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Cardio Exam 2 > Lec 22 Myocardial Infarction Path > Flashcards

Lec 22 Myocardial Infarction Path Flashcards

1
Q

What is ischemia?

A

injury from hypoxia induced by reduced blood flow

impaired inflow –> inadequate O2 and nutrients
impaired outflow –> insufficient removal of metabolites

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2
Q

Is ischemia reversible or irreversible?

A

depends on duration

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3
Q

What is major cause of myocardial ischemia?

A

reduced blood flow due to obstructive atherosclerotic coronary artery disease [CAD]?

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4
Q

What is MI?

A

irreversible muscle damage due to prolonged severe ischemia

= discrete focus of ischemic muscle necrosis

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5
Q

What part of heart is affected by left coronary artery LAD branch block?

A

anterior part of IV septum and anterior wall of LV

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6
Q

What part of heart is affected by right coronary artery block?

A

posterior part of IV septum and posterior wall of LV and right ventricle

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7
Q

What part of heart of affected by left coronary artery circumflex branch block?

A

lateral wall of lateral ventricle

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8
Q

What is most common site of infarcts?

A

LAD branch of left coronary artery

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9
Q

What is a transmural infarct?

A

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

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10
Q

What are some possible complications specific to transmural infarct?

A

pericarditis or ventricular wall rupture since it extends full thickness of wall

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11
Q

What is a subendocardial infarct?

A
  • ischemia limited to inner 1/3 or 1/2 of ventricular wall
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12
Q

What causes a regional subendocardial infarct?

A

transient obstruction of coronary artery
occurs in zone of perfusion of the artery
relieved before necrosis extends across the full thickness

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13
Q

What causes a circumferential subendocardial infarct?

A

something systemic = prolonged severe hypotension [shock]

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14
Q

What causes multifocal microinfarction?

A

due to pathology involving only smaller intramural vessels

  • due to microembolization
  • vasculitis
  • vascular spasm 2ndary to adrenaline, drugs, cocaine, etc
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15
Q

What is outcome of multifocal microinfarction?

A

either sudden cardiac death due to fatal arrhythmia or ischemic dilated cardiomyopathy

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16
Q

What happens to cells during early myocardial ischemia?

A

= 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
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17
Q

What happens to cells during late myocardial ischemia?

A

= non-reversible

  • disruptions in sarcolemma after 20 min of severe ischemia
  • intracellular molec leak out into blood
  • amorphous densities form in mitochondria
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18
Q

What happens to ATP and lactate levels in ischemic myocardium?

A
  • ATP drops and lactate rises in initial minutes of infarct and keep dropping/rising
19
Q

How long does it take after onset of infarct for myocardium to become non-functional/viable?

A

6-12 hours

20
Q

When does myocardium start to lose contractility in myocardial ischemia?

A

within 2 min

21
Q

How long for ATP to reduce to 50% of normal?

22
Q

How long after myocardial infarct does it take to see changes in heart on gross exam?

A

12 hours

–> in some pts with good coronary arterial collateral system due to chronic ischemia –> slower progression of necrosis

23
Q

What features do you see grossly 0-4 hours after MI?

24
Q

What features do you see grossly 4-12 hours after MI?

A

may see dark mottling due to stagnated trapped blood

25
What features do you see grossly 12-24 hours after MI?
see dark mottling due to stagnated trapped blood
26
What features do you see grossly 3-14 days after MI?
central yellow/brown softening | hyperemic border = granulation tissue at margins
27
What features do you see grossly > 2 mo after MI?
recanalized artery | gray/white scar
28
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
29
When do you start to see macrophages post MI?
starts ~ day 3; continues through day 14
30
When do you start to see neutrophils pos MI?
start around 12 hrs and most prominent days 1-3
31
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
32
What happens if ventricular free wall rupture?
get cardiac tamponade
33
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
34
What happens if rupture papillary muscle?
acute onset severe mitral regurgitation
35
What is an LV pseudoaneurysm?
happens at 3-14 days post MI | mural thrombus plugs hole wall in myocardium = time bomb
36
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
37
What causes pericarditis 1-3 days post MI?
= fibrinous pericarditis | - due to underlying inflammation extending to epicardium in transmural MI
38
What causes delayed pericarditis after MI?
dressler syndrome = autoimmune reactions | wks to mos post MI
39
What risks associated with large transmural MIs?
- cardiogenic shock - arrhythmias - late CHF
40
What risks associated with anterior transmural MI?
- rupture - expansion - mural thrombi - aneurysm
41
What risks associated with posterior transmural MI?
- conduction blocks | - RV involvement
42
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
43
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

Cardio Exam 2 (19 decks)

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