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Acquired heart conditions Flashcards

1
Q

Dilated cardiomyopathy–K9

General/lesions

A
  • Decreased myocardial contractiliy–systolic dysfunction–leading to progressive dilation of the L and/or R ventricle
  • Mild thinning of the walls
  • Can lead to eventual L or R-sided CHF
  • Histo lesions include
    • Lack of inflammation
    • Wavy myofibers
    • Fibro-fatty infiltration
    • Loss of myocytes and myocardial fibrosis
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2
Q

Dilated cardiomyopathy–K9

Pathophysiology

A
  • Idiopathic–diagnosis of exclusion, but poss. familial etiology in dobies, boxers, cockers, wolfhounds
  • End-stage of various other processes–L-carnitine or taurine deficiencies, toxicities (doxorubicin, alcohol), ischemia, infections, immunological, tachycardia and metabolic abnormalities
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3
Q

Dilated cardiomyopathy–K9

Doberman pinscher progression

A
  • Arrhythmogenic cardiomyoathy
    • Arrhythmias but normal L ventricular contractility
    • IWH may have lone AF
    • Dobies present w/ VDs, generally progresses to the next stage of dz
  • Occult DCM
    • Animals appear normal but have mophological changes (L ventricular enlargement), trending towards dec. contractility
    • Ventricular arrhythmias or AF common
  • Classic DCM: heart failure
    • L-sided more common
    • Ventricular enlargement, dec. contractility–systolic dysfunction
    • Ventricular arrhythmias or AF present
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4
Q

Dilated cardiomyopathy–K9

Taurine/L-carnitine deficiency

A
  • Bile acids are conjugated with taurine
  • Important moderator of Ca flux, reduces platelet aggregation, stabilizes neural membranes, + inotrope
  • Dogs can synthesize (those on lamb and rice diet have recently been diagnosed w/ deficiencies)
    • Recommend supplementing dogs on these diets w/ taurine and carnitine
    • Dogs which develop DCM can improve w/ medication and may eventually only need supplementation (will not reverse damage)
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5
Q

Dilated cardiomyopathy

Signalment

Usual history

A
  • Signalment
    • Seen in giant and some smaller breeds of dogs
    • Dif. gene pools may be over-represented in dif. countries
    • Most common in middle-aged males
  • History
    • Depends on ventricles involved
    • Wt. loss, exercise intolerance, weakness, syncope, etc.
    • Sudden death occurs in ~30% of dobies
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6
Q

Dilated cardiomyopathy–K9

Common abnormalities on PE

A
  • Poor BCS
  • Signs of heart failure
  • Muffled heart and lung sounds
  • Signs of A-fib
  • Systolic murmur from mitral regurg
  • S3 gallop sounds common
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7
Q

Dilated cardiomyopathy–K9

Abnormalities commonly found on special exam

A
  • Labwork
    • Pre-renal azotemia
    • Elevated liver enzymes
    • Low taurine or arnitine levels (rare)
    • Future–natriuretic and cardiac tropoin level testings (early diagnosis)
  • X-ray–generalized heart enlargement
  • Echo–definitive diagnosis
    • ​Ventricular enlargement w/ ‘flabby,’ thin walls
    • Reduced contractility and fractional shortening is decreased (~23% is normal for dobies)
  • M-mode–fractional shortening <20% (N = 25-45% in normal dogs)
  • Doppler–mitral valve insufficiency and reduced SV
  • ECG
    • VPDs–dobies
      • Up to 50/day ok
    • A-fib in other breeds
    • Signs of heart enlargement and ST segment depression
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8
Q

Dilated cardiomyopathy–K9

DDx

Prevention

Prognosis

A
  • DDx–pericardial effusion
  • Prevention–genetic markers should be available to detect animals at risk to keep them from breeding programs
    • Autosommal dominant in dobies–mutation in pyruvate dehydrogenase kinase (PDK4); commercial test available
    • Age of onset variable
  • Prognosis
    • Guarded to poor
    • Therapy will inc. quality of life
    • ACE inhibitors and pimobendan together improve life expectancy to 350 days
    • American cocker spaniels can recover completely w/ taurine and carnitine deficiency
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9
Q

Dilated cardiomyopathy–K9

Treatment: ACM

A
  • Arrhythmogenic CM
    • Treat if avg HR >90bpm or >250bpm w/ exercise
    • No evidence that treating will reduce risk of sudden death
    • Recommended to treat dogs w/ runs of VT, RonT phenomenon, or excessive VPDs
    • Lone A-fib
      • Beta blockers–atenolol, metoprolol
      • Control arrhythmias and ‘cardio-protection’
      • Diltiazem–control HR
    • Ventricular arrhythmias
      • Beta-blockers: sotalol
      • Combination of mexiletine and atenolol–reduce frequency of ventricular beats and runs
      • Indication to delay onset of further stages
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10
Q

Dilated cardiomyopathy–K9

Treatment: OCM

A
  • Ace inhibitors in dobies seem to delay onset of DCM
  • Same effect possibly with beta-blockers
  • Treat arrhythmias and moitor for dz progression
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11
Q

Dilated cardiomyopathy–K9

Treatment–DCM and CHF

A
  • Mild failure: furosemide, ACE inhibitors, pimobendan, and antiarrhythmics
  • Severe failure: hospitalized, oxygenated, and treated w/ injectable furosemide (monitor for hypo- K, Na, and Cl); observe RR and change administration of furosemide accordingly
  • Dobutamine can be used in cases of hypotension and markedly decreased contractility
  • Reduced preload w/ nitroglycerine ointment or sodium nitroprusside
    • Control w/ ACE inhibitors after
  • Pimobendan–(+) inotrope, inc. sensitivity to existing Ca w/o an inc. in myocardial oxygen demand
    • PDE III inhibitor–inc. contractility, general vasodilator
  • Digoxin + diltiazem–slow ventricular response rate in dogs w/ A-fib
    • Hypotension and heart block may occur
  • Dogs w/ clinical signs from ventricular arrhythmias, runs of VT, numerous VPDs w/ tachy, or RonT phenomenon–lidocaine followed by long-term mexiletine
    • No evidence that this will prevent sudden death
    • Reserve this trtmt for dogs w/ VT
  • Beta-blockers–dec. # and complexity of ventricular arrhythmias at low doses
    • High doses are (-) inotropes and cause severe decompensation
      • Should not be initiated until heart failure is controlled and standard therapy is in place
    • Metoprolol or carvediolol–dose should be gradually inc. until decompensation occurs, then back off
      • Optimal dose is unknown–low dose better than nothing
  • After discharge from hospital animal should set own activity level + restricted Na diet
    • Taper to lowest poss. dose of furosemide, start ACE inhibitors low and gradually inc. to max over a few weeks
  • Renal fx should be monitored/assessed after 3-7d (furosemide doseage)–dec. if BUN, Cr elevated
  • Supplement for any deficiencies ID’d
  • Fish oil improves cachexia in dobies
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12
Q

Dilated cardiomyopathy–feline

Pathophysiology

A
  • Characterized by ventricular dilation, thinning of ventricular wall, and dec. contractility
  • Majority of cases are due to taurine deficiency
    • Rare disease now
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13
Q

Dilated cardiomyopathy–feline

Signalment

Usual history

A
  • Signalment
    • Middle aged to older males
    • Burmese, siamese, abyssinian predisposed
  • History
    • Acute onset of paresis/paralysis due to ATE
    • Dyspnea, anorexia, lethargy, vomiting, and lung sounds
    • Gallop rhythms and murmur from AV valvular insufficiency common
    • Focal areas of retinal degeneration are suggestive of taurine deficiency
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14
Q

Dilated cardiomyopathy–feline

Common abnormalities on PE

DDx

Prevention

A
  • PE
    • Hypothermic, weak femoral pulses, poor CRT
    • Dyspnea, muffled heart and lung sounds
    • Gallop rhythms and murmur from AV valvular insufficiency common
    • Focal areas of retinal degeneration are suggestive of taurine deficiency
  • DDx–hypertrophic cardiomyopathy
  • Prevention–ensure cats receive adequate levels of taurine
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15
Q

Dilated cardiomyopathy–feline

Abnormalities on special exam

A
  • Labwork–low taurine or high T4
  • X-ray
    • Pleural effusion
    • Heart appears diffusely enlarged
    • Diffuse alveolar and interstitial patterns in lungs
  • Echo–definitive diagnosis
    • ​Dilated, thin-walled left ventricle w/ reduced contractility
  • M-mode
    • Inc. left atrial dimensions
    • Dec. ventricular wall thickness
    • Reduced fractional shortening
  • Doppler–mitral valve insufficiency, reduced stroke volume
  • ECG–normal or tall R waves in lead II
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16
Q

Dilated cardiomyopathy–feline

Treatment

Prognosis

A
  • Treatment
    • Treat pulmonary edema/pleural effusion if present
      • Oxygen, furosemide, venodilator therapy, thoracocentesis
    • ACE inhibitors can improve systolic fx
    • Treat ATE if present
    • Supplement taurine if found deficient
      • Will see echocardiographic improvement in ventricular performance by 6wks
    • Treat hyperthyroidism if present
  • Prognosis: fair if taurine deficient; if not, most cats die w/in 2 months regardless of treatment
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17
Q

Hypertrophic cardiomyopathy

Pathophysiology

A
  • Functional abnormalities in myocytes that leads to inc. cell stress and activation of trophic and mitotic factors–papillary musc. and left ventricular concentric hypertrophy (diffuse or focal)
  • Histo-myocytes are enlarged w/ fiber disarray
  • Intramural coronary arteriosclerosis and myocardial interstitial fibrosis
  • Primary and idiopathic in most cases
  • Hypertrophied and fibrosed L ventricular wall lacks compliance and cannot fill during diastole–diastolic failure; ventricular chamber non-existent in systole
  • Dynamic outflow tract obstruction by hypertrophied ventricular septum
  • Systolic anterior motion of the anterior mitral valve leaflets–misalignment of the mitral valve; anterior leaflets blocking outflow tract during systole
    • Can cause mitral insufficiency and regurg of blood back into atrium during systole = murmur
  • Lack of diastolic filling in L ventricle = inc. pressure in the L atrium –> chamber enlargement – L CHF signs
  • Blood stasis in the L atrium can predispose to clot formation
    • If dislodges–> iliac bifurcation of the aorta an dlodge–> ischemia in one/both hind limbs
      • Muscle necrosis, lameness
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18
Q

Hypertrophic cardiomyopathy

Signalment

Usual history

A
  • Signalment
    • Most common cardiomyopathy in cats; exclusion diagnosis
    • Middle-aged male cats
  • History
    • Most asymptomatic; only pick up murmur as incidental finding
    • Can trigger animal into heart failure if too stressful
    • Some may die suddenly–arrhythmias
    • Cats in heart failure resent w/ acute dyspnea–apear perfectly normal until then
    • Heart failure cats may also have painful hind limb lameness
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19
Q

Hypertrophic cardiomyopathy

Common findings on E

A
  • Pronounced apex beat on L side
  • S4 gallop rhythms and systolic murmurs common
  • Hind limbs may be cold to the touch, muscles hard and painful–lameness may be only sign
  • Remember that distress signs can mimic heart failure
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20
Q

Hypertrophic cardiomyopathy

Common abnormalities found on special exams

A
  • Labwork
    • Troponin-1 and pro-BNP biomarkers elevated
    • ATE–muscle necrosis and elevated ck AND ast
    • K+ may be elevated
    • Normal coag
  • X-ray
    • Valentine-shaped heart on DV
    • 50% have generalize heart enlargement–appear like DCM
    • Pulmonary edema present if in CHF
  • Echo
    • Marked thickening of the ventricular septum or L ventricular free wall
    • Papillary muscle hypertrophy
    • Reduced ventricular lumen
    • Can see regional or segmental hypertrophy
    • Can see dynamic outflow obstruction and SAM
  • Doppler
    • Turbulence in outflow tract
    • Can also see jets at mitral valve if insufficient
    • Spectral doppler will allow measurements of pressure gradients–determines severity of obstructions if resent
  • M-mode–thickened ventricular free wall and septum
  • Angio
    • Enlarged heart and septum, enlarged papillary muscles, dec. ventricular volume
    • Can be used to confirm ATE
  • ECG–normal or signs of L heart enlargement, dysrrhythmias or microscopic intramural myocardial infarction (MIMI)
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21
Q

Hypertrophic cardiomyopathy

DDx

Prevention

A
  • DDx–differentiate between primary and secondary HCM
  • Prevention–test for myosin binding protein 3 mutation in Maine Coon cats and 1 specific for Ragdolls–don’t breed cats that are +
    • May be other genes that cause dz–(-) test for MyBPC doesn’t mean the cats will never develop HCM
22
Q

Hypertrophic cardiomyopathy

Treatment

A
  • May remain asymptomatic and live normal lifespan
  • Beta-blockers
    • Atenolol–reduce pressure gradient in cases of LVOT obstruction
      • ACE inhibitors are given in cases w/ atrial enlargement–usually alongside a beta-blocker or dilitazem
  • Cats that are close to heart failure can be placed on ACE inhibitor and low-dose furosemide
    • Can start anti-coag therapy if indicated by imaging (‘swirling smoke’ in atrium)
    • Heparin or aspirin and plavix
  • Cats presenting in acute failure should be sedated, placed on oxygen, warmed (cardiogenic shock), and given dobutamine via CRI (reduce dose as animal improves)
    • Remove effusion via thoracocentesis and administer furosemide–taer as soon as RR improves (cats very sensitive to electrollyte imbalances caused by the drug)
  • Once stabilized, blace cats on beta blockers–propranolol (unless asthmatic) or atenolol
    • Beta-blockers promote ventricular relaxation and slow heart–improves passive ventricular filling, inc. stroke volume, and reduces pulmonary edema
    • Increased CO and slower rate will also improve myocardial perfusion and decrease oxygen req.
  • Diltiazem–Ca channel blocker–improves relaxation and reduces HR and contractility and O2 demand
    • Less effective than atenolol and has adverse side effects
  • Spironoloactone contraindicated–ulcerative facial dermatitis
  • ATE: can spontaneously recover via recanalization or collateral circulation
    • Sedation and analgesia required–painful
    • Reperfusion is sketch–hyperkalemia and acidosis from muscle damage (control w/ sodium bicarb)
    • Acepromazine + ACE inhibitor = hypotension–caution
    • Acepromazine used for anxiety and arteriodilation to improve collateral circulation
  • Thrombolytic therapy may seed up clinical recovery–expensive trtmts, lots of complications
  • Can control further thrombus formation w/ short term unfractionated hearin, lavix, warfarin (sketch), or daily inj. of low mo. wt. heparin (none are 100%)
  • Aspirin–no evidence of improvement
23
Q

Hypertrophic cardiomyopathy

Prognosis

A
  • Asymptomatic = guarded to good
    • Median 5 yr survival
    • Focal enlargements are better tolerated
    • Cats w/ more diffuse hypertrophies have worse prognosis
  • Cats presenting in heart failure have ~3mo
  • Cats w/ ATE and heart failure = very poor prognosis
    • Same w/ renal or celiac thromboembolism
24
Q

Feline hyperthyroidism

All the things

A
  • L ventricular concentric hypertrophy–w/ hypertension
  • Most have eccentric hypertrophy–high output and volume overload
  • Signs resolve w/ appropriate thyroid treatment
25
Q

Restrictive cardiomyopathy–feline

All the things

A
  • Endocardial, subendocardial or myocardial fibrosis or infiltrative disease which reduces diastolic filling
  • L ventricle involve–extreme L atrial enlargement
    • L heart failure signs
  • L atrium dilated, L ventricle relatively normal
  • Several etiologies
  • Poor prognosis
26
Q

Arrhythmogenic R ventricular cardiomyopathy in Boxers

Pathophysiology

A
  • Familial disease, autosomal dominant; incomplete penetrance
  • Extensive changes in right myocardium–inflammation, fibrosis, fat infiltration
  • Ventricular arrhythmias
  • VPDs originate from R ventricle
  • Sudden death possible at any stage
  • Possible etiology from dysfunctional gap junctions and Ca leakage
27
Q

Arrhythmic R ventricular cardiomyopathy of boxers

Signalment

Usual history

A
  • Signalment–boxers 1-15yrs (average 6-10yrs)
  • History
    • Sudden death
    • No abnormalities
    • Weakness
    • Syncope
    • Signs of R or L heart failure
28
Q

Arrhythmic R ventricular cardiomyopathy in boxers

Common findings on PE

Comm abnormalities on special exams

A
  • PE–normal, may hear VPDs
  • Special tests
    • Definitive diagnosis can only be made during necropsy after sudden death
    • Probable diagnosis based on familial history and any ossible clinical signs–weakness, syncope, etc.
    • Serum cTn-1 conc. elevated in affected animals
    • Holter monitoring to detect VPDs–anything over 100 episodes/day is suggestive
29
Q

Arrhythmogenic R ventricular cardiomyopathy in boxers

Treatment

Prevention

A
  • Treatment may decrease the complexity and # of VPDs–but no evidence this does anything to decrease risk of sudden death
  • Treat dogs w/ weakness and syncope, asymptomatic dogs with >1000 VPDs/day, VT, or RonT
    • Sotalol or mexiletine + atenolol
    • Evaluate treatment w/ holtor monitoring–effective if VPDs decrease by 85%
      • Beware of proarrhythmic effects
    • Omega-3 FA’s to help decrease # of VPDs
  • Prevention–dogs should be screened at ~1yr old and every year after to look for ARVC and sub-aortic stenosis
    • Dogs showing signs or suspect signs shouldn’t be bred
30
Q

Arrhythmogenic R ventricular cardiomyopathy in boxers

DDx

Prognosis

A
  • DDx–DCM or sub-aortic stenosis
  • Prognosis
    • Sudden death always possible
    • Severity of clinical signs does not correlate w/ # of VPDs (but more clinical signs are generally seen w/ inc. # of VPDs)
31
Q

Myxomatous atrioventricular valvular degeneration–endocardiosis

Pathophysiology

A
  • Thickening and contraction of the mitral valve leaflets cause it to become incompetent
  • Regurg of blood to the atrium in systole
  • Chordae tendinae become thickened–may rupture –> valve prolapse into the atrium during systole
  • Little regurg = heart compensation (by inc. sympathetic tone) –> minimal RAAS activation
  • Valvular degeneration progressive, inc. regurg causes L atrial enlargement–> compression of L main bronchus–> coughing
  • Volume overload in L ventricle = eccentric hypertrophy; may lead to CHF and pulmonary congestion
  • Rupture of chordae tendinae –> acute exacerbation w/ severe pulmonary edema
  • Jet lesions–> L atrial rupture, cardiac tamponade
32
Q

Myxomatous atrioventricular valvular degeneration–endocardiosis

Signalment

Usual history

A
  • Signalment
    • Older, male, small-medium dog breeds
    • Inherited condition in Cavalier King Charles spaniels
    • Slowly progressive dz and dogs usually die of something not heart-related
  • History–usually assoc. w/ variety of clinical syndromes
    • Asymptomatic murmur (louder w/ more regurg)
    • Large airway compression and coughing
    • Exercise intolerance
    • Weakness
    • Syncope
    • Left atrial rupture and acute cardiac tamponade
    • Acute heart failure w/ chordae tendinae rupture
    • Chronic CHF
33
Q

Endocardiosis

Common findings on PE

A
  • Dependent on stage of dz
  • Early
    • Murmur or systolic click
    • Click is early sign of mitral valve degeneration–> elongated chordae tendinae snap tight as degenerative valve protrudes into L atrium mid systole
  • Murmur is loudest on the L over the mitral valve/apex and radiates to the R
  • Advanced
    • L CHF signs
    • Mild to moderate lung edema
    • Inc. bronchovesicular sounds w/ crackles over ventral lung fields
  • Coughing in older dogs more commonly due to small airway dz (bronchial compression due to endocardiosis and/or progression to heart failure are less common)
34
Q

Endocardiosis

Common abnormalities on special tests

A
  • Labwork
    • Mild inc. in BUN and CR–> hypotension
    • Mild elevated liver enz. –> hepatic congestion
    • Natriuretic peptides and endothelin-1 blood levels rise w/ CHF (dogs coughing from CHF have even higher levels)
  • X-ray–depends on stage of dz
    • L atrial enlargement –> splitting of main stem bronchi and compression of L main bronchus in lateral
    • May be dif. to differentiate heart failure from compensated mitral regurg and chronic lung dz (best to compare previous rads)
  • Echo–fx usually remains normal
    • Contractility will be normal or enhanced: long standing cases the L ventricle may be dilated and hypocontractile
    • L atrium is usually enlarged and valves are club-shaped and thickened
    • Septal leaflet of mitral valve most commonly affected
    • Elongated chordae tendinae
  • Dopler–regurg and pulmonary tension
  • ECG–L atrial and ventricular enlargement
35
Q

Endocardiosis

DDx

Prognosis

Prevention

A
  • DDx–other causes of L-sided heart failure, primary respiratory dz
  • Prognosis
    • The larger the L atrium = the more severe the regurg
    • Most dogs will die of a condition unrelated to the valve insufficiency
    • If L heart failure occurs treatment can provide reasonable quality of life for ~1 yr
    • R CHF = poor prognosis
  • Prevention–None
    • ACE inhibitors may help
    • Pimobendan is deleterious if given before clinical signs of heart failure are present ($$$ for large dogs)
36
Q

Endocardiosis: treatment

Incidental?

Coughing but no CHF?

Mild-to-moderate heart failure?

A
  • Incidental–cannot stop/delay it; reference x-ray and echo useful
  • Coughing w/o CHF
    • Antitussives/bronchodilators (not in CHF dogs)
    • Arteriodilators (break cough cycle)
      • Hydralazine, ACE inhibitors
      • Lower systemic resistance to improve forward flow out of aorta and reduce regurg
  • Mild-to-moderate–at-home treatment
    • Furosemide (for pulmonary edema) + ACE inhibitors (vasodilation/control of RAAS)
    • Limited Na diet and restricted exercise
37
Q

Endocardiosis–treatment

Severe heart failure?

A
  • Hospitalization:
    • Oxygen
    • IV furosemide (initially, then dec. dose–hypokalemia)
    • Vasodilator (nitroP/nitroG/hydrazoline/ACE inhibitor)
  • Home
    • ACE inhib–usually enalapril (check Cr) + furosemide + dec. Na
    • Spironolactone
    • Pimobendan
  • Refractory–thiazides, dig, sildenafil, pimobendan
38
Q

Endocardiosis: ACIVM consensus statement

Stage A

Stage B? B1 vs. B2

A
  • A = At risk–CKCS or small breeds minus murmur
    • Diagnostics–yearly auscultation–vet/cardiologist
    • Treatment–no drugs
  • B = heart disease (murmur) w/ no signs
    • Diagnostics–rads, BP, echo (DCM?), blood work
    • B1: rads and echo normal
      • Yearly rechecks
      • No treatment needed
    • B2: Rads and echo abnormal
      • No consensus
      • ACE inhibitors, Na restriction, beta blockers, dig, spironolactone, amlodipine
39
Q

Endocardiosis: ACIVM consensus statement

Stage C

A
  • Past or current signs of heart failure
  • Acute (hospital)
    • Optimize preload, afterload, HR + contractility (improve CO)
    • Decrease regurg and releive clinical signs
    • Consensus = furosemide, free water, pimobendan, O2, thoracocentesis, good nursing, sedation (butorphanol), Na nitroprusside if severe
    • No consensus = ACE inhibitors, nitroglycerine
  • Chronic (at home)
    • Maintain acute goals, slow progression, inc. quality of life
    • Consensus: furosemide, ACE inh., pimobendan, good diet + dec. Na
    • No consensus = spironolactone, digoxin, minority beta blockers
40
Q

Endocardiosis: ECIVM consensus statement

Stage D

A
  • Refractory to standard therapy
  • Consensus = same as stage C +
    • Mechanical ventilation
    • Amlodipine, hydralazine
  • No consensus
    • Thiazides
    • Digoxin
    • Sildenafil
41
Q

Endocarditis

Pathophysiology

A
  • Develops during bacteremia when organisms colonize damaged endocardium and one of the heart valves–usually aorta b/c of the high pressure and force of blood–> leads to damaged endocardium
  • –> aortic and valvular insufficiency, L sided heart failure
    • Heart compensates for mitral insufficiency
  • Dysrhythmias–premature beats, tachy, heart block
  • Source of septic emboli = immunological joint dz, glomerulonephritis
  • Bartonella, staphylococcus, E. coli, corynebacterium, pseudomonas
42
Q

Endocarditis

Signalment

Usual history

A
  • Middle aged, male, large breed dogs
  • History
    • History of invasive diagnostic or sx procedure
    • urinary, skin, oral infection
    • Owners report signs of systemic infection: wt. loss, malaise, anorexia, shifting leg lameness, GI disturbances, fever, etc.
    • Can also be renal signs, seizures, CHF
43
Q

Endocarditis

Common findings on PE

A
  • Fever
  • Murmur (sudden onset; soft diastolic + systolic ejection murmur); may not be present
  • Bounding pulse–aortic insufficiency
  • Dysrhythmias, CHF
  • Joint swelling, renal, pnemonia, neuro, etc.
44
Q

Endocarditis

Common abnormalities on special tests

A
  • Labwork
    • Neutrophilic lekocytosis, left shift and toxic changes
    • Anemia of chronic inflammation, thrombocytopenia
    • Emboli–> elev. liver enzymes, BUN, Cr; hematuria, active urine sediments
    • Blood cultures (often neg.–mult. culture sites should be collected aseptically)
    • PCR–esp. Bartonella
  • X-ray–L heart enlargement
  • Echo: best diagnostic tool, but not 100% specific (can’t differentiate btn sterile or septic valvular changes)
  • Doppler–confirms aortic or mitral regurg
  • ECGs–VPD, VT, AV, bundle branch blocks
45
Q

Endocarditis

DDx

Prognosis

A
  • DDx
    • Systemic lupus srythmatosus
    • Rheumatoid arthritis
    • Occult neoplasia
    • Leukemia
    • Drux rxn
  • Prognosis–generally poor, but grave if heart failure develops
46
Q

Endocarditis

Treatment

Prevention

A
  • Treatment
    • Control arrhythmias + CHF
    • Sterilize heart and embolic lesions
    • Treat w/ bactericidal antibiotics–based on culture and sensitivity
  • Prevention
    • Animals w/ SAS might be predisposed
    • Prophylaxis is controversial
    • Monitor heart in animals w/ systemic bac. infections
47
Q

Pericardial effusion

Pathophysiology

A
  • Presence of abnormal amounts of fluid in ericardial sac
    • Caused by CHF, hypoalbuminemia, pericarditis, hemorrhage, neoplasia, or idioathic
  • Most commonly caused by neoplasia in dogs
  • Most commonly caused by FI and lymphoma in cats
  • Pressure from fluid prevents heart filling in diastole–cardiac tamponade
    • R CHF
  • Rate of formation NB
48
Q

Pericardial effusion

Signalment

Usual history

A
  • Signalment
    • GSDs
    • Goldens (predisposed to hemangiosarcomas)
    • Brachycephalics predisposed to paragangliomas
    • Large breed, middle/older animals present most commonly w/ idiopathic effusion
  • History
    • Wt. loss
    • Weakness
    • Exercise intolerance
    • Syncope
    • Dyspnea/orthopnea
    • Enlarged abdomen
49
Q

Pericardial effusion

Common findings on PE

A
  • Pale mm
  • Inc. CRT
  • Muffled heart sounds (no murmur)
  • Poor pulses
  • Jugular distention and ascites
50
Q

Pericardial effusion

Common abnormalities found on special tests

A
  • Labwork
    • Nucleated erythrocytes and schistocytes present (venous blood), normal hematocrit–hemangiosarcoma
  • X-ray
    • Cardiac silhouette enlarged and globose in shape (contours of cardiac chamber obscured)
    • Dilated caudal vena cava
    • Inc. interstitial lung density
    • Pleural effusion
  • Echo
    • Clear visualization of pericardial fluid
    • May outline a tumor if present
    • Hemangiosarcomas are on R auricle, atrium, or ventricle
    • Paragangliomas found at base of aorta
  • ECG
    • Dec. R waves, electrical alternans (alt. in height of R waves b/c heart is ‘swinging’ in pericardial sac)
51
Q

Endocarditis

DDx

Prognosis

A
  • DDx
    • Peritoneal–pericardial diaphragmatic hernia, contsrictive pericarditis
  • Prognosis
    • Idiotpathic pericardial effusions gen. have good prognosis (50% only need draining once)
    • Hemangiosarcoma–poor–most tumors don’t respond to chemotherapy
    • Heart base tumors grow slowly and w/ pericardectomy dogs can live for >1yr
52
Q

Pericardial effusion

Treatment

A
  • Cardiac tamponde = cardiac emergency
    • Diuretics contraindicated
    • Immediate pericardiocentesis is indicated
  • Pericardiocentesis–only sedate (carefully) if necessary (hypotension)
  • If fluid needs to be removed >4-5 times: pericardiectomy (sx also allows for more thorough inspection for neoplasia)
  • Recurrent pericardial effusions: percutaneous balloon pericardiotomy

SAM 1 (20 decks)

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