circulatory 2

Question 1

Myocarditis/myocardial
degeneration
- Etiology

Answer 1

◦ Myocardial degeneration (toxic/nutritional)
◦ Myocardial toxin
◦ Nutritional
◦ Infectious Myocarditis

Question 2

Myocardial toxins that can cause myocarditis

Answer 2

◦ Ionophores (monensin, lasolocid, salinomycin etc)
◦ Bacterial toxemia
<><><><>
◦ Gossypol toxicity (cotton seeds)
◦ Cassia occidentalis– India, South America
◦ Phalaris spp. (canary grass) – all continents

Question 3

nutritional causes of myocarditis

Answer 3

◦ Vitamin E / Se deficiency
◦ Excessive dietary molybdenum or sulfates

Question 4

Infectious Myocarditis - bacterial and viral causes

Answer 4

Bacterial
◦ Histophilus somni (formerly Hemophilus somnus)
◦ Truperella pyogenes (formerly Arcanobacterium, Actinomyces, Corynebacterium)
◦ Clostridial myocarditis - lambs
<><><><>
Viral
◦ Foot & Mouth Disease
◦ Bluetongue in sheep

Question 5

Myocarditis/Myocardial Degeneration
- Clinical signs: acute, chronic

Answer 5

Peracute /acute
◦ Sudden death
<><>
Chronic
◦ Heart failure (subacute to chronic cases)
◦ Arrhythmias
◦ Vitamin E / selenium deficiency
◦ Cases tend to die when exercised (unaccustomed)

Question 6

Myocarditis/Myocardial Degeneration
- Clinical pathology

Answer 6

◦ Depend on the underlying cause (toxic vs septic)
◦ Isoenzymes (LDH/CK) ??
<><>
◦ Cardiac Troponin I (structural protein) - cTpnI
◦ Indicative of active myocardial damage
◦ More sensitive, less cross-reactivity with skeletal muscle
◦ Myocardial necrosis had a cTnI concentration > or = 1.04 ng/mL.
◦ Experimental monensin toxicity cows.

Question 7

Myocarditis/Myocardial Degeneration
- Treatment

Answer 7

◦ Remove/treat underlying cause > Treat deficiencies
◦ Rest, minimize stress
◦ Anti-arrhythmics (usually not feasible)
◦ Anti-inflammatory medication for myocarditis > Cortiosteroids, NSAIDs (flunixin, meloxicam, ketoprofen)

Question 8

Myocarditis/Myocardial Degeneration
- PM lesions

Answer 8

◦ Gross PM often unrewarding
◦ Histology: degeneration, fibrosis, cellular infiltration
> Vit E/Selenium
> May see “characteristic” streaked pallor
◦ Myocarditis lesions may have abscesses
> But may be patchy on histology and may be missed

Question 9

Pericardial Disease
Most common in ruminants? less common?

Answer 9

Septic pericarditis
◦ Cows > Traumatic reticulitis/pericarditis
◦ Sheep, goats, calves > Component of septicemia
<><><><>
◦ Lymphoma (uncommon)

Question 10

Hardware-associated pericarditis
- pathogenesis

Answer 10

◦ Foreign body penetrates reticulum
◦ Distance to pericardium 1-1.5 cm
◦ Infectious pericarditis
◦ Mixed infection usually
◦ Intestinal organisms, May be gas producing

Question 11

Pericardial Disease
Clinical signs

Answer 11

◦ Muffled heart sounds > Fluid in pericardial sac interferes with sound transmission
◦ Weak and rapid peripheral pulse
◦ Decreased cardiac filling → decreased stroke volume→ decreased cardiac output
◦ Venous engorgement > Right heart cannot fill (thin walled), Compromised venous return
◦ Percussion (enlarged cardiac area)
◦ Jugular veins are often extremely distended
◦ Elbows abducted
◦ Pericarditis is often painful (mostly early in disease)
◦ May have a fever
◦ Friction rub sound (like an intense murmur)
◦ Hardware (TRP): history of anorexia, decreased milk production, poor rumen
motility, positive withers pinch
◦ May have splashing sound on auscultation

Question 12

Pericardial Disease
Friction rubs - what are these?
- what do they sound like?
- when can we no longer hear them?

Answer 12

◦ Fibrin layers on pericardium & epicardium rubbing together
<><>
Differentiation from murmurs
◦ Vary beat to beat
◦ In timing (i.e. cannot fix it to heart sounds: S1, S2)
◦ In character
◦ In intensity
<><>
◦ May be present at one examination, then absent, then reappear
◦ Disappear once effusion accumulates

Question 13

Pericardial Disease
Diagnosis

Answer 13

Clinical signs:
◦ Clinical diagnostic triad: muffled heart sounds, weak rapid pulse, venous engorgement
<><>
Ultrasound:
◦ Anechoic to flocculent fluid with fibrin strands and gas
◦ Thickness of pericardium
◦ Rectal probe may be useful (5-7 cm penetration depth)
<><>
ECG - Electrical Alternans
◦ Alternating large and small QRS complexes
◦ Change in ventricular axis due to presence of fluid
<><>
◦ Pericardiocentesis (best U/S guidance)

Question 14

Pericardial Disease
Treatment

Answer 14

◦ Systemic antibiotics alone not often enough
◦ Drainage of pericardial sac if causing enough signs
◦ Local instillation of antibiotics?
<><><><>
Surgery
◦ Rumenotomy: removal of foreign body through reticulum may work if pericardial involvement not
extensive.
◦ Once pericarditis well established often difficult to treat.
◦ Pericardectomy (usually a heroic effort)

Question 15

what is constrictive pericarditis?

Answer 15

◦ Fibrin formation organizes and forms fibrous tissue which restricts filling, may be a sequela or pericarditis

Question 16

Pericardial Disease
Post mortem examination
- what can we see? with hardware disease?

Answer 16

◦ Pericardium full of fluid
◦ Appearance of fluid varies with underlying disease
<><><><>
Hardware:
◦ Thickened pericardium
◦ Purulent, fibrinous fluid
◦ Communication with reticulum may be evident
◦ Foreign body may be present
◦ May have been withdrawn by magnet
◦ May have migrated further

Question 17

High Mountain Disease
- what is this?
- pathogenesis?
- what can make it worse?

Answer 17

Congestive heart failure occurring in cattle moved to and living at altitude
◦ Low atmospheric O2 causes alveolar hypoxia → reflex pulmonary arterial
vasoconstriction → pulmonary hypertension → right heart failure
Cor Pulmonale
(right heart failure secondary to pulmonary hypertension)
- Worsened by ingestion of locoweed: Oxytropis and Astragalus spp.

Question 18

High Mountain Disease
- who is susceptible?
- altitude?

Answer 18

Animals introduced to high altitude rather than
indigenous.
◦ Sheep, goats relatively resistant
◦ Holsteins appear predisposed
<><>
Elevation above see level?
◦ Variable depending on intercurrent disease, distance over
which animal must forage, nutrition.
◦ But generally, over 1800m above sea level.

Question 19

High Mountain Disease
- why are cows sensitive?
- compensation?
- additional effects?
- adaptation?

Answer 19

• Chronic low oxygen causes pulmonary arterioles to constrict > increased afterload
• Cows sensitive due to highly developed muscular media even in small pulmonary arterioles
• Compensatory mechanisms such as hyperventilation, polycythemia, increased cardiac output DO NOT develop
• Hypoxemia also causes myocardial damage
• Adaptation can occur if introduction to altitude is gradual

Question 20

High Mountain Disease - ‘Like’ conditions

Answer 20

Can have similar “syndrome” without altitude
◦ Severe pulmonary parasitosis
<><>
Severe pneumonia resulting in severe hypoxia
◦ Response to hypoxia can be the same and cor pulmonale can develop
◦ Can be exacerbated if with diseases such as diarrhea (eg. septic calves)
◦ Acidosis potentiates vasoconstriction

Question 21

High Mountain Disease
Post-mortem

Answer 21

◦ Congestive heart failure
◦ Concentric right ventricular hypertrophy!
◦ May need to weigh chambers to diagnose: Right ventricular free wall >30% heart weight

Question 22

High Mountain Disease
Management / Treatment, prognosis?

Answer 22

◦ Remove from altitude
◦ Minimize stress
◦ Diuretics may be of some benefit
◦ Usually die 3-4 weeks from onset of edema
◦ Slaughter/euthanasia

Question 23

Cardiomyopathy - what does this mean?

Answer 23

◦ Non-specific term
◦ Subacute or chronic
◦ Primary or intrinsic disorders of the myocardium.
◦ Reflect primary myocardial, biochemical and/or metabolic deficiencies
◦ Intrinsic myocardial disease (no other cardiac tissues affected)

Question 24

Bovine hereditary cardiomyopathy
- what is this?
- origins?

Answer 24

◦ Group of progressive degenerative disorders of the myocardium causing congestive heart failure and
subsequently death.
◦ Canadian Holstein sire Montwick Red Apple Sovereign (MRAS) > common ancestor

Question 25

Cardiomyopathy - what types do we see in cattle?
- what breeds? prognosis?
- associations?

Answer 25

Only dilated cardiomyopathy occurs in the bovine
<><>
Inherited forms:
◦ Polled Herefords
◦ Japanese black cattle
> Both breeds die very young (2-3 months)
<><>
Inherited form in Holsteins:
◦ Linked to the gene for red color
◦ Associated with diffuse myocardial fibrosis.
<><>
- Gene is also seen in black & white cattle therefore the disease can be seen with this color.
- Crossbreds can be affected
◦ Signs within 4 years of age

Question 26

Cardiomyopathy
Clinical signs

Answer 26

Right heart failure
◦ Tachycardia, tachypnea, +/- dyspnea
◦ Decreased: appetite, exercise tolerance and decreased production
◦ Venous engorgement
◦ Ventral edema (Brisket)
◦ Ascites
◦ Cool extremities
◦ Animal stands with elbows abducted
◦ Arrhythmias may occur but are uncommon

Question 27

Cardiomyopathy
- Diagnosis, PM

Answer 27

Rule out other causes of right heart failure
◦ Congenital heart disease, endocarditis, myocardial degeneration, traumatic
pericarditis
<><>
Clinical signs
◦ Otherwise healthy animal of target age/breed
<><>
PM: CHF + extensive myocardial fibrosis with ongoing cardiac
myocyte degeneration

Question 28

Estimated incidence of congenital heart disease in cattle

Answer 28

◦ Range from 0.08-1.7%
◦ Variability in:
◦ Age of subjects, postmortem techniques, interpretation of results, breed distribution

Question 29

Estimated incidence of congenital heart disease in sheep

Answer 29

1.3%

Question 30

Simple congenital heart diseases of cattle - what do we see most? what are some infrequent diseases?

Answer 30

◦ VSD (most common congenital heart defect)
◦ ASD, PDA less frequent
<><><><>
Complex anomalies infrequent
◦ Tetralogy of Fallot
◦ Persistent truncus arteriosus
◦ Pulmonic valve atresia
◦ Tricuspid valve atresia
◦ Hypoplastic left ventricle
◦ Hypoplastic right ventricle

Question 31

Congenital Heart Disease
- Left-to-right shunt results

Answer 31

◦ Workload both chambers is increased
◦ More left than right
◦ Animal has reduced cardiovascular functional capacity
◦ Failure to thrive/grow

Question 32

Congenital Heart Disease
- Right-to-left shunt results

Answer 32

◦ Added effect of hypoxemia (PaO2 25-30mmHg)
◦ Animals do poorly

Question 33

Congenital Heart Disease - clinical signs of simple and complex defects

Answer 33

Variable!
<><>
Simple defects
◦ Small and uncomplicated defects may be asymptomatic
◦ Incidental murmurs
◦ Larger defects may be initially without signs and then gradually progress
<><>
Complex defects
◦ Moderate to severe exercise intolerance
◦ May be associated with cyanosis due to right to left shunting

Question 34

Congenital Heart Disease
- what may cases present as?

Answer 34

• Cases may present as respiratory distress
• Must differentiate from pneumonia
• Previously stable case may present as sudden onset “pneumonia” following
  unaccustomed exercise
• Poor growth rate (common)
• Animals may decompensate with first calving (e.g. cow with larger VSD)

Question 35

Congenital Heart Disease
- Differentiating simple from complex

Answer 35

◦ Echocardiography
◦ Murmur of simple VSD usually loudest well forward on right side (membranous VSD)
◦ Murmur of VSD associated with complex anomaly often loudest on left (smooth septal)
◦ If hypoxia, then probably complex
◦ PDA murmur → consider complex
> PDA alone rare in ruminants
> PDA usually clinically significant, Other than in first couple hours after birth

Question 36

Congenital Heart Disease
- dx, prognosis

Answer 36

◦ Echocardiography > Definitive diagnostic technique aside from PM
◦ Clinical pathology unremarkable (other than blood gases)
◦ Prognosis grave other than for VSD
◦ Small VSD may have reasonable prognosis
> May predispose to endocarditis
> May become significant late in gestation/ early calving
> May have reduced production