8.2.4: Equine dysrhythmias

Question 1

Clinical signs of dysrhythmias

Answer 1

• (Sometimes no clinical signs)
• Poor performance - seen with atrial fibrillation, ventricular premature depolarisation (VPDs)
• Collapse - seen with multiple VPDs, ventricular tachycardia
• Death (rare) - seen when ventricular tachycardia progresses to ventriculr fibrillation

Question 2

How do we diagnose equine dysrhythmias?

Answer 2

• ECG
• Evaluation of underlying cause: blood tests, echocardiogram, etc.

Question 3

Conditions that might lead to myocardial dysfunction

Answer 3

• Electrolyte abnormalities
• Increased myocardial muscle mass
• Increased chamber size e.g. cardiomyopathy
• Myocarditis

Question 4

Aetiology of myocarditis

Answer 4

Myocarditis: inflammation of the myocardium
* Bacterial: Staph aureus, Strep equi, Clostridium chauveoi, Mycobacterium spp., Borrelia burgdorferi (causative agent of Lyme’s disease)
* Viral: FMD, equine infectious anaemia (EIA), equine viral arteritis (EVA), equine influenza virus (EIV), African horse sickness (AHS)
* Parasitic: large strongyles, toxoplasma, sarcocystis
* Thromboembolic disease due to any of the above

Question 5

Which forms of cardiomyopathy are seen in horses?

Answer 5

• Only DCM is reported in horses
• May be subacute/chronic condition
• The ventricle is dilated
• Myocarditis, or toxic causes of cardiomyopathy, are more common

Question 6

Evaluation of myocardium

Answer 6

• Echocardiography: assess myocardial appearace, fractional shortening at rest and following exercise etc.
• Dobutamine-atropine stress echocardiography: can evaluate the heart at increasing rates, stimulates exercise-like scenario
• Myocardial biopsies: can be done standing, ultrasound guided; insert biopsy instrument into heart via jugular vein

Question 7

Where do we place leads for ECGs in horses?

Answer 7

• One lead on right side of neck
• Second lead just behind triceps muscle on the left side of the thorax
• Only need 3 leads
• Telemetric/Holter systems are affordable and useful for 24hr monitoring/ monitoring at exercise

Question 8

Answer 8

Normal equine ECG at rest
There is a P for every QRS.
All the complexes are uniform and occurring at regular intervals.

Question 9

Answer 9

Normal equine ECG at exercise
* Much more difficult to interpret due to increased movement and heart rate
* Difficult to discern P and T waves in between each QRS
* R wave = downward projection -> look at the regularity of these

Question 10

Answer 10

Second degree AV block
* Most common dysrhythmia in horses
* Considered normal in horses
* Occurs due to high vagal tone (autonomic control of equine heart)
* In this case there are 4 regular PQRST then a P wave that does not result in ventricular depolarisation
* This P wave has been blocked by the AVN
* Audible as a missed beat on auscultation
* When horse stimulated e.g. exercise this will disappear and there will be normal sinus rhythm
* This is not of clinical concern

Question 11

What is the most important dysrhythmia in the horse?

Answer 11

Atrial fibrillation

Question 12

What can trigger atrial fibrillation in horses?

Answer 12

• Exercise
• Electrolyte/ acid-base imbalance
• Anaesthetic and drug administration esp drugs that cuase bradycardia

Question 13

Pathophysiology of atrial fibrillation in horses

Answer 13

• Horses are particularly susceptible especially large ones
• e.g. TBs, SBs, draught horses
• Due to large atrial mass -> more likely when atria are enlarged with disease e.g. mitral/ tricuspid regurgitation
• High vagal tone and low heart rate = risk factors

Question 14

How much does atrial contraction contribute to cardiac output and what is the impact of fibrillation at rest compared to exercise?

Answer 14

• Atrial contraction only contributes to 25% of cardiac output
• Atrial fibrillation therefore has no impact on cardiac output at rest, only at exercise

Question 15

Clinical signs of atrial fibrillation

Answer 15

• Sometimes none
• Exercise intolerance/ poor performance
• Epistaxis
• Weakness/ syncope - rare
• Myopathy - rare
• Colic - rare
• Congestive heart failure - rare

Question 16

What are the 2 types of atrial fibrillation

Answer 16

Paroxysmal
* Lasts less than 24-48hrs and spontaneously converts back to normal sinus rhythm
* More common in racehorses that spontaneously pull up during a race
* Sometimes associated with K+ depletion (e.g. furosemide) and administration of bicarbonate
* Always wait 24-48hrs before trying to convert these horses

Sustained atrial fibrillation
* More common form

Question 17

Physical exam findings of horse with atrial fibrillation

Answer 17

• Irregularly irregular rhythm, becoming less irregular with chronicity
• HR and pulse quality varies in intensity - booming B1, no S4 as this is associated with active atrial contraction, usually normal or decreased HR, occasionally increased
• Abnormally high HRs at exercise; may be associated with VPDs
• Should perform exercising ECGs on these animals esp if ridden exercise is to be continued

Question 18

Answer 18

Atrial fibrillation
* No P waves
* Normal QRS complexes at irregular intervals
* F (fibrillation) waves gives undulating baseline

Question 19

Treatment options for atrial fibrillation

Answer 19

• Quinidine suphate: administered orally via stomach tube every 2hrs up to 5-6 doses OR until toxic effects OR resolution of normal sinus rhythm. Many untoward side effects.
• DC cardioversion: wires put into heart of anaesthetised horse, positioned using ultrasonography and radiography, gradually administer increased current to try and stop the heart and convert to normal sinus rhythm

Question 20

Quinidine sulphate is
a) a positive ionotrope
b) a negative ionotrope

Answer 20

b) a negative ionotrope
This can be used to treat atrial fibrillation

Question 21

Side effects of quinidine sulphate

Answer 21

• Fatal dysrhythmias
• Colitis - drug is very irritant to mucosa
• Laminitis
• Nasal oedema
• Ataxia
• Hypotension

Use with caution: need repeated physical exam inc auscultation

Question 22

Prognosis of a horse with paroxysmal atrial fibrillation

Answer 22

• Excellent to good unless it keeps recurring
• Many convert back to normal sinus rhythm

Question 23

Prognosis of horse with sustained atrial fibrillation and heart failure

Answer 23

Poor to grave
Do not attempt to treat

Question 24

Prognosis of horse with sustained atrial fibrillation but no underlying cardiac disease

Answer 24

• <3 months - good with either quinidine sulphate or DC cardioversion
• > 3 months - better prognosis with DC cardioversion

Question 25

Prognosis of horse with sustained atrial fibrillation and underlying cardiac disease

Answer 25

* OK prognosis with DC cardioversion * These horses are more likely to re-fibrillate * Risk of refibrillation in horses with underlying cause e.g. structural cardiac disease, severe mitral regurgitation, lots of APCs present on ECG (APCs can trigger atrial fibrillation)

Question 26

Which equine dysrhythmias are not compatible with life?

Answer 26

* Asystole: complete lack of electrical activity * Ventricular fibrillation: often leads to sudden death, rare in horses

Question 27

Answer 27

**Ventricular premature depolarisation** * Tall, wide and bizarre QRS complex without obvious preceding P wave * Based on the R-R interval we can tell this complex occurs early * This is followed by a compensatory pause because depolarisation spreads across the heart and resets the SAN

Question 28

Dysrhythmia? Treatment?

Answer 28

**Ventricular tachycardia** * Complexes are wide and bizarre with no discernible P wave * Treat with lidocaine

Question 29

Dysrhythmia? Treatment?

Answer 29

**Torsades de pointes** * Undulating baseline with no complexes visible * PTS

Question 30

What characteristics make a tachyarrhythmia more dangerous?

Answer 30

* Very fast heart rate e.g. over 100bpm in adult horse * Multiform or polymorphic complexes * The presence of R on T phenomenon: R wave runs right into the T wave (means the ventricle is trying to depolarise when it is repolarising -> dangerous!!)

Question 31

Treatment of ventricular dysrhythmias

Answer 31

* Lidocaine -> IV boluses 0.5mg/kg every 5 mins up to total dose of 4mg/kg OR CRI 50mg/kg/min * Magnesium -> can be effective for refractory ventricular dysrhythmias * Procainamide - not in GP * Amiodarone - not in GP

Question 32

Adverse effects of lidocaine

Answer 32

* Nystagmus * Muscle twitching * Disorientation * Excitement * Convulsions * If suffering lidocaine toxicity: stop infusion, horse should quickly return to normal

Question 33

Metabolism and half life of lidocaine

Answer 33

* Lidocaine undergoes rapid hepatic metabolism * High level of first pass metabolism when given orally so should be given IV * Half life approx. 15mins * Take care using in animals with liver dysfunction or reduced hepatic blood flow * Less effective in hypokalaemia -> must correct any electrolyte imbalances before treatment

Question 34

What are the adverse effects of magnesium for treatment of ventricular dysrhythmias? When would you use it?

Answer 34

* Can be effective for refractory ventricular dysrhythmias * Mechanism of action not fully understood * Minimal adverse effects * Treatment of choice for quinidine-induce torsades de pointe in human patients * First line in treatment of ventricular tachycardia by some vets * Can be safely combined with other anti-arrhythmic agents and may potentiate the effects of lidocaine in patients with hypokalaemia

Question 35

Dysrhythmia and prognosis Below is exercise ECG. Horse is an international showjumper.

Answer 35

* Majority of trace shows normal sinus rhythm * Then there is a run of 3 wide and bizarre complexes that run one into the next (R on T phenomenon) * If this persists could be catastrophic for horse and rider as could lead to collapse/sudden death * A good indicator of why we must always perform an exercise ECG - this did not show at rest!

Question 36

This animal collapsed at rest.

Answer 36

* **Third degree AV block** (this is rare) * There is dissociation between P waves and QRS complexes * P waves are running at an underlying rate and not being conducted into the ventricles * The ventricles are contracting at their own rate, which is much slower * Bottom line = multiple P waves with no QRS - the ventricles are not contracting -> hence the collapse * Treatment: pacemaker implantation

Question 37

Treatment of bradyarrhythmias in the horse

Answer 37

* Not all need treatment - may be product of high vagal tone at rest * Relevance of advanced 2nd degree AV block at exercise remains controversial but if it persists at exercise probably warrants further investigation * Bradyarrhythmias an occur secondary to drug administration, electrolyte derangements, intestinal disease, primary myocardial disease -> where possible correct the underlying cause * Treatment: anticholinergics e.g. glycopyrrolate, atropine, hyoscine (which is in buscopan), or ventricular pacing