Myocardial and Feline Cardio Dz Flashcards
What is a common and extremely problematic complication of DCM with Dobermans? Why does it occur?
Sudden death - pathologic arrhythmias that weren’t addressed
What should you do with a patient with a syncopal history with irregular heart rhythms and pulse deficits?
RECORD THE ECG immediately so you can treat the arrhythmias before it causes sudden death
What age and breed does DCM commonly affect?
Middle aged male Dobermans
Do DCM dogs commonly have heart murmurs?
No
Top differentials for left sided heart disease in dogs
1) DCM - large breed and Spaniels
2) Mitral insufficiency due to valve disease - small breeds and Spaniels
3) Decompensated congenital defects
4) Endocarditis
What is dilated cardiomyopathy?
Abnormality of the HEART MUSCLE that is not due to other cardiac abnormalities or systemic disease
What are the three main characteristics that define DCM?
> > 3 D’s
- Decreased systolic function or contractility
- Dilation, ventricular and often atrial
- Dysrrhythmias
What two cardiac arrhythmias are most common with DCM?
1) Atrial fibrillation
2) Ventricular tachycardia
What form/cause of DCM is the most common?
Idiopathic - occurs in large breed dogs
Four etiologies of secondary DCM
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
Why does DCM lead to arrhythmias?
- Atrial stretch = atrial fibrillation and fibrosis
- Ventricular fibrosis and ischemia from idiopathic myocardial changes = v-tach
How does DCM lead to heart failure?
Ventricular fibrosis and atrial stretch > decreased contractility > decreased SV and CO > hypotension > SNS and RAAS activation = tachycardia and tacharrhythmias, Na/water retention, vasoconstriction
What is the number one diagnostic test to determine DCM?
- Echocardiography
- Hx and PE for CHF
- ECG for arrhythmias
What is compensated or occult DCM?
> > Dog looks completely normal and isn’t showing clinical signs
+ Gallop rhythm
+ Arrhythmias
+/- Relative systolic regurgitant murmurs may be present
+ Weak pulses
What is the difference between compensated/occult and decompensated DCM?
> > 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
What sign on your PE may help you differentiate DCM from valvular disease?
Pulse deficits = decreased stroke volumes, more common with DCM
Three main therapeutic targets with decompensated DCM?
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
Do we treat occult DCM? If so, with what?
- YES - pimobendan prolongs survival, +/- ACE-inhibitors
- Owner education to screen for progressive disease
Do we worry about A-fib causing sudden death?
No - just worsens clinical signs
Goals and treatment(s) for ventricular tachycardia
- 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
Is the AV node affected in DCM?
No - normal functioning, seeks to protect the ventricle from tachycardia, caused by the overwhelming production of atrial depolarization
Four components of a-fib
1) Tachycardia
2) Irregular rhythm
3) Supraventricular = narrow QRS
4) No P waves
Why is atrial fibrillation a problem? (2)
- Loss of coordinated atrial depolarization = decreased stroke volume
- Tachycardia = less time for ventricular filling = decreased CO
Can we cure the a-fib involved with DCM?
No - goal is to cause AV block (prolong PQ interval to produce a controlled ventricular response
Three drugs used to treat a-fib
1) Digoxin = mimics/enhances vagal tone
2) Ca++ channel blocker
3) Beta blockers
* Don’t use Ca++ and b-blockers together
Most common heart disease type in cats and dogs
- Dogs = valvular disease
- Cats = cardiomyopathies, most commonly HCM
When is the cardiomyopathic dysfunction in dogs and cats - systole or diastole
- Dogs = systole
- Cats = diastole
Do dogs or cats commonly present with cough as cardiac signs?
Dogs
Is the disease progression of heart disease gradual or acute in dogs and cats?
- Dogs = gradual
- Cats = acute, good at hiding clinical signs
Do dogs, cats, or both need echo to diagnose the type of heart disease?
- Dogs = often, sometimes only need signalment, history, and PE
- Cats = ALWAYS
True or false - CHF looks generally similar in cats, regardless of the etiology
TRUE - need echo for the specific causes, all get pleural effusion
Common history of cats with heart disease
- Signs of disease appear suddenly
- Often ADR, just “hiding” or acting “lethargic”
- May be acute dyspneic or lame due to thromboemboli
Common head/neck and thoracic findings of PE of cats with heart disease
- 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)
Are ECG’s helpful with diagnosing feline heart disease, yes or no?
- NON-SPECIFIC to the type of disease
- Includes: arrhythmias, axis shifts, conduction abnormalities, chamber enlargement
- May be NORMAL with severe disease
Things you can see on thoracic rads with feline heart disease (4)
- Chamber enlargements
- Pleural effusion
- Degree of cardiomegaly
- Non-specific edema patterns, starts caudodorsal, ventrocaudal, then cranial
What things can the echo tell you with heart disease? (2)
1) Anatomy - congenital malformations, acquired valvular or myocardial malformations
2) Function = chamber size/thickness, contractility
What is NT-proBNP and what can it tell us?
> 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
Who is NT pro-BNP more helpful in - dogs or cats?
Cats - easier to interpret
*Exception = DCM in dobermans
What is a cardiomyopathy?
> Acquired disease of the MYOCARDIUM
- Structural abnormality + functional abnormality
- Usually IDIOPATHIC = not due to systemic (Ex: hyperthyroidism) or infiltrative disease (LSA)
Breeds at risk for HCM (2)
- Maine Coon cats
- American shorthaired
What is the main diagnostic that differentiates between types of cardiomyopathies (i.e. HCM, DCM, etc)?
ECHO
What is the most common myocardial disease in cats?
Hypertrophic cardiomyopathy
Three hallmarks of HCM
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
What problems does thick and stiff ventricles pose? (2)
*Diastolic dysfunction = can’t relax
- Increased myocardial oyxgen needs = risk of ischemia
+/- Outflow obstructions by the mitral valve or septum
What problems does diastolic dysfunction pose? (3)
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
Differentials for left ventricular hypertrophy in cats (4)
- Congenital and valvular diseases are uncommon
- HCM
- Aortic stenosis
- Hyperthyroidism
- Hypertension secondary to hyperthryoidism or renal disease
What causes the atrial enlargement in HCM?
Poor diastolic function = atria doesn’t unload completely into the ventricle, has to push harder to unload during diastole
Three general goals with treatment of HCM
1) Improve muscle relaxation with positive lusitropes
2) Prolong filling time by slowing HR
3) Reduce outflow obstructions if present
What’s the number one med we use to treat feline HCM?
Atenolol = beta blocker, improves diastolic function AND arrhythmias by slowing the heart rate
Is there any benefit to treat asymptomatic HCM cats?
NO
Two hallmarks of DCM in cats
1) Dilation of left ventricle and atria
2) Poor systolic/contractile function
* Same as DCM in dogs
Etiology of DCM in cats
Usually IDIOPATHIC, may be due to taurine deficiency
Treatment of acute CHF in cats
1) Furosemide
2) LOW STRESS oxygen
3) Pimobendan
+/- Thoracocentesis
+/- Sedation
Treatment of arrhythmias in cats with and without CHF
- Without CHF = beta blockers
- With CHF = diltiazem (Ca++ channel blocker)
Do we use the same chronic CHF therapy in cats, as in dogs?
YES - ACE-i, furosemide, pimobendan, +/- spironolactone
Three reasons for thromboembolic events in cats
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
Pathology behind feline aortic thromboembolism
Hypercoagulability + underlying heart damage + turbulent blood flow = clot formation, embolizes to periphery and lodges (commonly in terminal aorta), causes ischemia AND releases vasoactive substances
Why does the formation of vasoactive substances play a role in the prognosis of feline aortic thromboembolisms?
Even if you remove the clot and reperfuse the tissue, the cytokines and PGFs can potentiate the tissue ischemia, may not help at all
History involved with feline aortic TE
- Acute in onset
- Unilateral or bilateral HL paresis
- R. forelimb paresis
+/- Signs of CHF
PE findings of a cat with aortic thromboemboli
>> 5 P's 1) Pain 2) Pallor 3) Pulselessness 4) Polar (cold) 5) Paresis \+/- Mutilation
What do you need to diagnose feline aortic TE?
*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
Acute treatment of FATE
- 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
Do we commonly treat FATE cats?
No - poor surgical candidates, risk of reperfusion injury, risk of mobilization of more emboli
Medical management of FATE (3)
1) Pain meds
2) Prevent further embolization - anticoagulants (aspirin), maintain hydration
3) Support collateral circulation with vasodilators and hydration
What is our cut-off for good/poor FATE prognosis cats?
Improvement by 7 days?
*Commonly not doing well due to additional infarcts to their kidneys or GI tract
What can we do to prevent FATE?
Not much - anticoagulants haven’t been proven effective
