Lec 22 Myocardial Infarction Path Flashcards
What is ischemia?
injury from hypoxia induced by reduced blood flow
impaired inflow –> inadequate O2 and nutrients
impaired outflow –> insufficient removal of metabolites
Is ischemia reversible or irreversible?
depends on duration
What is major cause of myocardial ischemia?
reduced blood flow due to obstructive atherosclerotic coronary artery disease [CAD]?
What is MI?
irreversible muscle damage due to prolonged severe ischemia
= discrete focus of ischemic muscle necrosis
What part of heart is affected by left coronary artery LAD branch block?
anterior part of IV septum and anterior wall of LV
What part of heart is affected by right coronary artery block?
posterior part of IV septum and posterior wall of LV and right ventricle
What part of heart of affected by left coronary artery circumflex branch block?
lateral wall of lateral ventricle
What is most common site of infarcts?
LAD branch of left coronary artery
What is a transmural infarct?
ischemic necrosis involving full thickness of ventricular wall
occurs in the distribution of a single coronary artery
occurs as a consequence of acute plaque change and suberimposed thrombosis w/ sustained obstruction
What are some possible complications specific to transmural infarct?
pericarditis or ventricular wall rupture since it extends full thickness of wall
What is a subendocardial infarct?
- ischemia limited to inner 1/3 or 1/2 of ventricular wall
What causes a regional subendocardial infarct?
transient obstruction of coronary artery
occurs in zone of perfusion of the artery
relieved before necrosis extends across the full thickness
What causes a circumferential subendocardial infarct?
something systemic = prolonged severe hypotension [shock]
What causes multifocal microinfarction?
due to pathology involving only smaller intramural vessels
- due to microembolization
- vasculitis
- vascular spasm 2ndary to adrenaline, drugs, cocaine, etc
What is outcome of multifocal microinfarction?
either sudden cardiac death due to fatal arrhythmia or ischemic dilated cardiomyopathy
What happens to cells during early myocardial ischemia?
= potentially reversible
- cells switch aerobic to anaerobic met
- decreased ATP –> failure of Na-K pump –> influx Na and H2O
- accumulation lactate
- glycogen depletion
- mild cell and mitochondria swelling
What happens to cells during late myocardial ischemia?
= non-reversible
- disruptions in sarcolemma after 20 min of severe ischemia
- intracellular molec leak out into blood
- amorphous densities form in mitochondria
What happens to ATP and lactate levels in ischemic myocardium?
- ATP drops and lactate rises in initial minutes of infarct and keep dropping/rising
How long does it take after onset of infarct for myocardium to become non-functional/viable?
6-12 hours
When does myocardium start to lose contractility in myocardial ischemia?
within 2 min
How long for ATP to reduce to 50% of normal?
10 min
How long after myocardial infarct does it take to see changes in heart on gross exam?
12 hours
–> in some pts with good coronary arterial collateral system due to chronic ischemia –> slower progression of necrosis
What features do you see grossly 0-4 hours after MI?
nothing
What features do you see grossly 4-12 hours after MI?
may see dark mottling due to stagnated trapped blood
What features do you see grossly 12-24 hours after MI?
see dark mottling due to stagnated trapped blood
What features do you see grossly 3-14 days after MI?
central yellow/brown softening
hyperemic border = granulation tissue at margins
What features do you see grossly > 2 mo after MI?
recanalized artery
gray/white scar
When does granulation tissue begin? What does it look like grossly?
by end of 1st week
appears as hypermic rim around yellow infarct; gradually progresses toward center of infarct by 2 wks
When do you start to see macrophages post MI?
starts ~ day 3; continues through day 14
When do you start to see neutrophils pos MI?
start around 12 hrs and most prominent days 1-3
What is myocardial rupture? Which part most commonly ruptures?
due to softened/weakened necrotic myocardium
most common = rupture of ventricular free wall w/ cardiac tamponade 2-4 days post MI when coagulative necrosis have weakened the walls
less common = IV septum rupture
least common = papillary muscle rupture
What happens if ventricular free wall rupture?
get cardiac tamponade
What happens if rupture IV septum?
acute ventricular septal defect –> get L to R shunt
can quickly lead to rapid combined ventricular failure and death
What happens if rupture papillary muscle?
acute onset severe mitral regurgitation
What is an LV pseudoaneurysm?
happens at 3-14 days post MI
mural thrombus plugs hole wall in myocardium = time bomb
What are some possible effects of true ventricular aneurysm?
- can have mitral valve shortening b/c of fibrosis –> incompetent valves
- can have stasis of blood –> mural thrombus
What causes pericarditis 1-3 days post MI?
= fibrinous pericarditis
- due to underlying inflammation extending to epicardium in transmural MI
What causes delayed pericarditis after MI?
dressler syndrome = autoimmune reactions
wks to mos post MI
What risks associated with large transmural MIs?
- cardiogenic shock
- arrhythmias
- late CHF
What risks associated with anterior transmural MI?
- rupture
- expansion
- mural thrombi
- aneurysm
What risks associated with posterior transmural MI?
- conduction blocks
- RV involvement
What are the 4 mech of reperfusion injury?
- oxidative stress from reoxygenation due to reactive O and N species
- intracellular Ca overload
- inflammation b/c with perfusion comes more neutrophils
- complement system activation
What are 2 common pathologic findings in reperfusion injury?
hemorrhage = b/c leakage from injured ischemic vessels
contraction bands = flooding new plasma Ca into leaky/damaged cell membranes get exagerated contraction of sarcomeres
