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Cardio Block > Ischemic Heart Disease - Pathology > Flashcards

Ischemic Heart Disease - Pathology Flashcards

1
Q

Define congestive heart failure.

What are the two ways it can occur?

A

It is when the heart cannot pump adequate blood to supply the body’s oxygen and nutrient requirements.

  1. low-output failure = heart can’t pump all the blood delivered to it by the venous system
  2. high-output failure = the heart pumps large volume of blood but for a non-cardiac reason (anemia) not enough O2 and nutrients are delivered
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2
Q

Define systolic dysfunction.

Define diastolic dysfunction.

A

Systolic dysfunction is when there is abnormality in myocardial contractility.
Diastolic dysfunction is when there is abnormality in myocardial relaxation

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3
Q

Define low-output failure and high-output failure.

A

Low output is when the heart cannot pump enough blood by volume to supply O2 and nutrients to tissue

High output failure is when enough the heart pumps enough blood to adequately supply the body but

  1. blood is insufficient (anemia)
  2. pumped inefficiently (AV malformations, bypass of capillaries)
  3. metabolic demands of tissue are too great and not met even by the high volume of blood
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4
Q

What is the difference between forward failure and backward failure?

A

Forward failure is when there is not enough CO.

Backward failure usually accompanies forward failure because when there is not enough CO, the blood pools in venous circulation causing congestion

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5
Q

What is the difference between compensated and decompensated heart failure?

A

Compensated: dilation and Frank-Starling mechanism (extra blood in the ventricle stretches the walls and causes a bigger contraction) to maintain adequate perfusion of the body’s organs

Decompensated: dilation and FS is not enough to maintain perfusion of tissue

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6
Q

What are the 3 major compensatory mechanisms used by the heart during heart failure?

A
  1. neurohumeral- increase contractility, BP, blood volume
  2. Frank-Starling
  3. myocardial hypertrophy
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7
Q

Describe the three major neurohumeral compensation mechanisms.

A
  1. NE is released to contract the heart and increase HR as well as contract vessels to increase BP
  2. Angiotensin II is activated by renin-angiotensin-aldosterone system to increase PVR and blood volume (aldo in the kidney)
  3. ANP is released when the heart has too much volume and the atrium is distended. This vasodilates and causes naturesis and diaresis to relieve volume/pressure
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8
Q

What is the Frank-Starling mechanism?

A

As ventricular volume increases, the end diastolic pressure will increase and the myocytes will be more stretched. This increases the strength of contractility of the heart.

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9
Q

What are the 2 forms of myocardial hypertrophy? What is each form in response to?

A
  1. Concentric hypertrophy is when the heart size increase is due to diameter of the myocytes increasing. It happens in response to increased pressure.
  2. Eccentric hypertrophy is when the increase of heart size is due to increased length of myocytes in response to volume.
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10
Q

What are the 4 main causes of left-sided heart failure?

A
  1. systemic hypertension
  2. ischemic heart disease
  3. mitral or aortic valve disease
  4. primary disease of myocardium
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11
Q

What are the causes of right-sided heart failure?

A

Most common cause is left-sided heart failure which backs up blood into the pulmonary venous circulation increasing pulmonary pressure.
Other causes would be diseases of pulmonary parenchyma or vasculature

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12
Q

What are the primary clinical findings of left-sided heart failure?

A

dyspnea, orthopnea, coughing, paroxysmal nocturnal dyspnea all due to venous pulmonary congestion and fluid leakage into the airspaces.

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13
Q

What are the classic morphological signs of left-sided heart failure?

A

All left sided heart failure has:
1. edema and congestion in the lungs
2. Hemosiderin-laden macrophages (heart failure cells)
The different causes of LHF will have different morphologies
1. Atherosclerosis of a vessel will show atherosclerosis in coronary arteries
2. Aortic stenosis will show hypertrophied muscle cells and calcification around the valve

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14
Q

What are the primary clinical findings of right-sided heart failure?

A
  1. peripheral edema
  2. ascites (fluid in peritoneal cavity)
  3. hepatosplenomegaly
  4. pleural effusions (fluid in pleural cavity NOT alveoli)
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15
Q

What is the most common morphological association with right sided heart failure?

A

Hepatosplenomegaly with nutmeg liver due to chronic passive congestion (blood not being able to return to vena cava from liver)

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16
Q

What are the two general forms of hypertension?

A
  1. Systemic hypertension - hypertrophied LV with no other cause (valve dysfunction, etc) and involve the entire body except lungs
  2. Pulmonary hypertension- increase in BP is in pulmonary vasculature
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17
Q

What is the criteria for the pathologic diagnosis of systemic hypertensive heart disease?

A
  1. LV hypertrophy with no other identified cause. NO LV dilation
  2. History or pathological evidence of hypertension (hyaline arteriosclerosis)
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18
Q

What are the clinical features of systemic hypertensive disease?

A
  1. Hypertrophied LV requires more blood making it more prone to ischemic injury
  2. systemic hypertension is a risk factor for atherosclerosis
  3. progressive renal failure
  4. cerebrovascular hemorrhage
  5. heart failure
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19
Q

What is cor pulmonale?

What is the criteria for pathologic diagnosis?

A

pulmonary hypertensive heart disease

It is diagnosed by hypertrophied RV with dilation caused by primary disorders of pulmonary parenchyma or vasculature

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20
Q

What are the 2 forms of cor pulmonale?

A
  1. Acute - following PE that obstructs >50% vasculature. Rapid onset of symptoms.
  2. Chronic- prolonged pressure overload by obstruction of pulmonary vasculature or obliteration of pulmonary septal capillaries. Insidious onset of symptoms
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21
Q

What are the 4 major causes of cor pulmonale?

A
  1. Disease of pulmonary parenchyma (COPD, diffuse pulmonary interstitial fibrosis, pneumoconiosis, CF)
  2. Diseases of pulmonary vessels (PE, pulmonary arteritis)
  3. Diseases affecting chest movement (kyphoscoliosis, obesity)
  4. Diseases that constrict arteries (metabolic acidosis, hypoxemia)
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22
Q

How can parenchymal fibrosis cause cor pulmonale?

A

Fibrosis of alveolar septae obliterate some capillaries and decrease vasculature available for RV to pump into so resistance increases and RV pressure increases and RV will hypertrophy if the condition is chronic

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23
Q

What is ischemic heart disease?

A

a group of disorders that CAUSE or RESULT FROM ischemic injury to the heart.
Ischemia is the lack of blood flow to the cells of the heart depriving them of O2 and nutrients and impairing removal of metabolic waste.

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24
Q

What causes the lack of blood flow that may cause ischemic heart disease?

A
  1. obstruction to a vessel (narrowing of coronary artery)

2. relative lack of blood flow due to increased demand of the heart or decreased O2 content of delivered blood

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25
Q

What are the 4 clinical syndromes associated with ischemic heart disease?

A
  1. Angina pectoris (unstable, stable, Prinzmetal)
  2. Acute MI
  3. Chronic Ischemic heart disease
  4. sudden cardiac death
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26
Q

What is acute coronary syndrome?

What are the 3 types?

A

Sudden or abrupt change in coronary vessel that can cause catastrophic ischemic heart disease.

  1. unstable angina
  2. acute MI
  3. sudden cardiac death
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27
Q

What is the most common cause of IHD and what 3 things have decreased the incidence of people affected by ischemic heart disease?

A

The most common cause is atherosclerosis in coronary arteries.

  1. smoking cessation
  2. control of DM
  3. control of hypertension
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28
Q

While an atherosclerotic plaque itself can partially, or completely obstruct a coronary aretery, acute changes like _______, __________, or ______ can contribute to the degree of occlusion.

A
  1. hemorrhage into the plaque
  2. vasospasm of the vessel
  3. thrombosis (usually after plaque rupture)
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29
Q

What percent of the vessel must be stenotic to cause ischemia?

A

With >70-75% of the vessel blocked, the heart can still pass enough blood at rest, but with increased demand (ex. exercise) the heart cannot increase flow appropriately and ischemia will occur

At 90% blockage, even at rest not enough blood can pass and ischemia will occur.

30
Q

How long dues the progression from 65% to 80% stenosis take if there is no acute coronary syndrome? What is the progression due to?

A

It can take months or years and is due to the accumulation of LDL and collagen production

31
Q

What is acute plaque change? What three things typically cause this change?
What happens after the plaque change?

A

It is a sudden change in the plaque caused by:

  1. rupture
  2. ulceration
  3. fissuring (tearing)
  4. exposure of the lipid core of the plaque to the blood is thrombogenic and can cause thrombosis.
  5. large neovascularized plaques can cause hemorrhage into the plaque expanding it
  6. Rupture can lead to intraluminal thrombosis
32
Q

Describe a plaque that would be prone to rupture.

What are these plaques called?

A

A plaque unable to stand stresses would be prone to rupture. They are called “vulnerable plaques”
This could be a plaque with a large/thick lipid core and a thin fibrous cap (less than 6.5micm)

33
Q

What affects the stability of a plaque? (3 main things)

A
  1. how vulnerable the structure is (thin cap, thick core= vulnerable)
  2. collagen remodeling (synthesis and degradation of collagen can affect the strength of the cap)
  3. Adrenergic stimulation (hypertension and vasospasm can put pressure on the plaque)
34
Q

What are the 3 main factors that affect the development of ischemic heart disease?

A
  1. inflammation–> atherosclerosis
  2. thrombus–> occlusive lesion–> ischemia/infarct
  3. vasoconstriction-> stenosis of the lumen
35
Q

How does a thrombus directly increase the size of a plaque? indirectly?

A

Directly- organization

Indirect- stimulate migration of smooth muscle into the plaque

36
Q

What stimulates vasoconstriction that can lead to increases stenosis of the lumen?

A

Adrenergic agonists (NE), thromboxane, and imbalances between vasoconstrictors and vasodilators

37
Q

What are the 3 main causes of Ischemic heart disease NOT related to atherosclerosis?

A
  1. Emboli
  2. coronary artery vasculitis
  3. coronary artery dissection
38
Q

What is angina pectoris?

What are the 3 main types?

A

chest pain due to non-sustained and reversible myocardial ischemia (NO INFARCT YET)

  1. Stable AP
  2. Unstable AP
  3. Prinzmetal angina
39
Q

What are the characteristics of stable angina?

when does it occur, what is the pain described as, what is it due to?

A

It occurs with exertion or increased myocardial demand but NOT with rest.
It occurs to the same degree each time (3rd flight of stairs and the pain starts each day)
It is crushing, pressure, squeezing.

It is due to a fixed plaque that occludes >75% of the lumen of the vessel

40
Q

What is Prinzmetal angina?

A

It is chest pain that occurs at rest due to vasospasm of a vessel. The vessel can be normal OR atherosclerotic

41
Q

What is unstable angina?

when does it occur, what is the pain described as, what is it due to?

A

It is not constant (increasing frequency and intensity) and can occur with exertion or at rest.
It has the same descriptions as stable angina - crushing, squeezing
It is due to an acute plaque change (hemorrhage, rupture, fissure).

42
Q

Is unstable angina reversible or irreversible?
What can it lead to?
What is the second name for unstable angina?

A

It is reversible but indicates an acute plaque change so can lead to:
increased stenosis-> prolonged ischemia->infarct

It is also called pre-infarction angina

43
Q

What is a myocardial infarction?

A

It is IRREVERSIBLE ischemic injury that has caused an infarct (irreversible cell injury or cell death)

44
Q

What is the most common cause of a MI? What are common risk factors?

A

Atherosclerosis due to:

smoking, diabetes, males, age, hypertension, hypercholesterolemia

45
Q

What are the two major kinds of MI?

A

Subendocardial (only a portion of the myocardium is affected)
Transmural (obstruction affects all layers of the vessel wall)

46
Q

What are the functional changes associated with a myocardial infarction?
Biochemical changes?
Morphologic changes?

A

Functional:
Decreased contractility
Electrical instability

Biochemical:
Loss of ATP
Loss of glycogen

Morphological:
cell swelling, necrosis, infarct

47
Q

The changes of myocardial ischemia can be reversible if perfusion is restored in _________.

A

20-40 minutes

48
Q

How can reversible injury cause death of an individual without causing death of cells?

A

Reversible ischemia is still associated with electrical instability and can cause a ventricular arrhythmia

49
Q

Describe the evolution of the infarct. What layer is affected first?

A

Subendocardial region is last to receive blood and is subject to higher amounts of stress from intramural pressure. It has a higher metabolic demand and is first to be affected by ischemia.
The infarct expands to the epicardium taking 3-6 hours.

50
Q

What determines the severity of an infarct?

A
  1. location
  2. severity
    3, rate of development of the occlusion
    4.size of vascular bed
  3. duration of occlusion
  4. metabolic demands of the tissue
  5. collateral circulation
51
Q

What region of the heart have the most MI?

A

LV and interventricular septum

52
Q

What is the difference between a transmural infarct and a subendocardial infarct?

A

Transmural is over 50% of the thickness of the vessel wall (STEMI)
Subendocardial is under 50% of the thickness of the vessel wall (NSTEMI)

53
Q

Describe the gross appearance of an infarct:

  1. before 12 hours
  2. after 2 months
A

Before 12 hours there is no signs of an infarct.

After 2 months there is dense scars

54
Q

Describe the microscopic appearance of an infarct:

  1. 0-4 hours
  2. 4-12 hours
  3. 12-36 hours
  4. 3-7 days
  5. 7-10 days
  6. 10-14 days
A
  1. nothing is apparent
  2. Coagulative necrosis
  3. neutrophilic infiltrate
  4. macrophages
  5. granulation tissue
  6. collagen deposition
55
Q

How do infarcts heal?

A

From outward in so the outer edge may appear to be a different age from the inside

56
Q

What is repurfusion? How can it damage tissue?

A

It is when blood flow starts back to an infarcted area after lysis of the clot and stenting of the vessel or coronary artery bypass.
It can produce ROS and cause contraction band necrosis.

57
Q

What is a silent MI? Who does it usually occur in?

A

It is when the normal symptoms of MI (substernal chest pain radiating to neck, jaw, left arm) is not experienced.
It usually happens in elderly and diabetics because of nerve damage

58
Q

What EKG abnormalities are associated with MI?

A

Transmural MI will have a Q wave, ST elevation, and potentially T wave inversion

59
Q

When is troponin I detectable after a myocardial infarction?

A

2-4 hours, peak at 48 hours, remains detectable for 7-10 days

60
Q

What are the three CK?
What ration is high in heart muscle and low in skeletal muscle?
When are they detectable after MI?

A

CK-MM, CK-MB and CK- BB

CKMB/CKMM is high in heart muscle.
Detectable at 2-4 hours, peak at 1-2 days, undetectable by 3 days

61
Q

What is the preferred marker for acute MI?

What are the drawbacks?

A

troponin I although it is not completely specific for AMI. It can also be caused by:

  1. CHF
  2. PE
  3. cardiopulmonary rescusitation
  4. sepsis
  5. cardiac trauma
  6. renal failure
62
Q

What are the complications associated with MI? (7)

A
  1. contractile dysfunction
  2. arrhythmia
  3. myocardial rupture
  4. infarct expansion
  5. mural thrombus
  6. ventricular aneurysm
  7. papillary muscle dysfunction
63
Q

How does MI cause contractile dysfunction?

A

LV failure causes hypotension due to forward failure and pulmonary congestion due to backward failure.
This makes the RV work harder and hypertrophy and dilate leading to CHF

64
Q

What are the 3 main places for myocardial rupture after an MI?
Which is clinically worst?

A
  1. free wall rupture- hemopericardium and cardiac tamponade. clinically worst
  2. interventricular rupture- L to R shunt
  3. Mitral valve papillary muscles- acute mitral insufficiency
65
Q

When do most ruptures due to MI occur?

What are common risk factors for rupture?

A

1-3 days (or 3-7 depending on who you ask) post-MI.

  1. over 60
  2. hypertension with no previous MI (no fibrosis yet)
  3. females after menopause
66
Q

When does pericarditis develop after an MI?

A

2-3 days after a transmural MI.

It is a reaction to inflammation in the myocardium

67
Q

Why can a myocardial infarction cause mural thrombus?

A

the loss of contractility in the LV alters linear flow of blood. This coupled with the inflammation of the tissue necrosis can lead to thrombus formation

68
Q

What is a ventricular aneurysm?

What do aneurysms make a person prone to?

A

With a transmural infarct, the wall develops into a thin fibrous scar that dilates outward and then becomes fibrotic.
Because it is fibrotic, an aneurysm wont rupture but it can assist in thrombi formation

69
Q

What is chronic ischemic heart disease?

A

It is heart failure as a result of prolonged ischemic injury.
It can arise from one or more past MIs or be due to diffuse ischemic injury

70
Q

What is the morphology of a heart with chronic ischemic heart disease?

A

Hypertrophied and dilated heart associated with coronary artery atherosclerosis.
Microscopically:
Fibrosis, hypertrophy, subendocardial vacuolization

71
Q

What is sudden cardiac death? What is the most common cause?

A

IT is when death occurs without symptoms or within 24 hours of symptoms.
The most common cause is atherosclerosis

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