ischaemic heart disease Flashcards

1
Q

Pathogenesis of IHD

A
  1. Reduced coronary blood flow
  2. Increased myocardial demand
  3. Availability of O2 in blood
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2
Q

4 clinical manifestations of IHD

A
  1. Angina Pectoris
  2. MI
  3. Chronic Ischaemic Heart Disease with Heart Failure
  4. Sudden Cardiac Failure
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3
Q

What is angina pectoris?

A
  • Episodic chest pain on exertion caused by transient ischaemia of the myocardium
  • Relieved by rest or vasodilators
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4
Q

What are the 3 types of angina pectoris?

A
  1. Stable Angina
    - chest pain on exertion
    - can be relieved by rest or vasodilators
  2. Prinzmetal Angina
    - due to arterial spasm
    - unrelated to physical activity, heart rate or BP
    - responds to vasodilators
  3. Unstable Angina
    - pain precipitated by lower levels of activity/rest
    - does NOT get better with rest
    - minimal effect from vasodilators
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5
Q

What are the early changes seen in myocardial ischaemia?

A
  1. Cessation of aerobic metabolism within seconds leading to inadequate production of high energy phosphate (ATP)
  2. Accumulation of noxious material eg Lactic Acid

As myocytes depend heavily on O2, severe ischaemia induces loss of contractility within 60s -> cessation of function can cause acute cardiac failure before myocytes completely dies

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6
Q

Occlusion of LCA will lead to

A

antero-lateral MI

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7
Q

Occlusion of LAD will lead to

A

antero-septal MI

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8
Q

Occlusion of RCA will lead to

A

posterior MI

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9
Q

Occlusion of LCX will lead to

A

lateral MI

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10
Q

What are the clinical diagnosis of MI?

A
  1. Symptoms: severe, crushing central chest pain that radiates to arm, neck with severe nausea and diaphoresis
  2. ECG changes:
    - transmural infarct: STEMI
    - subendocardial infarct: NO STEMI
  3. Elevated cardiac enzymes: troponin T, troponin I, creatine kinase M/B
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11
Q

What is the morphology of MI at 0-12h?

A

no visible macroscopic changes but triphenyl tetrazolium test is possible (stains cardiac muscle but dead muscles are unable to pick up stain)

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12
Q

What is the morphology of MI at 12-24h?

A

macroscopically: pale with blotchy discolouration
histologically: infarcted muscle brightly eosinophilic, loss of nuclei, intercellular oedema

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13
Q

What is the morphology of MI at 24-72h?

A

macroscopically: soft, pale, yellow colour
histologically: neutrophilic infiltrate

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14
Q

What is the morphology of MI at 3-10 days?

A

macroscopically: hyperaemic border around yellow area
histologically: granulation tissue forms

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15
Q

What is the morphology of MI at 6-8 weeks?

A

fibrous scar forms

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16
Q

What are the short term complications of MI?

A
  • LV failure
  • Arrhythmias
  • Rupture myocardium -> blood leaks out of inner pericardium sac -> blood accumulates in pericardial sac -> increased pressure in pericardial sac -> puts pressure on the heart -> compromises in diastolic filling of the heart -> cardiac tamponade
  • Thrombus formation
  • Acute pericarditis
  • Mitral valve incompetency
17
Q

What are the long term complications of MI?

A
  • Left heart failure
  • Aneurysm
  • Recurrent MI
  • Immune-mediated pericarditis
18
Q

What is chronic ischaemic heart disease with heart failure?

A

Chronic atherosclerotic narrowing of coronary arteries
Slow loss of myocardial fibres
Generalised myocardial fibrosis
Cardiac failure -> death

19
Q

What is the most common cause of sudden cardiac failure?

A

Ventricular fibrillation

20
Q

What are the other causes of sudden cardiac failure?

A

Pronounced stenosis of 1 or more major arteries
Acute plaque changes -> secondary thrombosis or massive MI