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M2 Cardiology > 14. Ischemic Heart Disease > Flashcards

14. Ischemic Heart Disease Flashcards

1
Q

Angina pectoris: what does it refer to?

A

chest pain experienced by most people during myocardial ischemia.

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2
Q

Does everyone with myocardial ischemia have angina?

A

no.

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3
Q

angina without coronary disease: what could be the cause?

A

ischemic heart disease due to something other than coronary artery narrowing. aortic stenosis, hypertrophic cardiomyopathy, HTN

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4
Q

define coronary disease

A

narrowing of the coronary arteries

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5
Q

define ischemic heart disease

A

one possible result from coronary disease.

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6
Q

coronary disease without angina

A

possible to not have chest pain with coronary disease if already ischemic: ischemic tissue can’t cause pain!

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7
Q

how much coronary artery obstruction do you have to have to cause myocardial ischemia?

A

> 75%.

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8
Q

silent myocardial ischemia: possible reason?

A

may be due to nerve fiber insensitivity, and is not uncommon in diabetics. may represent less severe ischemia but is dangerous bc patient doesn’t feel it.

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9
Q

how is the coronary circulation controlled?

A

autoregulation.

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10
Q

how does coronary autoregulation work?

A

inc in cardiac muscle activity leads to inc met activity, which leads to release of local metabolites, which dilate the coronary arteries.

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11
Q

what are the local metabolites that will dilate the coronary arteries as a result of met activity?

A

adenosine.

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12
Q

when does the majority of coronary perfusion take place?

A

during diastole, since the heart muscle is constricted during systole.

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13
Q

what is the most common cause of myocardial ischemia?

A

thrombosis. several hrs of ischemia may lead to infarction.

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14
Q

define ischemia

A

coronary flow becomes inadequate for the functional needs of the heart.

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15
Q

why is there a relatively large amt of ATP used in contraction of the heart?

A

large and numerous mitochondria

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16
Q

what consumes more energy: myocardial tension development, or myocardial fiber shortening?

A

tension development.

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17
Q

which is more vulnerable to ischemia, the subepicardium or the subendocardium?

A

subendocardium. because it is more interior and more subject to arterial compression with systole. also has to contract a greater % of total given the geometry of the heart.

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18
Q

what are the factors that decr 02 supply to the myocardium?

A

coronary atherosclerosis, coronary spasm, hypotension, hypoxia, anemia, tachycardia, LVH

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19
Q

atherosclerosis is seen as what kind of processes?

A

inflammatory

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20
Q

what is seen in the earliest lesions of atherosclerosis?

A

leukocytes, inflammatory markers (C reactive proteins).

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21
Q

what makes atherosclerotic plaques vulnerable

A

thinning of the fibrous cap that covers the lesions.

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22
Q

what happens when the cap on atherosclerotic plaques ruptures?

A

exposes tissue factor to bloodstream, yields further inflammation and thrombogenesis. net result can be enlargement of the plaque or occlusion of lumen.

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23
Q

Cardiac events: 3 things that define them/their progression

A
  1. early atherogenesis
  2. progression mediated by inflammation, promoted by risk factors
  3. acute thrombosis
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24
Q

describe the stages in progressive atherosclerosis

A
  • -fatty streak (endothelial dysfunction, plaque progression)
  • -fibrous plaque
  • -occlusive atherosclerotic plaque (may yield effort angina or claudication)
  • -rupture/fissure and thrombosis
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25
Q

describe fatty streaks

A

lipid accumulates in arterial intima in setting of normal risk factors

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26
Q

describe fibrous plaques

A

plaques enlarge under influence of risk factors and low level inf.

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27
Q

describe occlusive atherosclerotic plaque

A

lesions become large enough to cause significant luminal obstruction and symptoms (angina, claudication)

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28
Q

what is claudication?

A

muscle pain, ache, cramp, fatigue

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29
Q

describe the process of plaque rupture/fissure/thrombosis

A

plaque ruptures, leading to more acute conditions, unstable angina, infarct, sudden coronary death, stroke.

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30
Q

what is CRP?

A

c reactive protein – a marker of inflammation

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31
Q

CRP levels are higher in pts with acute coronary sx, or with stable angina?

A

acute coronary syndromes.

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32
Q

an unstable plaque will yield an EKG that has a Q wave or not?

A

no.

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33
Q

coronary thrombosis will yield an EKG that has a Q wave or not?

A

YES – Q wave infarct

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34
Q

what is typically the first real problem with a plaque?

A

a fissure of the fibrous cap overlying the plaque, which exposes the tissue to the bloodstream.

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35
Q

what happens after a fibrous cap fractures?

A

inflammatory response, that involves platelet activation and accumulation of vasoactive substances. this is the unstable plaque: –> unstable angina and myocardial infarction.

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36
Q

what happens with a coronary spasm?

A

another way for 02 supply to be decreased to myocardium. acute arterial spasm which can occlude a normal artery. usually transient

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37
Q

how does hypotension yield decr 02 supply to myocardium?

A

decr diastolic BP: decr coronary perfusion pressure. lower the pressure = lower coronary blood flow.

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38
Q

how does tachycardia yield decr 02 supply to myocardium?

A

absolute length of systole tends to be stable as HR increases, but diastole can be shortened. less time for diastolic coronary perfusion

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39
Q

how does LVH yield decr 02 supply to myocardium?

A

wall thickening means greater compressive forces, and a longer distance for blood to travel via intramural arteries to subendocardium

40
Q

what are the factors that increase myocardial 02 demand?

A
  1. tachycardia
  2. HTN
  3. increased preload
  4. increased inotropy
  5. LVH
41
Q

how does tachycardia increase myocardial 02 demand?

A

more contractions per minute means more 02 per minute. note tachycardia also decr 02 supply.

42
Q

how does HTN increase myocardial 02 demand?

A

increased systolic BP yields increased systolic wall tension –> costly in terms of 02 requirements.

43
Q

how does incr preload increase myocardial 02 demand?

A

preload = incr LV size. incr preload means that there is incr wall tension required by enlarged heart. remember Law of LaPlace: T = P x radius.

44
Q

how does incr inotropy increase myocardial 02 demand?

A

greater speed of contraction –> incr 02 demand

45
Q

how does LVH increase myocardial 02 demand?

A

incr myocardial mass requires greater blood supply

46
Q

what is the Double Product?

A

HR and BP (myo tension) are the most impt determinants of myocardial 02 demand. so the product of HR x systolic BP are a useful clinical parameter.

47
Q

what are 4 things that can result from myocardial ischemia?

A
  1. chest pain
  2. decr contractility
  3. myocardial infarction
  4. membrane changes
48
Q

What are 4 clinical effects of myocardial ischemia?

A
  1. chest pain
  2. LV dysfunction
  3. myocardial infarction/heart failure
  4. cardiac arrhythmia
49
Q

4 types of chest pain?

A
  1. typical/stable angina
  2. variant angina
  3. unstable angina
  4. acute myocardial infarction
50
Q

describe typical/stable angina

A

transient angina brought on my increase in myocardial 02 demand, with fixed coronary obstruction. usually due to exercise or anxiety (inc HR, inc BP). stable because brought on predictably by same amt of exercise.

51
Q

describe variant angina

A

transient angina at rest, due to decr in coronary blood flow. often due to coronary spasm. artery may be atherosclerotic, but may be normal.

52
Q

describe unstable angina

A

angina that changes in pattern, ie new onset, more frequently, with less exertion. usually due to plaque rupture.

53
Q

describe the angina associated with acute myocardial infarction

A

usually causes chest pain. initially, pain is same as variant angina. distinguishing feature = duration of pain.

54
Q

describe left ventricular dysfunction

A

transient ischemia can produce transient LV dysfunction, which is both systolic and diastolic.

55
Q

what is a myocardial infarction?

A

persistent ischemia leading to scarring –> persistent LV dysfunction. may be severe enough to yield heart failure. both systolic and diastolic failure.

56
Q

describe cardiac arrythmias

A

ischemia depolarizes myocardial cell membranes. produces ST-segment shifts on EKG and can also cause life-threatening arrhythmias.

57
Q

describe chronic coronary disease

A

one clinical syndrome in patients with coronary disease. fixed coronary obstruction, with or without prior infarction. may be asx, may have angina or other sx of heart failure. prognosis is good.

58
Q

describe acute coronary syndrome

A

usually the result of an acute lesion in a coronary plaque. can be: unstable angina, NSTEMI, or STEMI

59
Q

what is NSTEMI?

A

similar to unstable angina, but ischemia is severe enough to cause myocardial infarction. Not transmural (no ST elevation)

60
Q

what is STEMI?

A

coronary lesion is compounded by acute coronary thrombosis. leads to transmural ischemia and ST elevation, and a larger infarct.

61
Q

what is the most common cause of death in patients with coronary disease?

A

sudden cardiac death. arrhythmia leading to v-fib.

62
Q

character of typical angina: what is the description used by patients, and what is the gesture?

A

desc: various. gesture: Levine sign.

63
Q

typical angina location: where?

A

navel to nose. may radiate to jaw, arms

64
Q

typical angina: relation to activity?

A

most diagnostic feature of typical angina is its being brought on by exertion, relieved by rest.

65
Q

typical angina: duration?

A

relieved in minutes by rest and nitro.

66
Q

is pain lasting >30 min angina?

A

no

67
Q

3 features that can classifiy angina as typical?

A

chest discomfort is substernal. sx brought on by exertion, relieved within 30 min by rest or nitro

68
Q

physical findings during angina:

A

may have no sig abnormalities at baseline. but during attack, may have s4 gallop or murmur of mitral regurg.

69
Q

other, non-coronary causes, of chest pain

A

MSK, arthritis, pneumonia, pleurisy, valvular heart disease, pericarditis

70
Q

evidence of chronic LV dysfinction suggests what?

A

clue to previous infarction, contraindication to certain meds, or reason to consider surgery.

71
Q

what is the CASS registry?

A

table, showing probability of coronary artery disease based on age, sex, type of chest pain (definite/probable/non-angina)

72
Q

What are some diagnostic tests for coronary artery disease?

A

coronary arteriography, resting EKG, myocardial perfusion scan (Thallium scan)

73
Q

what are some problems with coronary arteriography?

A

used as the gold standard, but observer variability, underestimation of disease, artificial definition of “significant disease”, cost (5k), complications (1/1000)

74
Q

what on EKG is relatively specific for the diagnosis of infarction due to coronary disease?

A

pathological Q wave (at least 0.04 sec wide, 1/4th magnitude of R wave)

75
Q

what on EKG is relatively specific for the diagnosis of transmural ischemia due to coronary disease?

A

ST elevation.

76
Q

what on EKG is relatively specific for the diagnosis of subendocardial ischemia due to coronary disease?

A

ST depression. may also be seen in other circumstances (sensitive, but not specific).

77
Q

describe the myocardial perfusion scan/Thallium scan

A

IV injection of radioisotopes that are preferentially taken up by the myocardium. donut test. area of underperfused myocardium will fail to pick up the isotope.

78
Q

which is more specific for ischemia, the EKG or the Myocardial perfusion scan?

A

myocardial. (since ST depression is seen in other conditions as well)

79
Q

what information can come from a stress test?

A

ST segment shifts if concurrent EKG. exercise tolerance, HR response, BP response, exercise induced arrhythmias, symptoms, transient v fixed ischemia if compare Myocardial Perfusion Scan at rest w exercise.

80
Q

what is predicted max heart rate/how is it calculated?

A

MHR = 220-age

81
Q

when would a stress test be considered negative?

A

if HR reaches 90% MHR

82
Q

what is the predictive value of a diagnostic test?

A

the likelihood that a pt with a pos/negative test has/does not have the disease

83
Q

what does the predictive value of a test depend on?

A

the pre-test probability (the prob that the pt has a disease before the test results are known)

84
Q

when is stress testing most useful?

A

pts in whom the pre-test prob is intermediate. while stress test is helpful in diagnosis, may be even more helpful with prognosis

85
Q

what factors correlate with poor prognosis in pts with coronary disease?

A

severity of coronary dis
LV dysfunction
malignant ventricular ectopy
poor stress-test performance.

86
Q

what would define a poor stress test performance? an excellent?

A

Poor: inability to exceed 4 mets
Excellent: exceeds 10 mets

87
Q

what are 2 goals of treatment?

A

relieve symptoms, prolong life

88
Q

what are behavioral components of decreasing probability of coronary risk factors?

A

exercise
diet
smoking cessation
incr compliance with drugs

89
Q

what are 2 drugs that will lower risk factors of of coronary disease?

A

Anti-hypertensives

cholesterol lowering drugs (statins)

90
Q

what are general measures for patients with known CAD?

A 
risk factor modification
exercise conditioning
relaxation therapy
anticoags/antiplatelet
treat anemia/hypoxia
treat CHF if present
91
Q

what are some anti-anginal drugs?

A

nitrates
beta blockers
Ca channel blockers

92
Q

nitrates: MOA, effect on myocardium, side effects

A

vasodilation. lowers preload, decr myocardial 02 demand.

side effects: hypotension, headache

93
Q

beta blockers: MOA, effect on myocardium, side effects

A

reduce HR, BP. decr myocardial 02 demand.

side effects: heart failure, bradyarrhhthmias, fatigue, depression

94
Q

Ca channel blockers: MOA, effect on myocardium, side effects

A

incr myocardial 02 supply. (good for variant angina), some reduce HR, inotropy, BP (decr myocardial 02 demand)
side effects: headache, edema

95
Q

coronary bypass surgery (CABG): benefits and risks

A

benefits: relief of sx, prolongation of life
risks: immediate surg mortality, complications

96
Q

coronary angioplasty and stenting (PCI): benefits and risks

A

sx relief, prolongation of life,

risks: acute occlusion due to spasm, thrombosis or dissection; chance of re-stenosis may require repeat PCI.

97
Q

CABG shown to be most beneficial in what 2 groups?

A

pts with left main coronary disease

pts with 3 vessel disease and poor LV function

M2 Cardiology (32 decks)

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