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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?

A

10 min

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?

A

nothing

24
Q

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

A

may see dark mottling due to stagnated trapped blood

25
Q

What features do you see grossly 12-24 hours after MI?

A

see dark mottling due to stagnated trapped blood

26
Q

What features do you see grossly 3-14 days after MI?

A

central yellow/brown softening

hyperemic border = granulation tissue at margins

27
Q

What features do you see grossly > 2 mo after MI?

A

recanalized artery

gray/white scar

28
Q

When does granulation tissue begin? What does it look like grossly?

A

by end of 1st week

appears as hypermic rim around yellow infarct; gradually progresses toward center of infarct by 2 wks

29
Q

When do you start to see macrophages post MI?

A

starts ~ day 3; continues through day 14

30
Q

When do you start to see neutrophils pos MI?

A

start around 12 hrs and most prominent days 1-3

31
Q

What is myocardial rupture? Which part most commonly ruptures?

A

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
Q

What happens if ventricular free wall rupture?

A

get cardiac tamponade

33
Q

What happens if rupture IV septum?

A

acute ventricular septal defect –> get L to R shunt

can quickly lead to rapid combined ventricular failure and death

34
Q

What happens if rupture papillary muscle?

A

acute onset severe mitral regurgitation

35
Q

What is an LV pseudoaneurysm?

A

happens at 3-14 days post MI

mural thrombus plugs hole wall in myocardium = time bomb

36
Q

What are some possible effects of true ventricular aneurysm?

A
  • can have mitral valve shortening b/c of fibrosis –> incompetent valves
  • can have stasis of blood –> mural thrombus
37
Q

What causes pericarditis 1-3 days post MI?

A

= fibrinous pericarditis

- due to underlying inflammation extending to epicardium in transmural MI

38
Q

What causes delayed pericarditis after MI?

A

dressler syndrome = autoimmune reactions

wks to mos post MI

39
Q

What risks associated with large transmural MIs?

A
  • cardiogenic shock
  • arrhythmias
  • late CHF
40
Q

What risks associated with anterior transmural MI?

A
  • rupture
  • expansion
  • mural thrombi
  • aneurysm
41
Q

What risks associated with posterior transmural MI?

A
  • conduction blocks

- RV involvement

42
Q

What are the 4 mech of reperfusion injury?

A
  • 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
Q

What are 2 common pathologic findings in reperfusion injury?

A

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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