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
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
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
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)
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
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
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
- VPDs–dobies
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
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
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
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
-
High doses are (-) inotropes and cause severe decompensation
- 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
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
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
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
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
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
- Treat pulmonary edema/pleural effusion if present
- Prognosis: fair if taurine deficient; if not, most cats die w/in 2 months regardless of treatment
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
- If dislodges–> iliac bifurcation of the aorta an dlodge–> ischemia in one/both hind limbs
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
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
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)
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
- Atenolol–reduce pressure gradient in cases of LVOT obstruction
- 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
**Restrictive cardiomyopathy--feline**
All the things
* 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
**Arrhythmogenic R ventricular cardiomyopathy in Boxers**
Pathophysiology
* 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
**Arrhythmic R ventricular cardiomyopathy of boxers**
Signalment
Usual history
* Signalment--boxers 1-15yrs (average 6-10yrs)
* History
* Sudden death
* No abnormalities
* Weakness
* Syncope
* Signs of R or L heart failure
28
**Arrhythmic R ventricular cardiomyopathy in boxers**
Common findings on PE
Comm abnormalities on special exams
* 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
**Arrhythmogenic R ventricular cardiomyopathy in boxers**
Treatment
Prevention
* 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
**Arrhythmogenic R ventricular cardiomyopathy in boxers**
DDx
Prognosis
* 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
**Myxomatous atrioventricular valvular degeneration--endocardiosis**
Pathophysiology
* 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
**Myxomatous atrioventricular valvular degeneration--endocardiosis**
Signalment
Usual history
* 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
**Endocardiosis**
Common findings on PE
* 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
**Endocardiosis**
Common abnormalities on special tests
* 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
**Endocardiosis**
DDx
Prognosis
Prevention
* 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
**Endocardiosis****: treatment**
Incidental?
Coughing but no CHF?
Mild-to-moderate heart failure?
* 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
**Endocardiosis--treatment**
Severe heart failure?
* 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
**Endocardiosis: ACIVM consensus statement**
Stage A
Stage B? B1 vs. B2
* 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
**Endocardiosis: ACIVM consensus statement**
Stage C
* 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
**Endocardiosis: ECIVM consensus statement**
Stage D
* Refractory to standard therapy
* Consensus = same as stage C +
* Mechanical ventilation
* Amlodipine, hydralazine
* No consensus
* Thiazides
* Digoxin
* Sildenafil
41
**Endocarditis**
Pathophysiology
* 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
**Endocarditis**
Signalment
Usual history
* 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
**Endocarditis**
Common findings on PE
* 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
**Endocarditis**
Common abnormalities on special tests
* 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
**Endocarditis**
DDx
Prognosis
* DDx
* Systemic lupus srythmatosus
* Rheumatoid arthritis
* Occult neoplasia
* Leukemia
* Drux rxn
* Prognosis--generally poor, but grave if heart failure develops
46
**Endocarditis**
Treatment
Prevention
* 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
**Pericardial effusion**
Pathophysiology
* 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
**Pericardial effusion**
Signalment
Usual history
* 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
**Pericardial effusion**
Common findings on PE
* Pale mm
* Inc. CRT
* Muffled heart sounds (**no murmur**)
* Poor pulses
* Jugular distention and ascites
50
**Pericardial effusion**
Common abnormalities found on special tests
* 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
**Endocarditis**
DDx
Prognosis
* 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
**Pericardial effusion**
Treatment
* 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
