cardiovascular path 1

Question 1

The LV:RV thickness ratio

Answer 1

usually 2:1 or 3:1. It is 1:1 in fetuses and neonates.

Question 2

Common incidental findings to recognize and ignore for heart PM exam

Answer 2

• Endocardial and epicardial hemorrhages.
• Valvular hemocysts (esp on AV valves of calves)
• Blood clots in the cardiac ventricles
• Euthanasia drugs precipitate on the endocardial surface (following intrave- nous injection) or pericardial surface (fol- lowing intracardiac euthanasia) is recog- nized as gritty white material.

Question 3

Valvular Endocarditis
- what is it
- Why might bacterial infection become established on a heart valve?
- appearance

Answer 3

An inflammatory lesion caused by bacterial infection.
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* Bacteria in the blood (bacteremia) can colonize a heart valve that is damaged by the daily wear-and-tear of constant motion
* Conversely, a valve that is damaged by turbulent blood flow (eg aortic or pul- monic stenosis) is more readily colonized by the minor bacteremia that all of us occasionally experience.
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- focal thickening of a heart valve with a “vegetation”
> surface is rough and dull because the inflammation has destroyed the endothelium
> covered by fibrin and neutrophils

Question 4

endocarditis vs endocardiosis lesions

Answer 4

• Endocarditis - rough dull surface
• Endocardiosis - smooth and shiny

Question 5

endocarditis lesion progression

Answer 5

• can grow into a mass that protrudes from valve surface,
• or sometimes invades into the underlying myocardium

Question 6

if you see a mass on a heart valve, think:

Answer 6

Valve neoplasms are rare: if you see a mass on the valve, think endocarditis or endocardiosis

Question 7

sequelae of endocarditis

Answer 7

• heart failure due to valvular incompetence or stenosis
• Thromboembolism to lungs (from right- sided lesion) or kidneys, myocardium, etc. (from left-sided lesion)
• Bacteremia leading to polyarthritis, etc.

Question 8

Valvular Endocardiosis
- etiology
- most common anatomic location
- appearance

Answer 8

• Caused by degeneration of the heart valve over many years.
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• most commonly affects the left atrioventricular valve: this is called myxomatous mitral valve disease (MMVD)
  > can also affect both valves, or uncommonly only right side
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  Endocardiosis appears as nodular thickening and deformity of the atrioventricular valves, with a smooth shiny surface
• valve thickened by nodules of fibrous tissue and mucopolysaccharide
• endothelium is intact

Question 9

valvular endocardiosis consequences, lesions

Answer 9

• nodular distortions make the valve incompetent
  > during systole there is leakage of blood from the ventricle to the atrium
  > dilation of the atrium
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  Sometimes, there is a “jet lesion”: a focal white area of endocardial fibrosis where a jet of regurgitated blood repeatedly impacts the atrial endocardium.
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  Mild lesions are not functionally significant, but extensive lesions cause congestive heart failure: look for evidence of heart failure

Question 10

evidence of heart failure

Answer 10

• pulmonary edema and congestion
• hemosiderin-laden alveolar macrophages
• ascites
• etc.

Question 11

• MMVD disease progression
• lesions associated with faster course

Answer 11

• usually slow progressive course
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• sometimes there is unexpectedly rapid progression to heart failure or sudden death
• In these cases, we look for:
• Rupture of the chordae tendinae, which can cause rapid decompensation of a heart that is suffering both otherwise maintaining cardiac function. The rup- tured chordae tendinae usually have hemorrhage at the site of rupture, whereas hemorrhage would not be pres- ent if you accidentally cut the chordae during the necropsy examination.
• Myocardial ischemia, because reduced cardiac output leads to underperfusion of the myocardium.
• Left atrial rupture, resulting in hemoperi- cardium.

Question 12

sepsis effect on the endocardium or epicardium

Answer 12

increased vas- cular permeability induced by sepsis can cause severe ecchymotic hemorrhages of the endocardium or epicardium

Question 13

What happens in of heart failure?

Answer 13

1. Reduced cardiac output leads to:
2. Inability to move venous blood forward

Question 14

In heart failure, there is an inability to move venous blood forward
- what happens?

Answer 14

• The failing heart cannot deal with the venous blood presented to it, to adequately maintain forward flow
• Congestive heart failure may develop, with increased venous hydrostatic pressure
  > can be left or right sided

Question 14

reduced cardiac output in heart failure leads to:

Answer 14

1. Reduced cardiac output leads to:
   - decreased renal blood flow > activation of renin-angiotensin system > sodium and water retention, leading to:
   * Peripheral edema
   * Increased blood volume → increased workload on the failing heart exacerbates heart failure
   * ↓ Pulmonary blood flow → hypoxia → ↑ erythropoiesis leading to polycythemia
   * ↓ blood flow to the heart via coronary arteries → myocardial ischemia → exacerbates heart failure
   - Cardiac hypertrophy is a compensatory mechanism, but this may eventually inter- fere with myocardial perfusion.

Question 15

characteristic lesions of Left-sided congestive heart failure

Answer 15

• Left atrial dilatation
• Pulmonary congestion and edema
• Hemosiderin-laden macrophages in pul- monary alveoli (so-called “heart failure cells), as a result of leakage of erythro- cytes from congested blood vessels into alveoli, phagocytosis of erythrocytes by pulmonary alveolar macrophages, which degrade the hemoglobin to hemosiderin.
• Hydrothorax (in cats)

Question 16

Right-sided congestive heart failure characteristic lesions

Answer 16

• Subcutaneous edema, ascites, and (in cats) hydrothorax
• Hepatomegaly
• In cattle and occasionally dogs, “nut- meg” liver, characterized by congestion, fatty degeneration, necrosis, &/or fibro- sis of periacinar regions of liver.

Question 17

some common causes of left sided heart failure

Answer 17

• Left AV valve or aortic valve lesions: endocardiosis, endocarditis
• Myocardial disease: cardiomyopathy, myocardial necrosis, myocarditis
• Cardiac anomalies (SAS, PDA, VSD)

Question 18

some common causes of right sided heart failure

Answer 18

• Right AV valve or pulmonic valve lesions: endocardiosis, endocarditis
• Cor pulmonale due to increased resis- tance to pulmonary blood flow (high-alti- tude, widespread bronchiolar disease, interstitial lung disease, pulmonary vascular disease)
• Right heart failure can develop as a con- sequence of chronic left heart failure.

Question 19

Cor pulmonale is:

Answer 19

• an enlarged right ventricle in your heart that happens because of a lung condition.
• Pushing against high pressure in your pulmonary artery can cause your right ventricle to fail.

Question 20

Cardiac dilatation, causes:

Answer 20

• It dilates because it cannot contract, such as from myocardial necrosis or inflammation, or unknown causes (i.e. primary dilated cardiomyopathy)
• It dilates because it contains too much blood. This is volume overload—i.e., an increase in the amount of blood distend- ing the chamber, such as from a leaky valve (MMVD) or a shunt (PDA, VSD).
  > In this case, the ventricle receives an increased volume of blood, and dilates to accomodate this volume.
  > Concurrently, the heart works harder than normal, resulting in hypertrophy (increased mass of muscle).
  > Together, this results in “eccentric hypertrophy” or an increased myocardial mass with a dilated lumen.

Question 21

cardiac hypertrophy, common cause?
types and their causes.

Answer 21

• response to increased workload
• represents an attempt to compensate.
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• Eccentric hypertrophy: increased myocardial mass with a dilated lumen, caused by volume overload.
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  Concentric hypertrophy: increased myocardial mass with a small lumen, caused by pressure overload

Question 22

classic example of concentric hypertrophy

Answer 22

increased myocardial mass with a small lumen, caused by pressure overload
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- Subaortic stenosis is the classic example of concentric hypertrophy: the left ventricle has to work hard to push blood past the stenotic outflow tract and into the aorta
- the heart muscle hypertrophies but the lumen remains small because there is no increase in volume of blood within it

Question 23

concentric vs ecentric hypertrophy pathogenesis

Answer 23

Concentric Hypertrophy:
Stenosis of the outflow tract → pressure overload → concentric hypertrophy
(↑ mass, small lumen)
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Eccentric hypertrophy:
Shunt or leaky valves → volume overload → eccentric hypertrophy (↑ mass, big lumen)

Question 24

adverse effects of cardiac hypertrophy on the heart itself

Answer 24

if excessive, it may:
(i) prevent adequate perfusion of the myocardium
(ii) increase myocardial oxygen consumption, even though perfusion is becoming limited,
(iii) compromise the efficient laminar flow of blood within the ventricle, leading to inefficient turbulent flow, which in turn requires increased workload on the heart.
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As the primary heart lesion worsens (for example, the MMVD-affected valve becomes more nodular and leaky) these factors limit the ability of the myocardium to keep up with demand, and ultimately lead to ischemic necrosis of myofibres and dilata- tion of the ventricle.

Question 25

Cardiomyopathy, definition
- primary vs secondary

Answer 25

Cardiomyopathy is simply a disease of the heart muscle.
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1. When we say “cardiomyopathy”, we usually mean “primary cardiomyopathy”, which is a disease that is intrinsic to the myocardium
> often idiopathic
> can be inherited mutations of contractile protein genes, etc.
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2. If we can identify a cause = seconday cardiomyopathy, eg.
> Eccentric hypertrophy of the myocar- dium can result from leaky valves or congenital shunts (volume overload)
> Concentric hypertrophy can result from subaortic stenosis (pressure overload), hyperthyroidism (heart muscle works harder and hypertrophies), or an epi- nephrine-secreting pheochromocytoma (causes systemic hypertension and thus pressure overload)

Question 26

different forms of cardiomyopathies - main 3 +1 + 1

Answer 26

• hypertrophic cardiomyopathy
• restrictive cardiomyopathy
• dilated cardiomyopathy
• arrhythmogenic right ventricular cardiomyopathy
• unclassified cardiomyopathy