Cardiovascular

What is the most important principle when examining the heart at necropsy?

Observation comes before protocol and sampling — carefully orient and assess the heart before cutting.

What structure is used for orientation of the heart?

The right auricle is the key landmark for orientation

What chamber features must always be assessed?

• Size of the atria

• Wall thickness

• Chamber volume

Why is the septum important during examination?

The septum is your guide to distinguishing left vs right sides and assessing symmetry or hypertrophy

What is the correct directional flow to follow when examining chambers?

Atria → inflow → outflow

What learning tools are emphasized for mastering heart examination?

• Courselink videos

• Necropsies

Why is external orientation critical before cutting?

Incorrect orientation can lead to misidentification of chambers, vessels, or lesions

What are the two key external grooves used to orient the heart?

• Subsinuosal groove

• Paraconal groove

They correspond to interventricular septal orientation and help distinguish right vs left ventricular surfaces

Which groove on the heart is typically visible on the right side?

The subsinuosal groove

Which groove on the heart is typically visible on the left side?

The paraconal groove

What core steps should you mentally follow in an exam setting when identifying heart anatomy?

• Locate the right auricle

• Identify right vs left side

• Assess atria size

• Compare wall thickness and chamber volume

• Use septum as guide

• Follow atria → inflow → outflow

prevents random guessing and ensures systematic identification of lesions and chambers

What does a VSD cause physiologically?

Left-to-right shunt, increased pulmonary blood flow, volume overload

What are the two major endocardial diseases?

• Endocardiosis (degenerative)

• Endocarditis (infectious) → inflammation + thrombosis

What is endocardiosis (MMVD)?

Chronic degenerative disease of cardiac valves, especially mitral → Very common in dogs

• Shiny, smooth nodules → fibrous tissue over the valve

• Valve distortion

Valvular incompetence → volume overload

How do you tell if valvular disease is significant?

Look for secondary changes:

• Atrial dilation

• Ventricular hypertrophy

• Congestion or edema

Normal structures of the dog aortic valve

1. Nodule in centre

   of each cusp

2. Ventricular

   outflow: all muscle

   until annulus of

   valve cusp

• L atrium is larger → functionally significant, regurge of blood

• L ventricle is very big

• shiny nodules on valve

• jet lesion

• outside the heart → pulmonary congestion and edema, heart failure cells, effusion

Lesions of LEFT heart failure?

• Pulmonary edema & congestion

• Heart failure cells

• Pleural effusion (cats, both)

Lesions of RIGHT heart failure?

• Ascites

• Congested/enlarged liver

• Subcutaneous edema

• Pleural effusion

• Pulmonary Congestion

What findings indicate compensation (not failure)?

• Atrial dilation

• Eccentric or concentric hypertrophy

What is endocarditis?

Bacterial infection of valves with thrombosis and neutrophilic inflammation

Gross appearance

• Rough, dull, irregular vegetations

Sequelae

• Valvular insufficiency

• Septic emboli

• Heart failure

What is the lesion

Endocarditis in the dog → less severe

Causes of acute worsening in chronic heart failure?

• Myocardial ischemic necrosis

• Ruptured chordae tendineae

• Left atrial dilation, rupture, hemopericardium, tamponade

Ruptured vs. Cut chordae tendineae

What causes gritty endocardial lesions in dogs?

Barbiturate euthanasia artifact

Endocardial hemorrhages in horses indicate?

Often incidental, consider sepsis context.

Blood-filled cysts in neonatal calves?

Common and insignificant

How does myocardium compensate?

• ↑ Stroke volume → ↑ chamber size

• ↑ Heart rate

• ↑ Contractility → myocardial hypertrophy

• ↑ Sodium/water retention

Why is myocardium compensation inefficient?

• ↓ Diastolic filling

• ↑ Myocardial work

• ↓ Perfusion

What happens when myocardial compensation fails (decompensation)?

Decompensation leads to myocardial ischemia, resulting in:

• Decreased contractility, reducing cardiac output

• Ventricular dilation due to volume overload

• Atrial enlargement, secondary to impaired ventricular filling

• Venous congestion and edema, producing clinical heart failure signs

This marks the transition from adaptive hypertrophy to pathologic heart failure.

How do pressure overload and volume overload differ in their effects on myocardial hypertrophy?

• Pressure overload (e.g. subaortic stenosis, pulmonic stenosis, pulmonary hypertension):

  • Causes concentric hypertrophy

  • Wall thickness increases without chamber dilation

  • Reduces ventricular compliance → diastolic dysfunction

• Volume overload (e.g. valvular insufficiency, shunts):

  • Causes eccentric hypertrophy

  • Wall thickness increases with chamber dilation

  • Leads to systolic dysfunction over time

How does a ventricular septal defect (VSD) alter cardiac blood flow and workload?

A VSD causes left-to-right shunting due to higher left ventricular pressure, resulting in:

• Increased pulmonary blood flow

• Volume overload of the left heart

• Progressive eccentric hypertrophy

• Eventual pulmonary hypertension and heart failure if severe or chronic

How do compensation and left heart failure differ in myxomatous mitral valve disease (MMVD)?

• Compensated MMVD:

  • Atrial dilation

  • Eccentric ventricular hypertrophy

  • Maintained cardiac output

• Decompensated MMVD (left heart failure):

  • Pulmonary congestion and edema

  • Reduced forward output

  • Clinical respiratory distress

This slide emphasizes staging of disease, not just lesion presence

aortic stenosis causing pressure overload, where the left ventricle must generate abnormally high pressure to maintain normal cardiac output, leading to concentric hypertrophy

What is cardiomyopathy, and how are primary and secondary forms distinguished?

• Primary cardiomyopathy:

  • Intrinsic disease of cardiac myofibers

  • Often idiopathic or inherited

• Secondary cardiomyopathy:

  • Myocardial changes secondary to another condition

  • Causes include hyperthyroidism, nutritional deficiency, hypertension, congenital anomalies, or chronic heart failure

Major categories:

• Hypertrophic

• Dilated

• Restrictive

• Unclassified

• Arrhythmogenic right ventricular cardiomyopathy (ARVC)

What defines hypertrophic cardiomyopathy and which species is most affected?

HCM is characterized by concentric hypertrophy of the left ventricle, involving:

• Thickening of the free wall and interventricular septum

• Reduced ventricular compliance

• R/O hyperthyroidism, hypertension, subaortic stenosis, hypersomatotropism

• Heterogeneous >1 disease, clinical or subclinical

It is most common in cats, and uncommon in other species.

Why must hyperthyroidism be ruled out before diagnosing primary HCM?

Hyperthyroidism causes secondary concentric myocardial hypertrophy due to:

• Increased metabolic demand

• Chronic sympathetic stimulation

• Increased heart rate and contractility

This produces a phenotype indistinguishable grossly from primary HCM.

What are the gross and histologic lesions of hypertrophic cardiomyopathy?

Gross lesions:

• Marked left ventricular hypertrophy without dilation

• Increased heart weight

• LV : RV wall ratio >3:1 (often ~5:1)

• ± Left atrial dilation

Histologic lesions:

• Myocardial fibrosis

• ± Myofiber disarray

• Vascular changes contributing to ischemia

What functional impairments result from hypertrophic cardiomyopathy?

• Diastolic dysfunction due to stiff ventricular walls (most important)

• Electrical instability, predisposing to arrhythmias

• Myocardial ischemia, from reduced capillary density and increased oxygen demand

• Systolic function is often initially preserved

Why is myofiber disarray significant in hypertrophic cardiomyopathy?

Myofiber disarray:

• Disrupts coordinated contraction

• Increases electrical instability

• Predisposes to fatal arrhythmias

• Is a key histologic hallmark of primary HCM

How is restrictive cardiomyopathy defined and distinguished from HCM and DCM?

Not on exam

RCM is defined by restricted ventricular filling during diastole with:

• Normal ventricular wall thickness

• Marked atrial dilation

• Endocardial fibrosis ± synechiae

Unlike HCM or DCM, ventricles are neither thickened nor dilated

What are the causes of dilated cardiomyopathy?

Secondary causes: look for other gross and histo lesions, test levels in blood or diet

• Volume overload

• Myocarditis

• Myocardial necrosis

• Shunts

• Nutrition → Taurine or carnitine deficiency

Primary (idiopathic) DCM:

• Common in Dobermans, giant breeds, English Cocker Spaniels, and cats

How is diet linked to dilated cardiomyopathy?

Diet-associated DCM has been linked to:

• Taurine deficiency (especially in cats)

• Certain dog breeds with altered taurine metabolism

• Diets high in legumes, low protein, or unusual ingredients

Supplementation can partially or fully reverse disease in some cases

What are the key features of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

• Primarily affects Boxer dogs

• Causes sudden death due to arrhythmias → send in heart tissue especially R side

• Gross lesions may be minimal or show RV dilation

• Histology shows fibrofatty replacement of right ventricular myocardium

What are the major causes of myocardial necrosis?

• Ischemia

• Exertional injury, less likely in the heart, more SkM

• Nutritional deficienc

• Toxic injury (e.g. monensin)

• Distinguished from myocarditis via histopathology → cannot distinguish grossly

What causes white muscle disease and which tissues are affected?

White muscle disease is caused by vitamin E and selenium deficiency, leading to:

• Oxidative damage to cell membranes

• Necrosis of skeletal and/or cardiac muscle

• ± Mineralization of affected fibers

What causes atypical myopathy in horses?

Ingestion of box elder (Manitoba maple) toxins causes:

• Severe rhabdomyolysis

• Cardiac and skeletal muscle necrosis

• Often fatal acute disease

What infectious agents cause myocarditis?

• Viral: parvovirus, distemper, BVDV

• Protozoal: Toxoplasma, Neospora

• Bacterial: Histophilus somni, Clostridium chauvoei

• Immune-mediated: rheumatic fever (humans)

How does Histophilus somni cause myocardial injury?

Always effects papillary muscle of the L ventricle

Through:

• Bacteremia

• Vasculitis

• Infarction of myocardium
  Resulting in severe myocardial dysfunction.

What are the major categories of myocardial disease?

• Response to increased demand (hypertrophy)

• Cardiomyopathies (HCM, DCM, RCM, ARVC)

• Myocardial necrosis

• Specific diseases (white muscle disease, monensin toxicity, Histophilus somni)

Where does heart worm go?

Pulmonary artery

What structures and disease processes define pericardial pathology?

Pericardial diseases involve the pericardial sac and affect cardiac filling rather than myocardial contraction. Major processes include:

• Abnormal fat metabolism

• Fluid accumulation

• Hemorrhage

• Inflammation

These diseases primarily impair diastolic filling.

What is gelatinous transformation (serous atrophy) of fat, and why does it occur?

Serous atrophy of fat is caused by severe negative energy balance, leading to:

• Mobilization of fat stores

• Replacement of adipocytes with gelatinous, translucent material

• Commonly affects epicardial fat, bone marrow, and perirenal fat

It indicates chronic disease or starvation, not primary heart disease

What is hydropericardium and what causes it?

Hydropericardium is accumulation of non-inflammatory fluid in the pericardial sac, caused by:

• Hypoproteinemia

• Congestive heart failure

• Generalized edema states

It reduces cardiac filling but is usually secondary, not a primary cardiac disease

What is hemopericardium and why is it clinically significant?

Hemopericardium is blood accumulation in the pericardial sac, which can rapidly cause:

• Cardiac tamponade

• Reduced venous return

• Acute circulatory collapse

Severity depends on rate of bleeding, not volume alone

What are the most likely causes of hemopericardium in different animals?

• Newborn calf: trauma, coagulopathy

• Older dog: hemangiosarcoma (right auricle)

• Young adult dog: idiopathic (benign) pericardial effusion

• Horse: aortic rupture

How does aortic rupture lead to cardiac tamponade?

Rupture of the aorta causes rapid blood accumulation within the pericardial sac, resulting in:

• Acute increase in intrapericardial pressure

• Compression of the heart

• Inability of ventricles to fill during diastole

• Sudden death

What are the three routes by which infection reaches the pericardium?

• Hematogenous spread

• Extension from adjacent structures (lungs, myocardium)

• Direct penetration (foreign bodies)

What are common bacterial causes of pericarditis by species?

• Neonates: E. coli

• Pigs: Streptococcus suis, Glaesserella parasuis

• Cattle: hardware disease, Clostridium chauvoei

How do you determine the route of infection in pericarditis cases?

By evaluating:

• Lesion distribution

• Presence of foreign bodies

• Concurrent systemic infection

• Adjacent organ involvement

This determines whether spread was hematogenous, local extension, or penetrating

How does hardware disease cause pericarditis?

A sharp metallic foreign body penetrates the reticulum, diaphragm, and pericardium, causing:

• Bacterial contamination

• Severe inflammation

• Often fibrinopurulent pericarditis

What lesion pattern is typical of hardware ds

• Thick fibrin layers

• Purulent exudate

• Adhesions between pericardium and epicardium

• Progressive restriction of cardiac filling

Why is fibrinopurulent pericarditis termed “constrictive”?

Because fibrin and fibrosis:

• Physically restrict cardiac expansion

• Prevent normal diastolic filling

• Cause signs of right-sided heart failure

Which pathogens commonly cause fibrinous pericarditis in pigs?

• Streptococcus suis

• Glaesserella parasuis

• Mycoplasma hyorhinis

These typically spread hematogenously

What are the major causes of vasculitis and vascular necrosis?

• Immune complex deposition (Type III hypersensitivity)

• Infectious agents

• Physical injury (burns, frostbite)

• Hypertension

• Uremia

What are the major vascular pathologies introduced?

• Vasculitis → targets wall of vessel

• Aortic mineralization

• Arteriosclerosis & atherosclerosis

• Thrombosis and embolism

• Disseminated intravascular coagulation (DIC)

Which infectious agents commonly damage blood vessels?

• Bacteria: Erysipelothrix, Histophilus somni, Rickettsia rickettsii (RMSF)

• Viruses: EVA, FIP, BVD, MCF, PCV

• Fungi: Aspergillus

• Parasites: Strongylus vulgaris

How does acute BVD cause vasculitis?

Through:

• Endothelial injury

• Immune-mediated inflammation

• Fibrinoid necrosis of vessel walls

What is the primary vascular consequence of vascular injury: FIP and African horse sickness?

1. Edema

• Increased vascular permeability

• Leakage of protein-rich fluid

• Severe edema and effusions

2. Ecchymotic hemorrhages (DIC)

3. Peripheral infarcts (sepsis)

How does disseminated intravascular coagulation cause hemorrhage?

DIC causes:

• Widespread microthrombosis

• Consumption of clotting factors

• Secondary uncontrolled hemorrhage

What are the major outcomes of blood vessel injury?

• Thrombosis → ischemia, infarction

• Increased permeability → edema, hemorrhage, protein rich exudates, Fibrinoid necrosis

• DIC → consumptive coagulopathy, hemorrhages

What is the difference between metastatic and dystrophic vascular mineralization?

• Metastatic: due to systemic mineral imbalance (vitamin D toxicity, Johne’s)

  

• Dystrophic: occurs at sites of prior vascular injury

  

What defines hemangiosarcoma and why is it dangerous?

Hemangiosarcoma is a malignant endothelial tumor, commonly affecting:

• Right auricle

• Spleen

• Skin

It causes:

• Hemopericardium

• Cardiac tamponade

• Sudden death