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Cardiovascular > Equine Arrythmias > Flashcards

Equine Arrythmias Flashcards

1
Q

Are most causes of myocardial dysfunction in large animals 1* or 2*?

A 
2* 
- endotoxaemioa
- electrolyte disturbance (K, Ca, Mg) 
- acid-base disturbance (acidosis)
- hypoxia
- catecholamine induced
> horses with severe GI disease/URT obstruction during excerise may develop arrhythmia
> common and underdiagnosed in intensive care patients
- vagally induced
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2
Q

What are some potential 1* causes of myocardial disease/dysfunction?

A 
> infectious
- viral/bacterial/parasitic
> nutritional 
> others
- cardiomyopathy
- neoplasia
- immune mediated
- toxic
> idiopathic
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3
Q

Viral causes of 1* myocarditis?

A

> anything that causes a viraemia as part of its lifecycle

  • equine influenza
  • EHV
  • EVA
  • FMD
  • AHS
  • EIA`
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4
Q

Bacterial causes of 1* myocarditis?

A

> Bacterial

  • staph aureus
  • clostridium chauvoei
  • mycobacterium spp.
  • strep equi equi
  • actinobacillus spp.
  • rhodococcus equi
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5
Q

Parasitic causes of 1* myocarditis?

A
  • strongyles
  • onchocerca
  • toxoplasma
  • cysticerca
  • sarcocysta
  • borrelia burgdorferu (Lyme’s disease)
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6
Q

What nutritional deficiency may cause myocardial disease? what other form is possible? which species are most commonly affected?

A 
nutritional myodegeneration (white muscle disease) due to SELENIUM deficiency 
> cardiac form 
- neonates, acute or peracute 
- severe debilitation or sudden death 
- respiratory signs, arrhythmias 
> skeletal muscle form 
- slightly older animals
- weakness, stiffness and debilitation
- signs precipitated by stress 
> mostly ruminants, horses can be affected
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7
Q

How is diagnosis of nutritional myodegeneration confirmed? What would be seen at PM?

A
  • whole blood selenium concentrations
  • glutathione peroxidase levels decrease with deficiency
    > PM: pale streaky muscles with degeneration and fibrosis
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8
Q

Tx for nutritional myodegeneration?

A

Vit E and selenium IM

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9
Q

What is cardiomyopathy associated with in cattle? Does it occour in horses?

A
  • inherited
  • linked to red Holstein gene in Holstein-fresians
  • associated with curly coat in polled Herefords
    > occours sporadically in horses, cuases unknown
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10
Q

What type of neoplasia affects the heart in cattle and horses?

A

> cattle
- RA lesions from enzootic bovine leucosis virus
horses
- lymphoma and others

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11
Q

What may 1* myocardial inflammatory lesions and fibrosis be due to?

A
  • potentially immune mediated
  • toxins eg. halothane, erythromycin and ionophore ABx
  • idiopathic
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12
Q

What tests should be carried out when investigating arrhythmias?

A
  • haem and biochem (esp. hepatic and renal)
  • acid-base and electrolyte status
  • Se and glutathione peroxidase
  • viral serology
  • blood bacterial culture (rarely useful)
  • cardiac troponin 1 and cardiac isoenzymes to indicate cardiac damage
    > CK and LDH indicators of myocardial necrosis
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13
Q

When is echo indicated with arrhythmias?

A

Not unless there is a global myocardial problem

- but will rule outvalvular and congenital heart disease

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14
Q

How does the purkinje fibre system differ in LA to SA? What affect does this have clinically?

A
  • extensive
  • branches from endocardium to epicardium
  • depolarised wave conducted by purkinje fibres, NOT so much cell-cell spread as in carnivores
  • > small wavefronts, less influenced by myocardial mass than SA
  • > QRS size and duration does NOT accurately reflect shape and size of ventricular myocardium
  • do not overinterpret ECGs as they only show rate and rhythm
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15
Q

What configuration of ECG is used as standard in horses?

A

Base apex
- positive electrode left apex
- negative electrode left base (in front of shoulder)
- produces large P wave, clear QRST
> limb leads not used as horses don’t like them!

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16
Q

What other forms of ECG are available for practicality?

A

Radiotelemetry (instantaneous, good for exercise and intensive care)
Ambulatory (24hour recording, good for frequency of arrhythmias )

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17
Q

What are the 3 types of AV block?

A

1physiological
- delayed conduction through AV node
- slow, slightly variable HR
2 physiological
- intermittent conduction block though AV node due to increasingly high vagal tone (will reset once beat skipped)
- slow HR, pauses at regular intervals (will disappear with HR >60 at exercise)
- isolated 4th heart sound before block
-isolated but normally timed P waves on ECG
3* pathological
- dissociation of atria and ventricles
- due to pathology of AV node
- very slow ventricular rate, syncope and weakneszs

18
Q

What is the commonest pathological dysrhythmia in horses?

A

Atrial fibrillation

  • large atrial mass (found in normal horses, or atrial enlargement due to valve regurge or VSD
  • slow SA node rate (normal horses, ^ vagal tone)
  • variable refractory periods (due to high vagal tone, myocardial disease with electrolyte/pH change) allows re-entry to occour
19
Q

What is re-entry

A

When myocytes have variable refractory periods (due to high vagal tone) an impulse experienced an area of uni-directional block will be taken over by a passing electrical impule which will start to spread backwards, causing ‘eddie’ like areas of electrical flow

20
Q

What is the significance of atrial fibrillation?

A
  • CF. SA, AF IN HORSES CAN BE SPONTANEOUS AND NOT PATHOLOGICAL
  • atrial contraction only acocunts for 15% ventricular filling so not important at rest
  • CO only affected at exercise so intolerance only seen during periods of intense activity
  • in many horses can be an incidental finding 9eg. breeding horses, hackers, dressage)
  • can be paroxysmal or persistent (vets unlikely to see paroxysmal cases)
21
Q

Clinical signs of AF?

A
  • no clinical signs
  • exercise intolerance - poor performance or reluctance
  • irregularly irregular cardiac rhytm
  • no S4
  • variable pulse quality
  • variable intensity of heart sounds
  • EIPH due to pulmonary hypertension
22
Q

How can AF be distinguished from AV block?

A

AF S1,2,3 NO S4

AV block S4 with NO S1,2,3

23
Q

How does the presentation of AF differ in horse cf. dogs?

A

Dogs ^ HR -> jumbled chaotic sounding rhythm

- no ^ HR in horses

24
Q

How does AF appear on ECG?

A
  • random electrical activity in atria -> no P waves, f waves, random AV depolarisation, irregularly irregular R-R, NORMAL HR
25
Q

Tx of AF in horses?

A

> establish underlying heart disease
- AF usually spontaneous effect of heart failure (not cause)
check for signs of HF
- tachycardia >60bpm
- valve regurge esp. AV
- venous distension
- oedema
if incidental finding, no Tx necessary
if exercise intolerant: Quinidine (antiarrhythmogenic)
if in heart failure: palliative furosemide, digoxin, ACEI

26
Q

How does quinidine sulphate work? are there any side effects?

A
  • prolongs effective refractory period (slows fast Na+ channels)
  • promotes electrical homogeneity in the atria
    > crude side effects unwanted, especially tachycardia and hypotension -> ventricular hypoxia
  • vagolytic -> supra-ventricular tachycardia
  • a antagonist -> hypotension
  • neg inotrope -> v CO
  • ventricular arrhythmias
  • potentially fatal arrhythmias (monitor ECG carefully)
    -GI ulcers, D+, colic
  • nasal oedema
  • penile extrusion
  • ataxia
27
Q

What should be given alongside quinidine to prevent some side effects?

A
  • digoxin (delays ventricular tachycardia)
28
Q

Quinidine sulphate protocol?

A

10g/450kg every 2 hours until..

  • conversion
  • > 6 doses
  • colic, D+
  • QRS widened by more than 25%
  • tachycardia >100bpm
29
Q

How should quinidine induced hypotension be treated or managed?

A
  • due to a adrenergic antagonism
  • keep horse calm
  • no exercise
  • IV fluids
30
Q

When is emergency Tx required for rapid suprecentricular tachycardia as a side effect to quinidine?

A

ventricular rate >100bpm

  • give digoxin to slow conduction thorugh AV node
  • bicarbonate ^ protein binding and v effective plasma concentration
  • IV fluids to support blood pressure
31
Q

What drugs should be used to treat quinidine induced ventricular arrhythmias?

A
  • magnesium sulphate
  • propranolol
  • lignocaine
    > NOT procainamide (similar mechanism of action as quinidine)
32
Q

How should horses be managed after quinidine Tx?

A
  • 24 hour ECG normal before return to training
  • if supraventricular premature depolarisation present
    > rest? corticosteroids? digoxin? Don’t know
33
Q

What is prognosis of AF following quinidine tx related to?

A
  • prognosis proportional to time spent in AF before conversion (<6 months - worth treating??)
  • underlying cardiac disease (NB: AF is a result of heart failure NOT A CAUSE)
34
Q

What is an APC and When are APCs considered normal?

A 
> atrial premature complex
- abnormal P with normal QRS  
> non-conducted APC
- abnormal P with no QRS
* normal at rest 
* abnormal at exercise
35
Q

How is a VPC identified? What types exist?

A 
No P followed by abnormal QRS 
- uniform if constant QRS waveform
- multiform is variable QRS waveform 
< 4 in succession = isolated
> 4 in succession = supraventricular/ventricular tachycardia (SVT/VT)
36
Q

Do APCs require specific anti-arrhythmic tx?

A

No because ventricular rate not increased usually

  • investigate and treat underlying cause
  • if idiopathic give corticosteroids and rest (in case inflammatory cause)
37
Q

When is supraventricular tachycardia most commonly seen?

A

rarely except with quinidine toxicity

38
Q

Should ventricular premature complexes be investigated and treated?

A

YES! treat underlying cause

  • idiopathic: corticosteroids and rest
  • ventricular arrhythmias more likely to progress to fatal arrhythmias
  • establish when it occours (at rest and not at exercise, at rest and during exercise, at exercise only?)
39
Q

When should anti-arrhythmic therapy be considered for ventricular tachycardia?

A
  • clinical singns of low CO
  • ventricular rate >100bpm
  • polymorphic
  • R on T phenomenon
40
Q

What anti-arrhythmics can be used to treat ventricular arrhythmias?

A

> procainamide (1st choice in conscious horses)
quinidine gluconate (not in UK, USA only)
lignocaine (seizures, 1st choice in anaesthesia)
propranolol (rarely effective)
magnesium sulphate (Ca channel blocker, readily available, cheap, variable efficacy)

41
Q

What are the most important arrhythmias to identify?

A

2* AV block and AF

Cardiovascular (11 decks)

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