Atrial Fibrillation & Atrial Flutter
Atrial fibrillation is the commonest pathological dysrhythmia.
Atrial Fibrillation (AF): Occurs when many ectopic waves of depolarisation spread throughout the atria. While the atria fail to contract some of the disorganised depolarisation waves are conducted through the AV node, reaching the ventricles. As a result there is an irregular ventricular response. It can occur in absence of structural heart disease (primary/lone AF), or secondary to underlying cardiac disease. In animals with underlying heart disease, the ventricular response rate is usually elevated due to sympathetic predominance. In animals with primary 'lone' AF, ventricular response rate may be normal or only mildly elevated due to parasympathetic influence on the AV node.
Atrial Flutter: is similar to atrial fibrillation, but has sudden onset and termination and is therefore a transient arrhythmia. It may be seen as a precursor to atrial fibrillation. Ventricular response rate is variable, depending on the degree of physiological AV block.
Atrial fibrillation can occur in all species when there is atrial dilation secondary to other cardiac lesions.
This may be an incidental finding on clinical examination, especially if the horse is not used for highly athletic activities. The atrial contraction only contributes to around 15% of the ventricular filling, so signs of atrial fibrillation are only seen during vigorous exercise. If the horse is raced, hunted or an eventer, then signs may occur during exercise and include exercise intolerance, reluctance to exercise or a poor performance during exercise. It can be associated with exercise induced pulmonary haemorrhage, so this can be a clinical sign of the condition.
Signs generally relate to the underlying disease process, which in cows can range from gastrointestinal diseases such as a left-displaced abomasum, to uterine torsion.
Patients with primary atrial fibrillation are usually asymptomatic. However, there may be signs of haemodynamic compromise due to the rapid heart rate and a loss of atrial contribution to ventricular filling; which would usually account for up to 20% of cardiac output. This most commonly manifests as exercise intolerance.
Other signs are generally related to the underlying disease process or congestive heart failure. There may be a history of coughing, dyspnoea, tachypnoea, exercise intolerance, episodes of syncope.
History and physical examination may provide a presumptive diagnosis for this condition. Findings on clinical examination will include an irregularly irregular heart rhythm on auscultation with no fourth heart sound. The heart will sound 'chaotic'. There may also be a variable pulse quality and a variable intensity of heart sounds.
- No P waves
- Regular saw-tooth deflections of baseline
- Ventricular rate variable
- Sudden onset and termination
- No P waves
- Coarse oscillation of the baseline (F-waves)
- R-R interval irregular and chaotic
Echocardiography is recommended to determine the type and severity of any underlying structural heart disease. Mild left atrial enlargement may accompany the haemodynamic alterations imposed by the arrythmia.
In horses where the condition is found without other concurrent heart disease, treatment is with the drug quinidine sulphate. The necessity for this depends on the requirement of the horse to perform work, as horses can be retired or used as broodmares and can live a normal life with the condition.
Quinidine sulfate acts by prolonging the effective refractory period. The horse should be given quinidine sulphate concurrently with digoxin, which will have been started two days prior to commencing quinidine sulphate. Quinidine sulphate should be given every two hours by stomach tube until conversion to sinus rhythm, or until six doses have been given. There are some severe side effects which can occur with this treatment and they include ventricular tachycardia, colic, diarrhoea and hypotension.
There is a greater success with conversion in young horses and when conversion is attempted shortly following the onset of the arrythmia. If the arrythmia has been present for more than 4 months, therapeutic success is much less common and there is a higher recurrence rate.
Horses can also develop atrial fibrillation secondary to cardiac disease, such as mitral valve insufficiency, tricuspid valve insufficiency, or any acquired or congenital disease leading to atrial hypertrophy. Horses will usually develop congestive heart failure and have a resting tachycardia. These underlying conditions should be diagnosed and the congestive heart failure treated with diuretics and inotropes. These horses will have a poor prognosis for return to function and treatment is mainly to slow progression of disease.
Cattle are not usually treated with an antiarrythmic drug as the heart will revert to sinus rhythm following the correction of the underlying abdominal disorder.
The aim is to control heart rate to a level that is less likely to result in haemodynamic compromise (rarely conversion to normal sinus rhythm).
In dogs with AF secondary to structural heart disease, Digoxin is usually the first line of therapy. Digoxin slows conduction through the AV node. The goal is to keep the heart rate <150 bpm. Dogs should be re-assessed 5-7 days after starting Digoxin and serum Digoxin levels should be measured >8 hours post-administration. If the heart rate remains high and the serum Digoxin level is within target range, a calcium channel blocker such as Diltiazem can be added. If compliance is good and finances are not limited, there may be additional benefit of an ACE inhibitor, Spironolactone and Omega-3 fatty acids. These help reverse structural remodelling and modulate pro-inflammatory cytokines that perpetuate arrhythmias.
In dogs with primary 'lone' AF, Amioderone should be administered if electric cardioversion is an option. Amioderone increases the chances of remaining in sinus rhythm following cardioversion and some dogs may spontaneously convert to sinus rhythm with Amioderone alone. If electrical cardioversion is not an option, and the rate is >150bpm, then rate control is appropriate, using beta-blockers or Diltiazem. It is important to monitor these dogs for the development of structural cardiac disease, as AF may be seen in the occult phase of Dilated Cardiomyopathy.
In cats, atrial fibrillation usually indicates advanced structural heart disease with atrial dilation and is associated with a poor prognosis. The first-line drug of choice is Diltiazem.
In rabbits, Digoxin has been used anecdotally to slow the heart rate.
In all cases with concurrent severe heart disease and possibly congestive heart failure, efforts to control the disease by using diuretics such as Furosemide can be helpful in improving clinical signs. Calcium channel blockers and beta-blockers, both negative inotropes, should be used carefully in animals with myocardial failure (systolic dysfunction).
In horses, the likelihood of the rhythm remaining converted after the treatment depends on the duration of the condition before treatment; if it was diagnosed less than three months before treatment then it is more likely the treatment will be effective. Prognosis is poor if atrial fibrillation is caused by an underlying heart condition.
In cattle, prognosis depends on the underlying gastrointestinal condition and the treatment options chosen by the farmer.
In small animals, cases with primary atrial fibrillation and normal echocardiographic findings have a good prognosis. Animals with secondary atrial fibrillation associated with severe heart disease have a guarded to poor prognosis.
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