cardiovascular path 1 Flashcards
The LV:RV thickness ratio
usually 2:1 or 3:1. It is 1:1 in fetuses and neonates.
Common incidental findings to recognize and ignore for heart PM exam
- 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.
Valvular Endocarditis
- what is it
- Why might bacterial infection become established on a heart valve?
- appearance
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
endocarditis vs endocardiosis lesions
- Endocarditis - rough dull surface
- Endocardiosis - smooth and shiny
endocarditis lesion progression
- can grow into a mass that protrudes from valve surface,
- or sometimes invades into the underlying myocardium
if you see a mass on a heart valve, think:
Valve neoplasms are rare: if you see a mass on the valve, think endocarditis or endocardiosis
sequelae of endocarditis
- 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.
Valvular Endocardiosis
- etiology
- most common anatomic location
- appearance
- Caused by degeneration of the heart valve over many years.
<><><><> - 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
valvular endocardiosis consequences, lesions
- 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
evidence of heart failure
- pulmonary edema and congestion
- hemosiderin-laden alveolar macrophages
- ascites
- etc.
- MMVD disease progression
- lesions associated with faster course
- usually slow progressive course
<><><><> - 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.
sepsis effect on the endocardium or epicardium
increased vas- cular permeability induced by sepsis can cause severe ecchymotic hemorrhages of the endocardium or epicardium
What happens in of heart failure?
- Reduced cardiac output leads to:
- Inability to move venous blood forward
In heart failure, there is an inability to move venous blood forward
- what happens?
- 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
reduced cardiac output in heart failure leads to:
- 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.
characteristic lesions of Left-sided congestive heart failure
- 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)
Right-sided congestive heart failure characteristic lesions
- 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.
some common causes of left sided heart failure
- Left AV valve or aortic valve lesions: endocardiosis, endocarditis
- Myocardial disease: cardiomyopathy, myocardial necrosis, myocarditis
- Cardiac anomalies (SAS, PDA, VSD)
some common causes of right sided heart failure
- 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.
Cor pulmonale is:
- 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.
Cardiac dilatation, causes:
- 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.
cardiac hypertrophy, common cause?
types and their causes.
- response to increased workload
- represents an attempt to compensate.
<><><><> - 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
classic example of concentric hypertrophy
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
concentric vs ecentric hypertrophy pathogenesis
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)