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CAEM Pt. 2 > Myocardial and Feline Cardio Dz > Flashcards

Myocardial and Feline Cardio Dz Flashcards

1
Q

What is a common and extremely problematic complication of DCM with Dobermans? Why does it occur?

A

Sudden death - pathologic arrhythmias that weren’t addressed

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2
Q

What should you do with a patient with a syncopal history with irregular heart rhythms and pulse deficits?

A

RECORD THE ECG immediately so you can treat the arrhythmias before it causes sudden death

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3
Q

What age and breed does DCM commonly affect?

A

Middle aged male Dobermans

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4
Q

Do DCM dogs commonly have heart murmurs?

A

No

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5
Q

Top differentials for left sided heart disease in dogs

A

1) DCM - large breed and Spaniels
2) Mitral insufficiency due to valve disease - small breeds and Spaniels
3) Decompensated congenital defects
4) Endocarditis

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6
Q

What is dilated cardiomyopathy?

A

Abnormality of the HEART MUSCLE that is not due to other cardiac abnormalities or systemic disease

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7
Q

What are the three main characteristics that define DCM?

A

> > 3 D’s

  • Decreased systolic function or contractility
  • Dilation, ventricular and often atrial
  • Dysrrhythmias
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8
Q

What two cardiac arrhythmias are most common with DCM?

A

1) Atrial fibrillation

2) Ventricular tachycardia

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9
Q

What form/cause of DCM is the most common?

A

Idiopathic - occurs in large breed dogs

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10
Q

Four etiologies of secondary DCM

A

1) Nutritional deficiencies = taurine, carnitine, Se in horses
2) Toxic = monensin in horses, doxorubricin
3) SEVERE hypothyroidism
4) Consequence of primary cardiac disease = chronic volume or pressure overload

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11
Q

Why does DCM lead to arrhythmias?

A
  • Atrial stretch = atrial fibrillation and fibrosis

- Ventricular fibrosis and ischemia from idiopathic myocardial changes = v-tach

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12
Q

How does DCM lead to heart failure?

A

Ventricular fibrosis and atrial stretch > decreased contractility > decreased SV and CO > hypotension > SNS and RAAS activation = tachycardia and tacharrhythmias, Na/water retention, vasoconstriction

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13
Q

What is the number one diagnostic test to determine DCM?

A
  • Echocardiography
  • Hx and PE for CHF
  • ECG for arrhythmias
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14
Q

What is compensated or occult DCM?

A

> > Dog looks completely normal and isn’t showing clinical signs
+ Gallop rhythm
+ Arrhythmias
+/- Relative systolic regurgitant murmurs may be present
+ Weak pulses

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15
Q

What is the difference between compensated/occult and decompensated DCM?

A

> > CHF is present with decompensated
+ Arrhythmias, murmurs, gallop rhythm, weak pulses (like compensated)
+ PLUS signs of left/right heart failure
+ Cold feet/ears due to poor perfusion

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16
Q

What sign on your PE may help you differentiate DCM from valvular disease?

A

Pulse deficits = decreased stroke volumes, more common with DCM

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17
Q

Three main therapeutic targets with decompensated DCM?

A

1) Treat acute (FOP) and chronic CHF (pimo, ACE-i, furosemide, spironolactone)
2) Increase systolic function = pimobendan, decrease resistance with diuretics/ACE-i
3) Treat arrhytmias

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18
Q

Do we treat occult DCM? If so, with what?

A
  • YES - pimobendan prolongs survival, +/- ACE-inhibitors

- Owner education to screen for progressive disease

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19
Q

Do we worry about A-fib causing sudden death?

A

No - just worsens clinical signs

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20
Q

Goals and treatment(s) for ventricular tachycardia

A
  • Decrease frequency, repetitiveness
  • Control clinical signs
  • Decrease chance of sudden death

> Na channel or beta blockers

  • IV lidocaine
  • PO sotalol
  • PO mexiletine = first line tx at home
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21
Q

Is the AV node affected in DCM?

A

No - normal functioning, seeks to protect the ventricle from tachycardia, caused by the overwhelming production of atrial depolarization

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22
Q

Four components of a-fib

A

1) Tachycardia
2) Irregular rhythm
3) Supraventricular = narrow QRS
4) No P waves

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23
Q

Why is atrial fibrillation a problem? (2)

A
  • Loss of coordinated atrial depolarization = decreased stroke volume
  • Tachycardia = less time for ventricular filling = decreased CO
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24
Q

Can we cure the a-fib involved with DCM?

A

No - goal is to cause AV block (prolong PQ interval to produce a controlled ventricular response

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25
Q

Three drugs used to treat a-fib

A

1) Digoxin = mimics/enhances vagal tone
2) Ca++ channel blocker
3) Beta blockers
* Don’t use Ca++ and b-blockers together

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26
Q

Most common heart disease type in cats and dogs

A
  • Dogs = valvular disease

- Cats = cardiomyopathies, most commonly HCM

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27
Q

When is the cardiomyopathic dysfunction in dogs and cats - systole or diastole

A
  • Dogs = systole

- Cats = diastole

28
Q

Do dogs or cats commonly present with cough as cardiac signs?

A

Dogs

29
Q

Is the disease progression of heart disease gradual or acute in dogs and cats?

A
  • Dogs = gradual

- Cats = acute, good at hiding clinical signs

30
Q

Do dogs, cats, or both need echo to diagnose the type of heart disease?

A
  • Dogs = often, sometimes only need signalment, history, and PE
  • Cats = ALWAYS
31
Q

True or false - CHF looks generally similar in cats, regardless of the etiology

A

TRUE - need echo for the specific causes, all get pleural effusion

32
Q

Common history of cats with heart disease

A
  • Signs of disease appear suddenly
  • Often ADR, just “hiding” or acting “lethargic”
  • May be acute dyspneic or lame due to thromboemboli
33
Q

Common head/neck and thoracic findings of PE of cats with heart disease

A
  • Head and neck = cyanosis, panting, distended jugular veins
  • Thorax = dyspnea, tachypnea, GALLOP rhythms, heart murmurs, hypothermic (low CO), crackles (p. edema), muffled heart sounds (pleural effusion)
34
Q

Are ECG’s helpful with diagnosing feline heart disease, yes or no?

A
  • NON-SPECIFIC to the type of disease
  • Includes: arrhythmias, axis shifts, conduction abnormalities, chamber enlargement
  • May be NORMAL with severe disease
35
Q

Things you can see on thoracic rads with feline heart disease (4)

A
  • Chamber enlargements
  • Pleural effusion
  • Degree of cardiomegaly
  • Non-specific edema patterns, starts caudodorsal, ventrocaudal, then cranial
36
Q

What things can the echo tell you with heart disease? (2)

A

1) Anatomy - congenital malformations, acquired valvular or myocardial malformations
2) Function = chamber size/thickness, contractility

37
Q

What is NT-proBNP and what can it tell us?

A

> B-type naturietic peptide

  • Hormone released by the ventricle when it’s “stressed”
  • Increased with heart disease (+/- CHF)
  • May help differentiate between functional murmurs (non-pathologic) from murmurs due to heart disease
38
Q

Who is NT pro-BNP more helpful in - dogs or cats?

A

Cats - easier to interpret

*Exception = DCM in dobermans

39
Q

What is a cardiomyopathy?

A

> Acquired disease of the MYOCARDIUM

  • Structural abnormality + functional abnormality
  • Usually IDIOPATHIC = not due to systemic (Ex: hyperthyroidism) or infiltrative disease (LSA)
40
Q

Breeds at risk for HCM (2)

A
  • Maine Coon cats

- American shorthaired

41
Q

What is the main diagnostic that differentiates between types of cardiomyopathies (i.e. HCM, DCM, etc)?

A

ECHO

42
Q

What is the most common myocardial disease in cats?

A

Hypertrophic cardiomyopathy

43
Q

Three hallmarks of HCM

A

1) Ventricular thickening with left atrial enlargement
*Usually still has good systolic/contractile function
2) Poor relaxation = poor DIASTOLIC function
+/- Left ventricular outflow obstruction from bulging septum

44
Q

What problems does thick and stiff ventricles pose? (2)

A

*Diastolic dysfunction = can’t relax
- Increased myocardial oyxgen needs = risk of ischemia
+/- Outflow obstructions by the mitral valve or septum

45
Q

What problems does diastolic dysfunction pose? (3)

A

1) Decreased CO
2) Increased LA pressure –> CHF, atria has to push against the stiff ventricle (can’t relax well during diastole)
3) Secondary mitral insufficiency due to valve distortion following hypertrophy

46
Q

Differentials for left ventricular hypertrophy in cats (4)

A
  • Congenital and valvular diseases are uncommon
  • HCM
  • Aortic stenosis
  • Hyperthyroidism
  • Hypertension secondary to hyperthryoidism or renal disease
47
Q

What causes the atrial enlargement in HCM?

A

Poor diastolic function = atria doesn’t unload completely into the ventricle, has to push harder to unload during diastole

48
Q

Three general goals with treatment of HCM

A

1) Improve muscle relaxation with positive lusitropes
2) Prolong filling time by slowing HR
3) Reduce outflow obstructions if present

49
Q

What’s the number one med we use to treat feline HCM?

A

Atenolol = beta blocker, improves diastolic function AND arrhythmias by slowing the heart rate

50
Q

Is there any benefit to treat asymptomatic HCM cats?

A

NO

51
Q

Two hallmarks of DCM in cats

A

1) Dilation of left ventricle and atria
2) Poor systolic/contractile function
* Same as DCM in dogs

52
Q

Etiology of DCM in cats

A

Usually IDIOPATHIC, may be due to taurine deficiency

53
Q

Treatment of acute CHF in cats

A

1) Furosemide
2) LOW STRESS oxygen
3) Pimobendan
+/- Thoracocentesis
+/- Sedation

54
Q

Treatment of arrhythmias in cats with and without CHF

A
  • Without CHF = beta blockers

- With CHF = diltiazem (Ca++ channel blocker)

55
Q

Do we use the same chronic CHF therapy in cats, as in dogs?

A

YES - ACE-i, furosemide, pimobendan, +/- spironolactone

56
Q

Three reasons for thromboembolic events in cats

A

1) Sluggish circulation due to turbulent blood flow in dilated chambers
2) Underlying damage with overstretched atria = develop fibrosis
3) Hypercoagulability = cause that’s how cats are

57
Q

Pathology behind feline aortic thromboembolism

A

Hypercoagulability + underlying heart damage + turbulent blood flow = clot formation, embolizes to periphery and lodges (commonly in terminal aorta), causes ischemia AND releases vasoactive substances

58
Q

Why does the formation of vasoactive substances play a role in the prognosis of feline aortic thromboembolisms?

A

Even if you remove the clot and reperfuse the tissue, the cytokines and PGFs can potentiate the tissue ischemia, may not help at all

59
Q

History involved with feline aortic TE

A
  • Acute in onset
  • Unilateral or bilateral HL paresis
  • R. forelimb paresis
    +/- Signs of CHF
60
Q

PE findings of a cat with aortic thromboemboli

A 
>> 5 P's
1) Pain
2) Pallor
3) Pulselessness
4) Polar (cold)
5) Paresis
\+/- Mutilation
61
Q

What do you need to diagnose feline aortic TE?

A

*Can be done mostly by finding the 5 “P”’s on your PE
+/- Echo
+/- CK and AST elevation on chem
+/- K+ and Mg++ elevation following reperfusion

62
Q

Acute treatment of FATE

A
  • Priority = treat life threatening CHF or arrhythmias
  • Assess vascular, muscle, and neuro function
  • Assess metabolic and organ function (renal and lytes)
  • Tx = can attempt surgery or thrombolytic agents
63
Q

Do we commonly treat FATE cats?

A

No - poor surgical candidates, risk of reperfusion injury, risk of mobilization of more emboli

64
Q

Medical management of FATE (3)

A

1) Pain meds
2) Prevent further embolization - anticoagulants (aspirin), maintain hydration
3) Support collateral circulation with vasodilators and hydration

65
Q

What is our cut-off for good/poor FATE prognosis cats?

A

Improvement by 7 days?

*Commonly not doing well due to additional infarcts to their kidneys or GI tract

66
Q

What can we do to prevent FATE?

A

Not much - anticoagulants haven’t been proven effective

CAEM Pt. 2 (27 decks)

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