Ischemic Heart Disease/Myocardial Infarction Flashcards

1
Q

Ischemic heart disease can lead to what common manifestations?

A

angina
MI
Sudden Cardiac death
chronic ischemic heart dz/CHF

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2
Q

Patient presents with retrosternal chest pain when he exerts himself. What changes are expected on EKG?

A

ST segment DEPRESSION

stable+unstable angina = st depression

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3
Q

ST depression on EKG most commonly is from what type of ischemia?

A

subendocardial ischemia

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4
Q

Explain why subendocardial ischemia always presents first.

A

blood enters the epicardium, then myocardium, then endocardium

the myocardium is most metabolically active, so the area at the end of the myocardium (aka the endocardium) is where the oxygen is lowest

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5
Q

Subendocardial ischemia = what on EKG?

A

ST depression

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6
Q

If all 3 layers of the heart are ischemic, what will you expect to see on EKG?

A

ST elevation (transmural ischemia)

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7
Q

Pt presents to ER with severe resting retrosternal, jaw, and arm pain. EKG shows ST depression. Dx?

A

unstable angina

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8
Q

What is the biggest cause of unstable angina?

A

ruptured atherosclerotic plaque (exposed subendothelial collagen, forms a clot)

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9
Q

What is the vascular difference between an MI and unstable angina?

A

MI: total occlusion of artery
UA: partial occlusion

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10
Q

If a patient has a spastic coronary artery, what EKG changes are expected?

A

ST elevation (opposite to other 2 anginas)

Prinzemetal Angina

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11
Q

The injury to myocytes from angina is _________, for which the characteristic histologic finding is ________

A

reversible

cellular swelling

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12
Q

The pharmacologic tx for angina primarily does what to the vessels and heart?

A

Nitroglycerin

dilates VEINS mostly (arteries too @ hi dose)
reduces PRELOAD

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13
Q

The characteristic pathologic hallmark in a myocardial infarction is ________ of myocytes

A

necrosis/death

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14
Q

Rattle off the top 3 arteries for MI, and their distribution in the LV.

A

1: L anterior descending (ant wall+antseptal)

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15
Q

The most specific marker for MI is?

A

Troponin I

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16
Q

Pt presents with multiple reinfarctions after an acute MI. What marker would be most useful in this patient?

A

CK-MB

creatine kinase

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17
Q

What cardiac marker drops earliest post-MI?

A

creatine kinase

hence why its bettter than troponin I for dx reinfarction

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18
Q

What cardiac marker drops earliest post-MI?

A

creatine kinase

hence why its bettter than troponin I for dx reinfarction

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19
Q

What cardiac marker drops earliest post-MI?

A

creatine kinase

hence why its bettter than troponin I for dx reinfarction

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20
Q

Tx post-MI includes?

A

ASA/heparin
O2, nitrates, B-blockers, ACE-I
maybe fibrinolysis

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21
Q

Damage to myocytes post-MI via a Reperfusion injury is due to what molecules?

A

Free Radicals

reintroduction of blood brings in tons of O2, which gets converted to free radicals = more myocyte dmg

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22
Q

What artery is suspect with Q waves seen on leads V1-4?

A

LAD (#1)

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23
Q

What artery is suspect with Q waves seen on leads V4-6, I, and aVL?

A

L circumflex (#3)

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24
Q

What artery is suspect if leads II, III, and aVF show Q waves?

A

R coronary artery (#2)

25
Q

What artery is suspect with Q waves seen on leads V4-6, I, and aVL?

A

L circumflex

26
Q

Hours 0-4 after an MI, what changes are seen?

A

NONE

@ risk for arrhythmia/shock/CHF though

27
Q

State the 4 BASIC phases of an MI.

A

Ischemia
Coagulative Necrosis
Inflammation
Healing

28
Q

Hours 0-4 after an MI, what changes are seen?

A

NONE

@ risk for arrhythmia/shock/CHF though

29
Q

The phase of coagulative necrosis is primarily during what time?

A

FIRST DAY

lasts longer, but other changes happen

30
Q

The inflammatory phase is primarily during what time?

A

Day 2 until 1 week

31
Q

A heart on gross exam looks really DARK and mottled. How many days post-MI was the heart?

A

~1 day (darkness from release of necrotic cell contents)

32
Q

After day 1, what cell type first shows up?

A

Neutrophils (duh)

33
Q

A heart on gross exam looks really DARK and mottled. How many days post-MI was the heart?

A

~1 day (darkness from release of necrotic cell contents)

34
Q

After day 1, what cell type first shows up?

A

Neutrophils (duh)

35
Q

What general phase post-MI correlates with a YELLOW gross appearance?

A

inflammatory phase (after day 1, until 1 week)

36
Q

What is a risk caused by the early inflammatory response?

A

Fibrinous pericarditis

37
Q

A patient presents 2 days after an MI. He feels SHARP pains in his chest that get worse with inspiration and change with position. He also has a friction rub on auscultation. What is the mechanism of his pain?

A

NEUTROPHILS infiltrated the pericardium

=Fibrinous pericarditis

38
Q

Fibrinous pericarditis is associated with an infarct of what depth?

A

Transmural ONLY

subendocardial will not have neutrophils in the pericardium

39
Q

Neutrophils are replaced by what type of cell by the end of week 1?

A

macrophages

40
Q

Once macrophages show up, what characteristic tissue begins to be laid down?

A

Granulation tissue

41
Q

Granulation tissue is characterized by what triad?

A

fibroblasts
collagen
blood vessels

42
Q

The type of collagen present on day 8 post-MI is found where else in the body?

A

type III collagen

skin, bv, uterus, fetal tissue

43
Q

What genetic syndrome is a defect in the type of collagen found in granulation tissue?

A

Ehlers-Danlos syndrome (type III)

44
Q

As macrophages show up, what is a major risk to a post-MI patient?

A

RUPTURE of heart structure

45
Q

What characteristic gross finding is due to laying down of granulation tissue?

A

hyperemic border (new bv make a red ring)

46
Q

Patient presents 10 days post-MI. He has JVD, distant heart sounds, and is hypotensive. What type of cell is to blame for his findings?

A

Macrophages

they cause RUPTURE; here its a free wall rupture leading to cardiac tamponade

47
Q

Patient presents 10 days post-MI with an new finding: an early systolic decrescedo murmur. He has a high left atrial pressure. What type of cell is to blame for his new findings?

A

Macrophages

they cause RUPTURE; here its a papillary muscle rupture, causing mitral insufficiency

48
Q

Patient presents 10 days post-MI with an new finding: an early systolic decrescedo murmur. He has a high left atrial pressure. What artery was most likely occluded?

A

Right coronary artery

RCA supplies blood to the papillary muscle attached to the mitral valve, which is regurgitating by his signs

49
Q

When does a permanent scar begin to form after an MI?

A

1 month

50
Q

The formation of a scar characteristically is replacement of what?

A

type III collagen replaced by type I collegen

51
Q

A genetic defect of the collagen type found in a scar is called what?

A

Osteogenesis imperfecta (BBD: fx, blue sclera, hearing loss)

52
Q

The area of MI beigns to look _________ after a month

A

grey (scar forming)

53
Q

Sudden cardiac death is characterized by what?

A

death within 1 hr of onset of symptoms

54
Q

What is the most common cause of sudden cardiac death?

A

ventricular arrhythmia

55
Q

Chronic progressive ischemic heart disease is a ________ disease that results in ________

A

progressive

CHF

56
Q

What 2 big risks are present >1 month after an MI?

A

ventricular aneurysm/mural thrombus

Dressler syndrome

57
Q

A patient presents 1 month after an MI. He feels SHARP pains in his chest that get worse with inspiration and change with position. He also has a friction rub on auscultation. What is the mechanism of his pain?

A

autoimmune attack on the pericardium

aka Dressler syndrome; exposed areas of pericardium stimulate immune response

58
Q

Fibrinous pericarditis is a post-MI risk seen at what times?

A

few days after MI (due to neutrophils)

> 1 month after MI (due to autoimmune attack)