Equine cardiology

Atrial premature complexes

Pulses generated in a site other than then the SA node- ectopic

These occur prior to the normal SA impulse

Occasional APCs are normal

May predispose to SVT or AF during maximal exercise

When to investigate atrial premature complexes

Frequent at rest

Associated with runs of SVT

Associated with poor performance

Predisposing causes for atrial premature complexes

Atrial enlargement- blood leaking back in

Inflammation

Electrolyte abnormalities- colic, excess exercise

Hypoxia

Pyrexia

Sepsis/ toxaemia

ECG trace of APC

Different p wave configuration

QRS normal

R-R interval preceding to the complex- VPCs have compensatory pause

Occasionally not conducted- very early

Management of atrial premature complexes

Haematology and biochemistry to evaluate inflammation, electrolytes, infection

24 hour ECG

Exercising telemetry

Treatment of APCs

Treat underlying disease

Nothing specific needed if isolated or overdriven by exercise

Rest 1-2 months

Corticosteroids if myocardial inflammation is suspected

Supreventricular tachycardia

Rapid rhythm from ectopic focus in atrial or AV node

Atrial/ junctional tachycardia

Paroxysmal or sustained

Primary heart disease or secondary to systemic disease

SVT on ECG

Difficult to distinguish from sinus tachycardia

Transition on ECG trace ver time

P wave- different configuration, sometimes lost in preceding T wave

Inconsistent conduction of P waves to the ventricle

Management of SVT

Blood work

Echo if cardiac disease suspected

Severe signs- use digoxin to control the ventricular response rate

Atrial fibrillation

Most common arrhythmia affecting performance in horses

Lack of coordinated atrial contraction

Causes of AF

No underlying cardiac disease

Large atria, high vagal tone

Electrolyte imbalances

Symptoms of atrial fibrillation

None at rest

At peak exercise atria contribute up to 25% to ventricles- decreased performance, acute onset= slowing, ataxia, EIPH

Types of atrial fibrillation

Paroxysmal- go in and out of AF

Persistent

Permanent- can't fix

No Pwave

Diagnosis of AF

Paroxysmal- difficult, reverts spontaneously in 24-48 hours

Auscultation- regularly irregular, so S4

ECG: no p waves, undulating basline- f waves; highly irregular R-R; normal QRS

Blood work- fibrinogen, electrolytes

Echocardiogram- underlying cardiac disease- atrial enlargement

When to treat atrial fibrillation

None- if convert within 24-48 hours

How to treat AF

Conversion- of no significant underlying cardiac disease

Chemical- quinidine sulphate (+digoxin)- 22mg/kg by NGT every 2 hard- max 40-60g- many side effects, monitor QRS length- increase of >25%- sign of toxicity not best

Trans venous electrical cardioversion- under GA best

Echo and 24 hour ECG post conversion

Rest before return to work

Success of AF treatment- TEC

90% successful, recurrence 25% (4 month duration before treatment- consider last normal auscultation and viruses in yard)

Treatment of quinidine toxicity

Sodium bicarbonate

Lido/ MgSO4 to treat Vtach

Quinidin highly irritant

Consequences of not treating AR

Breeding animals- ok

Mild athletic activity- perform exercising ECG to look for ventricular ectopic

Ventricular premature complex's

Ectopic focus in ventricle

If one found at rest- cardiac work up

At exercise may progress to vent tachycardia- exercise ans syncope

QRS complex wide and bizarre

VPC causes

Electrolyte imbalances

Systemic disease

Diagnosis of VPCs

Auscultation

ECG- QRs wide and bizarre, not preceded by p wave, following T wave is of different polarity than other T waves, compensatory passes- next sinus impulse is blocked

Uniform or multi form

Blood work including cardiac isoenzymes

24hr and exercising ECG

Echocardiography

Treatment of VPC

Occasional- 1 per hour- not significant; no treatment

Frequent or multiform- suggests myocarditis pathology

- rest 4-8 weeks

corticosteroids

Prognosis if VPC

Occasional at rest/ exercise- only ridden by informed adult

Horses with complex ectopic- rest and treat and re-examine

Horses withVPCs nd underlying cardiac disease- not suitable for work

VT

4 + VPCs in a row

Paroxysmal or sustained

Causes of VT

Systemic disease- colic, toxaemia

Electrolyte imbalances

Cardiac disease

VT on clinical exam

Rapid rhythm >60bpm- regula/ irregular

If sustaines HR >120: signs of CHF; venous distension, jugular pulse, oedema

If HR> 150- syncope, pulmonary oedema

Weak pulse with deficits

Diagnosis of VT

ECG- AV dissociation (regular P, different rate of ventricles), P-P interval regular and normal rate,

R-R interval may e regular, or paroxysmal, periodically irregular,

R on T may be seen (QRS begins on T wave of previous beat)- thes3 can progress to ventricle fibrillation

Treatment of VT

Treat underlying disease

Anti-arrhythmic therapy if- high HR, rhythm multiform, R on T present

Pulmonary oedema- furosemide 1-2mg/kg

Lidocaine 0.5mg/kg slowly can pre-treat with diazepam

Procainamide MgSO$ if no response

Prognosis of VT

Primary cardiac disease- poor prognosis

Convert to NST- rest for 4 weeks and re-evaluate with exercising ECG

Follow up annually

Acquired valvular disease

Aortic regurgitation

Mitral regurgitation

Tricuspid regurgitation

Valvular endocarditis

Aortic regurgitation

Common in older house- age-related regurgitation

Murmurs: decrease rod, hol-diastolic, musical

PMI over left heart base, may radiate right

Bounding arterial pulses- significant

Intensity not good indicator- need echo; flow jet and chamber size

Left sided volume overload eventually, may be slow

Progressive exercise intolerance

Prognosis of aortic regurgitation

Mid AR with no exercise intolerance or CHF- safe to ride

Bounding pulses- do exercising EG- decreased myocardial perfusion = ventricular arrhythmias

Use echo to make prognosis for future athletic activity

Regular echo exams to monitor progress

Eventually, LA enlargement and risk of AF

Mitral regurgitation presentation

Middle aged to older;degenerative schanges

Pan or holosystolic murmur, band-shaped, PMI over left apex

Radiates towards heart base

No variation with exercise

Murmurs >grade 2- usually more severe, but auscultation unreliable

Echo indicated in all cases for atrial enlargement, flow size, and depth

Exercising ECG in moderate to severe MR- follow up q6 months or 1 year

Prognosis of MR

Progression may be very slow

Moderate Mr likely yo limit performance

Low grade with no EI of CS of heart disease- safe to ride

Monitor with serial exam

Sequelae of MR

Left sided HF, pulmonary hypertension of RSHF

Tricuspid regurgitation

Common

Pan/ holosystolic band shaped with PMI over the RHS (DIFFERENTIATE FROM VSD)

Radiates cranially no change with exercise

Pulmonary hypertension or right sided hypertrophy may predispose

Progreses slow of at all

Sequelae or TR

Rarel associated with deceased performanc or heart failure

Exercise intolerance, AF and RHF- venous distension, jugular pulse, pedema, ascites, hepatic congestion

Valvular endocarditis

Pare

Bacterial infection of endocardium, causing damage to vales- aortic and mitral most common

CS: systemic illness

Murmur may be severe

APC or VPC may be resent

Jugular phlebitis sometimes involved

Diagnosis of valvular endocarditis

Bloody. Ultrasound, blood culture

Prognosis of valvular endovcarditis

Grave- treatment often unrewarding

Damage to leaflets may be permanent-

High dose, prolonged broad spectrum antimicrobials

Antithrombotic therapy

Repeat echo

Types of acquired cardiac disease

Myocardial disease

Pericardial failure

CHF

Myocarditis causes

Inflammatory, degenerative, toxic (monensin)

Viral or idiopathic in athletic roses

CS of myocarditis

Poor performance, exercise intolerance, sudden death

Arrhythmias

HR may be normal at rest, but elevated during exercise

Prolonged recovery

Pericarditis

Rare

Idiopathic- viral, bacterial associated with pleuropneumonia

Clinical signs of pericarditis

Poor performance- acute heart failure

Pericardial effusion

Muffled heart sounds, tachycardia, pericardial friction rubs, absent lung sounds vetrally

Diagnosis of pericarditis

Echocardiography

Severe pericarditis

Life threatening, drainage is requires- paricardiocentes

Antibiotics, anti-inflammatory drugs

Congestive heart failure presentation

Rare due to large cardiac reserve

History of progressive exercise intolerance

Weight loss, weakness, lethargy, CRT prolonged tachycardia >45bpm, weak pulses deficits if arrhythmia, jugular distension/ pulse, oedema, tachypnoea, murmur

Diagnosis of CHF

Echocardiogram

ECG

Treatment of CHF

Antiarrhythmic therapy

Diuretics- furosemide

Ace inhibitors- enalapril

Positive inotropic drugs- dioxin

Prognosis for CHF

6 mo

Ventricular sceptical defect

Most common congenital defect in horses

Usually just below aortic valve

May occur with TOF

Murmur: pansystolic, band-shaped murmur, RHS, crescendo-de crescendo murmur on LHS, one grade softer

Significance of VSD

Large defects- CHF shortly after birth

Smaller defects- poor performance when starting trainfin

Ver small may be asymptomatic

Diagnosis of VSD

Echocardiography

Prognosis of VSD

Less Han 2.5cm may be asymptomatic and may perform at high intensity

Larger defects- more like;y to develop performance/ life limiting CHF

Exercising ECG >2.5 cm

PDA

Usually causes by 72 hours

Defect rarely seen in isolation poor prognosis

Volume overload of PA, LA, LV

Continuous machinery murmur and thrill

Diagnosis- echocardiography

Tetralogy of fallout

Grade prognosis

Overriding aorta, pulmonic stenosis, RV hypertrophy

Reduced blood to lungs; deoxygenated blood to systemic circulation

Clinical signs of tetralogy of fallout

Ill thrift, exercise intolerance

Tachycardia, tachypnoea, cyanosis after exercise

Loud pan-systolic murmur- both sides PMI