Arrhythmias in Large Animals Flashcards

(53 cards)

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
2nd degree atrioventricular block
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
3rd degree atrioventricular block
always pathological complete block of conduction (dissociation) due to pathology at the AV node very slow ventricular rate, syncope, weakness
27
2nd degree atrioventricular block - ECG appearance
``` 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
atrial fibrilation
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
atrial fibrilation - significance
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
atrial fibrilation - clinical signs
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
paroxysmal atrial fibrilation
Atrial fibrillation may spontaneously resolve minutes-hours duration exercise-induced, mainly immediately post strenuous exercise horses and cattle with gastrointestinal disease
32
atrial fibrillation - ECG appearance
``` Random electrical activity in atria no P wave f waves random depolarisation of AV node irregularly irregular R-R note: rate is normal ```
33
atrial fibrillation - treatment
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
quinidine sulphate
``` 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
quinidine treatment - protocol
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
Quinidine sulphate - side-effects
``` Hypotension Decreased cardiac output Supraventricular tachycardia Ventricular arrhythmias Potentially fatal arrhythmias ```
37
quinidine - induced hypotension
due to alpha adrenergic antagonism – Keep the horse calm
38
rapid supraventricular tachycardia
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
quinidine - induced ventricular arrythmias - treatment
``` Proarrhythmic effect Magnesium sulphate Propanolol Lignocaine NOT PROCAINAMIDE (same as quinidine) ```
40
quinidine sulphate - extra-cardiac side effects
``` diarrhoea colic flatulence nasal oedema penile protrusion ataxia usually dose dependent GI effects are the main cause of treatment failure ```
41
prognosis
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
normal QRS with abnormal P
APC (atrial premature complexes)
43
abnormal P with no QRS
non-conducted APC
44
abnormal QRS with no P
VPC (ventricular premature complexes)
45
VPC with constant QRS waveform
uniform
46
VPC with variable QRS waveform
multiform
47
< 4 in succession
Isolated APC or VPC
48
> 4 in succession
``` Supraventricular tachycardia (SVT) Ventricular tachycardia (VT) ```
49
APC's
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
supraventricular tachycardia
rare except with quinidine toxicity
51
Ventricular premature complexes (VPC) and VT
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
ventricular tachycardia
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
Anti-arrhythmics used to treat ventricular arrhythmias
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