Cardiology Flashcards
What is the most common cardiac defect reported in large animals? What is the most common location of this defect?
Ventricular septal defect (VSD).Perimembranous VSDs are more common than muscular.
Define a ventricular septal defect (VSD).
Opening in the inter ventricular septum that creates a communication between the left and right ventricles.
In what breeds of cattle are VSDs heritable?
Herefords and Limousins.
In what breeds of horses are VSDs most common?
Welsh Mountain Pony (Type A), Arabian, Standardbred, Quarter Horse.
What is the embryologic defect that results in formation of a VSD?
- Failure of fusion of the endocardial cushion and muscular ventricular septum, or- Failure of fusion of the truncal and conal septa.
What is the most common direction in which blood is shunted in large animals with VSDs?
Left to right.Because pressure in LV exceeds pressure in RV.
List the factors which influence the size of the shunt.
- Size of the defect.- Pressures in the RV, LV and pulmonary a.
Describe the murmur(s) heard in patients with VSD.
Loud, harsh, pancystolic murmur with PMI over tricuspid v on RHS and softer, holosystolic murmur with PMI over pulmonic v on LHS.+/- palpable thrill.+/- split S2.
If the murmur is loudest on the LHS in an animal with VSD what should be suspected?
A subpulmonic VSD or a complex anomaly.
What CSx may be seen in large animals with VSD, in addition to a cardiac murmur?
Poor growth, lethargy, dyspnoea, exercise intolerance, CHF (by 5yo).Small defects may be asymptomatic.
List three differential diagnoses for VSD.
- Tetralogy of Fallot.- Mitral or tricuspid valvular anomalies.- Neonate flow murmur.
Describe echocardiographic findings in patients with VSD.
- Typical perimembranous VSD: long-axis LVOT view, located underneath the right and/or non-coronary leaflet of the aortic v and central to septal leaflet of the tricuspid v.- Subpulmonic VSD (calves>foals): short axis view in septum between the LVOT and RVOT.- Large/mod VSDs –> LA and LV enlargement, RV enlargement and pulmonary a dilation +/- aortic valve prolapse and aortic regurgitation.
Horses can race with VSDs = ______.
- = 4.5m/s peak velocity.
Haemodynamically significant VSDs (i.e. resulting in CHF and death) have > _____ diameter, peak shunt velocity _______.
- > 3.5cm diameter.- 0.3 VSD:Ao root.-
What changes occur within the heart in patients with very large VSDs?
Pressure in LV and RV are almost equalised –> RV, pulmonary circ, LA and LV must compensate for volume overload –> dilation of cardiac chambers and pulmonary hypertension.
What happens to pulmonary resistance in patients with concurrent VSD and pulmonary disease of LHF and what effect does this have on the RV?
Increased pulmonary resistance –> chronic volume AND pressure overload on RV –> reversed direction of shunt (i.e. R-L) = Eisenmenger Complex (more common in cattle).
VSDs can create turbulent blood flow within the heart. What cardiac disease does this predispose to?
Endocarditis secondary to endocardial damage.
Identify which type of valvular regurgitation in most like to occur in patients with VSD and why.
Aortic regurgitation, due to the location of the VSD resulting in loss of structural support for the aortic valve cusps.
Define an atrial septal defect (ASD) and list the most common ASD described in large animals.
A connection between the left and right atrial at the septal level.Most common is patent foramen ovale (PFO).
In which species is PFO seen commonly and what other congenital cardiac defect is it often seen with?
Calves and PDA.
What is the embryologic origin of a PFO?
Failure of the septum primum to adhere to the crista dividens after birth.
Describe the murmur presents in patients with PFO?
Holocystolic, crescendo-decrescendo at the left heart base.
In which direction in the shunt most commonly in PFO?
Left to right.
PFO are frequently asymptomatic in large animals. In the case of a large defect, however, congenital remodelling may occur. What changes may be seen on echo in this case?
RA, RV and LA enlargement.
Define a patent ductus arteriosus (PDA).
Persistent potency of the vessel that connects the pulmonary arterial system to the aorta.
When should a PDA normally close after birth in calves and foals and why does it close?
- Very shortly after birth in calves, and within 4 days in foals.- Closes in response to decreasing pulmonary vascular resistance, increased systemic vascular resistance, increased blood vol and increased LV pressure when breathing begins.
Describe the murmur in an animal with a PDA.
Continuous, high-pitched, ‘machinery murmur’ on the left and right; PMI 3rd/4th ICS at the level of the point of the shoulder.Murmur may be absent with large PDAs.
What clinical signs may be seen in animals with PDAs in addition to a cardiac murmur?
- Bounding pulses (due to run-off of blood from systolic to pulmonary circulation).- Cyanosis (if shunt reversed).- Stunted growth.
Describe diagnostic imaging findings in an animal with a PDA.
- Rads: may see enlarged cardiac silhouette and pulmonary congestion.- Echo: may see PDA, enlarged LA and LV, enlarged LA:Ao root ratio.- Angiography provides definitive diagnosis.
Describe changes which occur in the heart secondary to the presence of a PDA.
PDA –> L-R shunt –> LV overload –> LV dilation and hypertrophy +/- CHF.Pulmonary hypertension and congestion can occur –> RV hypertrophy.
When does a right to left shunt occur in PDA patients?
When pulmonary resistance exceeds systemic vascular resistance.
What is the prognosis for large animals with PDA?
May remain asymptomatic if small; poor prognosis if large.
Is PDA a heritable condition in large animals?
No evidence at this time that it is a heritable defect.
List the four components of a Tetralogy of Fallot (ToF).
- Overriding (biventricular origin) aorta.- VSD.- Pulmonic stenosis.- RV hypertrophy.
What congenital anomaly is present, in addition to the 4 present in cases of ToF, to make the condition a Pentalogy of Falot?
- ASD, plus…- Overriding (biventricular origin) aorta.- VSD.- Pulmonic stenosis.- RV hypertrophy.
What is the embryologic origin of a ToF?
Abnormal development of the conal septum.
Describe the typical murmur in animals with ToF.
Crescendo-decrescendo murmur or pulmonic stenosis, or harsh, plateau-shaped murmur of VSD.
What clinical signs may be seen in animals with ToF in addition to a cardiac murmur?
- Small size or slow growth.- Marked exercise intolerance –> dyspnoea and collapse.- Cyanosis of the MMs, skin and nose.
List differential diagnoses for oxygen-responsive cyanosis in young large animals.
- NARDs.- CNS Dz.- Heart failure with pulmonary oedema.
List differential diagnoses for non-oxygen responsive cyanosis in young large animals (i.e. R-L shunt)
- ToF or PoF.- Reverse PDA.- Reverse VSD.- Tricuspid or RV atresia.- LV hyperplasia.- Truncus arteriosus.- Pseudotruncus arteriosus.
Describe diagnostic findings suggestive of ToF.
- Echo: visualisation of defects and colour Doppler flow abnormalities.- CBC: PCV, RBCC and Hg conc increased in some cases.- Blood gas: arterial hypoxaemia (degree depends on amount of shunting).
In which large animal species is ToF most common and is it an hereditary condition in large animal species?
- Calves > foals.- No evidence of a hereditary link at this time.
What is the most common primary heart tumour of large animals?
Lymphosarcoma.
What breeds of horses display the highest incidence of atrial fibrillation?
Standardbreds, Warmbloods, draught horses.
Describe the pathophysiology of atrial fibrillation in horses.
- CO at rest in normal in most horses with AF, however, maximal CO during exercise is limited because the atrial contribution to filling is most important at higher HRs.- In AF, the loss of coordinated fronts of electrical activity in the atria results in loss of both coordinated mechanical activity and atrial contraction. –> CO dec by up to 20%. - In addition, the irregular ventricular rhythm results in variable cardiac fill, further reducing cardiac performance.- Variable HR: ventricular rate response depends on the refractory period of the AV node and freq and strength of atrial stimuli. - In the otherwise healthy horse with AF vagal tone will be high and symp tone low at rest therefore ventricular rate will be close to normal or slightly increased.- If sympathetic activity is increased or if vagal activity is blocked then the ventricular rate response will increase as the AV nodes refractory period shortens.- AF can induce atrial electrical, structural and functional remodelling that may be responsible for the self perpetuating, progressive and recurrent nature of AF (changes are more likely to be reversible if tx promptly).
Define the three classifications of atrial fibrillation in horses.
- Paroxysmal AF: - Often assoc with a single episode of poor performance.- Arrhythmia usually disappears spont within 24-48hrs. - May be associated with transient K depletion (especially in horses tx with furosemide or bicarb).- Most often unrelated to other clinical or echocardiographic abnormalities of heart disease. 2. Persistent AF: arrhythmia terminates after tx. 3. Permanent AF: - Arrhythmia is sustained and resistant to therapy. - Many horses do not have significant cardiac dz on PE and echo exam, however ultrastructural and functional myocardial pathology may be present predisposing to AF.
What are the clinical signs in horses with atrial fibrillation?
- The arrhythmia is often detected as an incidental finding in horses with no overt CSx.- Exercise intolerance is the most common CSx seen; more common in high-performance horses (racehorses, polo ponies, endurance horses, Grand Prix SJ) than show hunters, dressage, pleasure, endurance horses.- EIPH, respiratory distress, CHS, ataxia, collapse and myopathy have all been reported with AF.- Horses with AF usually have normal resting HRs, although the HR usually decreases after conversion.
What are the diagnostic test findings in horses with atrial fibrillation?
- Auscultation: normal HR or tachycardia, irregularly irregular heart rhythm, variable intensity heart sounds and an absent fourth heart sound.- Arterial pulses vary in intensity and pulse deficits may be present, esp when the ventricular rate is high.- ECG: ➢ Characterised by an absence of P waves, instead fibrillation (f) waves are seen in the baseline. ➢ f waves may be coarse (large) or fine (small) and the number of atrial pulses/min usually >500.➢ QRS-T complexes: normal morphology and duration.➢ The ventricular rate response is variable, although periodicity may be observed infrequently.- If resting tachycardia is present you should look for intercurrent cardiac lesions or a disorder that increases symp tone e.g. pain, anaemia, fever, infection.- Echo: usually normal, unless concurrent valvular or ventricular myocardial dz is noted. Not abnormal for LV shortening fraction to be slightly reduced then return to normal post-conversion.
Describe quinidine sulphate therapy for cardioversion in horses with atrial fibrillation.
- Blocks vagal activity; typically admin via NGT because of its irritating effects on the MMs. - IV quinidine gluconate can be successful if AF is of recent onset or NGT delivery is not feasible but failure does not necessarily predict the response to oral tx.- E.g. regimen: 22mg/kg via NGT q2h for 2-4 tx then q6h until horse converts or horse dev signs of toxicosis. - If conversion has not occurred in 24hrs then digoxin 0.0055-0.0011mg/kg PO BID may be added for a further 24 48hrs (drugs interact → doubled serum conc of digoxin). If >24hrs the lowest end of the dose range should be used and serum digoxin conc should be measured.- When tx of >12-24hr is required adequate hydration and electrolyte balance (esp K and Mg) must be ensured by oral or IV fluid admin because most horses on tx will become depressed and inappetent, will show reduced water intake and may develop mild dxa.- Careful clinical and continuous ECG monitoring should be performed during tx. Prolongation of QRS duration by >25% of the pre-tx value is an indication of toxicity → stop therapy. Supraventricular tachycardias, ventricular arrhythmias (multiform VT, VPCs) can also occur → stop therapy and tx (IVF to improve perfusion, IV sodium bicarb to reverse Na channel blocking effect of quinidine, adrenaline if critical hypotension develops, lignocaine or MgSO4 for ventricular arrhythmias).- CSx of toxicosis: ataxia, colic and nasal oedema → resp stridor. Depression, dxa and paraphimosis occur in many horses tx with quinidine but resolve after discontinuation of the drug.
Describe transvenous electrovardioversion for treatment of atrial fibrillation in horses.
- 1° tx or for horses that respond adversely or inadequately to quinidine tx.- Must be performed under GA with the horse well padded because shock results in a sudden jolt of the body.- Involves transcutaneous placement of two specialised electrode catheters transvenously (one catheter tip in the left PA and the other in the RA cavity) and application of an electric shock.- Complications appear to be low → one report of transient complete AV block; GA/electric shock risks.
What is the prognosis for horses with atrial fibrillation?
- Excellent Px for conversion (>95%) if HR
Describe the signalment and aetiology of bacterial endocarditis in horses.
- Most cases in horses
Describe the pathophysiology of bacterial endocarditis in horses.
- Predisposing factors are often not recognised in horses.- Bacteraemia is fairly common in horses but bacterial endocarditis is rare. - Interplay of a number of factors is probably required for dev of lesions, incl status of the endothelial surface of the valve, haemodynamics, host immune system, adherent properties of the bacteria, events that initiate bacteraemia. - In humans infective endocarditis is usually preceded by nonbacterial thrombotic endocarditis = a platelet-fibrin complex forms on a damaged valve and is a good medium for bacterial growth; unknown if this occurs in horses.- Lesions consist of platelets, fibrin, bacteria, inflam cells.- Clinical signs result from three aspects of the disease: damage to the cardiac valves and the resulting pathophysiologic responses; septic embolisation of fragments to other organs with resulting dysfunctional infection of the valves and other sites (metastatic abscess formation).- Mitral valve > aortic > tricuspid > pulmonic.
List the clinical signs of bacterial endocarditis in horses.
- Most common signs: fever and heart murmur.- Other presenting signs: lameness, thrombophlebitis, diarrhoea, cough, oedema, seizures, depression, colic, poor growth, laminitis and umbilical infection.- Auscultation: L apical systolic = MV lesion, R apical systolic = TV, L/R diastolic = AV, murmurs caused by PV regurg are rare because the pressure gradient and velocity of regurgitant flow are low.- If infective endocarditis affected the chordae tendinae or myocardium a murmur will not be heard.- If L CHF: exercise intolerance, lethargy, inc RR and effort, nostril flare, cough and inappetence +/- abnormal lung sounds; froth at the nostrils/mouth = grave Px indicator.- Septic jugular thrombophlebitis is a risk factor for tricuspid valve endocarditis → R CHF, incl venous (esp jugular) distension, jugular pulses and abdominomegaly secondary to hepatic congestion and ascites.- MV/AV can → systemic thromboemboli in organs incl kidneys, myocardium and CNS.- TV/PV can → thromboemboli in the lungs, metastatic pneumonia can be severe.
Describe clinicopathologic findings in horses with bacterial endocarditis.
- CBC: hyperfibrinogenaemia, leucocytosis, neutrophilia, hyperglobulinaemia and anaemia of chronic disease.- MBA: cTnI may be inc; may be evidence of end organ damage incl azotaemia and proteinuria.- Blood culture: may or may not be positive due to variable shedding of the organism, previous antimicrobial admin and fastidiousness of organisms in growth media. Should be collected over 3-24h from at least 3 aseptically prep sites.- Definitive dx = confirmation of microorganisms in a valvular lesion by culture or histo evaluation (=PM).
Describe electrocardiogram and echocardiogram findings in horses with bacterial endocarditis.
- ECG: usually reveals tachycardia regardless of whether the horse is in heart failure or not; arrhythmias are not uncommon and are usually ventricular in origin.- Echo: – Imaging modality of choice, enables assessment of valve structure, cardiac dimensions and function. – The degree of regurg or stenosis can be evaluated with Doppler ultrasound.– Acute lesions: hypoechoic, irregular and shaggy.– Chronic lesions: appear more regular and echogenic.– Valve thickening or ruptured chordae tendinae of the affected valve may be seen.– It is possible to make false –ve or false +ve dx on ultrasound, however in a study there was high correlation between echo findings and PM findings.
How is bacterial endocarditis treated in horses?
- Goals: eradicating the organism and addressing complications of the infection.- Organisms within vegetative lesions are protected from the immune system and have slow metabolism therefore ABs should be admin IV, bactericidal and prolonged. - Ideally C&S but likely organisms are gram +ve/-ve sp pen gent whilst awaiting results. - Humans: IV for 4-6 weeks then oral for 3mo; too expensive in horses –> IV 1-2 weeks then swap to antibiotics with similar spectrum incl TMPS/rif, PPG, enro.- Antithrombotics may slow continued adhesion of platelets to the infective lesion on the valve and dec the risk of thromboembolic events – aspirin 10-25mg/kg PO SID.- Other medical management as indicated: CHF → diuretics (furosemide 1-2mg/kg PO BID), vasodilators (hydralazine 1mg/kg PO BID; more research req to determine if ACE inhibitors are effective) and inotropes (digoxin). If arrhythmias are haemodynamically sig anti-arrhythmias should be used (lignocaine, MgSO4).
What is the prognosis for horses with bacterial endocarditis?
- Very poor; 10% survival in one case series.- Px very grave for L-sided lesions, particularly aortic valve lesions; better for R sided lesions (can even return to work).- Multiple reasons for tx failure: high cost (long tx and usually first 1-2weeks in hosp) + poor Px → euth, bacteriologic cure is difficult to achieve even if the best tx is attempted because the infective organisms are well sequestered from the horse’s immune system and ABs by the lesions matrix of fibrin and platelets → may result in relapse of CSx within 2mo of stopping tx; even if cure is achieved the affected valve with remodel and scar, possibly resulting in even worse valvular regurg over time and inc risk of heart failure.
What is the mechanism of action of monensin?
Monensin is produced by the fungus Streptomyces cinnamonensis. It is selective in transporting Na and K ions between the intracellular and extracellular spaces
Describe the proposed toxic mechanism of monensin in horses.
- Hypothesis one for toxic action: – Monensin interacts with the mechanisms regulating K entry into cell organelles, esp the mitochondria.– Low conc → net accum of K within the cell, high conc → net loss of K from the cell. – The effect of monensin might therefore be inhibition of ATP hydrolysis in mitochondria (requires K) → decreased cell energy production → loss of cell function and death.2. Hypothesis two for toxic action:– Inc intracellular calcium is responsible for cell death.– Increased intracellular Ca conc → Ca sequestered by mitochondria to maintain Ca homeostasis → inhibition of oxidative phosphorylation and less energy produced to pump Ca out of cell → critical level of Ca in cell → release of degenerative enzymes, swelling of mitochondria and sarcoplasmic reticulum → cell necrosis and death.
Describe pathologic changes in the internal organs of horses with monensin toxicity.
- Myocardial lesions are charac by pale myofibres, loss of fibre striation, multifocal vacuolar degeneration and scattered areas of necrosis –> replaced by fibrous tissue.- Result is a structurally weakened heart that can succumb to stress and cause acute death.- Other lesions may be present incl pericardial, pleural and peritoneal effusions; haemopericardium and epicardial haemorrhage.- Chronically affected horses may have hepatic congestion with centrilobular necrosis and hydropic degeneration of the renal tubules.
What are the clinical signs of monensin toxicity in horses.
- Peracute toxicity: progressive, severe haemoconc, hypovolaemic shock and death within a few hours.- Acute toxicity: partial to complete feed aversion, abdominal pain, occasional water dxa, intermittent profuse sweating, stiffness, progressive muscle weakness (esp HL), progressive ataxia, tachycardia, hypotension, dyspnoea and polyuria; death may occur 1-4 days after onset of CSx.- Horses surviving sublethal doses: reduced athletic performance, unthriftiness, cardiac failure (arrhythmias especially atrial fibrillation and tachycardia, jugular pulse, pericardial and pleural effusions); intravascular haemolysis may occur to a limited degree.
How is monensin toxicity diagnosed in horses?
- Suspected when horses show CSx of feed refusal, colic, muscle weakness and heart failure and when possible exposure to contaminated feed has occurred.- Test feeds, serum, liver, GI contents, faeces for monensin.- CBC/MBA: non pathognomonic; may include: early evidence of severe haemoconc and dehydration in peracute phase; serum K and Ca may be decreased moderately in the first 12-16hrs but then return to normal limits; azotaemia in acutely affected animals; elevated CK, AST, cTnI.
Outline the treatment of monensin toxicity in horses.
- There is not a specific antidote for monensin toxicity.- Decontamination: activated charcoal to dec absorption, mineral oil to hasten bowel evacuation.- IVFT to combat haemoconc and hypovol shock, measure electrolytes and acid-base and correct deficiencies. - Se and Vit E have been shown to be somewhat protective against the effects of monensin tox in swine. - Never administer digitalis glycosides or calcium! Can → myocardial cell death. - Critically evaluate cardiac function of any horse that was previously affected before return to work.
List the causes of acquired valvular disease in cattle.
- Degenerative changes.- Infection (bacterial or viral endocarditis or myocarditis).- Inflammation.- Trauma.- Myocardial dz (cardiomyopathy).- Neoplasia (esp lymphoma).- Idiopathic.
Chronic bacterial infection can predispose to bacterial endocarditis. List three common chronic bacterial infections that have been linked with endocarditis in cattle.
- Foot abscesses.- Rumenitis.- Reticular abscesses.
What is the most common bacterial isolate from bacterial endocarditis lesions in cattle?
Trueperella pyogenes.
Which valve is most commonly affected in cattle with bacterial endocarditis?
Tricuspid valve.
List the clinical signs of valvular disease in cattle.
- Murmur: varies with valve affected; often quiet to no murmur in cattle with bacterial endocarditis.- Cardiac enlargement –> greater area for auscultation +/- arrhythmias e.g. a fib.- CHF: tachycardia, coughing, respiratory distress, jugular v distension, abnormal jugular pulsation, subcutaneous oedema, mammary v distension, crackles/moist lung sounds; wt loss, anorexia, fever, mastitis.
Describe echocardiographic findings in cattle with acquired valvular disease.
Regurgitant jet, increased chamber dimensions, valvular lesions.Valvular insufficiency: mild jet 2/3 receiving chamber.
List potential CBC, MBA and urinalysis findings in cattle with bacterial endocarditis.
- CBC: anaemia, neutrophilia, hyperfibrinogenaemia.- MBA: hyperglobulinaemia, inc liver enzymes.- Urinalysis: pyuria or haematuria.
Describe the pathophysiology of congestive heart failure (CHF) in cases of acquired valvular disease in cattle.
Valvular incompetence –> volume overload of recipient chamber –> increased EDV –> compensatory dilation and increased ED pressure +/- hypertrophy –> decreased contractile ability –> CHF.
Describe the pathophysiology of bacterial endocarditis in cattle.
Localised infection –> bacterial endocarditis –> disseminated sepsis –> cull.
List the components of bacterial valvular vegetative lesions in cattle.
Blood cells, fibrin, necrotic tissue, bacteria.
Outline the treatment and prognosis for bacterial endocarditis lesions in cattle.
- Antibiotics (gram +ve), aspirin/LMWH to prevent platelet adhesion, furosemide if CHF, digoxin to improve contractility. - Px is guarded to poor (they present with advanced dz).
Define High Mountain Disease (a.k.a. Brisket Dz) of cattle.
Hypoxic vasoconstriction from high altitude dwelling.
What factors can exacerbate the signs of HMD and what does this combination of factors lead to?
- Pneumonia, lungworms, prolonged exposure to cold temperatures, ingestion of locoweed.- HMD + factors above –> cor pulmonale (effect of lung dysfunction on the heart).
Describe the pathophysiology of HMD in cattle.
High altitude (>6000ft) +/- respiratory dz +/- locoweed –> pulmonary a constriction in response to hypoxia –> pulmonary hypertension –> pressure overload on RV –> RV hypertrophy, dilation or failure.
List the latin name and toxic principal of Locoweed.
- Plant: different oxytropis and astragalus species.- Toxin: swainsonine; causes myocardial damage.
List the clinical signs of Brisket Disease in cattle.
- Subcutaneous brisket oedema, oedema of ventral thorax, limbs, submandibular space.- Lethargy, weakness, pulling eyes, diarrhoea, collapse, death, jugular v distension or pulsations, dyspnoea, tachypnoea.- Auscultation: tachycardia, +/- gallop rhythm, +/- split S2, +/- murmur related to tricuspid or pulmonic regurg.
List four differential diagnoses for Brisket Disease in cattle.
- Bacterial endocarditis of the tricuspid valve.- Cardiomyopathy.- Lymphoma.- Traumatic reticuloperitonitis-pericarditis.
Describe the epidemiology of HMD in cattle.
- Occurs in 0.5-5% native high-altitude cattle; higher % if lowland cattle moved to high altitudes.- Mainly occurs in calves and yearlings.- Complex inheritance with breeds/pedigrees resistant or susceptible.
Outline the treatment and prognosis for HMD in cattle.
- Remove from high altitude, treat primary dz process, InO2 +/- digoxin, furosemide. - Px poor once CHF has developed; can potentially reverse for pulmonale.
Outline methods to prevent HMD in cattle.
Select cattle for breeding at high altitudes that are resistant to HMD, remove susceptible cattle to low altitudes, avoid locoweed, vaccinate against respiratory viruses, deworm to prevent lungworm.
Define myocarditis.
Inflammation of the myocardium.Occurs secondary to bacteraemia, septicaemia, pericarditis, endocarditis.
List the infectious organisms capable of causing myocarditis in cattle.
- Bacterial: Clostridium chauvoei, Mycobacteria.- Fungal: FMD.- Parasitic: Toxoplasmosis, Cysticercosis, Sarcocystis.
Define cardiomyopathy.
Subacute or chronic disease of the ventricular myocardium without valvular disease, congenital abnormalities or pulmonary disease.
In what breed of cattle is hereditary Dilated Cardiomyopathy (DCM) reported?
Holstein-Friesian.
In what breed of cattle is a hereditary (non-DCM) cardiomyopathy reported?
Curly-coated Poll Hereford.
Which neoplasia may cause a cardiomyopathy through myocardial invasion in cattle?
Lymphoma or fibrosarcoma.
List toxins associated with the development of cardiomyopathies in large animals.
Monensin, lasolacid, salinomycin, cassia occidentalis (coffee senna), gossypol (cotton), phalaris, vitamin E/selenium deficiency, copper deficiency (primary or secondary to high sulphates), excessive molybdenum.
List the clinical signs associated with myocarditis in cattle,
- CSx depend on extent of disease, location of inflammation and systemic illness.- +/- fever, cardiac arrhythmias (supraventricular or ventricular), gallop rhythm, murmur, signs of CHF.
List the clinical signs of DCM in cattle.
- Heart-related: peripheral oedema, jugular dilation/pulse, tachycardia, arrhythmias, murmurs, tachypnoea, pleural/pericardial effusion.- Extra-cardiac: poor exercise tolerance, decreased milk production, increased liver enzymes, DA, diarrhoea, anorexia.
List differential diagnoses for cardiomyopathies in cattle.
Bacterial endocarditis, congenital heart defects, for pulmonale, nutritional myodegeneration, cardiac neoplasia, thoracic abscess, pericarditis, pleuritis, diaphragmatic hernia.
Outline diagnostic tests which should be performed in cattle with suspected myocarditis or cardiomyopathies.
- CBC/MBA: +/- neutrophilia, dec albumin, inc BUN, inc creatinine, inc GGT, inc SDH, inc TBili, inc CTnI.- Echo/ECG: variable - WNL or changes consistent with DCM, CHF, arrhythmias. - Urinalysis: haemoglobinuria is suggestive of monensin, gossypol, nutritional myodegeneration.- Test serum for BLV, alpha-tocopherol, glutathione peroxidase and Cu; test whole blood for Se.
Describe the treatment and prognosis for cattle with myocarditis or cardiomyopathies.
- Myocarditis: tx underlying dz if recognised, control complications (arrhythmias, CHF, shock), Vit E if ionophore toxicity, corticosteroids may be beneficial.- Px for myocarditis good if no CSx CHF, guarded if CHF.- DCM: +ve inotrope (digoxin), diuretics (furosemide), vasodilators (ACE-I), rest.
Define pericarditis.
Inflammation of the pericardium, resulting in accumulation of fluid or exudate between the visceral and parietal pericardium.
List the causes of pericarditis in cattle.
- Traumatic reticuloperitonitis-pericarditis (TRP).- Neoplasia.- Idiopathic.
Describe typical cardiac auscultation findings in a cow with pericarditis.
Tachycardia, muffled heart sounds, absent lung sounds in the ventral thorax; ‘washing machine murmur’: splashing sounds attributed to gas and fluid accumulation in the pericardium secondary to anaerobic infection.
Describe the clinical signs seen in cattle with pericarditis.
- Non-specific: fever, inappetence, depression, weight loss.- More specific: peripheral oedema, jugular distension and pulses, tachypnoea, dyspnoea, elbow adducted, expiratory grunt, reluctance to move.
How do you diagnose a case of pericarditis in large animals?
- CBC/MBA: variable findings dependant on underlying disease and chronicity.- Elevated CTnI or myocardial CK/LDH.- Rads: in TRP metallic FB and fluid and gas accumulation may be identified.- Echo: confirms Dx –> fluid, fibrin, gas in pericardial sac.- Fluid analysis following pericardiocentesis: TRP –> mixed bacteria, yellow, could odour, TP >3.5g/dL, WBC >2500/ul; idiopathic: hemorrhagic, sterile.
Describe the pathophysiology of pericarditis.
Fluid accumulates in the pericardial sac –> increased pericardial pressure –> increased end diastolic pressure -> impaired ventricular filling, increased atrial pressure, decreased venous return, decreased diastolic perfusion to myocardium –> decreased contractibility, SV, CO –> CHF.
Describe the treatment for TRP in cattle.
Px is poor; salvage procedures only: drain pericardium, perform rib resection at 5th intercostal space.
Describe the treatment of Idiopathic Haemorrhagic Pericarditis in cattle.
Drain pericardial sac.Corticosteroids may result in resolution in some cases.
How common are cardiac neoplasias in large animals?
Uncommon. More common to see secondary involvement from adjacent structures i.e. lungs, pleura, LNs, diaphragm.
What is the most common cardiac neoplasia of cattle and where in the heart is it most commonly observed?
Lymphoma.Right atrium.
List the clinical signs observed in cattle with cardiac neoplasia.
Non-specific and related to chronic disease; progress to cardiac signs related to involvement of pericardium or myocardium.
How is cardiac neoplasia diagnosed in cattle?
- CBC/Chem: non-sepcific changes.- Test for BLV: only 1-5% BLV positive cattle develop lymphosarcoma.- Echo.- Definitive diagnosis via histopathology following necropsy.
What is the prognosis for cattle with cardiac neoplasia?
Hopeless.
Which heart sound(s) (in addition to S1 and S2) can be heard in normal, healthy camelids?
S4.S3 is heard in camelids with diastolic dysfunction and HF.
Describe the physiologic murmur that is commonly heard in crias (and occasionally adults).
Soft (grade 1-2/6) systolic ejection murmur at the left heart base.
What is the most common congenital heart defect described in camelids?
Ventricular septal defect.NB muscular defects commonly observed!!!
What non-pathologic arrhythmia is common in camelids?
Sinus arrhythmia.Some evidence that some healthy alpacas demonstrate second-degree AV block at rest.
What is the prevalence of arrhythmias in camelids?
Low e.g. 1.2% in a retrospective study examining 663 ECGs from llamas.
What arrhythmias may occur in camelids with gastrointestinal, neurologic, ocular or respiratory disease and why?
First- and second-degree AV block.Due to vagal influences.
