Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

SA Cardiology > Canine myocardial disease > Flashcards

Canine myocardial disease Flashcards

(75 cards)

Start Studying
1
Q

Primary canine cardiomyopathies

A

Idiopathic diseases

Dilated cardiomyopathy (DCM)

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

Hypertrophic cardiomyopathy

Atrial myopathy

Restrictive cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dilated cardiomyopathy (DCM) - incidence

A

The most common canine cardiomyoathy with a prevalence of up to 60% in some breeds (Dobermann)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC) - breeds

A

Prevalent in boxers and english bulldogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hypertrophic cardiomyopathy - incidence

A

Rare in dogs

Terriers possibly over-represented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Atrial myopathy - incidence

A

Rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Restrictive cardiomyopathy - incidence

A

Rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Secondary canine cardiomyopathies

A

Arrhythmia-induced cardiomyopathy

Nutrition-associated cardiomyopathies

Congenital cardiac disease

Endocrinopathies

Chronic myocarditis

Systemic inflammation

Drug/toxin induced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Arrhythmia induced cardiomyopathy

A

Chronic tachycardia and arrhythmias can lead to a severe myocardial failure mimicking DCM.

This is potentially reversible with control of the arrhythmia

Increased myocardial oxyegn demand, reduced ventricular filling time and reduced coronary perfusion

Decreased systolic function and cardiac output, and left ventricular dilation

Severity of dysfunction dependent on the type of arrhythmia and duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Nutrition-associated cardiomyopathies

A

Taurine deficiency:
- key roles in calcium handling and excitation-contraction coupling within the myocardium
- Deficiency may cause DCM phenotype
- Described in American Cocker spaniels, Golden retrievers, and Newfoundlands
- Potentially reversible with supplementation

Grain-free/legume rich diets:
- Increasing prevalence of DCM associated
- mechanism not understood
- diet change may give some improvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Congenital cardiac disease (cardiomyopathy)

A

Any cardiac disease causing left-sided volume overload

May mimic DCM

E.g. mitral valve dysplasia, large left-to-right PDA, and left-to-right VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Endocrinopathies causing cardiomyopathy

A

Hypothyroidism (association rather than causation?)

Hyperadrenocorticism (possiblereverse remodelling with treatment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Chronic myocarditis (cardiomyopathy)

A

Characterised by non-specific inflammation of the myocardium

Can result in DCM phenotype

Cardiac troponin I is typically markedly elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Systemic inflammation and cardiomyopathies

A

Left ventricular systolic dysfunction

Can occur in systemis inflammatory response syndrome and steroid responsive meningitis arteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Drug/toxin cardiomyopathies

A

Doxorubicin (chemotherapy) can have cardiotoxic effects

Manifests as myocardial failure and/or arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dilated cardiomyopathy

A

Second most common cardiac disease in dogs

Most prevalent in large and giant breeds

Presents with structural and/or electrical alterations

Charaterised by left ventricular dilation (+/- right) and systolic dysfunction

Diagnosis of exclusion

Occult/preclinical phase and then progressed to congestive heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Occult or preclinical phase of DCM

A

Characterised by an abscence of clinical signs or ECG alterations

Duration of the phase is variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What can cause sudden death in a dog suffering from DCM?

A

Typically due to ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Aetiology of DCM

A

Primary DCM thouhgt to be inherited

Gene associations in in Dobermanns, boxers, and irish wolfhounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathology of DCM

A

Dilation of the left ventricle and left ventricular systolic dysfunction

Metabolic dysfunction or defects in contractility at a cellular level

Leads to overt systolic dysfunction and eccentric ventricular hypertrophy

Dilation of the mitral annulus can lead to mitral regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Histopathology of DCM

A

There are two distinct described in DCM:

A fatty infiltration- degenerative type (mainly in Dobermanns and Boxers)

An attenuated wavy fibre type (more common in giant breeds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathophysiology of DCM

A

Impaired systolic function -> progressive eccentric hypertrophy of L ventricle -> reduced CO -> activation of compensatory mechanisms (RAAS) -> further myocardial hypertrophy and chamber dilation

Increased left-sided volumes result in progressively increased left atrial pressures -> pulmonary oedema

Ventricular arrhythmias and atrial fibrillation are common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Occult/preclinical phase of DCM

A

Presence of echocardiographic and/or electrical changes without signs of CHF

Slowly progressive over several years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical phase of DCM

A

Progression to CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Staging of DCM

A

Very similar to staging of MMVD

(A, B1, B2, C, D)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Signalment of DCM
Adult dogs (usually 5-7) Large and giant breeds Portugese water dogs can get a juvenile onset form of DCM
26
History - preclinical DCM (stage B)
Family history of cardiac disease Diet history Most dogs will be asymptomatic +/- exercise intolerance, collapse, syncope
27
History of clinical DCM (stage C: CHF)
Exercise intolerance, lethargy Collapse/syncope Elevated respiratory or effort Cough Abdominal distension (if right sided CHF)
28
Physical examination of pre-clinical DCM (stage B)
May be unremarkable Soft murmur due to mitral regurgitation Arrhythmias +/- pulse deficits may be present
29
Physical examination of clinical DCM (stage C: CHF)
Murmur - soft Tachycardia, arrhythmias, pulse deficits, weak pulses Tahcypnoea +/- dyspnoea Pulmonary crackles Reduced/absent lung sounds Jugular distension, positive hepatojugular reflux, abdominal distension with fluid thrill Weakness, collapse Cardia cachexia
30
Diagnostics for DCM
Echocardiography Radiography ECG Holter Cardiac biomarkers Systolic blood pressure Exclusion of disease mimickers
31
What is echocardiography used for in DCM?
Assess the severity of systolic dysfunction Assess the severity of left ventricular +/- left atrial dilation and the likelihood of CHF Assess the right heart also Monitor progression of the disease Exclude secondary causes of a DCM phenotype
32
Typical echo findings in DCM
Rounded, dilated left ventricle (increased volumes and diameter) Left atrial dilation Mild mitral regurgitation Reduced ejection fraction and fractional shortening
33
Echo findings of Stage B1 DCM
Relatively normal or equivocal echo (but presence of arrhythmias)
34
Echo findings of Stage B2 DCM
Evidence of left ventricular systolic dysfunction (reduced ejection fraction, fractional shortening and end systolic volume) As disease advances: progressive left ventricular dilation (increased end diastolic volume and diameter) and progressive left atrial dilation (increased LA:Ao)
35
Echo of Stage C DCM
Same as B2 but more advanced dilation and systolic function, large left atrium, and evidence of elevated left sided filling pressures. May see B lines suggestive of pulmonary oedema May have signs of right-sided CHF
36
Radiography for DCM
Gold standard for diagnosis of pulmonary oedema and so CHF Assesses for: - cardiomegaly with left atrial enlargement - distension of the pulmonary veins - lung pattern
37
ECG for DCM
Common arrhythmias include: Ventricular arrhythmias - Ventricular premature complexes - Ventricular tachycardia Atrial fibrillation Supraventricular premature complexes
38
Holter for DCM diagnosis
24hr holter advised Can detect VPCs Presence of over 300 VPCs in 24hrs in a Dobermann is diagnostic (or two holters in 12mo with 50-300) Signs of malignancy used to determinewhether antiarrhythmic treatment is required - coupling intervals (R-R intervals) exceeding 260/minute - frequent couplets or triplets
39
Cardiac biomarkers for DCM diagnosis
Ancillary screening tool (can't replace echo and holter) NT-proBNP Cardiac troponin I
40
NT-proBNP for DCM diagnosis
Indicator of myocardial stretch and strain May help assess the severity of disease and monitor disease progression Identify dogs that would benefit from further screening False positives are possible Poor sample handling may lead to reduced levels Daily variation and breed variation
41
Cardiac troponin I for DCM diagnosis
Indicator of myocardial cell damage Prognostic indicator, monitor disease progression Can be elevated in some non-cardiac disease
42
Systolic blood pressure in clinical DCM
120mmHg
43
Clinical pathology in DCM
Pre-renal azotaemia is a common finding Elevated liver enzymes due to liver congestion (in right-CHF) Consider T4/TSH and basal cortisol Consider plasma or whole blood taurine
44
Screening for DCM
Annual screening advised from three years old in at-risk breeds Echo and 24-hr holter ECG +/- cardiac biomarkers Genetic testing
45
Sequelae of DCM
Left sided congestive heart failure Forward failure Right-sided congestive heart failure Arrhythmias - atrial fibrillation - ventricular arrhythmias and sudden cardiac death - sustained tachyarrhythmias
46
Treatment of pre-clinical DCM
Pimobendan Antiarrhythmic therapy
47
Key points of CHF treatment
Standard therapy: pimobendan, diuresis, RAAS inhibition Aims are to reduce preload (diuretics, venodilators), provide inotropic support (pimobendan) and reduce RAAS stimulation Furosemide and torasemide are licensed in dogs Renal parameters and electrolytes should be monitored ACE-inhibitors in combination with spironolactone, can be initiated once recovered from acute CHF event
48
Acute CHF (in-hospital treatment)
Oxygen Furosemide IV Pimobendan Sedation/antianxiety (butorphanol)
49
Additional hospital treatment for more advanced/refractory acute CHF cases
Vasodilators - nitro-glycerine (venodilator) - sodium nitroprusside CRI (ateriodilator and venodilator) Further inotropic support - Dobutamine CRI Mechanical ventilation
50
At home treatment for chronic CHF
Pimobendan Diuretics - furosemide PO - torasemide PO - thiazides considered in refractory cases ACE-i - benazepril - combined with spironolactone Spironolactone - potassium sparing (aldoseterone antagonist) - Combined with benazepril
51
Treatment for ventricular arrhythmias
Lidocaine (mergency treatment of V tach) Solatol (oral treatment) Mexiletine (minimal depression of systolic dysfunction, may have marked GI effects) Amiodarone (minimal myocardial depression)
52
Solatol
Oral treatment for chronoic ventricular arrhythmias Peak effect within 2-4 hours of administration Negative inotrope- use with care in severe systolic dysfunction
53
Mexiletine
Oral treatment for ventricular arrhythmias Minimal effect on systolic function Adverse effects: GI (anorexia, vomiting, diarrhoea)
54
Amiodarone
Oral therapy for ventricular arrhythmias Takes several weeks to reach steady serum levels Adverse effects: hepatopathy and thyroid dysfunction
55
Lidocaine
Treatment for sustained ventricular tachycardia Na channel blocker IV only
56
Amiodarone
Treatment for sustained ventricular tachycardia Adverse effects: hepatic and thyroid dysfunction
57
Treatment for atrial fibrillation
Diltiazem Digoxin
58
Diltiazem
Treatment for atrial fibrillation Calcium channel blocker Mild negative inotropic effect, so care of high doses in cases with CHF
59
Digoxin
Treatment for atrial fibrillation Narrow therapeutic window Check serum levels 5-7 days post initiation of treatment, or dose change 6-8hrs post pill Lower doses required in patients with renal disease Monitor potassium
60
Treatment for stage A DCM
No treatment
61
Treatment of stage B1 DCM
+/- Antiarrhythmics
62
Treatment of stage B2 DCM
Pimobendan +/- antiarrhythmics
63
Treatment of stage C DCM
Diuretics Pimobendan ACE-i Spironolactone
64
Treatment of stage D DCM
Diuretics Pimobendan ACE-i Spironolactone + additional diuresis + K supplementation
65
Prognosis of DCM
Highly variable due to long pre-clinical phase Prognosis of DCM with CHF is generally guarded, median survival times following progression to CHF of typically 6-12months Median survival is shorter when there is concurrent atrial fibrillation Sudden caridac death affects up to 25-30% of dogs with DCM
66
Arrhythmogenic right ventricular cardiomyopathy ARVC
Myocardial disease primarily affecting right ventricle - may involve LV Progressive loss of myocytes with fatty or fibro-fatty replacement Best described in Boxers (and english bulldogs) Primarily an electrical disease sometimes associated with myocardial dysfunction Results in ventricular arrhythmias High risk of syncope and sudden cardiac death
67
Aetiology of arrhythmogenic right ventricular cardiomyopathy (ARVC)
Likely to be genetic Disease of the desmosome
68
Pathophysiology of ARVC
Fibrofatty tissue replacement particularly in the right ventricle Fatty tissue and scarring may be seen grossly Replacement of cardiomyocytes with adipose, fibrosis, and inflammatory cells Right +/- left ventricular dilation and systolic dysfunction seen in some
69
Signalment of ARVC
Best described in Boxers, also reported in English Bulldogs Adult onset (usually 5-7)
70
Three clinical categories of ARVC
Asymptomatic Symptomatic Arrhythmias and DCM phenotype
71
Asymptomatic ARVC
Arrhythmias detected incidentally on clinical examination/ECG
72
Symptomatic ARVC
Present with clinical signs associated with ventricular arrhythmias (syncope, weakness, collapse, exercise intolerance) Echocardiography may show right ventricular dilation and reduced right ventricular function Left ventricular size and function remain normal
73
Diagnosis of ARVC
Family history or history of syncope warrants screening Echocardiography - normal or signs of right ventricular dilation Holter - identifies the presence of ventricular arrhythmias and assess the severity of these. Annual holter advised in breeding dogs and those with family history
74
Treatment of ARVC
Palliative Aims at controlling ventricular arrhythmias and ameliorating any associated clinical signs Solatol - first line antiarrhythmic Pimobendan - indicated in cases with structural or functional changes
75
Prognosis of ARVC
Syncope seen in approx 1/3 of Boxers with ARVC - associated with worse prognosis Risk of sudden death Many dogs without significant echo changes can have good long term prognosis

SA Cardiology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions