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Cardio Exam 1 > 9 - Cardiovascular Pathology I > Flashcards

9 - Cardiovascular Pathology I Flashcards

1
Q

What is the number one cause of death worldwide?

A

Cardiovascular disease

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2
Q

What percentage of this burden occurs in developing countries?

A

80%

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3
Q

How many people in the US die each year from cardiovascular disease?

A

750,000

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4
Q

What is the yearly economic burden of ischemic heart disease in the US?

A

$100 billion

It is very costly and is preventable

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5
Q

List the locations of blood flow starting where blood first enters the heart

A
  • Right atrium
  • Tricuspid valve
  • Right ventricle
  • Pulmonic valve
  • Pulmonary arteries
  • Pulmonic veins
  • Left atrium
  • Mitral valve
  • Left ventricle
  • Aortic valve
  • Aorta
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6
Q

What is the role of gap junctions?

A

That are important for rapid communication between cells

This is important for action potentials traveling through the heart so that muscle contracts in a uniform way

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7
Q

What are the four cardiac valves?

A

1 - Tricuspid
2 - Pulmonary
3 - Mitral
4 - Aortic

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8
Q

What is the purpose of cardiac valves?

A

To maintain unidirectional blood flow through the heart

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9
Q

What changes in cardiac valves can affect function?

A
  • Valve mobility
  • Valve pliability
  • Structural integrity

The flaps are delicate and are made up of elastic fibers and connective tissue

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10
Q

What is the only valve with two cusps?

A

Mitral valve (bicuspid)

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11
Q

What are the first branches off of the aorta?

A

Coronary arteries

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12
Q

What is the role of the autonomic nervous system in controlling the conduction system?

A

The ANS controls the rate of firing of the SA node

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13
Q

Describe the path of conduction in the heart starting with the SA node

A

SA node → AV node → bundle of His →right and left bundle branches

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14
Q

Where do Purkinje fibers come into play?

A

The right and left bundle branches then form Purkinje fibers to help the muscle contract in a uniform way

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15
Q

What does the right coronary artery supply?

A

Supplies blood to the right atrium, right ventricle, bottom portion of the left ventricle and back of the septum

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16
Q

What does the left coronary artery branch into?

A

Circumflex artery and left anterior descending artery

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17
Q

What does the circumflex artery supply?

A

Supplies blood to the left atrium and the side and back of the left ventricle

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18
Q

What does the left anterior descending artery supply?

A

Supplies blood to the front and bottom of the left ventricle and the front of the septum

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19
Q

How prevalent is congestive heart failure (CHF)?

A

CHF affects nearly 5 million individuals and is the leading discharge diagnosis in patients over 65 years of age in the United States

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20
Q

When does CHF occur?

A

CHF occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure

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21
Q

When do we see CHF?

A

It can appear during the end stage of many forms of chronic heart disease

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22
Q

What is the definition of CHF?

A

CHF is characterized by variable degrees of decreased cardiac output and tissue perfusion, as well as pooling of blood in the venous system which may cause pulmonary edema, peripheral edema, or both

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23
Q

What is the most common cause of heart failure?

A

Coronary artery disease

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24
Q

Why does coronary artery disease cause heart failure?

A

CAD causes an MI which then leads to damaged heart tissue, scar formation and an inability to contract well

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25
Q

What is the other most common causes heart failure?

A

Sustained high blood pressure

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26
Q

What are other structural or functional causes of heart failure?

A
  • Cardiomyopathy
  • Congenital heart disease
  • Heart valve disease
  • Heart tumor
  • Lung disease
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27
Q

What is cardiomyopathy?

A

There are different types

  • Dialated cardiomyopathy
  • Hypertropic cardiomyopathy (thickened heart muscle)
  • Restrictive cardiomyopathy (rigid heart muscle)
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28
Q

What makes you at risk for developing heart failure?

A

You are also at increased risk for developing heart failure if you are overweight, have diabetes (drives atherosclerosis), smoke cigarettes, abuse alcohol, or use cocaine (heart rate will rapidly increase with cocaine use).

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29
Q

What are the two types of heart failure?

A

Acute and chronic

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30
Q

Describe the onset of acute heart failure

A

Develops rapidly (hours/days) and can be immediately life threatening because the heart does not have time to undergo compensatory adaptations.

Sudden event like a heart attack is an example

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31
Q

What are some examples of acute heart failure?

A
  • Cardiopulmonary by-pass surgery
  • Acute infection (sepsis)
  • Acute myocardial infarction
  • Valve dysfunction
  • Severe arrhythmias.
  • Endocarditis (vegetation on valves)
32
Q

Describe chronic heart failure

A

A long-term condition (months/years) that is associated with the heart undergoing adaptive responses (dilation, hypertrophy) to a precipitating cause.

33
Q

What is the long-term effect of compensatory measures in chronic heart failure?

A

These adaptive responses can be deleterious in the long-term and lead to a worsening condition.

  • End stage heart failure
  • Either get a transplant or die
34
Q

How is ultrasound used in diagnosing heart failure?

A
  • Echocardiography is commonly used to support a clinical diagnosis of heart failure
  • This modality uses ultrasound to determine the stroke volume
35
Q

Describe the values used to determine the existence of heart failure

A
  • SV = the amount of blood in the heart that exits the ventricles with each beat)
  • EDV = End-diastolic volume, the total amount of blood at the end of diastole)

The SV in proportion to the EDV gives us a value known as the ejection fraction (EF)

36
Q

What is a normal ejection fraction (EF)?

A

Normally, the EF should be between 50% and 70%

37
Q

In systolic heart failure, what is the ejection fraction?

A

In systolic heart failure, it drops below 45%

38
Q

What is systolic dysfunction?

A
  • Dilated ventricles (enlarged with thin walls)
  • More volume is present in the ventricles at the end of diastole
  • The heart does not pump out a lot of blood
  • There is a lot of left over blood in the heart after contraction
  • High end systolic volume and low stroke volume means very poor ejection fraction
39
Q

What is diastolic dysfunction?

A
  • Ejection fraction is normal
  • You can’t pump enough out to meet the demands of the body
  • Not able to fill enough of the ventricles because they are thick and rigid
40
Q

What are the four stages of CHF?

A

Stage A
Stage B
Stage C
Stage D

41
Q

Describe stage A of CHF

A

Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder.

42
Q

Describe stage B of CHF

A

Stage B: a structural heart disorder but no symptoms at this stage.

43
Q

Describe stage C of CHF

A

Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment.

44
Q

Describe stage D of CHF

A

Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

  • Ejection fraction below 25%
  • Without a transplant, they will die
45
Q

What are three ways in which the neurohumoral system contributes to compensation in congestive heart failure? Why is this helpful in diagnosis?

A
  • Norepinephrine
  • RAAS
  • Atrial natiuretic peptide

We can actually measure these things in the blood

46
Q

Describe the release of norepinephrine

A

Release of norepinephrine by adrenergic cardiac nerves of the autonomic nervous system (which increases heart rate and augments myocardial contractility and vascular resistance)

  • Heart will beat stronger with sympathetics
  • Peripheral vasculature will begin constricting
47
Q

Describe the activation of RAAS

A

Activation of the renin-angiotensin-aldosterone system (RAAS).

  • The flow to the kidney is reduced, and senses it as a low volume state in order to retain water and increase volume
  • This will cause problems with edema (that’s why we give diuretics)
48
Q

Describe the release of atrial natriuretic peptide

A

Release of atrial natriuretic peptide. B-Type Natriuretic Peptide (BNP >100 pg/mL)

49
Q

What will you see in left sided CHF?

A

SYMPTOMS will be present because the lungs are filling with fluid

50
Q

What will you see in right sided CHF?

A

SIGNS will be present which you will see during physical diagnosis (edema, venous distention)

51
Q

What is biventricular CHF

A

When a patient has R and L sided CHF

52
Q

How does biventricular CHF typically occur?

A
  • Have symptoms of lungs filling with fluid which then puts pressure on the right heart
  • Most common cause of R heart failure is L sided heart failure from an MI
53
Q

Symptoms of left-sided CHF

A
  • Pulmonary congestion and edema
  • Presences of heart failure cells (hemosiderin-laden macrophages)
  • Dilation of L atrium
  • Increased risk of a-fib
  • Dyspnea (difficulty breathing)
  • Orthopnea (while laying down)
  • Paroxysmal nocturnal dyspnea (while sleeping)
  • Reduction in renal perfusion (only in severe L sided CHF)
  • Reduction in CNS perfusion (only in severe L sided CHF)
54
Q

What is the cause of right-sided heart failure?

A
  • Cor pulmonale is usually due to conditions in pulmonary hypertension
  • Lung disease causing the right heart to fail (resistance in the lungs makes it hard for the R heart to pump blood to the lungs)
55
Q

Describe what happens and what the symptoms are in R heart failure

A
  • Blood backs up into the venous system
  • JVD
  • Pitting edema
  • Congestive hepato-splenomegaly
  • Pleural effusion
  • Pericardial effusion
  • Peritoneal effusion
  • Congestion of kidney and CNS
56
Q

On a cellular level, where does congestion occur?

A

In the alveolar space

  • Heart failure cells
  • Edema
57
Q

What is the treatment for CHF?

A
  • Diuretics
  • Angiotensin converting enzyme inhibitors (ACEi)
  • Beta blockers (to reduce HR)
  • Mechanical assistance
  • Heart transplant
58
Q

What is ischemic heart disease mostly the result of?

A

Chronic atherosclerosis

- Develop plaques over time

59
Q

Describe the epidemiology of ischemic heart disease

A

Ischemic heart disease (IHD) is the leading cause of death worldwide for both men and women.

60
Q

What is the cause of ischemic heart disease?

A
  • Due to an imbalance between the supply (perfusion) and demand of the heart for oxygenated blood.
  • In more than 90% of cases reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries (coronary artery disease - CAD).
61
Q

What are the non-modifiable risk factors for atherosclerosis?

A

Non-modifiable are things you can’t do anything about

  • Age
  • Male
  • Family history (events under 55)
  • Genetic abnormalities (hyperlipidemia)
62
Q

What are the modifiable risk factors for atherosclerosis?

A

Modifiable are things that can be changed and treated

  • Hyperlipidemia
  • Hypertension
  • Cigarette smoking*****
  • Diabetes
  • C-reactive protein

Minor

  • Inactivity
  • Stress
  • Obesity

** = MAJOR risk factor

63
Q

Describe the pathogenesis of ischemic heart disease

A

Insufficient coronary perfusion relative to myocardial demand, due to chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries, and variable degrees of superimposed acute plaque change, thrombosis, and vasospasm

64
Q

What is the part of the heart that gets perfused last?

A

The most vulnerable area of the heart that gets perfused last is the endocardium – the tissue that dies the first in an MI

65
Q

How long does it take for chronic atherosclerosis to develop?

A
  • Develops over decades
66
Q

Can the clinical manifestations of ischemic heart disease be explained by the anatomic burden alone?

A

No

67
Q

What is generally required to cause symptomatic ischemia (angina)?

A

Generally, obstructing 75% or greater of the lumen is generally required to cause symptomatic ischemia

68
Q

What is generally required to cause inadequate coronary blood flow at rest?

A

Obstruction of 90% of the lumen

69
Q

Can multiple coronary vessels be involved?

A

Yes

70
Q

Describe the pathophysiology of atherosclerosis

A

Pathophysiology

  • Macrophages and chronic inflammatory cells are present because there is a type of endothelial injury
  • Foam cells can be formed very easily when LDL and modified LDLs are taken up by the immune cells
  • Foam cells form a fatty plaque in the artery, leading to the atherosclerosis
  • Collagen can cover this layer
  • The muscular layers of the vessel can become involved – proliferation of smooth muscle cells occurs
71
Q

Describe fatty streaks/atherosclerotic plaques

A
  • Cells undergo necrosis
  • Necrotic cores are present with macrophages and other immune cells
  • A fibrous cap will form over the top
  • This is an atherosclerotic plaque
  • Can do an ultrasound to determine the presence of atherosclerosis of arteries
72
Q

What is a grumous?

A

A component of a coronary plaque

  • Cholesterol and fatty material come together to form crystals
  • Neovascularization of this area can occur
  • A lot of inflammatory cells are preset in this region
73
Q

What is a vulnerable plaque?

A

Plaques that are prone to rupture due to plaque hemorrhage (bleeding into the plaque) or due to fibrous cap disruption

A plaque that will send off a chunk which will get lodged in a smaller vessel and occlude it

74
Q

Describe the qualities of a vulnerable plaque

A
  • Soft with a lipid-filled core
  • Most often eccentric (not in the core of the body)
  • Most often only 40-60% stenotic (narrowed)
75
Q

What happens to a vulnerable plaque?

A
  • Atherosclerotic material gets to a smaller vessel
  • Thrombotic occlusion of coronary artery
  • Acute myocardial ischemia/infarction
76
Q

Why are vulnerable plaques hard to detect and treat prophylactically?

A
  • Only moderate stenosis

- Can’t detect them because there isn’t a closed vessel which you could see

Cardio Exam 1 (15 decks)

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