Acquired heart conditions

Question 1

Dilated cardiomyopathy–K9

General/lesions

Answer 1

• 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

Question 2

Dilated cardiomyopathy–K9

Pathophysiology

Answer 2

• 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

Question 3

Dilated cardiomyopathy–K9

Doberman pinscher progression

Answer 3

• 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

Question 4

Dilated cardiomyopathy–K9

Taurine/L-carnitine deficiency

Answer 4

• 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)

Question 5

Dilated cardiomyopathy

Signalment

Usual history

Answer 5

• 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

Question 6

Dilated cardiomyopathy–K9

Common abnormalities on PE

Answer 6

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

Question 7

Dilated cardiomyopathy–K9

Abnormalities commonly found on special exam

Answer 7

• 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

Question 8

Dilated cardiomyopathy–K9

DDx

Prevention

Prognosis

Answer 8

• 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

Question 9

Dilated cardiomyopathy–K9

Treatment: ACM

Answer 9

• 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

Question 10

Dilated cardiomyopathy–K9

Treatment: OCM

Answer 10

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

Question 11

Dilated cardiomyopathy–K9

Treatment–DCM and CHF

Answer 11

• 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

Question 12

Dilated cardiomyopathy–feline

Pathophysiology

Answer 12

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

Question 13

Dilated cardiomyopathy–feline

Signalment

Usual history

Answer 13

• 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

Question 14

Dilated cardiomyopathy–feline

Common abnormalities on PE

DDx

Prevention

Answer 14

• 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

Question 15

Dilated cardiomyopathy–feline

Abnormalities on special exam

Answer 15

• 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

Question 16

Dilated cardiomyopathy–feline

Treatment

Prognosis

Answer 16

• 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

Question 17

Hypertrophic cardiomyopathy

Pathophysiology

Answer 17

• 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

Question 18

Hypertrophic cardiomyopathy

Signalment

Usual history

Answer 18

• 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

Question 19

Hypertrophic cardiomyopathy

Common findings on E

Answer 19

• 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

Question 20

Hypertrophic cardiomyopathy

Common abnormalities found on special exams

Answer 20

• 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)

Question 21

Hypertrophic cardiomyopathy

DDx

Prevention

Answer 21

• 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

Question 22

Hypertrophic cardiomyopathy

Treatment

Answer 22

• 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

Question 23

Hypertrophic cardiomyopathy

Prognosis

Answer 23

• 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

Question 24

Feline hyperthyroidism

All the things

Answer 24

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

Question 25

Restrictive cardiomyopathy–feline

All the things

Answer 25

• 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

Question 26

Arrhythmogenic R ventricular cardiomyopathy in Boxers

Pathophysiology

Answer 26

• 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

Question 27

Arrhythmic R ventricular cardiomyopathy of boxers

Signalment

Usual history

Answer 27

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

Question 28

Arrhythmic R ventricular cardiomyopathy in boxers

Common findings on PE

Comm abnormalities on special exams

Answer 28

• 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

Question 29

Arrhythmogenic R ventricular cardiomyopathy in boxers

Treatment

Prevention

Answer 29

• 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

Question 30

Arrhythmogenic R ventricular cardiomyopathy in boxers

DDx

Prognosis

Answer 30

• 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)

Question 31

Myxomatous atrioventricular valvular degeneration–endocardiosis

Pathophysiology

Answer 31

• 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

Question 32

Myxomatous atrioventricular valvular degeneration–endocardiosis

Signalment

Usual history

Answer 32

• 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

Question 33

Endocardiosis

Common findings on PE

Answer 33

• 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)

Question 34

Endocardiosis

Common abnormalities on special tests

Answer 34

• 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

Question 35

Endocardiosis

DDx

Prognosis

Prevention

Answer 35

• 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)

Question 36

Endocardiosis: treatment

Incidental?

Coughing but no CHF?

Mild-to-moderate heart failure?

Answer 36

• 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

Question 37

Endocardiosis–treatment

Severe heart failure?

Answer 37

• 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

Question 38

Endocardiosis: ACIVM consensus statement

Stage A

Stage B? B1 vs. B2

Answer 38

• 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

Question 39

Endocardiosis: ACIVM consensus statement

Stage C

Answer 39

• 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

Question 40

Endocardiosis: ECIVM consensus statement

Stage D

Answer 40

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

Question 41

Endocarditis

Pathophysiology

Answer 41

• 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

Question 42

Endocarditis

Signalment

Usual history

Answer 42

• 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

Question 43

Endocarditis

Common findings on PE

Answer 43

• 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.

Question 44

Endocarditis

Common abnormalities on special tests

Answer 44

• 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

Question 45

Endocarditis

DDx

Prognosis

Answer 45

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

Question 46

Endocarditis

Treatment

Prevention

Answer 46

• 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

Question 47

Pericardial effusion

Pathophysiology

Answer 47

• 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

Question 48

Pericardial effusion

Signalment

Usual history

Answer 48

• 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

Question 49

Pericardial effusion

Common findings on PE

Answer 49

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

Question 50

Pericardial effusion

Common abnormalities found on special tests

Answer 50

• 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)

Question 51

Endocarditis

DDx

Prognosis

Answer 51

• 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

Question 52

Pericardial effusion

Treatment

Answer 52

• 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