CANINE CARDIOMYOPATHIES Flashcards

1
Q

respiratory signs patient - what diagnostic tests to prioritize?

A
  • thoracic radiographs > most important to rule out many things
  • ECG > we hear tachyarrhythmia, but need to know more about rhythm diagnosis
  • CBC/biochem > may need to treat with diuretics, want to know kidney function
  • BP > weak femoral pulses; identify if hypotensive
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2
Q

if a patient presents and we have a suspicion of heart failure, what a good first step?

A

if congestive heart failure is anywhere in my Ddx, will probably benefit from furosemide to get fluid off their lungs
> will not be bad if eg. pneumonia anyways

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3
Q

Atrial fibrillation - typical ECG appearance

A
  • Absence of P waves
  • Irregular rhythm
  • Usually tachycardic
  • (+/- f waves)
  • Typically narrow QRS complexes (supraventricular origin)
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4
Q

Atrial fibrillation (AF)
- prevalence in dogs and cats
- most common cause in small animals?

A
  • Most common clinically relevant arrhythmia in dogs (esp. large/giant breeds)
  • Rare in cats > as their small atria cant easily attain critical mass
  • Requires critical atrial mass to
    initiate and sustain AF
  • Pathologic atrial dilation is most common cause in small animals
    > E.g. 2° to DCM, MVD
  • Primary (“Lone”) AF
    > Giant breeds (Irish wolfhounds, Great Dane)
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5
Q

Consequences of AF

A
  • No atrial contribution to filling
  • Tachycardia (↓ diastolic filling time)
    <><>
    Resulting in:
  • ↓ cardiac output
  • ↑ filling pressures
  • ↑ myocardial oxygen demand
  • Worsening of CHF
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6
Q

thoracic radiographs for DCM

A
  • Left atrial enlargement
  • Left ventricular enlargement
  • Pulmonary venous distension
  • Diffuse bronchointerstitial pulmonary pattern > Worse caudodorsally
    <><><><>
  • Radiographic diagnosis: left-sided cardiomegaly & cardiogenic pulmonary edema
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7
Q

Development of pulmonary edema, pathogenesis (related to left sided congestive heart failure)

A
  • Left atrial enlargement
  • Pulmonary Venous Distention
  • pulmonary capillary hypertension
  • interstitial pulmonary edema
  • alveolar pulmonary edema
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8
Q

echocardiogram observation for DCM

A
  • rounded, dilated ventricle and decreased systolic function
  • reduced contractility
  • this test gives us a definitive diagnosis of DCM
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9
Q

Dilated Cardiomyopathy (DCM) Phenotype, prevalence? what dogs get it more commonly?

A
  • Dilation of left +/- right ventricle
  • Decreased contractility
  • Second most common canine acquired cardiac disease (second to degenerative mitral valve disease)
  • More common in large/giant breeds
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10
Q

DCM etiologies

A

Primary
* genetic > doberman
<><>
Secondary
* Nutritional
* Tachycardia-induced
* Toxicity > E.g. doxorubicin
* Infectious
> Trypanosoma cruzi (Chagas dz)
> Viral (e.g. parvovirus)

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11
Q

nutritional DCM - may be related to what? who may be predisposed?

A

Taurine deficiency
* Impaired energy metabolism
* Cocker spaniels, Golden Retrievers
* Cats

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12
Q

Progression of Canine DCM

A

NORMAL Stage A
- Normal heart and Free of clinical signs
<><>
PRECLINICAL Stage B
- Abnormal heart and Free of clinical signs
- usually lasts 2-4 years
<><>
CLINICAL/CHF Stage C and D
- stage C: onset of CHF, possible sudden death
- More abnormal heart and With clinical signs
- stage D: Development of refractory heart failure
- can have CHF death, sudden death, CHF euthanasia
- usually lasts 4-6 months in dobermans, or ~1 year for others
<><><><><>
- A: at risk
- B and on: Development of evidence of heart disease/cardiomegaly
- C and on: Development of signs of heart failure
- D: Development of refractory heart failure

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13
Q

Determinants of myocardial performance:

A
  • Preload
  • Afterload
  • Contractility
    > these 3 all contribute to stroke volume
    <><><><>
  • Distensibility
    <><><><>
  • Heart rate
    <><><><>
  • stroke volume and heart rate determine cardiac output
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14
Q

Determinants of myocardial performance: how they change with DCM

A
  • Preload up
  • Afterload up
  • Contractility down
  • Distensibility down
  • Heart rate up
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15
Q

Therapeutic plan for DCM

A
  • Preload: high > Furosemide, ACEi
  • Furosemide most important!
  • reduce preload, get fluid out of the lungs
    <><><><>
  • Afterload: high > ACEi, Pimobendan
  • has some vasodilatory effects, can help decrease afterload
    <><><><>
  • Contractility: low > Pimobendan
    <><><><>
  • Distensibility: low
    > ACEi (?)
    > Spironolactone (?)
    <><><><>
  • Heart Rate: high
    > Treat if pathologic tachyarrhythmia
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16
Q

Treatment of stage B (preclinical) DCM in dogs:

A
  • pimobendan has shown benefit
  • benazepril (ACE inhibitor) seems to lengthen time to clinical signs
    > these studies both done in dobermans, but we use these for other breeds too
17
Q

ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY
- breed?

A
  • boxers, but also reported in other breeds
18
Q

ARVC - pathogenesis and result

A
  • Progressive fibrofatty replacement of the right, and to some degree the left, ventricular myocardium
  • Manifests as right ventricular (RV) origin arrhythmias (may see LV origin as well)
19
Q

ARVC clinical presentation
- age?
- types?
- ECG and signs?

A
  • Any age (commonly 6-10yrs)
    <><>
    3 subtypes:
  • Asymptomatic
    > Incidental detection of arrhythmia
  • Exercise intolerance or syncope
    > Associated with ventricular arrhythmia
  • Systolic dysfunction and CHF
    > Rare (10% of ARVC cases)
    <><>
    Vast majority of cases show arrhythmia only with NORMAL echo
20
Q

How to best diagnose ARVC?

A
  • ECG
  • Holter (24 hour ambulatory ECG)
  • +/- Echocardiogram
    <><>
    Gold standard: myocardial biopsy… but high risk of complications
21
Q

possible ECG findings for ARVC?
important considerations for diagnosis?

A
  • isolated VPCs or doublets / triplets
  • runs of ventricular tachycardia
    <><>
  • Rule out other causes of ventricular arrhythmias! use other tests
22
Q

ARVC Treatment
* When to treat? how?
* Goals of treatment?
* caveat?

A

When to treat?
* Symptomatic due to
ventricular arrhythmia
* If asymptomatic, if arrhythmia severe in frequency/complexity
How:
* Sotalol
* Mexiletine
* Combo
<><><><>
Goals of treatment:
* Reduce frequency & complexity of ventricular arrhythmias, reduce symptoms
<><><><>
* No treatment has been proven to prevent sudden death, which can be unpredictable