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CRH II > Feline Cardiomyopathy > Flashcards

Feline Cardiomyopathy Flashcards

1
Q

describe feline cardiomyopathies

A
  1. primary disease of the cardiac muscle:
    -hypertrophic cardiomyopathy!!
    -restrictive cardiomyopathy
    -dilated cardiomyopathy
    -arrhythmogenic RV cardiomyopathy
    -nonspecific
  2. secondary disease of the cardiac muscle
    -hyperthyroidism
    -systemic hypertension
    -dietary
    -tachycardia-related
    -acromegaly
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2
Q

describe hypertrophic cardiomyopathy (HCM)

A
  1. the most common feline cardiomyopathy!!
  2. pathology:
    -ventricular thickening
    -typically LV wall and IVS
    -papillary hypertrophy
    -may be asymmetric hypertrophy
    -LA enlargement
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3
Q

describe HCM pathophysiology

A
  1. thickened, noncompliant ventricular walls cause DIASTOLIC dysfunction
  2. decreased cardiac output from reduced diastolic filling
  3. geometric changes in the ventricle and papillary muscles cause mitral regurgitation
  4. increased LA pressure leads to congestion (pulmonary edema, pleural effusion, pericardial effusion)
  5. increased myocardial O2 consumption and decreased perfusion leads to myocardial ischemia
  6. LV outflow obstruction may occur
    -systolic anterior motion (SAM) of the mitral valve (MV pulled into LV outflow tract)

diastolic dysfunction caused increased LA pressure and leads to CHF

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4
Q

describe clinical findings of HCM

A
  1. compensated:
    -cats may have clinically silent disease
    -murmur, typically sternal or parasternal
    -gallop!! very sensitive for occult cardiomyopathy in cats!!
    -arrhythmias, femoral pulse deficits
  2. decompensated:
    -panting, tachypnea, dyspnea
    -cyanosis (MM color variable: normal, pale, cyanotic)
    -jugular vein distension
    -crackles if pulmonary edema
    -decreased/muffled lung sounds if pleural effusion
    -ascites is rare
    -evidence of arterial thromboembolism
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5
Q

what are different characteristics of feline cardiac disease/heart failure from dogs?

A

dogs:
-primary valvular most common
-CM: systolic dysfunction
-cough: frequent presenting sign
-signs gradually worsen
-frequently ascites
-echo may not be needed for dx

cats:
-cardiomyopathies most common
-CM: diastolic dysfunction
-very rare to cough with cardiac disease
-signs appear acutely (hide signs until super severe)
-frequently pleural effusion, less often ascites
-echo typically is necessary for definitive diagnosis

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6
Q

describe radiographic findings of HCM in cats

A
  1. generalized cardiomegaly
    -VHS >7.75-8.0
    -heart > 2.5-3.5 ICS
  2. left atrial enlargement
  3. left ventricular enlargement
  4. CHF:
    -distended pulmonary veins
    -interstitial to alveolar infiltrates
    -pleural effusion
    -rare ascites
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7
Q

describe ECG of HCM in cats (3)

A

look for

  1. conduction abnormalities
  2. axis shifts
  3. signs of chamber enlargement
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8
Q

describe genetics of HCM in cats

A
  1. maine coon and ragdoll cats:
    -mutations: MYBPC3
    -can do genetic testing to see if patients have mutations that predispose to HCM!
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9
Q

describe echocardiography of HCM

A
  1. LV wall and septal thickening
    -may be asymmetric or regional

-LV concentric hypertrophy differentials: systemic hypertension, hyperthyroid heart disease, so measure blood pressure and obtain T4

  1. +/- LVOT obstruction:
    -fixed or dynamic (systolic anterior motion)
  2. +/- LA enlargement: if massive LA enlargement, may add plavix?
  3. +/- smoke or intracardiac thrombus
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10
Q

describe acute therapy for CHF due to HCM

A
  1. oxygen
  2. IV furosemide: decrease preload
  3. +/- pimobendan (PO) or dobutamine (IV) to increase contractility
  4. +/- sedation: butorphenol
  5. thoracocentesis if pleural effusion
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11
Q

describe chronic therapy for CHF due to HCM

A
  1. furosemide: loop durietic
  2. ACE-inhibitor: enalapril or benazepril
    -NEVER GIVE IN ACUTE: could cause AKI
  3. +/- pimobendan: indodilator
  4. +/- spironolactone: aldosterone antagonist; also not for acute setting!
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12
Q

describe follow up from acute presentation of CHF due to HCM

A
  1. recheck in 5-7 days
  2. thoracic rads
  3. renal panel
  4. blood pressure
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13
Q

describe NT-proBNP for HCM patients

A

100% specific for distinguishing healthy from cardiomyopathy

-use in combo with history, PE, and echo!

-good for the cat that comes in with gallop and arrhythmia, plus some enlargement on rads, if NT-proBNP is high = very likely underlying HCM

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14
Q

contrast restrictive cardiomyopathy to end stage HCM on echo

A

RCM:
-normal wall thickness
-atrial enlargement
-diastolic dysfunction

end stage HCM:
-walls may be normal
-dilated chambers
- +/- myocardial infarction

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15
Q

describe DCM on echo in cats

A
  1. left ventricular dilation and systolic dysfunction
  2. primary DCM is rare
    -secondary can be from taurine deficiency
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16
Q

describe sequelae of CM in cats

A

feline arterial thromboembolism! (ATE)

17
Q

describe pathophysiology of ATE

A
  1. commonly associated with feline CM
  2. damaged cardiac endothelium
  3. hypercoagulable state
  4. intracardiac blood stasis
  5. thrombus leave the heart and embolizes to peripheral vasculature
    -distal blood supply is disrupted
    -thrombi cause release of vasoactive substances
  6. acute event causes pain, then ischemia leads to necrosis of muscles or organs
  7. reperfusion injury can occur
18
Q

describe ATE in the heart

A
  1. impaired relaxation (diastolic dysfunction)
  2. left atrial enlargement and left auricular enlargement cause blood stasis
    -smoke: spontaneous echogenic contract
  3. thrombus formation: endothelial injury, platelet activation
  4. superficial portions of an intracavitary thrombus can break off
    -most common site: terminal abdominal aorta/saddle thrombus
  5. alternate sites:
    -brachial infarction
    -cerebral infarction
    -renal infarction
    -splanchnic infarction
19
Q

what are the 5 P’s of ATE saddle thrombus in cats?

A
  1. pain
  2. pulselessness
  3. pallor
  4. paresis
  5. polar (cold extremities)
20
Q

describe clinical signs of ATE

A
  1. cats may regain some to all motor function within 4-6 weeks
    -reestablishment of a collateral vascular network
    -intrinsic dissolution of the embolus
    -recanalization of the obstructed aorta
  2. chronic complications from aortic infarction
    -self mutilation of necrotic limb
    -limb necrosis requiring amputation
  3. renal: acute renal failure, renal pain
  4. central neurologic:
    -stupor, seizures, sudden death
  5. mesenteric: severe abdominal pain, vomiting
  6. additional:
    -hypothermia
    -murmur
    -gallop
    -arrhythmia
    -CHF: in up to 60%
21
Q

describe diagnostic tests for ATE

A
  1. chemistry:
    -hyperglycemia: due to stress
    -hypoglycemia in affected limb
    -azotemia: hypoperfusion, embolism
    -increased CK
    -increased AST/ALT
    -hyperkalemia
  2. chest rads: rule CHF in or out
  3. echocardiogram: LA size and content
22
Q

describe prevention of ATE

A
  1. if see left atrial enlargement or spontaneous echo contrast in LA
    -start clopidogrel or aspirin!
23
Q

describe management strategies of HCM in cats when ATE is suspected

A
  1. analgesia!!
  2. maintain hydration/perfusion
    -judicious use of fluids, however caution if patient has CHF
  3. manage CHF
  4. thrombolytic therapy (tPA): for hemorrhage, to avoid reperfusion injury
  5. anticoagulant therapy: heparin, low molecular weight heparin
    -heparin: unfractionated: inhibits Xa and IIa
    -low molecular weight heparin: pricier
24
Q

describe prognosis of HCM in cats with ATE

A
  1. guarded
    -survival rates 33-39%
  2. single limb affected: improved survival compared to bilateral pelvic limb infarction
  3. acute prognosis is more clear after 24-72 hours

CRH II (45 decks)

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