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Pathophys II MHM - Exam 1 > Cardiac Module 5 > Flashcards

Cardiac Module 5 Flashcards

1
Q

Describe myocardial ischemia

A
  • Myocardial cells become oxygen deprived
  • Results in loss of contractility, conduction changes, lactic acid accumulation
  • If flow is NOT restored, infarction occurs
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2
Q

MC cause of myocardial ischemia?

A

Atherosclerosis in the form of CAD

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3
Q

Stable angina

A
  • Transient episode of blood flow impairment
  • Recurrent episodes lasting 3-5 mins
  • Relieved with rest
  • Classic symptom = angina pectoris
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4
Q

Angina pectoris

A

Substernal chest discomfort (heaviness, pressure, pain)

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5
Q

Silent angina

A
  • Ischemia that does not cause obvious signs/symps

- Common following conditions/surgical procedures (transplant, CABG, emotional stress, etc)

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6
Q

Acute coronary syndromes include:

A
  • Unstable angina

- MI

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7
Q

Unstable angina

A
  • Thrombus breaks up before cell death, allows for reperfusion
  • “Reversible” ischemia (no cell damage)
  • 20% will have MI or death from MI within 30 days
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8
Q

MI

A
  • Thrombus occludes blood flow causing irreversible necrosis/cell death
  • Damaged cells release “markers”
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9
Q

Changes immediately to 10-20 minutes after acute MI

A
  • Loss of contractility (hypokinesis)
  • Dysrhythmia (EKG changes w/in 30-60 secs)
  • Lactic acid accumulation
  • Increased catecholamine release
  • AT II release
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10
Q

Why does lactic acid accumulation occur during an MI?

A

After 6-10 secs, anaerobic metabolism takes over (producing lactic acid) for survival until blood flow is restored

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11
Q

When does hyperglycemia occur in relation to an MI?

A

72 hours s/p MI

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12
Q

What occurs within 15-30 minutes after MI?

A

Process of necrosis (cell death) begins

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13
Q

Where does myocardial necrosis begin within the tissue?

A

Usually in sub-endothelium

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14
Q

When are cellular/histological changes of necrosis visible?

A

Not until 6 hours after

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15
Q

What occurs 3-6 hours post MI?

A

Necrosis expands “outward” toward epicardium

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16
Q

What is a transmural infarct?

A

Infarct affects the complete thickness of ventricular wall

17
Q

What is the basis for classifying a STEMI?

A

Transmural infarct

18
Q

What occurs 6-12 hours after MI?

A
  • Degree of cell damage becomes increasingly irreversible

- Biomarkers begin to be released into bloodstream (myoglobin, troponin T and I, CK-MB)

19
Q

What are the biomarkers for MI?

A
  • Myoglobin
  • Troponin T and I
  • CK-MB
20
Q

What is the biomarker of choice to assess MI?

A
  • Troponins

- Best predictor

21
Q

Myoglobin

A
  • Very early marker of MI

- Rises within 2 hours

22
Q

Troponins T and I

A
  • Marker of choice for MI
  • Rises within 3 hours, peaks at 18-48 hours depending on MI size
  • Best predictor
23
Q

CK-MB

A
  • Used to be marker of choice prior to troponins

- May begin to rise within 3 hours, peak 18-24 hours

24
Q

What occurs 3-4 days after MI?

A
  • Soft scar formation

* At risk of fatal rupture during first 1-2 weeks! Accounts for 10% of MI mortality

25
Q

What occurs 2-3 months after MI?

A

Mature scar formation

*Dilation and hypertrophy may result

26
Q

Myocardial stunning

A
  • Cell unable to contract after reperfusion
  • Occurs even though the cell hasn’t suffered irreversible damage
  • Transient (may last hours to days)
27
Q

Hibernating myocardium

A
  • Contractile function is reduced in a “healthy” myocardial cell that is experiencing ischemia
  • Returns to normal after perfusion is restored
28
Q

Ischemic preconditioning

A

Myocardial cell adapts to brief episodes of ischemia by increasing “tolerance” to infarction

29
Q

Reperfusion injury

A
  • May occur after a hypoxic area is re-perfused

- Reintro of blood flow may create excess oxygen free radical production leading to inflammation cascade

30
Q

What does a reperfusion injury contribute to?

A

“Final” size of infarct (area of permanent damage)

31
Q

4 stages of plaque development

A
  1. Endothelial injury
  2. Fatty streaks
  3. Fibrous plaque formation
  4. Complicated/unstable plaques
32
Q

What is the earliest gross pathological lesion in atherosclerosis?

A

Fatty streaks (full of LDL)

33
Q

What makes a plaque “complicated”?

A

If it ruptured

34
Q

What is prinzmetal angina?

A
  • Coronary spasm

- A cause of myocardial ischemia

35
Q

What are the acute coronary syndromes (ACS)?

A

Unstable angina

Myocardial infarction

36
Q

What are the clinical manifestations of myocardial ischemia?

A

Stable angina

Silent angina

Pathophys II MHM - Exam 1 (9 decks)

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