Equine dysrhythmias Flashcards

1
Q

what is the differnce between endocardial and myocardia disease inthe horse?

A

Endocardial disease
* Valvular regurgitation
* Jet lesions
MANIFEST AS CARDIAC MURMURS

Myocardial disease
* Disruption to action potential propagation
* Abnormalities in contraction
MANIFEST AS CARDIAC DYSRHYTHMIAS
* Collapse/sudden death

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2
Q

how does mycoardial disease present in the horse? how is it diagnosed?

A
  • No clinical signs
  • Poor performance
    ◦ Atrial Fibrilation (AF)
    ◦ Ventricular Premature Depolarisation (VPD)
    ◦ ventricular tachycardia (VT)
  • Collapse
    ◦ Multiple VPDs
    ◦ VT
  • V rarely death
    ◦ VT to Ventricular fibrillation (VF)

Cardiac dysrhythmias:
* Diagnosis - ECG
* Evaluation of underlying cause - Blood tests, echocardiogram, other

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3
Q

what conditions lead to myocardial dysfunction?

A
  • Electrolyte abnormalities
  • Increased myocardial muscle mass
  • Increased chamber size - Cardiomyopathy
  • Myocarditis
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4
Q

what are the causes of myocarditis in the horse?

A

Inflammation of the myocardium
* Bacterial
◦ Staph aureus
◦ Strep equi
◦ Clostridium chauvoei
◦ Myocobacterium spp.
◦ Secondary to sepsis, pericarditis, endocardititis
* Borrelia burgdorferi (Lyme disease)
* Viral
◦ Foot and Mouth Disease, Equine infectious Anaemia, Equine Viral Arteritis, Equine Influenza Virus, African Horse Sickness
* Parasitic
◦ Large strongyles, Toxoplasma, Sarcocystis
* (Thromboembolic – due to above)

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5
Q

what cardiomyopathy affects horses?

A

Only Dilated Cardiomyopathy reported/important in LA
* Subacute or chronic
* Dilated ventricle

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6
Q

what is used to assess myocardial function?

A

Echocardiography
* Assessment of myocardial appearance
* Long and short axis

Fractional shortening
* At rest and following exercise
* to evalute the myocardial function and the ability of the hear to contract and pump blood

Dobutamine-atropine stressechocardiography​
* give the horse dobutamine and atropine and therefore can evaluate theheart at increasingheart rates​ - stimulate exercises

Myocardial biopsies​
* Can now be donestanding​
* Ultrasound guided​
* Biopsy instrumentinto heart via jugular vein

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7
Q

what dysrhthmia is physiological in horses, why does this occur??

A

2nd degree AtrioVentricular Block
* Considered normal in horses, due to high vagal tone in the autonomic control of the equine heart, done to lower BP

p wave blocked by AV node - electrical signal not transferred to the ventricles

  • when exercised this rhythm will disappear and return back to normal sinus rhythm and these are of no clinical concern in these horses.
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8
Q

what is the most important cardiac dysrhythmia in the horse? what can cause it?

A

Atrial fibrillation
* Lack of coordinated atrial electrical activity
* Can be triggered by electrolyte/acid-based imbalances, anaesthetic and drug administration (that causes bradycardia, exercise

  • Horses particularly susceptible (esp large ones), TBs, SBs, Draught horses
    ◦ Large atrial mass (more likely when enlarged with disease – Mitral Regurgitation /Tricuspid Regurgitation)
    ◦ High vagal tone and low heart rate
  • No effect on cardiac output at rest, only when exercised as atrial contraction only contributes 25% of CO - during exercise need the last bit of atrial contraction to maintain cardiac output
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9
Q

what are thetwo typed of atrial fibrilation?

A

Paroxysmal – lasts less than 24-48hrs and spontaneously converts back to sinus rhythm
* Sometimes associated with K+ depletion (furosemide) and administration of bicarbonate

Sustained - more common in horses

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10
Q

what is seen on clinical exam of horses with atrial fibrialtion?

A
  • Irregularly irregular rhythm
    ◦ Becomes less irregular with chronicity
  • HR and pulse quality varies in intensity
    ◦ Booming S1 on auscultation
    ◦ No S4 – active atrial contraction
    ‣ Helps distinguish from other dysrhythmias
    ◦ Usually normal or decreased HR; occ increased and will be increased if associated Heart Failure
  • Abnormally high heart rates at exercise
    ◦ Can be associated with VPDs at exercise
    **Should perform exercising ECGs on these animals - for safety **
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11
Q

what does atrial fibrilation look like on ECG?

A

◦ No P waves
◦ Normal QRS complexes
◦ F (fibrillation) waves - undulating baseline

red - f waves

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12
Q

what is the treatment of atrial fibrilation?

A

Pharmacological
* Quinidine sulphate orally via stomach tube, every 2 hours, 5-6 doses given or until signs of toxic effects, or conversion to normal rhythm
* Many untoward side effects
◦ Fatal dysrhythmias
◦ Colitis – drug very irritant to mucosa
◦ Laminitis/nasal oedema/ataxia
◦ hypotension
Use with caution
* Need repeated physical examinations
* Auscultation
* Continuous ECG monitoring (At time of treatment and for 24hrs after)
* Check acid-base and electrolytes prior to treatment

Monitor toxicity by assessing prolongation of QRS complex
* >25% of pre-treatment value makes untoward effects more likely - treatment stopped at this point

Alternative treatment - DC Cardioversion
* Wires into heart of anaesthetized horse - Positioned using ultrasound and radiography
◦ wires placed via the jugular vein under standing sedation as makes imaging easier
◦ then GA horse
* Increased current to try and stop heart and convert to sinus rhythm

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13
Q

what is the prognosis of atrial fibrilation?

A
  • Paroxysmal – excellent to good – unless keeps recurring
  • Sustained, no underlying cardiac disease
    ◦ <3months – good either technique
    ◦ >3months – better with DC cardioversion
    ◦ Risk of re-fibrillation – if there is underlying cause eg: structural cardiac changes, severe mitral regurgitation causing atrial enlargement, atrial premature contractions
  • Sustained, underlying cardiac disease
    ◦ Average prognosis with DC conversion
    ◦ More likely to re-fibrillate
  • Sustained, heart failure
    ◦ Poor to grave prognosis
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14
Q

what does ventricular premature complexes look like on ECG?

A

(third complex)
- no obvious P wave
- shortened R-R interval (between second and third complex)
- ventricular premature depolarisation - tall and wide , with inverted T wave, no discernible p wave (suggests it has not come from the sinoatrial node), followed by a compensatory pause (as the impulse from this depolarisation resents the sinoatrial node, therefore return of sinus rhythm after)

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15
Q

what is this an example of?

A

ventricular tachycardia - wide and bizarre complexes with no discernible P wave

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16
Q

what is the treatemt of ventricualr tachdsyrhythmias?

A
  • Lidocaine - first line
  • Magnesium - can be effective for refractory ventricular dysrhthmias that fale to respond to lidocaine, ess advers effects
  • Procainamide - often not available in GP practice
  • Amiodarone - often not available in GP practice
17
Q

Pharmacologic management of acute tachyarrhythmias are indicated when?

A
  1. There is evidence of poor cardiac function manifesting with either clinical signs (eg, depression, weakness, collapse, syncope, severe systemic hypotension) OR
  2. There are laboratory parameters indicating poor peripheral perfusion (azotemia (reduction in renal perfusion) or hyperlactatemia (anaerobic resp)) OR
  3. A malignant arrhythmia is present that may worsen if left untreated, including:
    a. Rates over 100 bpm (in the adult horse) OR
    b. Multiform or polymorphic complexes (different complexes from beat to beat) OR
    c. The presence of the R-on-T phenomenon (QRS complexes running straight into the T wave)
18
Q

when dose 2nd degree AV block in the horse need to be treated? how is it treated?

A
  • Relevance of advanced second degree AV block controversial
    ◦ Persistence at exercise – requires further investigations as if the HR is not able increase appropriately to exercise then compromises cardiac output
  • can occur secondary to Drug administration, electrolyte derangements, intestinal disease, primary myocardial disease - therefore these need to be investigated first before embarking on treatment

Treatment –
◦ Anticholinergics
‣ Glycopyrrolate, atropine, hyoscine (scopolamine)
◦ Ventricular pacing

19
Q

what does a 3rd degree AV bloock looklike in horses?

A

disassociation between the P and the QRS, P waves are running at an underlying rate. And these are not being conducted into the ventricles. The ventricles are creating their own rate, which is much slower. And so you’ll see that the QRS complexes are slightly irregular.