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Cardiac Ischemia (Boards and Beyond) (EKG changes (Poor R wave progression…
Cardiac Ischemia (Boards and Beyond)
caused by coronary atherosclerosis
O2 demand exceeds O2 supply = Ischemia
Clinical syndromes resulting
Stable angina
"stable" atherosclerotic plaque
no plaque ulceration
no thrombus
symptomatic if plaque occludes 75% of lumen
stable symptoms: angina upon exertion, alleviate w/ rest
Acute Coronary Syndromes
Rupture of atherosclerotic plaque : :text
results: thrombus formation
can cause Subtotal Occlusion
Unstable angina: unstable pattern of symptoms
or MI non-ST elevated MI
or Total occlusion (100%)
STEMI
Complication
Sudden Death
#1 common cause of death (older adults)
Sign of plaque rupture
arrhythmia
#
Risk Factors
Major: prior coronary disease
Coronary risk equivalents (risk of CAD is just as high as prior coronary disease)
Diabetes
peripheral arterial disease
chronic kidney disease
others
HTN
Hyperlipidemia
Family Hx
first relative (nuclear family)
M<50
F<60
modifiable risk
Obesity/sedentary
smoking
typical symptoms
chest pain (angina)
dyspnea
diaphoresis
Extent of Ischemia pathological patterns
Transmural Ischemia
complete 100% obstruction (STEMI)
entire wall is necrotic
Subendocardial Ischemia
obstruction w/ some flow
seen in stable angina
unstable angina
or NSTEMI
area of infarction is limited to subendocardium
endocardium can get O2 from ventricle
subendocardium must get O2 from coronary aa.
EKG changes
ST depressions
classic Subendocardial ischemia
when subendocardium is ischemic: depolarization. Upward deflection seen.
Also small waves of depolarization move away from ischemic zone at rest. Elevates baseline.
ST depression is actually the rest of the ventricle depolarizing back to baseline
T wave inversion
many causes other than CAD
ventricular hypertrophy
normal in BBB
resolving pericarditis
raised ICP intra cerebral pressure (cerebral T wave)
recall repolarization away from lead is positive
but ischemic zone repolarizes first, while epicardium depolarizes LATER. So inverted T wave
ST elevations
only seen in Transmural ischemia
entire wall sends waves of depolarization AWAY while at rest
depolarization of ventricle returns to baseline
repolarization moves back to a depression from baseline
Evolution of EKG in STEMI (vessel occlusion)
normal
Acute: ST elevation
Q wave appears
any time Q wave seen: active infarct in that portion of heart
Inversion of T wave after days
ST segments return to baseline
after 1 wk, can only see Q wave. Persists for many years
"Age indeterminate infarct"
Dead myocardium doesn't repolarize
18 hours
6 hrs
Minutes
Takeaway: Q wave can be either acute or old infarct because of progression
Hyperacute T waves
seen in transmural ischemia (early:before ST elevations)
often w/ ST depressions
Poor R wave progression
R wave increases in size from V1-V6
R waves normally > S waves in V3
example: R wave smaller than S wave in V3
indicative of
anterior ischemia (acute or prior
)
normal R wave
Treatment
terms
Revascularization
restore blood to myocardium when there is a blockage
Indications
angina
MI
systolic dysfunction
hibernating myocardium: severely deprived of O2
still alive
not contracting normally
Angioplasty
reshaping blood vessels
Percutaneous Coronary intervention PCI
Balloon angioplasty
Coronary stenting is 1 way
complications:
Restenosis
inflammation from stent: slow steady growth of scar tissue over a stent
1 more item...
Reocclusion of vessel
rarely lifethreatening
slow return of angina
Stent thrombosis
acute closure of stent by thrombus
metal in stent serves as nidus for thrombus
1 more item...
assd. with missed medication doses
1 more item...
Prevention:
2 more items...
Coronary bypass
bypass delivers blood flow from aorta beyond obstruction
Ischemic Pathological Changes: Myocardium
0-4 hours
4-12 hrs
12-24hrs
5-10d
7wk
Gross: gray-white scar
micro:scar
Gross: Central Yellowing
Micro: Surrounding tissue inflammation
Gross: Hyperemia
Micro: Surrounding tissue inflammation
Gross: mottled appearance
Histo: Necrosis, edema, hemorrhage
no changes
Complications of ischemia
First 4 days
Arrhythmia
Major cause of death
e.g Vtach
5-10d
weeks later
Ventricular Aneurysm
myocardial scar tissue bulges.
see the arrow noting thin scar tissue thats not red
blood stasis
thrombus
strokes or peripheral embolism
Ventricular Pseudoaneurym
rupture contained by pericardium/scar tissue
not true aneurysm: no endocardium/myocardium
pooling blood pushes out from the pericardium, as opposed to stretching
may rupture
presents as chest pain or dyspnea
more common in inferior wall
location and timing of pseudo vs true aneurysm is different
True: anterior wall, takes weeks to occur
Pseudo: inferior wall!, less than 2 weeks to occur
just another version of a free wall rupture
Dressler's Syndrome
form of pericarditis (weeks to months)
clinical signs
chest pain
friction rub
Immune mediated phenomenon
Treatment: NSAIDS or steroids
Free wall rupture
usually fatal--sudden death
cardiac tamponade
Papillary muscle rupture
acute mitral regurgitation
holosystolic murmur
severe: leads to
HF
respiratory distress
more common in INFERIOR MI
Infralateral papillary muscle has single blood supply
Septal rupture VSD
Loud, holosystolic murmur (maybe w/ thrill)
overloading RV from LV
hypotension
RH failure
incr JVP
edema
Fibrinous Pericarditis (post MI)
#
not autoimmune
extension of myocardial inflammation into pericardium
not life threatening
secondary prevention of CAD
pts have high risk of recurrent events
STEMI
NSTEMI
stable angina
preventative therapy even in asymptomatic patients
ASA
Statins
BB
used in pts with prior infarct
