L42 Ischemic Heart Disease Flashcards

1
Q

What is the leading cause of mortality worldwide?

A

Cardiovascular disease (25% of US deaths)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens in heart failure (also known as congestive heart failure)?

A

The heart is unable to pump blood sufficiently to meet the needs of the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two types of heart failure?

A

Diastolic (inability of the heart chamber to relax, expand, and adequately fill during diastole; ventricle is unable to fill with blood)

Systolic (inadequate myocardial contractile function; the ventricle is unable to eject blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In which type of heart failure does the ejection fraction decrease?

A

Systolic heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What increases in heart failure?

A

End diastolic ventricular volume, end diastolic pressures, venous pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens in right sided heart failure?

A

Engorgement of the systemic and portal venous circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens in left sided heart failure?

A

Damming of blood in the pulmonary circulation and diminished peripheral blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some causes of left sided heart failure?

A

Ischemia, hypertension, aortic and mitral valve diseases, and non-ischemic myocardial diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the causes of right sided heart failure?

A

Left sided heart failure, cor pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some signs and symptoms of right sided heart failure?

A

Edema, dark purple legs (blood pooling), ascites, hepato/splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some signs and symptoms of left sided heart failure?

A

Dyspnea, orthopnea, no edema, no ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes ischemic heart disease?

A

Decreased perfusion (coronary blood flow) and increased myocardial demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are four syndromes caused by ischemic heart disease?

A
  1. Angina pectoris
  2. Acute myocardial infarction
  3. Chronic ischemic heart disease/heart failure
  4. Sudden cardiac death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the three types of angina pectoris?

A
  1. Stable
  2. Unstable
  3. Prinzmetal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe stable angina pectoris.

A

Result of chronic stenosing coronary atherosclerosis; leads to increased cardiac demand and workload needs unmet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the lumenal obstruction in stable angina pectoris.

A

> 75% reduction of lumen area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the symptoms of stable angina pectoris?

A

Substernal chest pressure during physical activity and emotional excitement that is relieved with rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe unstable angina pectoris (aka crescendo agina, pre-infarction angina)

A

Caused by atherosclerotic plaque disruption; atheroma cap is breached, exposing the core, leading to platelet activation and aggregation; vasospasm may also occur. Eventually, there is a partially occluding thrombus formed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the lumenal obstruction of unstable angina pectoris.

A

50-75% (less than stable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms of unstable angina pectoris?

A

Anginal symptoms, but they occur frequently with less effort/at rest for a longer duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What types of plaques are vulnerable?

A

Lipid rich atheromas with thin fibrous caps and lots of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe Prinzmetal variant angina.

A

Caused by a coronary artery spasm unrelated to physical activity, heart rate, and blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the pathogenesis of myocardial infarction.

A

Plaques are disrupted. Platelets adhere/aggregate/activate. Vasospasms occur. Coagulation is activated. Ultimately, an occlusive thrombus forms.

(There are other possible mechanisms).

24
Q

Describe the development of acute coronary syndromes.

A

Atherosclerosis causes a fixed coronary obstruction (typical angina). This plaque can be disrupted/healed, leading to severe fixed coronary obstruction (chronic ischemic heart disease) or to thrombus formation.

25
Q

What are the acute coronary syndromes?

A

Unstable angina, acute myocardial infarction

26
Q

When does reversible ischemia become irreversible and progress to coagulative necrosis?

A

After 30 minutes

27
Q

What is the difference between a transmural and nontransmural infarction?

A

Transmural: entire thickness of the wall is infarcted

Non-transmural: only a portion of the myocardium is infarcted

28
Q

When a coronary artery is obstructed, which part of the heart infarcts first?

A

The part of the heart furthest from it (except a thin portion of the lumenal myocardium that is spared)

29
Q

Describe the morphology of the myocardium after 0.5-4 hours.

A

No gross or light microscopic changes

30
Q

Describe the morphology of the myocardium after 4-12 hours.

A

Beginning of coagulative necrosis, hemorrhage (eosinophilia of cytoplasm, loss of some nuclei, some hemorrhage)

31
Q

Describe the morphology of the myocardium after 12-24 hours.

A

Gross: dark mottling (hemorrhage)
Histology: Ongoing coagulative necrosis, pyknosis of nuclei (very pink fibers, RBCs)

32
Q

Describe the morphology of the myocardium after 1-3 days.

A

Gross: mottled myocardium
Histology: loss of nuclei and myocytes, neutrophil infiltrate

33
Q

Describe the morphology of the myocardium after 3-7 days.

A

Myocyte disintegration, dying neutrophils, phagocytosis of dead cells

34
Q

Describe the morphology of the myocardium after 7-10 days.

A

Well-developed phagocytosis and early granulation tissue

35
Q

Describe the morphology of the myocardium after 10-14 days.

A

Granulation tissue

36
Q

Describe the morphology of the myocardium after 2-8 weeks.

A

Scar formation

37
Q

What are the symptoms of MI?

A

Crushing substernal chest pain, dyspnea, diaphoresis, tachycardia, pulmonary congestion, edema

38
Q

What laboratory evaluations can be done to look for an MI?

A

Myoglobin (first), creatinine kinase (second), and troponin (third) all increase

39
Q

What is a triphenyletrozolium chloride stain used for?

A

Stains LDH red (yellow when it isn’t there); this enzyme is depleted in MI

40
Q

How can MI’s be treated?

A
  1. Aspirin/anti-platelet agents (counteract thrombus formation)
  2. Heparin (counteract coagulation cascade)
  3. Thrombolytic therapy (counteract thrombus formation)
  4. Beta blockers (slow heart rate/contractility, decrease demand of heart)
  5. ACE inhibitors (decrease remodeling)
  6. Nitrates (vasodilation)
  7. Oxygen (decrease demand)
41
Q

What is the goal of therapy in the setting of an MI?

A

Myocardial salvage

42
Q

What is reperfusion injury?

A

Restoration of blood flow leads to local myocardial damage (free radical production, hypercontracture due to increased intracellular calcium, leukocyte aggregation, and mitochondrial dysfunction)

43
Q

What are 5 serious MI complications?

A
  1. Cardiogenic shock
  2. Arrhythmia
  3. Rupture
  4. Acute pericarditis
  5. Ventricular aneurysm
44
Q

What happens in cardiogenic shock?

A

Severe pump failure in 10-15% of patients who have very large infarctions

45
Q

Why does arrhythmia occur in the setting of an MI?

A

Myocardial irritability, conduction disturbances

46
Q

When does myocardial rupture typically happen after MI?

A

After 3-7 days

47
Q

Where can the myocardial rupture occur?

A

Free wall (leading to hemopericardium or cardiac tamponade), ventricular septum, or papillary muscle

48
Q

Ventricular aneurysm is a late complication of MI. What is a complication of the aneurysm?

A

Mural thrombus

49
Q

What is remodeling?

A

Alteration in the structure of the heart in response to hemodynamic load and/or cardiac injury in association with neurohormonal activation

50
Q

Describe the process of remodeling.

A

Hypertension (pressure overload), valvular disease (pressure/volume overload), and MI (regional dysfunction with volume overload) all increase cardiac work. This increases wall stress. Cells stretch and hypertrophy and/or dilate.

51
Q

What is the mechanism of sudden cardiac death in ischemic heart disease?

A

Lethal arrhythmia caused by myocardial irritability from ischemia or fibrosis

52
Q

What are the effects of hypertension/left-sided hypertensive heart disease?

A

Hypertrophy of the left ventricle (can even be caused by mild BP elevation)

53
Q

Compare a normal heart weight/LV wall thickness to that of someone with systemic hypertension and aortic stenosis.

A

Normal: 250-350 gm, 1.5cm thick

HTN: 500+ gm, 2+cm thick

Aortic stenosis: 800 gm

54
Q

What can happen to someone with left-sided hypertensive heart disease?

A
  1. Asymptomatic
  2. CHF
  3. Arrhythmias/A Fib
55
Q

What causes cor pulmonale (pulmonary hypertensive heart disease)?

A

Pulmonary HTN (caused by COPD, pulmonary fibrosis, chronic pulmonary thromboembolism, primary pulmonary HTN, increased resistance)