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20 Cards in this Set
- Front
- Back
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List 5 primary causes of equine arrhythmias.
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1. Infectious causes
2. Nutritional causes 3. Idiopathic 4. Toxic causes 5. Cardiomyopathies |
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List five secondary causes of equine arrhythmias. Note that secondary causes are the most common causes!
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1. Endotoxaemia
2. Acid-base/electrolyte disturbances 3. Hypoxia 4. Catecholamine induced 5. Vagally induced |
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What nutritional myopathy may cause arrhythmias (more of a problem in farm animals than horses)?
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White muscle disease. Caused by animals grazing selenium deficient pastures. Leads to oxidative damage of muscle due to a lack of peroxidase activity.
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How do you diagnose and treat white muscle disease?
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Dx: Blood selenium or blood glutathione peroxidase concentrations.
Tx: IM injection of Vit E and Selenium |
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Which toxins may be associated with arrhythmias in horses?
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Halothane, ionophores, erythromycin
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How do you work up an equine arrhythmia case?
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Take a thorough history and do a Physical exam.
Do Clin path. Bloods for biochem and haematology, acid base and electrolyte status, look for cardiac isoenzymes such as CK and LDH as they are indicators of myocardial cell death. Echo is only useful if murmurs are present. Good for checking the valves and for the presence of congenital defects. ECG is very important for diagnosis of arrhythmias! |
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How does the purkinje fibre system of herbivores differ from those of carnivores and how does this affect an ECG trace?
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In herbivores, the purkinje fibre system is much more extensive. Its spreads from the endocardium right out to the epicardium. There is less cell-cell spread than there is in carnivores.
Because of this, the waves produced in an ECG trace are not influenced by myocardial mass. Thus, the QRS size and duration does NOT accurately reflect the shape and size of the ventricular myocardium as it can in small animals. |
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Describe the morphology of the ECG waves in normal horses.
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The P wave is double peaked
QRS is small T wave is variable |
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Describe first degree AV block.
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This is a normal physiological response. It means there is delayed conductance through the AV node. The horse will have a slow and variable heart rate.
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Describe second degree AV block.
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This may also be a physiological response to high vagal tone. Can be normal in fit horses when theyre at rest. Will see intermittent block through the AV node, ie: some P waves that are not followed by QRS complexes. The block will occur at regular intervals and will always disappear when the horse is exercising.
Note: This is ABNORMAL when it occurs at heart rates > 60bpm! |
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Describe third degree AV block.
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This is always pathological. It means there is complete block through the AV node due to pathology at the node. There will be a slow ventricular rate, syncope and weakness.
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Why are horses anatomically and physiologically predisposed to developing spontaneous atrial fibrillation?
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Because they have large atrial masses,
they have naturally slow SA nodes (high vagal tone), and they have variable refractory periods. |
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Compare and contrast A-fib in small animals and in horses.
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In small animals, A-fib is caused by cardiac dz and can cause heart failure.
In horses, A-fib is commonly spontaneous, not occurring due to cardiac dz, and it does not cause heart failure either. |
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What is the significance of A-fib in horses?
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Atrial contraction in the horse contributes to 15% of ventricular filling. In fibrillation this 15% is lost. In a resting horse this isnt really a problem, but in an exercising horse it will be! It will cause exercise intolerance!
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What will an ECG trace look like from a horse with A-fib?
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There will be no P waves, there will be F waves, there will be random AV node depolarizations leading to irregularly irregular R-R intervals.
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How do you treat A-fib in horses?
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First check to see if it is spontaneous or due to underlying heart disease. If it is an incidental finding then theres no need to treat. If it is causing decreased performance, the most common treatment is Quinidine sulphate PO.
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How does Quinidine sulphate work and what are some unwanted side effects of its use?
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It prolongs the refractory period in the atria by slowing down the fast Na channels. It therefore promotes electrical homogeneity of the atria.
Side effects include: ventricular tachycardia, hypotension, decreased CO, and GI ulceration. |
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What precautions should you take to decrease the adverse effect of Quinidine treatment?
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Pretreat with Digoxin to decrease ventricular tachycardia, do not move from the box during treatment, be vigilant about screening for side effects, monitor ECG continuously during treatment and stop treatment immediately if needed.
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Describe the significance of atrial premature complexes.
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These are common in fit horses post exercise. They rarely require anti-arrhythmics because they do not cause ventricular tachycardia. Most are idiopathic. Treat with rest +/- corticosteroids.
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When are you most likely to find ventricular premature complexes in a horse?
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If it has endotoxaemia or an acid-base/electrolyte imbalance. Always look for and treat the underlying cause!
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