circulatory 2 Flashcards

1
Q

Myocarditis/myocardial
degeneration
- Etiology

A

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

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2
Q

Myocardial toxins that can cause myocarditis

A

Ionophores (monensin, lasolocid, salinomycin etc)
◦ Bacterial toxemia

<><><><>
◦ Gossypol toxicity (cotton seeds)
◦ Cassia occidentalis– India, South America
◦ Phalaris spp. (canary grass) – all continents

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3
Q

nutritional causes of myocarditis

A

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

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4
Q

Infectious Myocarditis - bacterial and viral causes

A

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

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5
Q

Myocarditis/Myocardial Degeneration
- Clinical signs: acute, chronic

A

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

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6
Q

Myocarditis/Myocardial Degeneration
- Clinical pathology

A

◦ 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.

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7
Q

Myocarditis/Myocardial Degeneration
- Treatment

A

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

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8
Q

Myocarditis/Myocardial Degeneration
- PM lesions

A

◦ 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

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9
Q

Pericardial Disease
Most common in ruminants? less common?

A

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

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10
Q

Hardware-associated pericarditis
- pathogenesis

A

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

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11
Q

Pericardial Disease
Clinical signs

A

◦ 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

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12
Q

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

A

◦ 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

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13
Q

Pericardial Disease
Diagnosis

A

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)

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14
Q

Pericardial Disease
Treatment

A

◦ 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)

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15
Q

what is constrictive pericarditis?

A

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

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16
Q

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

A

◦ 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

17
Q

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

A

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.

18
Q

High Mountain Disease
- who is susceptible?
- altitude?

A

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.

19
Q

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

A
  • 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
20
Q

High Mountain Disease - ‘Like’ conditions

A

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

21
Q

High Mountain Disease
Post-mortem

A

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

22
Q

High Mountain Disease
Management / Treatment, prognosis?

A

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

23
Q

Cardiomyopathy - what does this mean?

A

◦ 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)

24
Q

Bovine hereditary cardiomyopathy
- what is this?
- origins?

A

◦ 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

25
Cardiomyopathy - what types do we see in cattle? - what breeds? prognosis? - associations?
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
26
Cardiomyopathy Clinical signs
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
27
Cardiomyopathy - Diagnosis, PM
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
28
Estimated incidence of congenital heart disease in cattle
◦ Range from 0.08-1.7% ◦ Variability in: ◦ Age of subjects, postmortem techniques, interpretation of results, breed distribution
29
Estimated incidence of congenital heart disease in sheep
1.3%
30
Simple congenital heart diseases of cattle - what do we see most? what are some infrequent diseases?
◦ 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
31
Congenital Heart Disease - Left-to-right shunt results
◦ Workload both chambers is increased ◦ More left than right ◦ Animal has reduced cardiovascular functional capacity ◦ Failure to thrive/grow
32
Congenital Heart Disease - Right-to-left shunt results
◦ Added effect of hypoxemia (PaO2 25-30mmHg) ◦ Animals do poorly
33
Congenital Heart Disease - clinical signs of simple and complex defects
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
34
Congenital Heart Disease - what may cases present as?
- 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)
35
Congenital Heart Disease - Differentiating simple from complex
◦ 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
36
Congenital Heart Disease - dx, prognosis
◦ 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