Ischemic Heart Disese - Jarzembowski

Question 1

Define Ischemic Heart Disease.

Answer 1

Imbalance (generally shortage) between supply & demand of oxygen, nutrients, and waste removal of heart tissue.

Question 2

Why is ischemia worse than hypoxia?

Answer 2

Ischemia involves a lack of nutrient delivery & metabolite removal in addition to interrupted oxygen supply.

Question 3

Give four possible causes of heart ischemia.

Answer 3

1. Fixed obstruction
2. Acute plaque change
3. Thrombosis/embolism
4. Vasospasm

Question 4

What is the consequence of a >90% obstruction of coronary flow?

Answer 4

>90% results in resting ischemia, as opposed to exertional only (>70%)

Question 5

What vessels are most susceptible to fixed atherosclerotic obstruction?

Answer 5

LAD (left anterior descending) > LCX (left circumflex) > RCA (right coronary)

Question 6

What factors contribute to the risk of acute plaque changes?

Answer 6

Intrinsic: eg Foam cells, lipid, inflammation, cap integrity.

Extrinsic: eg Adrenergic stimulation

Question 7

What are the typical outcomes of total and partial coronary thromboses?

Answer 7

Total = Acute transmural MI and/or sudden cardiac death.

Partial = Unstable angina, subendocardial infarction, embolization. Sudden death still possible.

Question 8

Recall where lipids deposit in an atherosclerotic plaque.

Where does the calcification occur?

Answer 8

Lipid deposition in the intima.

Calcification also occurs in intima (as opposed to media)

Question 9

What factors contribute to inappropriate coronary vasoconstriction?

How would this present clinically?

Answer 9

Adrenergics, platelet & mast cell contents, endothelial dysfunction.

Severe, but transient angina.

Question 10

Distinguish between the outcomes typical of immature/vulnerable plaques and mature/stable ones.

Answer 10

Immature/vulnerable may undergo acute changes >> thrombus or embolization >> acute MI.

Stable results in severe fixed obstruction >> chronic ischemic heart disease.

Question 11

What are the four clinical syndromes of heart ischemia?

Answer 11

Angina pectoralis

Myocardial infarction

Chronic ischemic heart disease

Sudden cardiac death

Question 12

Recall the 3 types of Angina pectoralis.

Which can occur at rest? Which is most dangerous?

Answer 12

Stable - Elicited by exertion or emotional response.

Prinzmetal - Due to artery spasm, can occur at rest.

Unstable - Progressively worsening plaque, will eventually occur at rest and often precedes acute MI.

Question 13

What is the difference between angina pectoralis and myocardial infarction?

Answer 13

In angina pectoralis, pain is elicited from reversible ischemia of heart tissue. In myocardial infarction, ischemia is severe enough to cause irreversible damage (necrosis).

Question 14

Distinguish between transmural and subendocardial infarctions.

Answer 14

Transmural - Usually results from complete vessel obstruction; full thickness necrosis confined to one vessel’s territory.

Subendocardial - Milder obstruction; necrosis limited to inner 1/3 of myocardium but may extend laterally.

Question 15

Why is the inner 1/3 of the myocardium most susceptible to necrosis in myocardial infarctions?

Why is the subendocardium affected, and not the whole endocardium?

Answer 15

Perfusion pressure there is lower, and subendocardial resistance is higher.

Innermost layers of endocardium receive oxygen from the blood in the ventricle.

Question 16

What occurs almost immediately upon infarction?

After how long is the ischemic damage irreversible?

Answer 16

Ceasing of contraction of the infarcted area.

20-40min until the ischemia results in necrosis.

Question 17

An infarction results in the death of the left lateral wall of the left ventricle. What vessel was occluded?

What ischemic outcome results from global hypotension?

What would cause multiple intramural infarctions?

Answer 17

Left lateral wall supplied by Left circumflex branch.

Global hypotension can cause infarction of the entire circumferential subendocardium. (pressure inadequate to reach subendocardium)

Hypertension or multiple emboli from an upstream thrombus can cause multiple intramural infarctions.

Question 18

Describe the changes in gross morphology of an infarcted heart.

Answer 18

<12hrs: Subtle. Tetrazolium stain reveals pale areas.

12-24hrs: Dark red-blue mottling from clotting blood.

1-14days: Yellow-tan area with peripheral hyperemia.

>14days: Grey-white scar.

Question 19

What does a tetrazolium stain detect?

Answer 19

Tetrazolium stains dehydrogensase enzymes red. This can reveal dead tissue as pale.

Question 20

Describe the changes in histology of an infarcted heart.

Answer 20

4-12hrs: Wavy fibers.

12hrs-7days: Coagulative necrosis (loss of nuclei, eosinophilia), neutrophil infiltration.

7-14days: Granulation tissue present.

>14days: Dense fibrous scar. (blue trichrome stain)

Question 21

How does reperfusion injury occur?

Answer 21

Reperfusion of infarcted tissues results in damage from leukocyte ROS, platelet/complement activation, and microvascular injury.

Question 22

How does a typical MI patient present?

Answer 22

With severe chest pain (“crushing”, may radiate to L arm or neck). Weak pulse, diaphoresis, dyspnea.

(Labs: Elevated cardiac enzymes, CRP)

Question 23

How many MIs are silent?

What patient population is especially prone to these?

Answer 23

10-15%.

Heart transplant patients (since the heart isn’t innervated)

Question 24

Describe 3-4 possible complications that result form MIs.

Answer 24

Contractile dysfunction (severe >> cardiogenic shock)

Arrhythmias (>> sudden death)

Myocardial rupture

Pericarditis

Question 25

Distinguish between the consequences of myocardial ruptures at the following sites:

Free wall

Ventricular septum

Papillary muscle

Answer 25

Free wall: Hemopericardium/tamponade.

Ventricular septum: L>R shunt.

Papillary muscle: Mitral regurgitation.

Question 26

How does fibrinohemorrhagic pericarditis present?

Answer 26

Friction rub (can be auscultated).

Question 27

What is a mural thromboembolism?

Answer 27

A thrombus that forms in the unmoving area around the infarction, which may embolize to circulation (L/R).

Question 28

What factors influence the prognosis of acute MI?

Answer 28

How large the infarct is, where it is, how much tissue is involved, how extensive the necrosis is (how much time has passed). How much funciton remains?

Question 29

What are some causes of chronic ischemic heart disease?

Describe these hearts.

Answer 29

Cardiac decompensation secondary to infarction, or severe coronary obstruction.

Enlarged, usually with LV hypertrophy & dilation.

Question 30

What is Sudden Cardiac Death? Why does it usually occur?

Answer 30

Unexpected death from cardiac causes; usually due to arrhythmias & related to heart ischemia.

Question 31

What arrhythmias are potentially fatal?

Answer 31

Asystole and Ventricular Fibrillation (V-Fib)

Question 32

When is contraction band necrosis seen?

Answer 32

In reperfusion injury of infarcted tissue (due to calcium return; not seen without reperfusion!)