Equine - Cardiac Disease Flashcards
1
Q
What is the most common primary heart tumour of large animals?
A
Lymphosarcoma.
2
Q
What breeds of horses display the highest incidence of atrial fibrillation?
A
Standardbreds, Warmbloods, draught horses.
3
Q
Describe the pathophysiology of atrial fibrillation in horses.
A
- 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).
4
Q
Define the three classifications of atrial fibrillation in horses.
A
- 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. - Persistent AF: arrhythmia terminates after tx.
- 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.
5
Q
What are the clinical signs in horses with atrial fibrillation?
A
- 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.
6
Q
What are the diagnostic test findings in horses with atrial fibrillation?
A
- 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.
7
Q
Describe quinidine sulphate therapy for cardioversion in horses with atrial fibrillation.
A
- 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.
8
Q
Describe transvenous electrovardioversion for treatment of atrial fibrillation in horses.
A
- 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.
9
Q
What is the prognosis for horses with atrial fibrillation?
A
- Excellent Px for conversion (>95%) if HR
10
Q
Describe the signalment and aetiology of bacterial endocarditis in horses.
A
- Most cases in horses
11
Q
Describe the pathophysiology of bacterial endocarditis in horses.
A
- 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.
12
Q
List the clinical signs of bacterial endocarditis in horses.
A
- 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.
13
Q
Describe clinicopathologic findings in horses with bacterial endocarditis.
A
- 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).
14
Q
Describe electrocardiogram and echocardiogram findings in horses with bacterial endocarditis.
A
- 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.
15
Q
How is bacterial endocarditis treated in horses?
A
- 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).
