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)
adverse effects of cardiac hypertrophy on the heart itself
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.
Cardiomyopathy, definition
- primary vs secondary
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)
different forms of cardiomyopathies - main 3 +1 + 1
- hypertrophic cardiomyopathy
- restrictive cardiomyopathy
- dilated cardiomyopathy
- arrhythmogenic right ventricular cardiomyopathy
- unclassified cardiomyopathy
