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EQUINE > 8.2.4: Equine dysrhythmias > Flashcards

8.2.4: Equine dysrhythmias Flashcards

1
Q

Clinical signs of dysrhythmias

A
  • (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
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2
Q

How do we diagnose equine dysrhythmias?

A
  • ECG
  • Evaluation of underlying cause: blood tests, echocardiogram, etc.
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3
Q

Conditions that might lead to myocardial dysfunction

A
  • Electrolyte abnormalities
  • Increased myocardial muscle mass
  • Increased chamber size e.g. cardiomyopathy
  • Myocarditis
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4
Q

Aetiology of myocarditis

A

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

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5
Q

Which forms of cardiomyopathy are seen in horses?

A
  • Only DCM is reported in horses
  • May be subacute/chronic condition
  • The ventricle is dilated
  • Myocarditis, or toxic causes of cardiomyopathy, are more common
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6
Q

Evaluation of myocardium

A
  • 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
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7
Q

Where do we place leads for ECGs in horses?

A
  • 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
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8
Q
A

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

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9
Q
A

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

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10
Q
A

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

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11
Q

What is the most important dysrhythmia in the horse?

A

Atrial fibrillation

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12
Q

What can trigger atrial fibrillation in horses?

A
  • Exercise
  • Electrolyte/ acid-base imbalance
  • Anaesthetic and drug administration esp drugs that cuase bradycardia
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13
Q

Pathophysiology of atrial fibrillation in horses

A
  • 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
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14
Q

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

A
  • Atrial contraction only contributes to 25% of cardiac output
  • Atrial fibrillation therefore has no impact on cardiac output at rest, only at exercise
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15
Q

Clinical signs of atrial fibrillation

A
  • Sometimes none
  • Exercise intolerance/ poor performance
  • Epistaxis
  • Weakness/ syncope - rare
  • Myopathy - rare
  • Colic - rare
  • Congestive heart failure - rare
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16
Q

What are the 2 types of atrial fibrillation

A

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

17
Q

Physical exam findings of horse with atrial fibrillation

A
  • 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
18
Q
A

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

19
Q

Treatment options for atrial fibrillation

A
  • 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
20
Q

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

A

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

21
Q

Side effects of quinidine sulphate

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

Use with caution: need repeated physical exam inc auscultation

22
Q

Prognosis of a horse with paroxysmal atrial fibrillation

A
  • Excellent to good unless it keeps recurring
  • Many convert back to normal sinus rhythm
23
Q

Prognosis of horse with sustained atrial fibrillation and heart failure

A

Poor to grave
Do not attempt to treat

24
Q

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

A
  • <3 months - good with either quinidine sulphate or DC cardioversion
  • > 3 months - better prognosis with DC cardioversion
25
Q

Prognosis of horse with sustained atrial fibrillation and underlying cardiac disease

A
  • 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)
26
Q

Which equine dysrhythmias are not compatible with life?

A
  • Asystole: complete lack of electrical activity
  • Ventricular fibrillation: often leads to sudden death, rare in horses
27
Q
A

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

28
Q

Dysrhythmia? Treatment?

A

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

29
Q

Dysrhythmia? Treatment?

A

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

30
Q

What characteristics make a tachyarrhythmia more dangerous?

A
  • 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!!)
31
Q

Treatment of ventricular dysrhythmias

A
  • 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
32
Q

Adverse effects of lidocaine

A
  • Nystagmus
  • Muscle twitching
  • Disorientation
  • Excitement
  • Convulsions
  • If suffering lidocaine toxicity: stop infusion, horse should quickly return to normal
33
Q

Metabolism and half life of lidocaine

A
  • 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
34
Q

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

A
  • 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
35
Q

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

A
  • 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!
36
Q

This animal collapsed at rest.

A
  • 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
37
Q

Treatment of bradyarrhythmias in the horse

A
  • 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

EQUINE (59 decks)

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