Rumi CVS

sihirlifil's version from 2018-04-29 13:25

CVS Exam

Question Answer
First step of the exam:Distance! Difficulty breathing, dyspnic, resp rate, open mouth? Swollen LN, D+ (Johne’s)? Then move animal gently (weakness, exercise intolerance, collapse)
Predominant CS:
Weight loss (cardiac cachexia)
Ddx: cancer, Johne’s, GI parasite
Predominant CS:
Bottle jaw (edema)
Ddx: poor teeth, parasites, other PLE
Predominant CS:
Brisket disease
Poke with finger first. Solid: mass, abscess; pitting = edema
Predominant CS:
Ddx: Hydrops, urolithiasis w/ ruptured bladder
Cardiac auscultation can be difficult, why?Muscle or body fat muffles sounds
Restraint system gets in the way
Patient demeanor

Brisket edema (but skin is flabby so check)
Jugular distention
Neck extended
What is this?? how’s it related to CVS failure? (hint… not the front end)
Rectal prolapse! Coughing from CHF, 2ry effect of edema
CS of CV diseaseEdema, pleural effusion, ascites
Muffled heart sounds
Exercise intolerance, weakness, syncope
Venous distention/pulsations
Painful peripheral swelling
Edema: results from?Increased vascular permeability
Increased capillary hydrostatic pressure
Decreased vascular oncotic pressure
Increased tissue oncotic pressure
(Edema) Inc vasc permeability: caused by?Trauma, infection, endotoxemia, allergic vasculitis (activation of complement --> liberation of cytotozins (O2 radicals, leukotrienses, H2O2, PAF, lysosomal enzymes, etc)
(Edema) Incr capillary hydrostatic pressure: caused by?CHF (e.g. Se def’y w/ cardiomyopathy)
Tricuspid valve insufficiency
Venous thrombosis
Liver dz (portal vein obstruction)
Mediastinal masses
(Edema) Decr vascular oncotic pressure: caused by?(TP < 5g/dL, Alb< 1.5g/dL)
Decreased production (starvation, liver dz)
Increased loss (PLN, PLE, peritonitis, pleuritis, etc)
Hemodilution (iatrogenic)
(Edema) Incr tissue oncotic pressure: caused by?(Not really an issue) Infection, topical counterirritants
(Edema) Lymphedema: caused by?Blocked lymphatics (tumors, trauma, increased CVP)
Arrhythmias: types? how do they occur?Via abnormal generation or conduction
Benign: sinus arrhythmia, sinus bradycardia (usually assoc w/ lack of feed intake)
Pathologic: Atrial fibrillation, premature depolarization (assoc w/ GIT disease: e-lyte or A/B disturbance)
(Arrhythmias: other causes)LSA, valvular dz, myocardial dz, pericarditis, cor pulmonale, fever, toxemia, e-lyte abnormalities
Arrhythmias: DiagnosticsChem: check electrolytes
ECG (often impossible in field)
ECG most useful for?Arrhythmias: A-fib, AV conduction disturbances, ventricular arrhythmias
Not diagnostic for chamber enlargement
**The most common arrhythmia in ruminant =A-fib
Underlying GIT dz, metabolic alkalosis, e-lyte abnormalities
**ECG in large animals best done by using…Base apex
Positive electrode L thorax in ICS 5; negative in right jugular furrow 2/3 distance from ramus to thoracic inlet; ground electrode any site away from heart (e.g. ear)
Where is the bovine cardiac electrical axis?Directed dorsally! (more of a spontaneous depol of ventricles, unlike dogs & cats with progressive depol wave)
Is this normal?
Yes! Bifid (‘notched’) P wave normal in horse & some rumis
Murmurs: caused by? predisposed by?Turbulence (vs. laminar flow)
Increased velocity or decreased viscosity (anemia) predisposes
Murmurs: how do we characterize?Via part of cardiac cycle, intensity, shape/frequency, PMI, radiation
(Systolic btw S1 & S2; diastolic btw S2 & S1; continuous)
(Murmur grading)
Murmurs: ejection =Innocent
Anemia, fever
Aortic/Pulmonic stenosis
ASD, VSD, Tetrology
Murmurs: regurgitant =Mitral regurg
Tricuspid regurg
VSD, Tetrology
Muffled heart sounds: due to?Displacement: pericardial effusion
Soft tissue masses: abscesses, tumor
Air: pneumothorax, pneumomediastinum, emphysema
Fat, muscle
Muffled heart sounds: which diagnostics are available?Echocardiography (pericardial/pleural effusion)
Thoracic rads
Equipment limitations due to size, demeanor, armpit access; clinic vs. field setting!
Exercise intolerance/weakness: ManifestationsFailure to perform or produce
Cough on exertion
Respiratory distress
Recumbency, reluctance to rise or move
Venous distention: what’s normal?Jugular pulse <1/3 up the neck with head up
What’s wrong with this guy
Jugular distention
Venous distention: root?Increased resistance to right ventricular filling
Venous distention and pulsations: caused byRHF
Constrictive pericarditis
Venous distention and prominent pulsations: caused byTricuspid regurg
Arrhythmias associated w/ atrial contraction against closed AV valve

Congenital Dz

Question Answer
What’s going on? what else you wanna do?
Microphthalmia (etiology: genetic, BVD)
Look for other congenital abnormalities! Cleft palate, atresia coli, atresia ani, cardiac defects… often seen with VSD, tailless, dome head, cheiloschisis, wedge & hemivertebra
** Dx of congenital defectsAuscultation (sometimes murmur appears as they age)
Necropsy :(
Tx of congenital defectsNot recommended… may be found dead, euthanize (poor-doer). Discourage use as breeding animals
** Most commonly reported congenital dz =VSD
VSD: cause? presentation?Unknown, suspected heritable
Alone or part of complex anomaly. Usually in membranous septum, ventral to 3cuspid (can be in apex in camelids)
VSD: CSVary depending on size, shunt direction, concurrent valve/myocardial problems
Clinically normal --> poor growth, dyspnea, etc. Bilat, harsh, plateau, pansystolic murmur, PMI R tricuspid, L pulmonic, usually palpable thrill
What is Eisenmenger’s Syndrome? results in?R heart resistance --> VSD L-R shunt becomes R-L shunt
ASD: assoc with? CS?Often assoc w/ PDA!
Freq asymptomatic. Holosystolic crescendo-decrescendo at L heart base, shunt usually L-R
PDA: cause? CS?Ductus arteriosus fails to close (decr pulm vasc resistance & incr systemic vasc resistance)
CS depend on size, direction of shunt, concurrent defects
Continuous, high-pitched, machinery murmur on L (loudest) & R 3-4 ICS (large ones can exist w/o murmur)
Tetralogy of Fallot: what are the defects?Overriding aorta, VSD, obstruction of PA flow, RV hypertrophy (ASD = pentalogy)
Tetralogy of Fallot: caused by? CS?Abnormal development of conal septum in embryo
Loud pansystolic murmur w/ thrill, L 3-4 ICS
Tetralogy of Fallot: common cause of?Cyanosis
R/O respiratory dz (has murmur), CNS dz (no other neuro manifestations)
(Other congenital defects)Pulmonic stenosis
Tricuspid atresia
Mitral chordae rupture
Ventricular hypoplasia
Truncus or pseudotruncus arteriosus
Aortic anomalies
Ectopia chordis cervicalis (relatively common in cattle)
(BVDV association)

Endocardial Dz

Question Answer
Valvular disease: how does it happen? causes?Chronic active infxn --> sustained bacteremia (Cattle: Truperella pyogenes > Strep & Helococcus. Pigs: Erysipelothrix, Strep)
Foot rot, abscesses, ruminitis, other septic processes (Prelim valve dmg not necessary)
Neoplasia (rare): LSA
Valvular dz manifests byRegurgitation murmur
PMI over affected valve
Most common valvular disease =Bacterial endocarditis
Single most important factor in DX of endocarditis is?High lvl of suspicion (any animal showing CS is considered candidate)
Pathogenesis of endocarditisHemodynamics: ‘jet/venturi effect’
Endothelial dmg (VSD, PDA, catheters, nematode migration, mammary vein lacerations)
Bacteremia (commensal in mouth & genitourinary, arise from septic focus)
Agglutinins (antibodies cause clumping)
Bacterial adherence
What is this lesion? where?
Endocarditis lesion (endothelial dmg); at sites where relatively low pressure, & where high pressure streams of blood produce ‘jet lesions’
Heart valves most freq affected in RUMI?Tricuspid, mitral
Heart valves most freq affected in PIGS?Mitral
**Why is the tricuspid valve affected more freq in ruminants?
first place blood goes to, low flow area (blood hangs out there more)
CS of endocarditisWeight loss, exercise intolerance
PE: Tachycardia, febrile (intermittent, coincides with emboli shower), 50% have heart murmur
Metastatic dz makes hard to dx
Dx of endocarditisCS, cardiac exam
Blood culture
CBC/Chem: anemia, hyperproteinemia from high globulins (findings not specific
Have it on ddx list
Endocarditis: US findings?Irregular, thickened tricuspid leaflets
Endocarditis: how effective is blood culture? how to collect?5 blood cultures over 48h period will ID 90% of organisms in bacterial endocarditis cases (indicative but not definitive)
Sample when pyrexic, before antibx therapy, sterile, both aerobic & anaerobic
Prognosis of valvular dzDepends on etiology, onset, duration, severity. Generally guarded-poor
Tx of bacterial endocarditisLong-term -Cidal based on C&S (Penicillin, if g(-) pen-aminoglycoside combo)
Aspirin, low dose heparin
Furosemide, Digoxin to stabilize CHF
What is this sequel of endocarditis? Thromboembolism
Aortic valve endocardial lesion w// fibrin clot entering a coronary sinus (red = recent dmg, white = past)

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