Atrial fibrillation is a relatively common tachyarrhythmia among canines with serious cardiac disease. It is very rare in feline patients, but when seen it tends to result from severe end stage heart disease. Among dogs with atrial fibrillation, there is a small subset without concomitant structural heart disease. The ventricular rate in these dogs tends to be far lower than the majority of dogs with atrial fibrillation. This subset is mainly composed of certain giant and large breed dogs and they are said to have "lone" atrial fibrillation. The remainder of this discussion and the lecture will focus on the more common and challenging clinical situation--dogs with rapid atrial fibrillation and significant structural and/or functional cardiac disease. These dogs tend to have significant cardiac disease that has led to atrial dilation among other changes. When atrial fibrillation is first noted in these patients the underlying cardiac disease will likely have already been present for a significant time. While many of these patients will be known to have had heart disease due to murmurs, radiographic changes or clinical signs noted on prior visits, atrial fibrillation can be the first clinical abnormality noted in some animals. This happens not infrequently in canine patients with dilated cardiomyopathy or certain congenital cardiac abnormalities, which can be associated with a very quiet or no murmur and speaks to the importance of a careful auscultation.
While untreated atrial fibrillation auscults as a rapid and chaotic rhythm, it is not unique in sounding this way and an electrocardiograph is necessary to differentiate atrial fibrillation from other tachyarrhythmias. The defining electrocardiographic characteristics of untreated atrial fibrillation include an irregular tachycardia of supraventricular origin with no discernible P waves (the exception to the tachycardia being the less common slower variety described above). Because the tachycardia is of supraventricular origin the QRS complexes generally are of normal appearance (with the rare exception being a patient who has both atrial fibrillation and a ventricular conduction disturbance such as a bundle branch block). Keep in mind that patients with atrial fibrillation commonly have ventricular arrhythmias (e.g., VPCs), but the underlying rhythm is still atrial fibrillation if the above conditions are met. Another ECG finding often seen with atrial fibrillation is the fine, irregular baseline undulations known as f waves. These f waves are not always seen and their absence, in the setting of an irregular supraventricular tachycardia with no P waves, does not change the ECG interpretation.
The hemodynamic deficits associated with atrial fibrillation are related to the loss of normal atrioventricular coordination and the rapid ventricular rate. In a normal sinus rhythm, there is a well-timed and efficient contraction of the atria that occurs just prior to ventricular systole. This atrial contraction, also called an atrial "kick", can provide twenty-five percent of ventricular filling at a normal heart rate. As ventricles can only deliver that which they receive, the atrial kick contributes significantly to overall cardiac output. In atrial fibrillation, there is complete absence of coordinated atrial contraction. Another major reason for the hemodynamic insult of atrial fibrillation is the rapid, irregular ventricular rate that occurs in response to the even more rapid and chaotic atrial impulses. The rapid heart rate causes shortened periods of diastole which further limits ventricular filling. These combined effects decrease cardiac output which can contribute to or exacerbate heart failure. Moreover, the rapid ventricular rhythm increases myocardial oxygen demands, while limiting myocardial oxygen supply due to the abbreviated and irregular periods of diastole. This imbalance can lead to further clinical deterioration over time.
Thankfully, the ventricle does not "see" all of the supraventricular impulses because the AV node has limits on how many impulses it can conduct per minute due to relative and absolute periods of refractoriness. The relatively slow conduction of the AV node and these refractory periods create an electrical bottleneck which helps to limit the number of impulses the ventricle receives during atrial fibrillation. Much of our treatment of this and other supraventricular tachycardias is designed to pharmacologically manipulate the AV node to further limit the degree of ventricular exposure to supraventricular impulses. The resultant desired decrease in heart rate is termed a decrease in the ventricular response rate, as hundreds of impulses a minute will continue to arrive at the AV node. This decrease in the ventricular response rate will help to mitigate the decrease in cardiac output caused by the arrhythmia. A return to a sinus rhythm with medications or electrical cardioversion might be ideal, but long-term and safe conversion has been challenging in small animals. With this information as background, the lecture will briefly describe proposed mechanisms of atrial fibrillation and then focus the majority of the lecture on treatment strategies for various clinical scenarios--including pharmaceuticals and cardioversion.