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Selected Canine Medicine > CVHD (L1-2) > Flashcards

CVHD (L1-2) Flashcards

1
Q

What two broad categories do we think about regarding the origin of heart disease?

A

Heart versus blood vessels

Congenital* versus acquired

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2
Q

In small dogs, the most common category of heart disease is …

A

Chronic valvular heart disease (mainly mitral)

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3
Q

Puppies and kittens presented with

signs of heart failure are likely to have …

A

Congenital defects such as haemic disorders

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4
Q

Young puppies and kittens have more or less viscous blood? How is this relevant?

A

Less. Low viscosity fluid breaks into turbulence at a low

velocity. Innocent murmurs are perfectly normal as a result

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5
Q

Are cardiomyopathies more or less rare than degenerative valvular disease?

A

More

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6
Q

What is the most common canine cardiac disease?

A

Chronic valvular heart disease

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7
Q

Chronic valvular heart disease is especially common in what breeds?

A

King Charles cavalier spaniels, and they are infected young.

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8
Q

Dilated cardiomyopathies are generally more common in…

A

Large or giant breed dogs

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9
Q

What is a feature of heart failure in the majority of cases related to HR?

A

Tachycardia

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10
Q

Stages of heart failure?

A

Stage A – Patient is at high risk for the development of heart
disease but currently has no identifiable structural disorder of
the heart (e.g. all Cavalier King Charles spaniels)
Stage B – Patient has evidence of structural heart disease (e.g. a
significant heart murmur) but has never developed clinical
signs of heart failure. B1: no radiographic or echocardiographic
evidence of cardiac remodelling. B2: evidence of heart
enlargement
Stage C – Patient with past or current clinical signs of heart
failure associated with structural heart disease. Signs may be
acute or chronic.
Stage D – Patient with end-stage cardiac disease. Clinical
signs of heart failure are refractory to “standard therapy”

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11
Q

List the order of most commonly affected valves in chronic valvular heart disease

A

mitral > (mitral + tricuspid)&raquo_space; tricuspid

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12
Q

What tends to happen to animals that have had endocardiosis for a long period of time which suddenly gets dramatically worse?

A

Cordae tendinae rupture

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13
Q

Outline the origin of endocardiosis

A

Uncertain, may be a genetic predisposition regarding dyscollagenosis, a response to primary lesions or inherited.

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14
Q

What is the thinking behind the inherited
predisposition in cavalier King Charles spaniels?
and small dogs in general?

A

These dogs have been bred to be smaller.
Viscosity of the blood is the same in a
smaller dog, but the way it flows is still the
same, hence the response to injury is still
there.

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15
Q

Detailed incidence of chronic valvular heart disease?

A

Present in ~33% of small breed dogs by 10
years of age. % keeps going up. Accounts
for 75-80% of all canine cardiac disease

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16
Q

Outline the path pathophys of chronic valvular heart disease?

A

Valvular lesions grow and eventually lead
to leakage / insufficiency / regurgitation of
blood from ventricle into atrium.
The valve leaflets can’t coapt or close completely.
Now we may hear a murmur.
Gradual nodule progression over years.

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17
Q

What is the result of leakage in chronic valvular heart disease?

A

Extra vol regurgitating back into atrium with each beat gradually leads the atrial walls to stretch and remodel. Atrial pressure does not rise much for quite some time.

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18
Q

What would happen if the LA increased in size with chronic worsening regurgitation BUT with a rise in pressure?

A

Pulmonary oedema

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19
Q

Why are dogs with chronic valvular heart disease (and softly audible murmurs) not showing signs of heart failure?

A

The atrium enlarges, atrial pressure remains reasonably low.

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20
Q

The amount of blood passing ineffectually from _____ to ______ and back will ______ over time

A

From atrium to ventricle will increase over time.

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21
Q

What does volume overload lead to?

A

Ventricular dilatation and eccentric hypertrophy

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22
Q

What results due to enlargement and damage to the heart muscles

A

Spontaneous depolarisations are more likely, and rhythm disturbances are more possible.

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23
Q

Are rhythm disturbances in chronic valvular heart disease likely to be Supraventricular or ventricular?

A

Supraventricular

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24
Q

What is meant when chronic valvular heart disease is described as a “vicious cycle”?

A

The enlarged chambers lead to enlarged AV annulus (AV ring), and the leaflets have even more difficulty meeting in the middle, worsening the leak. Aortic output suffers, sympathetic tone increases, RAAS kicks in, and we increase the workload on the already failing heart (a forward fucking failing fucked up fucking system fuck).

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25
Q

The heart can adapt for some time, but what eventually happens?

A

The atrium and veins draining into it are unable to remodel/dilate further, or rapidly enough. We start to see lymphatic drainage and a bit of pulmonary oedema building up around the hilus

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26
Q

What happens on the left side regarding a lost ability of the atrium and veins to stretch/dilate further?

A

Pulmonary lymphatic drainage increases to compensate. Eventually this is not enough and pulmonary oedema begins to develop (little at first). Venous pressure rises and the animal is in “congestive” heart failure.

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27
Q

What happens when the right side fails in chronic valvular heart disease (or in general)? Explain what you may see regarding the jugular pulses

A

It is normal for a small dog to have a jugular pulse at the most ventral portion of the neck, but in heart failure this comes up 1/3 of the way. We can detect excessive pulses on physical exam (especially if we press on the abdomen). The liver will gradually get larger (capsular stretch and remodel). Eventually ascites develops.

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28
Q

When may we see pleural effusion in cases of chronic valvular heart disease?

A

Believe to see this with biventricular failure (L & R fucked)

29
Q

What is a jet lesion?

A

Damage resulting in endothelium loss; turbulent blood flow being the causative factor

30
Q

What sudden changes may we see in chronic valvular heart disease?

A

Ruptured chordate tendinae
Atrial tear
Sudden tachyarrhythmia (likely supraventricular)
Supervening other diseases/stress

31
Q

What is the effect and presentation of a ruptured chordae tendinae?

A

Collapse, dyspnoeic, leak worsened, pulmonary oedema within 10 minutes as there’s no fucking time to adapt

32
Q

What do we see when an atrial tear occurs?

A

Ventricle gets too big, tears, may tear septum. These animals may go directly into right sided heart failure and suddenly develop ascites. If it tears under the pericardium, we see sudden electrical phenomenon.

33
Q

List various sites for damage to occur that relate to Supraventricular issues

A

AV node, SA node, AV bundle, intermodal pathways, others.

34
Q

Will you see a cough before or after pulmonary oedema?

A

Long before, generally

35
Q

List prominent clinical features in dogs with chronic valvular disease

A

Depends on stage, but …

Murmur
Cough
Exercise intolerance
Weakness
Syncope
Dyspnoea/tachypnoea/Orthoptera
Sudden death
36
Q

What might you notice on your physical exam in dogs with suspected chronic valvular heart disease?

A

Low capillary refill, poor mm colour
APical beat/thrill (squirting, dayummmm)
Heart rate and rhythm
Arterial pulse char & rhythm may have deficits
Heart and lung sounds (oedema? Muffled?)
Jugular pulses (>1/3 of the way up the neck?) distended?

37
Q

What is meant by a hyperkinetic pulse character? When do we see it?

A

Strong, chronic anaemia

38
Q

What is meant by a hypoxic ethic pulse character? When do we see it?

A

Dehydration, weak

39
Q 
The 4 pulse characters are ...
Hyperkinetic
Hypo kinetic
\_\_\_\_\_\_\_\_\_\_
\_\_\_\_\_\_\_\_\_\_
A

Weak and slow rising

Variable from beat to beat (pericardial effusion)

40
Q

If pulse strength is variable from beat to beat, what may this suggest?

A

Pericardial effusion

41
Q 
Average heart rate values for:
General:
Large:
Small:
Cats:

Tachycardia:
Dogs
Cats

A

160 in small dogs

> 220 in cats (stressed?)

42
Q

Explain heart sounds S1 - S2

A 
S1 (first heart sound).
- Closure of AV valves, loudest over heart apex
S2
- Closure of aortic and pulmonic
- Loudest over heart base
43
Q

Explain heart sounds S3 - S4

A

S3
- Not normally heard. Rapid ventricular filling before next beat. Low pitched, best heard over mitral area
S4
- Fourth sound, not normally heard
- Atrial contraction forcing blood into an already over-full or stiff ventricle. Aortic or pulmonic area just prior to S1

44
Q

What parameters do we use to characterise a murmur?

A

Intensity, character and timing, point of max intensity (PMI), radiation

45
Q

How do we describe murmurs?

A

Loudness/grade (out of 5?6? Where lower is subtle)
When? During cardiac cycle/duration
Where? PMI left or right, base of apex, IC space, etc.
Quality? Musical, blowing, frequency

46
Q

Explain grades 1 - 6 of murmurs

A

1 - very soft, only in quiet surroundings after long listening
2 - soft but easily heard
3 - Moderate intensity
4 - Loud murmur but no pre cordial thrill
5 - Loud murmur with a palpable pre cordial thrill
6 - Loud murmur with precordial thrill; heard with stethoscope lifted from chest wall

47
Q

What is a gallop rhythm?

A

Not a rhythm, it is an extra (third) sound with each beat.

48
Q

Explain a gallop beat

A

S3 or S4 which are not normally heard, are now heard. S3 - low frequency vibrations at the end of ventricular filling. S4 - low frequency vibrations associated with blood flowing into ventricles during atrial contraction

49
Q

Outline coughing in chronic valvular heart disease (CVHD, cbf repeatedly typing)

A

Compression of L. Main stem bronchi by LA.
Dry, almost honking
Pulmonary oedema (moist, +/- dyspnoea)
Concurrent respiratory tract disease may be present (chronic bronchitis is common in older dogs).

50
Q

What questions might we ask to distinguish CVHD from chronic bronchitis in terms of cough?

A

What time of the day? CVHD - morning. Dogs with chronic bronchitis cough when stimulated. CHronic bronchitis involves an increase in goblet cells –> MOIST cough

51
Q

What are some causes of syncope?

A

Brandy arrhythmia, tachyarrhythmia with low CO, long bout of coughing, severe left main stem bronchus collapse.

52
Q

Mechanism of syncope?

A

Isn’t enough time to allow the heart to fill up with blood, not sending blood to the brain, faint. Coughing can do this

53
Q

DDx for CVHD. Go

A 
Primary resp. Disease (coughing, dyspnoeic, tachypnoea). 
CMO
Ineffective endocarditis
Sick sinus syndrome
Late presenting congenital disease
54
Q

What’s one major way (other than cough questions) that we can distinguish CVHD from chronic bronchitis (assuming we don’t have simultaneous occurrence)

A

Is the dog tachycardia and/or has sinus arrhythmia

55
Q

Is the murmur relevant or is something else causing the resp. Disease?

A

Don’t fucking forget this

56
Q

How do we diagnose CVHD?

A

Depends on stage presented.

  • Systolic murmur (esp. Mitral) in small or med sized dog.
  • Cough, exercise intolerance, weakness, syncope, dyspnoea and/or tachypnoea, lung crackles, ascites
  • Radiography (looking for cardiomegaly)
  • ECG, echocardiography
57
Q

What do I do if I hear a murmur in a happy, healthy dog?

A

Offer the client:

  • Baseline thoracic rads
  • Arterial blood pressure measurement
  • Baseline basic blood work (PCV/TPP/Creatinine at a minimum) and a urinalysis
58
Q

What do I do if my baseline work is normal in a dog with early CVHD?

A

Nothing. Re-examine in 6-12 months. If abnormal, consider some other options

59
Q

What are the treatment principles of CVHD

A

Control signs of CHF
Limit excessive neuro hormonal activation contributing to disease progression
Decrease LV size
Promote forward flow of blood

60
Q

What is treatment dependent on?

A

Stage presented

  • Disease in the absence of clinical signs?
  • Mild to moderate failure?
  • Severe and life-threatening?
61
Q

What are some recommendations (that may or may not be helpful due to lack of clear evidence) for CVHD dogs with no clinical signs

A 
Client education
Routine monitoring and maintenance
Avoid high salt foods (Mild NA restriction)
Avoid exuberant exercise
Consider AceI and B-blockers
62
Q

What may influence our decision to treat a patient with undeveloped clinical signs?

A

Heart size

Large dogs with CVHD progress more rapidly than small dogs

63
Q

How do we treat mild to moderate heart failure?

A 
Exercise restriction
Furosemide (enough to improve breathing) 
ACEI (oppose RAAS)
Moderate dietary salt restriction
\+/- digoxin for arrhythmias
64
Q

Problems with frusemide in CVHF dogs?

A

Give minimum needed. On its own, it activates RAAS. Use with ACEI

65
Q

When treating dogs with CVHD, outline your protocol for diuretic usage and ACEI usage

A

Frusemide, increase dose over many months. Eventually need to introduce another diuretic. One week after starting or increasing ACEI, check the drug has not raised serum creatinine substantially/

66
Q

When treating a CVHD dog with ACEI and Frusemide, and creatinine markedly increase, what do you do?

A

Back off ACEI

67
Q

How do we treat severe, acute CVHD

A

Supplemental O2
Cage rest
IVfrusemide
Oral primo ending (+/- Oral ACEI)
Nitro glycerine ointment (Monday morning head, yeeeeee vasodilator)
Nitroprusside infusion (vasodilator)
Dopamine/dobutamine infusion (+Ve inotrope)

68
Q

What’s your prognosis?

A

Excellent when caught early, years of high quality life.

Guarded to poor if advanced, non-responsive or severe, acute exacerbate of chronic, stable disease

69
Q

Difference between heart disease and heart failure?

A 
Disease = harmful cardiac finding
Failure = overwhelmed compensatory mechanisms

Selected Canine Medicine (6 decks)

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