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CEP > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

Cardiovascular disease (CVD) includes

A
  • coronary heart disease
  • heart failure
  • hypertension
  • stroke
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2
Q

What is the leading cause of death in the United States?

A

CVD

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3
Q

Approximately 50% of all CVD deaths are from

A

CHD

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4
Q

Every 42 seconds in the US

A

someone suffers a heart attack

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5
Q

Avg age of first MI for men

A

65

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6
Q

Avg age of first MI for women

A

72

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7
Q

Why is the age of MI later for women than for men?

A

estrogen is cardioprotective and women have more estrogen

added benefits of protection only lasts until menopause when estrogen starts to plummet

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8
Q

Acute coronary syndromes include

A
  1. Unstable angina pectoris
  2. Acute myocardial infarction
  3. Potentially sudden cardiac death
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9
Q

Unstable angina pectoris (chest pain) is the result of

A

ischemia (decreased blood flow/oxygen)

random, no rhyme or reason, occurs at rest or with exertion. more dangerous

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10
Q

Acute MI

A

death of cardiac muscle cells due to prolonged ischemia

tissue undergoes necrosis. cannot be regenerated

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11
Q

Endothelium protects against…

A

innermost layer of artery

atherothrombosis

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12
Q

Intima

A

thin layer of connective tissue on top of endothelium

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13
Q

What is the formation site of atherosclerotic lesions?

A

intima

they don’t form at endothelium

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14
Q

Media

A

located on top of intima; contains mainly smooth muscle cells along with some connective tissue

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15
Q

Adventitia

A

outermost layer;
contains connective tissue, fibroblasts, and a few smooth muscle cells

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16
Q

Lumen

A

opening of the vessel

17
Q

What happens when the endothelium gets damaged?

A

endothelium is very thin, when it gets damaged, the layer is wiped away from the inner part of the vessel. What is left remaining is the intima. When intima is exposed, cells catch on and plaque starts to form

18
Q

Atherogenesis

A

formation of plaque

19
Q

Atherogenesis:

Endothelial injury

A

everyone has endothelial injury, but for most it is not chronic or excessive

Chronic or excessive injury

20
Q

Atherogenesis:

Inflammatory response

A

after endothelial injury

immune response leads to inflammation

  • product of chronic injury
  • platelet formation into a cluster
  • monocyte (immune cell) accumulation
  • LDL-C accumulation (LDL-C platelet response for patching)

these build up on top of one another

21
Q

Atherogenesis:

Endothelial dysfunction

A
  • product of chronic injury
  • increased adhesiveness of platelets and monocytes to artery wall
  • increased permeability to lipoproteins in the blood
  • impaired vasodilation/ increased vasospasm

lose ability to contract and expand… location of injury cannot function like normal vessel

22
Q

Atherogenesis:

Plaque formation

A
  • growth factors from platelets exacerbate growth and proliferation of plaque
  • lesion progresses from intima to other layers and leads to eventual narrowing of lumen
  • firm, pale gray plaque with a fibrous cap
  • cap breaks off and leads to free-floating inflammation… can lead to a stroke
23
Q

Progression of atherogenesis

A

smaller plaques = less stable and more likely to break off

newer formations = less stable

24
Q

Plaque rupture or fissuring of the fibrous cap is a risk for

A

embolus

25
Q

2/3 of individuals with ACS have a high risk for

A

vulnerable atherosclerotic lesions

26
Q

Rupture-prone lesions are ____ before becoming disrupted

A

<50% occlusive

27
Q

Blood draw for ACS

A

cardiac troponin
2nd draw 3-6 hours later, if MI, then significantly lower

most accurate measure of a heart attack

28
Q

Echocardiogram

A

identify area of heart damage

29
Q

chest x ray

A

heart size, pulmonary edema

30
Q

Electrocardiogram

A

ST elevation (STEMI), nonspecific t-wave abnormalities

31
Q

Diagnosis of acute myocardial infarction

A

at least 2 of the following
- chest pain for more than 30 min
- ECG showing ST segment or T-wave changes
- Presence of biomarker of myocyte necrosis

32
Q

classification of myocardial infarction in regards to prognosis

A

ST-segment elevation (STEMI)

Non ST-segment elevation (NSTEMI)

33
Q

ST-segment elevation (STEMI)

A

occluded coronary artery

extensive damage and worse prognosis

34
Q

Non-ST-segment elevation (NSTEMI)

A

less damage (typically due to clot dissolution)

better prognosis

35
Q

Nitroglycerin

A

slows down the onset of heart attack. systemic vasodilator

try to restore blood flow first intervention

36
Q

beta blocker

A

slows HR/BP by inhibiting epinephrine

37
Q

ACE-inhibitor

A

slow BP by dilating vessels

38
Q

Antiplatelet therapy/ anticoagulants

A

decrease amount of plaque formed. blood thinner

39
Q

Factors associated with poor ACS prognosis

A

LVEF less than or equal to 35% or congestive heart failure

poor exercise capacity, <5 METS

Evidence of extensive myocardial ischemia during exercise or pharmacologic stress testing

Complications such as renal failure, stroke

CEP (2 decks)

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