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Equine arrhythmias Flashcards

1
Q

How can myocardial disease be broadly classified?

A

PRIMARY: infectious, nutritional, others, idiopathic

SECONDARY (most commonly)

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2
Q

List secondary causes of myocardial disease in LA - 6

A 
Endotoxaemia
Electrolyte disturbances - K, Ca, Mg
Acid-base disturbances
Hypoxia
Catecholamines
Vagally-induced
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3
Q

List primary causes of myocardial disease in LA

A

INFECTIOUS: viral, bacterial, parasitive
NUTRITIONAL
OTHERS: cardiomyopathy, neoplasia, immune-mediated, toxic

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4
Q

T/F: any infectious agent that has a blood bourne phase can cause myocardial damage

A

True - probably cause ischaemia and fibrosis - acts as an irritant focus and trigger arrhythmias

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5
Q

List viral causes of primary myocardititis - 6

A 
EIV
EHV
EVA
FMDV
AHS (african horse sickness)
EIA
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6
Q

List bacterial causes of primary myocardititis - 6

A 
S. aureus
Clostridium chauvoei
Mycobacterium spp.
Strep. equi subspp equi
Actinobacillus spp
Rhodococcus equi
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7
Q

List parasitic causes of primary myocarditis

A 
Strongyles
Onchocerca
Toxoplasma
Cysticerca
Sarcocysta
Borrellia burgdorferi (Lyme's disease)
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8
Q

Outline white muscle disease (WMD) - 2 different forms

A

Ruminants, less commonly horses grazing Se deficient patstures. Oxidative (ROS) injury to mm.

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.

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9
Q

Diagnosis - WMD

A

Whole blood Se concentrations

Glutathione peroxidase concentrations

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10
Q

Treatment - WMD

A

Vitamin E and Se as an IM injection

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11
Q

PME - WMD

A

Pale streaky mm

Degeneration and fibrosis of muscles

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12
Q

Outline cardiomyopathy in cattle

A

Inherited - linked to red Holstein gene in Holstein-Friesians. Associated with curly hair coat in polled Herefords.

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13
Q

Outline cardiomyopathy in horses

A

Occurs sporadically, causes unknwon

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14
Q

Outline cardiac neoplasia - cattle

A

Right atrial lesions extending into the remainder of the heart and heart base area. Adult form enzootic bovine leukosis

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15
Q

Outline cardiac neoplasia - horses

A

Lymphoma and other neoplastic conditions occur sporadically

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16
Q

Outline inflammatory lesions and fibrosis as a primary myocardial pathology

A

Focal or generalised

Aetiology unknown - perhaps immune-mediated?

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17
Q

What toxins can induce primary cardiomyopathy

A

Halothane (GA gas, now largely replaced with isoflurane)

ABs - erythromycin, ionophores (coccidiostats)

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18
Q

Outline how catecholamines cause secondary myocardial disease and dysfunction

A

Horses with severe GIT disease and upper airway obstruction during exercise may develop arrhythmias. Fairly common and often unrecognised (ICU patients)

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19
Q

What is the aim of diagnostic investigations?

How? 5

A

Confirm that myocardial disease/dysfunction is present
Identify specific or underlying causes.

ACHIEVED BY:
Clinical history and exam
Clinical pathology
Echo (rule out murmurs)
ECG
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20
Q

What may be conducted as part of the clinical pathology work up of diagnosis? 8

A 
Haematology and general blood biochemistry
Acid-base and electrolyte status
Se and glutathione peroxidase 
Viral serology
Blood bacterial culture
Cardiac troponin 1
Cardiac isoenzymes (CK and LDH)
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21
Q

When do you do echo?

A

Only if murmur is concurrently present.
Identifies global myocardial dysfunction
But doesn’t rule out concurrent: valvular disease or congenital heart disease

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22
Q

Outline Purkinje fibre system in LA

A

extensive - branches from endocardium to epicardium: depolarising wave conducted mainly by 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 doesn’t accurately reflect the shape and size of the ventricular myocardium.

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23
Q

What is the conventional position for ECG?

A

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)

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24
Q

Describe QRS in horses

A

Negative

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25
Describe T wave in horses
positive, negative or neutral (with positive and negative elements). Very variable between horses and sometimes between beats in an individual horse - doesn't indicate a myocardial problem like it would in SA).
26
What is radiotelemetric ECG?
ECG attached to horse with surface contact electrodes. ECG sent to distant monitor by radio. Instantaneous USES: exercise, ICU
27
What is ambulatory ECG? Uses?
ECG is recorded digitally or onto magnetic tape on small monitor for up to 24 hours - subsequently analysed by dedicated computer system. Horse can be left unattended, removing environmental influences. Provides more accurate indication of the frequency of arrhythmias than standard ECG - assess prognosis, follow efficacy of therapy.
28
What are the different AV blocks?
1st degree - physiological 2nd degree - physiological 3rd degree - always pathological
29
Outline 1st degree (physiological) AV block
Delayed conduction through AVN | Slow, slightly variable HR
30
Outline 2nd degree (physiological) AV block
intermittent block of conduction through the AVN (high vagal tone) Slow HR with pauses at regular intervlas Isolated 4th heart sound heard before block Isolated, normally-timed P waves on ECG ECG: P waves without associated QRST P waves normal shape P waves occur at expected time May have more than 1 blocked P wave (usually no more than 1 in 3) Frequency of block varies (1 in 3 upwards)
31
Outline 3rd degree AV block
complete block of conduction (dissociation) due to pathology of the AVN very slow ventricular rate, syncope, weakness
32
Describe AF
Commonest pathological dysrhythmia
33
What does initiation of AF require? 3
Large atrial mass Slow SAN rate Variable refractory periods
34
When might you get variable refractory periods?
High vagal tone Myocardial disease, Electrolyte or pH change Allows 're-entry' to occur
35
How does AF in dogs differ?
In all dogs, except giant breeds, AF usually occurs secondary to ventricular dilation and overload (this CAN happen in the horse but AF is more commonly spontaneous)
36
What is the significance of AF? 5
- Atrial contraction contributes to approx. 15% ventricular filling. The loss of this in AF means CO is affected only at exercise. - In horses with no other cardiac disease, AF only causes signs of exercise intolerance if the horse is engaged in vigorous exercise. - In many horses it is an incidental finding - Frequently spontaneous and not due to cardiac disease (contrasts with SA) - May be paroxysmal or peristent
37
Clinical signs - AF - 5
- Depending on use (none to exercise intolerance, poor performance, reluctance to exercise) - Irregularly-irregular cardiac rhythm (run of beats variable with variable pauses, no 4th heart sounds but S1-3 heard. No compensatory increase in HR unlike dogs) - Variable pulse quality - Variable intensity of heart sounds - EIPH
38
Describe paroxysmal AF
AF may spontaneously resolve (i.e. it is transient) Minutes - hours Exercise-induced (mainly immediately post strenuous exercise) Horses and cattle with GIT disease
39
AF appearance on an ECG - 5
- No P wave - F waves (recording of Eddy currents cycling through the atria. They are fast, variable intensity depolarisations) - Random depolarisation of AVN - Irregularly irregular AVN - Rate is NORMAL
40
AF - first steps in treatment principles
Establish if underlying heart disease is present (AF usually spontaneous and AF is an effect, not cause, of HF) CHECK FOR SIGNS OF HF: resting tachycardia (>60bpm), valve regurgitation (esp mitral or tricuspid), venous distension, oedema.
41
AF - treatment: 1. ) Incidental finding 2. ) Competition horse with exercise intolerance 3. ) Heart failure
1. ) No treatment 2. ) Quinidine sulphate (an anti-arrhythmic) 3. ) Palliative furosemide, digoxin and ACEI
42
How does quinidine sulphate work?
PROLONGS THE EFFECTIVE REFRACTORY PERIOD: class 1a anti-dysrhythmic, slows Na+ fast channels, promotes electrical homogeneity in the atria.
43
What are the unwanted effects of quinidine sulphate treatment?
Vagolytic (ventricular tachycardia), >100bpm Alpha-adrenergic antagonist (hypotension) Negative inotrope (decreases CO) GIT ulceration Colic, diarrhoea QRS widened by 25% The first 2 of these are a bad combination as they are likely to give you ventricular ischaemia and death.
44
Outline quinidine sulphate treatment protocol
Pre-treat with digoxin (5mg/450kg) on day -2 to +1 Don't remove from box during treatment Then quinidine sulpate by stomach tube (10g/450kg) every 2 hours until conversion or stop if 6 doses and no conversion OR signs of toxicity appear
45
Cardiovascular side effects of quinidine sulphate - 5
``` Hypotension Decreased CO Supraventricular tachycardia Ventricular arrhythmias Potentially fatal arrhythmias ```
46
Outlien quinidine-induced hypotension
Due to alpha-adrenergic antagonism: Keep horse calm Don't allow any exercise following Tx IV fluids possibly
47
Outline quinidine-induced supraventricular tachycardia
DUE TO VAGOLYTIC EFFECT: Emergency Tx required if ventricular rate >100bpm Digoxin to slow conduction through AVN Bicarbonate: increases protein binding to reduce effective plasma concentration IV fluids: support BP
48
Outline quinidine-indued ventricular arrhythmias
``` Due to proarrhythmic effect Magnesium sulphate Propanolol Lignocaine NOT procainamide (similar mechanism of actuion s quindine) ```
49
What are extra-cardiac side effects of quinidine sulphate?
``` Diarrhoea Colic Flatulence Nasal oedema Penile protrusion Ataxia Usually dose-dependent but can be acute and not dose-dependent. GIT effects = main cause of Tx failure ```
50
Management of AF after Tx
Normal 24 hour ECG - then return to training | Supraventricular premature depolarisations - rest, corticosteroids or digoxin.
51
Prognosis - AF
Depends on underlying cardiac disease DURATION PRIOR TO TREATMENT: < 3 months - recurrence rate of 15% > 3 months - recurrence rate of 60% and higher prevalence of side effects associated with prolonged duration of treatment Don't treat horses with AF > 6 months duration (?)
52
What characterises an APC?
normal QRS with abnormal P
53
What characterises a non-conducted APC?
abnormal P with no QRS
54
What characterises a VPC?
abnormal QRS with no P
55
What if there are <4 APCs or VPCs in succession?
They are considered to be isolated APCs or VPCs?
56
What if there are > 4 APCs or VPCs in succession?
It is known as: supraventricular tachycadraia (SVT) OR ventricular tachycardia (VT)
57
What happens in an atrial premature complex (APC)?
APC may or may not be conducted into ventricle because the AVN may be refractory when the P wave arrives.
58
Tx - APCs?
Rarely require specific anti-arrhythmic therapy because ventricular rate is not increased. Investigate and treat underlying cause Idiopathic cases - corticosteroids and rest are used in the hope that this may be effective in a sub-population with an inflammatory pathogenesis (viral?)
59
When may SVT occur?
Rarely occurs except in association with quinidine toxicity.
60
T/F: Ventricular arrhythmias are more likely to progress into fatal arrhythmias
True
61
What should you do if you detect an arrhythmia?
Establish if arrhythmia occurs: at rest only at rest and during exercise during exercise only
62
What should you do with ventricular tachycardia (VT)?
Assess the likelihood that the rhythm will destabilise to ventricular fibrillation.
63
When should you consider anti-arrhythmic therapy for VT? 4
- CSs of low CO output - Ventricular rate is > 100bpm - Polymorphic (2 different types of ectopic complex) - R-on-T phenomenon (R waves occuring immediately after the preceding T wave)
64
Outline anti-arrhythmics used to treat ventricular arrhythmias - 5
PROCAINAMIDE - 1st choice for conscious horse QUNIDINE GLUCONATE - USA only LIGNOCAINE - seizures, 1st choice if under anaesthesia PROPANOLOL - rarely effective in horses MAGNESIUM SULPHATE = physiological calcium channel blocker) - readily available, inexpensive, variable efficacy
65
T/F: arrhythmias often develop in association with non-cardiac disease
True - especially GIT disease (pH and electrolyte disturbances)
66
What are the most important arrythmias to ID?
2nd degree AV block | AF
67
What are anti-arrhythmic agents used for? 2
In some ventricular arrhythmias and AF.
68
Outline quinidine sulphate pharmacology
Peak concentration = 131 minutes Rapid plasma to tissue distribution Elimination 1/2 life = 3.3 -12.5 hours (mean = 6.6 hours) Therapeutic plasma concentrations = 2-5mg/ml Toxic plasma concentration = >5mg/ml

Cardiovascular (22 decks)

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