Cardio3- Misc Feline Cardiomyopathies

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  1. What is feline RCM?
    myocardial disease characterized by diffuse LV endocardial fibrosis or LV myocardial fibrosis, causing progressive LV diastolic dysfunction.
  2. What are causes of primary RCM in cats?
    genetic causes- mutation of contractile elements causing severe relaxation delay
  3. What are causes of secondary feline RCM? (2)
    amyloidosis, endomyocarditis, others
  4. PE findings with feline RCM. (2)
    loud gallop sounds, NO MURMUR (a murmur will never be RCM ever)
  5. What are  radiographic findings with feline RCM? (4)
    severe LA and RA enlargement +/- CHF, valentine heart
  6. Echo findings with feline RCM. (7)
    severe bi-atrial enlargement, normal LV wall thickness, normal LV chamber dimension, endocardial hyperechogenicity, false tendons, low normal to decrease LV systolic function, severe LV diastolic dysfunction (restrictive filling Doppler pattern)
  7. Cats with HCM and RCM complicated by myocardial infarction and reparative scar tissue can lead to ______________ on echo.
    thinning and scarring of LV free wall
  8. What does restrictive filling look like on Doppler?
    very tall E wave, very small/non-existent A wave (blood rushes in at very high velocity in early diastole--> column of blood flow stops abruptly)
  9. What will you hear on auscultation of a cat with RCM?
    S3 gallop (early ventricular filling) [no S4 because atrial kick is ineffective]
  10. What is feline ARVC?
    primary myocardial disease characterized by progressive RV and RA dilatation, arrhythmias, and RV systolic dysfunction.
  11. Feline ARVC occurs most commonly in __________, although it is a rare disease in general.
    older cats
  12. _____________ is common with feline ARVC, and ___________ may occur.
    RV ectopy; atrial standstill/ fibrillation
  13. Severe feline ARVC end up leading to __________.
    R-CHF
  14. What is "triangle of dysplasia" and with what disease does it occur?
    area where fatty infiltration typically starts at apex of RV; occurs with feline ARVC
  15. What is feline UCM (unclassified cardiomyopathy)?
    myocardial disease that does not fit the characteristics of HCM, RCM, DCM, and ARVC- i.e. we don't know what to call it
  16. Describe echo findings with feline UCM. (3)
    • w/ no obvious reason, no abnormal auscultation
    • LA/RA enlargement
    • LV diastolic dysfunction
  17. What is feline DCM?
    primary myocardial disease characterized by left/right ventricular eccentric hypertrophy (dilatation) and lV systolic dysfunction.
  18. Systolic dysfunction is common secondarily to... (4)
    chronic volume overload, ischemic heart disease, myocarditis, and taurine deficiency.
  19. What are PE findings with feline DCM? (3)
    gallop sounds, hypokinetic pulses, +/- CHF
  20. What are ECG findings associated with feline DCM? (3)
    [non-specific] cardiac enlargement pattern. tachyarrhythmia, complete heart block
  21. What are radiographic findings common with feline DCM? (2)
    generalized cardiomegaly (pumpkin heart), +/- signs of CHF (pleural effusion)
  22. Generally with feline DCM, BP is _________.
    low
  23. What are echo findings common with feline DCM? (4)
    • severe LA and often RA enlargement
    • LV dilatation with decreased wall thickness
    • Decreased LV systolic function (low SF)
    • Severe LV diastolic dysfunction/ restrictive filling
  24. What is commonly the SF with feline DCM?
    <30%
  25. What are some necessary diagnostics for a cat with DCM? (2)
    • measure whole blood taurine levels (in taurine deficiency, taurine is usually <20nmol/mL)
    • cTI- ischemic myocardial dz and myocarditis are detected by this method and may be associated with systolic dysfunction
  26. Do murmurs develop with DCM?
    sometimes but it is never louder than 2/6 (b/c if the heart cannot contract well, it cannot develop a loud murmur)
  27. Cardiomyopathy due to high-output disease is caused by ... (3)
    massive RAAS activation, as with anemia, hyperthyroidism. [pump well and are still in failure]
  28. What do you see on echo with cardiomyopathy of high-output disease? (4)
    eccentric LV and RV hypertrophy, LA and RA enlargement, LV hyperkinesia, increased LV diastolic function (w/ hyperthyroidism)
  29. Low PCV activated RAAS because...
    vessels dilates to try and get more oxygen to muscles; RAAS is activated to try and retain fluids and increase plasma volume to increase BP.
  30. FATE is a common problem in feline cardiomyopathy with _________.
    LA enlargement
  31. What are the 3 factors required for clot formation?
    [Virchow's Triad] endothelial injury, blood stasis, coagulopathy
  32. What is the cause of saddle thrombus?
    clot forms in enlarged LA/ auricle--> embolus breaks off and travels downstream--> gets lodged at aortic trifurcation
  33. What are predilection sites for FATE? (2)
    aortic trifurcation, right front leg
  34. What is an echocardigraphic indication of FATE?
    smoke- blood stasis
  35. The clinical signs of FATE depend on... (4)
    location, degree of occlusion, duration, collateral circulation
  36. What is the classic presentation of FATE? (10)
    • [Five P's] pain, paresis, pulselessness (in femoral a.), pallor, polar (cold limbs)
    • cyanotic nail beds, signs of CHF, volcalization, tachypnea (from pain), open mouth breathing
  37. What are other differentials for FATE? (3)
    • spinal cord disease, peripheral neuropathy, central brain lesion
    • feel the pulses--> weak or absent?--> FATE!
  38. What are the goals of FATE management? (5)
    pain relief, supportive therapy, manage heart failure +/- renal failure, prevent additional clot formation and sudden death
  39. With the treatment of FATE, sudden death may occur due to ____________.
    acute reperfusion
  40. What is the acute therapy for FATE? (6)
    • pain medication- Methadone, Oxymorphone, Bupenorphine, Fentanyl
    • prevent thrombus expansion- Heparin
    • inhibition of platelet aggregation- Plavix
    • +/-Thrombolysis- tissue plasminogen activator (under investigation)
    • CHF therapy
    • Regulate electrolytes
  41. If the cat survives the acute episode of FATE, what is chronic therapy and prevention of further clots? (3)
    Plavix, Aspirin, treat underlying condition
  42. With acute reperfusion, _________ occurs, which can lead to ___________.
    K+ spike; fatal arrhythmias
  43. What is the prognosis for FATE?
    • Poor
    • 3 expected outcomes: discharge, death, euthanasia (high chance of recurrence)
  44. What is the mechanism of steroid-induced heart failure?
    possibly related to hyperglycemia and secondary volume overload or fluid retention related to the use of Depo-Medrol in cats [remember DM is a side-effect of Depo]
  45. How can you avoid steriod-induced CHF in cats? (2)
    echo should be done on all cats before injection with Depo-Medrol to identify occult cardiomyopathy; monitor respiratory rate in cats receiving Depo
  46. What is "moderator band" cardiomyopathy?
    endocardial type of RCM in cats, characterized by a prominent false tendon in the LV lumen--> progressive LV diastolic dysfunction and restrictive filling
  47. Describe the genesis of pleural effusion in cats with L-CHF.
    L-CHF--> impaired diastolic function--> increased LV pressure--> pulmonary hypertension--> increased hydrostatic pressure in pulmonary veins (usually drain into LA), increased pressure in pulmonary arteries--> pleural effusion and pulmonary edema.
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318463
Card Set
Cardio3- Misc Feline Cardiomyopathies
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vetmed cardio3
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