Cardio: Ischemic Heart Disease and MI Flashcards

1
Q
  • Secondary to atherosclerosis; exertional chest pain in classic distribution
  • Usually w/ ST depression on ECG
  • Resolves w/ rest
A

Stable Angina

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2
Q
  • Occurs at rest, secondary to Coranary artery spasm
  • Transient ST elevation
  • A/w tobacco, cocaine, and triptans
  • Treat w/ Ca2+ channel blockers, Nitrates, and Smoking cessation
A

Variant Angina (Prinzmetal)

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3
Q
  • Thrombosis with incomplete coronary artery occlusion
  • ST depression
  • Increasing frequency and intensity of chest pain
A

Unstable Angina

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4
Q
  • Distal to Coronary stenosis, vessels are maximally dilated at baseline
  • Administration of vasodilators (dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas
    → ↓ flow and ischemia in the poststenotic region
  • Principle behind pharmacologic stress tests
A

Coronary Steal Syndrome

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5
Q
  • Most often Acute Thrombosis due to Coronary Artery Atherosclerosis w/ complete occlusion of Coronary Artery and Myocyte necrosis
  • Cardiac biomarkers are diagnostic
  • Transmural, ECG will show ST elevations
  • Subendocardial, ECG will show ST depression
A

Myocardial Infarction

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6
Q

Evolution of MI: 0 - 4 hr

A
  • Gross: None
  • Microscope: None
  • Complications:
    • Arrhythmia, HF, Cardiogenic shock, Death
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7
Q

Evolution of MI: 4 - 12 hr

A
  • Gross:
    • Occluded artery → Dark mottling w/ tetrazolium stain
  • Microscope:
    • Early coagulative necrosis, release of necrotic cell contents into blood; edema, hemorrhage, wavy fibers
  • Complications:
    • Arrhythmia, HF, Cardiogenic shock, Death
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8
Q

Evolution of MI: 12 - 24 hr

A
  • Gross: Occluded Coronary Artery
  • Microscope:
    • Neutrophil migration starts
    • Reperfusion injury may cause contraction bands due to free radical damage
  • Complications:
    • Arrhythmia, HF, Cardiogenic shock, Death
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9
Q

Evolution of MI: 1 - 3 days

A
  • Gross: Hyperemia
  • Microscope:
    • Extensive Coagulative necrosis
    • Tissue surrounding infarct shows acute inflammation w/ Neutrophils
  • Complications: Fibrinous pericarditis
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10
Q

Evolution of MI: 3 - 14 days

A
  • Gross:
    • Hyperemic border; central yellow-brown softening - maximally yellow and soft by 10 days
  • Microscope:
    • Macrophages, then granulation tissue at margins
  • Compications:
    • Free wall rupture → tamponade; papillary muscle rupture → Mitral regurgitation; interventricular septal rupture due to macrophage-mediated structural degradation
    • LV Pseudoaneurysm (Mural thrombus “plugs” hole in myocardium → “time bomb”
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11
Q

Evolution of MI: 2 weeks to several months

A
  • Gross: Recanalized artery w/ Gray-white scarring
  • Microscope: Contracted scar complete
  • Complications:
    • Dressler syndrome, HF, Arrhythmias, True ventricular aneurysm (outward bulge during contraction), “Dyskinesia”
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12
Q

Cardiac Troponin I

A
  • Rises after 4 hrs and is ↑ for 7 - 10 days
  • More specific than other protein markers
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13
Q

CK-MB

A
  • Predominantly found in myocardium but can also be released by skeletal muscle
  • Useful in diagnosing Reinfarction following Acute MI because levels return to normal after 48 hrs
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14
Q

Q waves: V1 - V4

A

Anterior wall infarct - LAD

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15
Q

Q waves: V1 - V2

A

Anteroseptal infarct - LAD

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16
Q

Q waves: V4 - V6

A

Anterolateral infarct - LAD or LCX

17
Q

Q waves: Lead I, aVL

A

Lateral wall infact - LCX

18
Q

Q waves: Lead II, III, aVF

A

Inferior wall infarct - RCA