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MHD > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What is the general problem in diastolic heart failure?

A

Heart cannot sufficiently fill with blood (Ventricle is stiff and cannot relax enough)

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2
Q

What is the general problem in systolic heart failure?

A

Heart cannot pump/eject blood sufficiently to meet demands of the body
Low ejection fraction

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3
Q

What is a normal ejection fraction?

What is the ejection fraction in a patient with systolic heart failure?

A

Normal is 60-70%

Systolic heart failure - lower EF (40% or even lower)

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4
Q

What are some of the compensatory mechanisms that act during CHF?

A

Frank Starling
Adrenergic nervous system
Renin-angiotensin-aldosterone
Cardiac remodeling

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5
Q

List some of the consequences of L sided heart failure

A

Less peripheral blood flow
Blood pools in the pulmonary circulation

Symptoms: SOB, orthopnea, ischemic changes and symptoms in the pulmonary circulation

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6
Q

What are some symptoms that could lead to L sided heart failure?

A

Ischemia
HTN
Aortic/mitral valve disease

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7
Q

What are some consequences of R sided heart failure?

A

Systemic and portal venous circulation engorgement
Peripheral edema (increased pressure in capillaries and veins)
Ascites

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8
Q

What is the top cause of R sided heart failure?

A

L sided heart failure

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9
Q

What is it called when the R side of the heart is failing, but not the L side?

A

Cor pulmonale

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10
Q

List the three types of angina pectoris

A

Stable Angina
Unstable Angina
Prinzmetal Angina

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11
Q

Describe how a person develops stable angina

A

Growth of atherosclerotic plaques in the lumen of the blood vessel over many years. Over 75% of the original lumen becomes obstructed and the person feels substernal chest pain when they have increased cardiac demand.
Their coronaries cannot meet the needs of increased cardiac demand

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12
Q

How should a person relieve symptoms of stable angina?

A

Rest

Vasodilators (like nitroglycerin)

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13
Q

Describe the pathogenesis of unstable angina

A

Atherosclerotic plaque disruption in the coronary arteries. Fissure or ulceration of the atheromatous plaque causes platelets to activate and aggregate. Thrombus forms and it PARTIALLY occludes the blood vessel, causing chest pain

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14
Q

How do the symptoms of unstable angina differ from stable angina?

A

Unstable angina has frequent chest pain that occurs with less effort (or at rest) and with longer duration

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15
Q

What causes Prinzmetal Variant Angina?

A

Coronary artery spasm

NOT related to HR, blood pressure, or physical activity

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16
Q

How should you treat Prinzmetal angina?

A

Vasodilators

17
Q

Describe the basic pathogenesis of a Myocardial Infarction

A

Plaque disruption in a coronary artery leads to platelet adhesion, aggregation, and activation. An occlusive thrombus is formed, blocking blood flow to an area of myocytes

18
Q

What is the critical time amount by when we must reverse the ischemia from an MI?

A

30 min.

After 30 min, reversible ischemia becomes irreversible, coagulative necrosis

19
Q

What is the difference between a transmural and a nontransmural MI?

A

Transmural MI infarcts the full thickness of the myocardium.

Nontransmural MI does not affect the full thickness of the wall (usually the subendocardium is the infarcted portion)

20
Q

Within the first 30 min to 4 hours after an MI, what gross changes will you see in the heart? What microscopic changes?

A

No gross or light microscopic changes

21
Q

4-12 hours after an MI, what microscopic changes will you start to see? What gross changes?

A

Coagulative necrosis
Eosinophilia

No gross changes

22
Q

12-24 hours after an MI, what microscopic changes will you start to see? What gross changes?

A

Gross- Dark mottling of the heart

Coagulative necrosis is ongoing
See pyknosis of nuclei

23
Q

1-3 days after an MI, what microscopic changes will you start to see? What gross changes?

A

Gross changes - mottled red-yellow appearance

Loss of nuclei and myocytes
Neutrophil infiltrate

24
Q

3-7 days after an MI, what microscopic changes will you start to see? What gross changes?

A

Myocyte disintegration
Lots of PMN infiltrate

Myocardium appears yellow grossly due to PMN infiltrate

25
Q

7-10 days after an MI, what microscopic changes will you start to see? What gross changes?

A 
Early granulation tissue will form (new vascularization developing)
Scar formation (NO collagen seen yet)
26
Q

10-14 days after an MI, what microscopic changes will you start to see? What gross changes?

A

Granulation tissue continues to form

Some mature collagen may be seen on Trichrome stain

27
Q

2-8 weeks after an MI, what microscopic changes will you start to see? What gross changes?

A

Well developed scar formation in the myocardium (Dense blue collagen seen)

28
Q

What is the typical clinical presentation of an MI?

A

Crushing substernal chest pain
Dyspnea
Diaphoresis (sweating)
Tachycardia

29
Q

What substances in the blood may indicate an MI? When do they appear?

A

Troponin
CK-MB
Both peak around 20-24 hours after MI

30
Q

What is LDH? Why is it important?

A

LDH is an enzyme released by myocytes into the circulation during an MI. You can do a triphenyltetrocolium chloride stain to visualize this grossly.

31
Q

How do you treat an MI?

A 
Aspirin
Heparin
Thrombolytic therapy
Catheter/Stent Intervention
Beta blockers
ACE inhibitors
Nitrates
Oxygen
32
Q

What is reperfusion injury?

A

Restoration of blood flow leads to local myocardial damage because you carry harmful free radicals to undamaged myocytes

33
Q

What is cardiogenic shock?

A

Severe pump failure of the heart. Occurs in large infarcts

34
Q

When is the myocardium at greatest risk of rupture after an MI? Why?

A

3-7 days after an MI.
At that point, the myocardium is composed of dead myocytes and PMNs (no collagen yet), so there is no strength to support the myocardium.

35
Q

In progressive heart failure, what changes do you see?

A

Series of infarcts leads to lessened myocardial contraction over time. Remaining myocytes will hypertrophy in response. Ultimately, the hypertrophied heart will start to fail

Expression of fetal genes (hypertrophy)
Deposition of ECM
Abnormal proteins present

36
Q

What is the basic mechanism of sudden cardiac death?

A

Lethal arrhythmia

Usually not due to an acute infarction

37
Q

How will the L side of the heart respond to hypertension?

A

It will hypertrophy (and eventually fail)

38
Q

What will you see in the histology of a hypertrophied LV pumping against HTN?

A

Enlarged nuclei and myofibrils

Interstitial deposition of collagen because there has been some damage to the myocytes

39
Q

In what clinical situations would a person be at increased risk of developing Cor Pulmonale?

A

Cor Pulmonale = Isolated R heart failure

Seen in COPD, pulmonary fibrosis, chronic thromboemboli to the pulmonary vessels

MHD (57 decks)

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