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CRP- Cardiology > CAD and MI > Flashcards

CAD and MI Flashcards

1
Q

What is ischemic heart disease (IHD)?

A

group of syndromes related to myocardial ischemia; IHD is the leading cause of death in the U.S. This also results from reduced nutrient substrates and inadequate removal of metabolites.

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2
Q

What is myocardial ischemia?

A

imbalance between oxygen supply and demand

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3
Q

What is the most common cause of ischemia?

A

reduction of coronary blood flow from atherosclerotic CAD, occurring after decades of slow accumulation of atheromas.

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4
Q

What are the 4 types of Ischemic Heart Disease (IHD)?

A
  1. Angina= less severe (stable, Prinzmental, unstable)
  2. MI= most important
  3. Sudden Cardiac Death
  4. Chronic Ischemic Heart Disease= w/heart failure
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5
Q

Is there clinical heterogeneity of IHD?

A

YES: elderly that are asymptomatic with severe atherosclerosis to young people with minimal CAD presenting with acute MI or sudden death.

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6
Q

On what does clinical morphology of IHD depend?

A

plaque changes= erosion, ulceration, fissuring, rupture, hemorrhage, superimposed thrombus

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7
Q

Do pts with CAD typically have more than one affected vessel?

A

YES >90%. Slowly developing lesions can stimulate the development of collateral circulation protecting against ischemia.

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8
Q

What coronary arteries are most commonly affected with CAD?

A

LAD, LCX, RCA

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9
Q

What is stable angina?

A
  • chest pain that arises with exertion or emotional stress due to atherosclerosis of coronary arteries with >70% stenosis; decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion.
  • relieved by rest or nitroglycerin
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10
Q

What will an EKG show with stable and unstable angina?

A

ST-segment depression due to subendocardial ischemia.

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11
Q

What is unstable angina?

A
  • chest pain that occurs at rest, usually due to rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery.
  • high risk of progression to MI
  • relieved by nitroglycerin
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12
Q

What is Prinzmetal angina?

A
  • episodic chest pain unrelated to exertion, due to coronary artery VASOSPASM.
  • relieved by nitroglycerin or calcium channel blockers
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13
Q

What will an EKG show with Prinzmetal angina?

A

ST-segment elevation due to transmural ischemia.

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14
Q

What are some influences that can affect plaques?

A
  • intrinsic influences= plaque structure and composition itself
  • extrinsic influences= BP, platelet reactivity. Plaque often cannot withstand mechanical stresses.
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15
Q

What are vulnerable plaques?

A
  1. plaques with large areas of foam cells and extracellular lipid.
  2. fibrous cap plaques, which are thin or contain few smooth muscle cells or clusters of inflammatory cells.
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16
Q

What are some changes that can occur to plaques?

A
  • fissures= occur at junction of the fibrous cap and normal plaque free arterial segment where stresses are greatest.
  • collagen made by smooth muscle cells can be degraded by metalloproteinases made by macrophages.
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17
Q

What does inflammation do to plaques?

A

destabilizes it

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18
Q

What will adrenergic stimulation do to plaques?

A

stress plaque by hypertension and vasospasm.

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19
Q

Can a minimally occluded coronary artery result in occlusion with plaque change?

A

YES. (Textbook number says 75% occlusion to be clinically significant).

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20
Q

How does inflammation lead to CAD?

A

initial lesion needs interaction between endothelial cells and leukocytes. Endothelial cells will then release chemokines and increase their expression of adhesion proteins (ICAM, VCAM..). T cells produce cytokines that activate macrophage filled with oxidized LDL.

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21
Q

As what marker may c-reactive protein serve?

A

a potential marker of atherosclerosis, because it is a marker of inflammation in general.

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22
Q

Where does a coronary thrombus typically occur?

A

on a disrupted plaque, causing a previously anti-coagulant surface to become pro-coagulant. These may embolize.

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23
Q

Of what are thrombi potent activators?

A

growth related signals, promoting growth of atheromas :(

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24
Q

What is the role of vasoconstriction in CAD?

A

compresses lumen increasing mechanical forces that can disrupt the plaque, augmenting the issue.

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25
Q

What stimulates vasoconstriction?

A

adrenergic agents (ex. cocaine), released platelet contents, impaired secretion of NO by eNOS, mediators released from perivascular inflammatory cells

26
Q

Why is cocaine so bad?

A

it is an adrenergic agent that increases HR, BP and metabolic demand of the heart, but induces vasospasm, which decreases O2 supply to the heart causing severe stress on it. Additionally it is a pro-arrthymogenic agent causing arrhythmias.

27
Q

Where will an infarct occur if the LAD is occluded?

A

anterior wall of the LV

28
Q

Where will an infarct occur if the LCX is occluded?

A

left lateral wall of the LV

29
Q

Where will an infarct occur if the RCA or its posterior branch is occluded?

A

posterior wall of left ventricle

30
Q

If an infarct is not transmural, where is the first place ischemia will occur?

A

the place that is farthest from the blood supply, which is the subendocardium (innermost wall of the heart).

31
Q

What are the 3 different patterns of infarction?

A
  1. transmural= entire thickness of wall
  2. subendocardial= innermost portion
  3. multifocal= scattered infarcts throughout the heart
32
Q

What normally causes a transmural infarction?

A

a combination of chronic coronary artery atherosclerosis, acute plaque change, and superimposed thrombosis.

33
Q

What can cause a subendocardial infarction?

A

reduction in systemic blood flow (shock) superimposed on chronic coronary stenosis.

34
Q

What can cause multifocal infarctions?

A

micoembolization, vasculitis, vasospasm of smaller vessels and often due to endogenous catecholamines or drugs such as cocaine.

35
Q

What is a proximal infarct of the LAD (meaning closer to the aorta) called?

A

the widow maker

36
Q

What happens to ATP as ischemia progresses?

A

it reduces, obviously

37
Q

What are some important points that determine MI location, size, severity, and morphology?

A

size of vascular bed, duration of occlusion, O2 demands, extent of collateral vessels, presence of vasospasm, BP, HR, rhythm…

38
Q

** How does MI morphology change with specific time progressions following obstruction?

A

-

39
Q

Will damaged heart tissue be replaced by myocardial cells?

A

NO, it cannot be regenerated so it will be replaced by fibrosis (scar tissue).

40
Q

What happens to the remaining myocytes following a well healed infarction?

A

they hypertrophy to make up for the loss of other myocytes.

41
Q

What are the general complications of contractile dysfunction and arrhythmias due to MI?

A
  • contractile dysfunction: causing hypotension, vascular congestion, pulmonary edema, cardiogenic shock.
  • arrhythmias: causing conduction disturbances and myocardial irritability, sinus bradycardia, asystole (no cardiac electrical activity), heart block
42
Q

***What are the specific complications that can occur due to MI?

A
  • PAPILLARY MUSCLE DYSFUNCTION and rupture= 3 days post MI causing mitral regurgitation.
  • VENTRICULAR RUPTURE= 4-7 days post MI causing cardiac tamponade.
  • SEPTAL RUPTURE= acute ventricular septal defect with a left to right shunt.
  • MURAL THROMBI= due to abnormality in contractility and endocardial damage, producing prothrombotic surface, which can embolize.
  • ACUTRE PERICARDITIS= 1-3 days post MI due to inflammation.
  • VENTRICULAR ANEURYSMS= bulging of fibrous myocardium.
43
Q

What are some clinical features of MI?

A
  • substernal chest pain
  • radiation into the left arm, neck, jaw
  • silent MI in diabetics or those with hypertension
44
Q

What are the laboratory tests for MI detection?

A
  • creatine kinase MB (CK-MB)= dimer composed of isoforms M and B.
    MM= homodimer found mostly in cardiac and skeletal muscle.
    BB= homodimer found in brain, lung and other tissues
    MB= heterdimer found in CARDIAC TISSUE.
  • Troponin I= most sensitive and specific marker (gold standard).
45
Q

Is CK-MB a sensitive and specific test?

A

Sensitive yes, but NOT specific since it can be seen in some skeletal muscle injury as well.

46
Q

What happens to CK-MB with time?

A

begins to rise over 3-12 hours and peaks at 24 hours before returning to normal over 48-72 hours.

47
Q

What happens to troponin I levels with time?

A

rises within 3-12 hours, peaks between 12-48 hours and returns to normal over 5-14 days.

48
Q

What is spontaneous coronary artery dissection (SCAD)?

A

rare emergency condition that results due to separation of the arterial wall layers (usually between media and adventitia) leading to compression of the coronary artery lumen and thus ischemia, infarction, and possible death.

49
Q

What are the risk factors for spontaneous coronary artery dissection (SCAD)?

A

atherosclerosis, peripartum state (period shortly before, during, and immediately after giving birth) due to hormonal changes, connective tissue and autoimmune diseases, or may be idopathic (we don’t know).

50
Q

What will you see with postpartum SCAD?

A

eosinophilic infiltration in the adventitia, and their release of lytic enzymes such as collagenase, peroxidase, and acid phosphatase.

51
Q

What is chronic ischemic heart disease?

A

progressive CHF due to ischemic myocardial damage. Most cases involve prior myocardial infarcts or coronary artery interventions.

52
Q

What is sudden cardiac death?

A

unexpected death due to cardiac disease; occurs without symptoms or

53
Q

What is the most common etiology (cause) of sudden cardiac death?

A

acute ischemia. 90% of pts have preexisting severe atherosclerosis.

54
Q

What EKG associations are seen before sudden cardiac death?

A

prolonged QT (associated with variety of channelopathies).

55
Q

What is long QT syndrome?

A

results from prolonged ventricular repolarization and can be inherited or acquired following medications (anti-psychotic antiarrhythmics or allergy medications).
Symptoms present with rigorous physical exercise.

56
Q

Are males or females more likely to experience symptoms of long QT syndrome?

A

females

57
Q

What is Brugada syndrome?

A

inherited ion channelopathy (gene SCN5A) that causes unexplained sudden death commonly seen in middle-aged males of south-east Asia. EKG may reveal RBBB.

58
Q

What is catecholaminergic polymorphic ventricular tachycardia?

A

defective Ca++ channels associated with sudden unexplained death with exercise seen in Finnish and Italian families.

59
Q

What is short QT syndrome?

A

associated with sudden cardiac death and premature atrial fibrillation.

60
Q

*What is Commotio Cordis?

A

lethal disruption of heart rhythm due to sudden blunt impact to the precordial area causing abnormal cardiac ventricular activity (usually V-fib). More in kids (think baseball hitting them right in the chest).

61
Q

With what vulnerable time period does Commotio Cordis coincide?

A

vulnerable period of ventricular repolarization

CRP- Cardiology (49 decks)

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