Myocardial Infarction Flashcards
Cause of MI ?
- Rupture of the atherosclerosis with thrombosis
- Complete occlusion of coronary artery
- CA vasosapsm
- Prinzmetal angina
- Emboli
- Vasculitis-Kawasaki Disease
Cell injury in MI ?
Necrosis of cardiacx] myocytes
Dyspnea manifesto in MI ?
Total function oif heart is impaired = Pulmonary congestionnand edema = Dyspnea
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Presenations of MI ?
- Chest pain = >20minutes
- Diaphoresis
- Pain radiates left arm — jaw
- Dyspnea
Not releived by nitroglycerine
Involvement in MI ?
- LV
- RV
- Both atria are spared
EKG changes in MI ?
- Initially = Subendocardial ischemia = ST depression
- Severe ischemia = Traansmural ischemia = ST elevation
Occlusion in MI ?
- Left ant descending artery = ant wall & ant septum of LV = 45%
- Right coronary artery = post wall & post septum & papillae muscle LV
- left circumflex artery = lateral wall of LV
Mmembrane damage fate in MI ?
Leakage of cardiac enzyme s= Marker of MI
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Hallmark of MI ?
Membrane damage
Cardiac marker in mI ?
- Troponin I
- CK-MB
Troponin I details time—
Rise 2-4 hr after infraction
peak = 24 hr
normal = 7-10 day
CK-MB????
Level rise =4-6 hr
peak = 24 hr
normal = 72 hr
creatinine kinase MB
Tx of MI ?
- Aspirine/Heparin = Limit thrombosis
- O2 = minimize ischemia
- Nitrates = vasodialtion
- Beta blocker = dec O2
- ACEi = dec LV dilation
- Fibrinolytic /angioplasty = open blocked vessels
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Reperfusion of irreversibly = C ainflux = Hypercontraction of myofibrills == Contraction band necrosis
in MI
Further damaging myocytes
after return of O2 + inflammatory cells create = Free radicles
Reperfusion injury
Which kind of necrosis in MI ?
Coagulative necrosis
Day 1 necrosis time ?
<4 hour = changes = No changes
Complications of MI ___+++
74 Whole CHART IN PATHOMA-
Coagulative necrosis features ?
- Pyknosis
- Kariokinesis’
- Kryptosis
3 feature of CN
Day1 —– Week 1 ?
Inflammation by Neutrophil + Macrophage
1-3 days heart condition ?
Fibrinous pericarditis
(Chest pain + Friction rub )
4-7 days infarction ?
Rupture of ventricular wall
-cardiac temponade
-papillary muscle rupture
-mitral insufficiency
-IV septum defect = Shunt
Granulation tissue with plump fibrosis blood vessels seen in ?
1-3 weeks
red border emerge
After months complications ?
- White scar
- Fibrosis
- Mural thrombus
- Dressler syndrome
Dressler syndrome?
AB against own pericardium
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Cause of sudden cardiac death ?
- Fatal ventricular arrhythmia
- Mitral valve prolapse
- Cardiomyopathy
- Cocaine abuse
Chronic ischemic heart disease progression ?
CHF
CHRONIC ischemic damage +/- ischemia = ????
CIHD
Irreversible cell injury typical sign ?
UWorld
Mitochondrial Vacuolization
UW
Leads of ST elevation and Q waves indication ??
Left circulflex artery = Lateral wall of LV = Infraction =
UW
I aVL
UW
Free wall rupture results in –
UW
- Cardiac temponade
- Hypotension
- Shock
- Cardiac arrest
Autpsy of MI ????
UW
Slitlike tear at the site of infarction in the LV wall
uW
Inferior wall lead in ECG ?
UW
II III aVF
Which chamber is relatively protected from MI ?
UW
RV
Devastating but uncommon complications of transmural MI ?
UWorld
LV free wall rupture
UW
Which factors protect RV from MI ?
UW
- Small muscle mass with high capacity to increase O2 extraction
- Perfusion throughout the cardiac cycle
- Heightened ischemic preconditioning
same shit revise»_space;»
UW
ST-elevation myocardial infarction involves transmural (full-thickness) infarction of the myocardial wall, and usually
results from acute atherosclerotic plaque rupture with the development of overlying thrombus that fully occludes the
coronary artery lumen. It classically presents with sudden-onset substernal chest pain that is not relieved by rest or
short-acting nitrates. ECG demonstrates ST elevation in the affected leads with subsequent development of Q waves.
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After the onset of severe ischemia leading to myocardial infarction (MI), early signs of coagulative necrosis do not
become apparent when ??
UWorld
Light microscopy untill 4 hours after the onset of MI
UWorld
cellular and
mitochondrial swelling that is observed histologically why ?
UW
=Ion pump failure
=ATP deficiency during ischemia
=Intracellular accumulation of Na & Ca
=Draw free water into the cell
=Cellular swelling
UWorld
Why papillary muscle rupture in MI ?
UW
Papillary muscle = Supplied solely by Pst Decending Artery
Its susceptible to ischemic rupture
How fibrosis after MI occur ??
UW
Transforming growth factor-Beta = Reduce inflmmation = Promote tissue remodelling = Fibroblast proliferation = collagen deposition
UWorld
Life threatening complication of MI that occurs 3-5 days after ??
UW
Papillary muscle rupture
