8.2.4: Equine dysrhythmias Flashcards
Clinical signs of dysrhythmias
- (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
How do we diagnose equine dysrhythmias?
- ECG
- Evaluation of underlying cause: blood tests, echocardiogram, etc.
Conditions that might lead to myocardial dysfunction
- Electrolyte abnormalities
- Increased myocardial muscle mass
- Increased chamber size e.g. cardiomyopathy
- Myocarditis
Aetiology of myocarditis
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
Which forms of cardiomyopathy are seen in horses?
- Only DCM is reported in horses
- May be subacute/chronic condition
- The ventricle is dilated
- Myocarditis, or toxic causes of cardiomyopathy, are more common
Evaluation of myocardium
- 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
Where do we place leads for ECGs in horses?
- 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
Normal equine ECG at rest
There is a P for every QRS.
All the complexes are uniform and occurring at regular intervals.
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
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
What is the most important dysrhythmia in the horse?
Atrial fibrillation
What can trigger atrial fibrillation in horses?
- Exercise
- Electrolyte/ acid-base imbalance
- Anaesthetic and drug administration esp drugs that cuase bradycardia
Pathophysiology of atrial fibrillation in horses
- 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
How much does atrial contraction contribute to cardiac output and what is the impact of fibrillation at rest compared to exercise?
- Atrial contraction only contributes to 25% of cardiac output
- Atrial fibrillation therefore has no impact on cardiac output at rest, only at exercise
Clinical signs of atrial fibrillation
- Sometimes none
- Exercise intolerance/ poor performance
- Epistaxis
- Weakness/ syncope - rare
- Myopathy - rare
- Colic - rare
- Congestive heart failure - rare
What are the 2 types of atrial fibrillation
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
Physical exam findings of horse with atrial fibrillation
- 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
Atrial fibrillation
* No P waves
* Normal QRS complexes at irregular intervals
* F (fibrillation) waves gives undulating baseline
Treatment options for atrial fibrillation
- 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
Quinidine sulphate is
a) a positive ionotrope
b) a negative ionotrope
b) a negative ionotrope
This can be used to treat atrial fibrillation
Side effects of quinidine sulphate
- Fatal dysrhythmias
- Colitis - drug is very irritant to mucosa
- Laminitis
- Nasal oedema
- Ataxia
- Hypotension
Use with caution: need repeated physical exam inc auscultation
Prognosis of a horse with paroxysmal atrial fibrillation
- Excellent to good unless it keeps recurring
- Many convert back to normal sinus rhythm
Prognosis of horse with sustained atrial fibrillation and heart failure
Poor to grave
Do not attempt to treat
Prognosis of horse with sustained atrial fibrillation but no underlying cardiac disease
- <3 months - good with either quinidine sulphate or DC cardioversion
- > 3 months - better prognosis with DC cardioversion
Prognosis of horse with sustained atrial fibrillation and underlying cardiac disease
- 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)
Which equine dysrhythmias are not compatible with life?
- Asystole: complete lack of electrical activity
- Ventricular fibrillation: often leads to sudden death, rare in horses
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
Dysrhythmia? Treatment?
Ventricular tachycardia
* Complexes are wide and bizarre with no discernible P wave
* Treat with lidocaine
Dysrhythmia? Treatment?
Torsades de pointes
* Undulating baseline with no complexes visible
* PTS
What characteristics make a tachyarrhythmia more dangerous?
- 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!!)
Treatment of ventricular dysrhythmias
- 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
Adverse effects of lidocaine
- Nystagmus
- Muscle twitching
- Disorientation
- Excitement
- Convulsions
- If suffering lidocaine toxicity: stop infusion, horse should quickly return to normal
Metabolism and half life of lidocaine
- 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
What are the adverse effects of magnesium for treatment of ventricular dysrhythmias? When would you use it?
- 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
Dysrhythmia and prognosis
Below is exercise ECG. Horse is an international showjumper.
- 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!
This animal collapsed at rest.
- 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
Treatment of bradyarrhythmias in the horse
- 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
