Arrhythmias in Large Animals Flashcards

1
Q

Pathogenesis of myocardial disease

and dysfunction in large animals - primary

A
Infectious causes
Nutritional
cardiomyopathy
neoplasia
immune mediated
toxic
Idiopathic
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2
Q

primary myocarditis - viral

A

equine influenza, equine herpes virus, equine viral arteritis
foot and mouth disease, african horse sickness, equine infectious anaemia

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3
Q

Pathogenesis of myocardial disease

and dysfunction in large animals - secondary

A
most common 
Endotoxaemia
Electrolyte disturbances
Acid-base disturbances
Hypoxia
Catecholamine-induced
Vagally-induced
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4
Q

primary myocarditis - bacterial

A

Staphylococcus aureus, Clostridium chauvoei, Mycobacterium spp.
Strep. equi subsp equi., Actinobacillus spp, Rhodococcus equi

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5
Q

primary myocarditis - parasitic

A

strongyles, onchocerca, toxoplasma, cysticerca, sarcocysta, Borrelia burgdorferi (Lyme’s disease)

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6
Q

Nutritional myodegeneration

A

(white muscle disease)
ruminants and, less commonly, horses grazing selenium deficient pastures
oxidative (ROS) injury to muscle

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7
Q

nutritional myodegeneration - cardiac form

A

Neonates
Acute or peracute
Severe debilitation or sudden death
Respiratory signs, arrhythmias

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8
Q

nutritional myodegeneration - skeletal muscle form

A

Slightly older animals
Weakness, stiffness and debilitation
Signs precipitated by stress

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9
Q

nutritional myodegeneration - diagnosis

A

whole blood selenium concentrations

glutathione peroxidase concentrations

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10
Q

nutritional myodegeneration - treatment

A

Vitamin E and selenium (i.m. injection)

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11
Q

nutritional myodegeneration - post mortem

A

pale streaky muscles

degeneration and fibrosis of muscles

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12
Q

cardiomyopathy

A

Horses - occurs sporadically, causes unknown

cattle - inherited, breed associated

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13
Q

cardiac neoplasia

A

Cattle - right atrial lesions extending into the remainder of the heart and heart base area, adult form enzootic bovine leukosis
Horses - lymphoma and other neoplastic conditions occur sporadically

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14
Q

inflammatory lesions + fibrosis

A

focal or generalised
aetiology unknown
immune-mediated?

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15
Q

toxins

A

halothane (not used in the UK)

antibiotics

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16
Q

secondary myocardial disease + dysfunction

A
Endotoxaemia
Hypoxia
Electrolytes– potassium, calcium, magnesium
Acidosis
Catecholamines
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17
Q

clinical pathology

A
Haematology and general blood biochemistry (esp hepatic and renal)
Acid-base and electrolyte status
Selenium and glutathione peroxidase
Viral serology
Blood bacterial culture
Cardiac Troponin I
Cardiac isoenzymes
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18
Q

cardiac isoenzymes

A
creatine kinase (CK) and lactate dehydrogenase (LDH)
released into the circulation with myocardial cell death
indicators of myocarditis/myocardial necrosis
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19
Q

echocardiography

A

identifies global myocardial dysfunction – frequently unremarkable with focal myocardial disease (i.e. not all that useful)
rules out concurrent – valvular disease, congenital heart disease

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20
Q

electrocardiography in large animals

A

cardiac rate and rhythm only
in large animals the Purkinje fibre system is extensive - branches from endocardium to epicardium
depolarising wave is conducted mainly via Purkinje fibres with much less cell-cell spread through myocardium than in carnivores
this produces small wavefronts which are less influenced by myocardial mass than in SA
therefore, in contrast to SA, the QRS size and duration does not accurately reflect the shape and size of the ventricular myocardium

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21
Q

electrocardiography

A

Conventiona l– Base-apex lead -Positive electrode - left apex, Negative electrode - left base (in front of shoulder), Produces large P wave, clear QRST
Most horses resent the leads on their body less than on their limbs, Limb leads not used
Radiotelemetry
Ambulatory

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22
Q

radiotelemetric ECG

A

ECG monitor is attached to horse with surface contact electrodes
ECG is sent to a distant monitor by
radio – instantaneous, exercise, intensive care

23
Q

ambulatory ECG

A

ECG is recorded digitally or onto magnetic tape on small monitor for up to 24 hours
horse can be left unattended, removing environmental influences
provides more accurate indication of the frequency of arrhythmias than standard ECG

24
Q

1st degree atrioventricular block

A

physiological
delayed conduction through the AV node
slow, slightly variable heart rate

25
Q

2nd degree atrioventricular block

A

physiological
intermittent block of conduction through the AV node (high vagal tone)
slow heart rate with pauses at regular intervals
isolated fourth heart sound heard before block
isolated, normally-timed P waves on ECG

26
Q

3rd degree atrioventricular block

A

always pathological
complete block of conduction (dissociation)
due to pathology at the AV node
very slow ventricular rate, syncope, weakness

27
Q

2nd degree atrioventricular block - ECG appearance

A
P waves without associated QRST
P waves are normal shape 
P waves occur at expected time
may have more than 1 blocked P wave
frequency of block varies (1 in 3 upwards)
28
Q

atrial fibrilation

A

commonest pathological dysrhythmia
initiation of AF requires:
•large atrial mass, normal horses, atrial enlargement (valve regurgitation, VSD)
•slow SA node rate - high vagal tone
•variable refractory periods - effect of high vagal tone, also in myocardial disease, electrolyte/pH change, allows ‘re-entry’ to occur

29
Q

atrial fibrilation - significance

A

atrial contraction contributes approx 15% of ventricular filling; loss only affects cardiac output at exercise
horses with no other cardiac disease atrial fibrillation only causes signs of exercise intolerance if the animal is engaged in vigorous exercise in many types of horse it can be an incidental finding
in contrast to SA, equine AF is frequently spontaneous and not due to cardiac disease
AF may be paroxysmal but may be persistent

30
Q

atrial fibrilation - clinical signs

A

exercise intolerance/poor performance/reluctance to exercise
irregularly-irregular cardiac rhythm – runs of beats (variable) with variable pauses, no fourth heart sound
variable pulse quality
variable intensity of heart sounds
exercise-induced pulmonary haemorrhage

31
Q

paroxysmal atrial fibrilation

A

Atrial fibrillation may spontaneously resolve
minutes-hours duration
exercise-induced, mainly immediately post strenuous exercise
horses and cattle with gastrointestinal disease

32
Q

atrial fibrillation - ECG appearance

A
Random electrical activity in atria
no P wave
f waves
random depolarisation of AV node
irregularly irregular R-R
note: rate is normal
33
Q

atrial fibrillation - treatment

A

establish whether there is underlying heart disease
check for signs of heart failure
quinidine - if competing horse with exercise intolerance
heart failure - palliative, furosemide, digoxin, ACE inhibitors

34
Q

quinidine sulphate

A
prolongs effective refractory period– class 1a antidysrhythmic, slows Na+ fast channels, promotes electrical homogeneity in the atria
unwanted effects – vagolytic (ventricular tachycardia), alpha-adrenergic antagonist (hypotension),  negative inotrope (decreases cardiac output), gastrointestinal ulceration
35
Q

quinidine treatment - protocol

A

treat with digoxin (5mg/450 kg) on day -2 to +1 do not move from box during treatment
quinidine sulphate by stomach tube at 10g/450 kg every 2 hours until conversion occurs or stop if - 6 doses and no conversion, signs of toxicity appear

36
Q

Quinidine sulphate - side-effects

A
Hypotension 
Decreased cardiac output
Supraventricular tachycardia
Ventricular arrhythmias
Potentially fatal arrhythmias
37
Q

quinidine - induced hypotension

A

due to alpha adrenergic antagonism – Keep the horse calm

38
Q

rapid supraventricular tachycardia

A

Due to vagolytic effect
emergency treatment required if ventricular rate > 100 /min
digoxin to slow conduction through the AV node
bicarbonate to increase protein binding to reduce effective plasma concentration
intravenous fluids to support blood pressure

39
Q

quinidine - induced ventricular arrythmias - treatment

A
Proarrhythmic effect
Magnesium sulphate
Propanolol
Lignocaine 
NOT PROCAINAMIDE (same as quinidine)
40
Q

quinidine sulphate - extra-cardiac side effects

A
diarrhoea
colic
flatulence
nasal oedema
penile protrusion
ataxia
usually dose dependent
GI effects are the main cause of treatment failure
41
Q

prognosis

A

Depends on – underlying cardiac disease + duration prior to treatment
less than 3 months – recurrence rate 15%
greater than three months – recurrence rate 60% higher prevalence of side-effects associated with prolonged duration of treatment

42
Q

normal QRS with abnormal P

A

APC (atrial premature complexes)

43
Q

abnormal P with no QRS

A

non-conducted APC

44
Q

abnormal QRS with no P

A

VPC (ventricular premature complexes)

45
Q

VPC with constant QRS waveform

A

uniform

46
Q

VPC with variable QRS waveform

A

multiform

47
Q

< 4 in succession

A

Isolated APC or VPC

48
Q

> 4 in succession

A
Supraventricular tachycardia (SVT) 
Ventricular tachycardia (VT)
49
Q

APC’s

A

Rarely need specific anti-arrhythmic therapy as ventricular rate not incr
Investigate + treat underlying cause
Idiopathic - corticosteroids + rest are used for an inflammatory pathogenesis

50
Q

supraventricular tachycardia

A

rare except with quinidine toxicity

51
Q

Ventricular premature complexes (VPC) and VT

A

Investigate and treat underlying cause
idiopathic - corticosteroids + rest - anti-infl removes undelying cause
Ventricular arrhythmias more likely to progress into fatal arrhythmias
Establish if the arrhythmia occurs - At rest only + not during exercise, At rest + during exercise or During exercise only

52
Q

ventricular tachycardia

A

Assess likelihood that the rhythm will destabilise to ventricular fibrillation
Consider anti-arrhythmic therapy if – clinical signs of low cardiac output, Ventricular rate > 100, Polymorphic, R-on-t phenomenon

53
Q

Anti-arrhythmics used to treat ventricular arrhythmias

A

Procainamide – Drug of first choice in conscious horses
Quinidine gluconate – USA only, not UK
Lignocaine - Seizures, drug of first choice under anaesthesia
Propanolol – Rarely effective in horses
Magnesium sulphate (physiological calcium channel blocker) – Readily available + inexpensive but variable efficacy