive cardiomyopathy
diuretics and aldosterone antagonists
pacer for av block
corticosteroids, melphan, autologous stem (for amyloidosis)
iron depletion (treatment for hemochromatosis)
cardiac transplant
implantable cardioverter-defibrillator
takotsubo broken heart syndrome
acute cardiac syndrome
left ventricular ballooning
often precipitated by acute emotional or physical stress
symptoms of broken heart syndrome
cheat pain and st elevations
management of broken heart syndrome
spontaneous recovery
ef guides treatment (ef less than 45% and complications are considered high risk)
beta blockers and ace inhibitors
follow up care is a must