Atrial Fibrillation

Pathophysiology

March 20, 2016

Introduction
Atrial Fibrillation, commonly known as A-Fib or AF, is the most common type of persistent cardiac arrhythmia. AF effects only 2% of the population under the age of 65, but 9% of those over the age of 65 (Centers for Disease Control and Prevention [CDC], 2015). Many other cardiac diseases are seen with AF, either as a cause, or as a result of the atrial fibrillation. Left untreated, AF can result in tachycardia that causes ventricular dysfunction and/or heart failure, along with a significantly increased risk of thromboembolic stroke. I recently conducted an interview with my father who has had AF for nearly 20 years and I compared my findings in the literature against his experiences with the disease.
Pathophysiology
Atrial Fibrillation is a supraventricular tachyarrthymia. In the heart, ventricular rate is controlled by the conduction and refractory properties of the AV node and the progression of wave fronts entering the AV node. Calcium channels are accountable for the major depolarizing current in AV nodal cells. Beta-adrenergic receptor stimulation boosts AV nodal conduction, whereas vagal stimulation impedes AV nodal conduction. Sympathetic activation and vagal withdrawal, as with illness or exertion, speeds up the ventricular rate. After each atrial excitation wave that depolarizes AV nodal tissue, those cells become refractory for a time, preventing subsequent impulses from propagating in the node (American College of Cardiology/American Heart Association/Heart Rhythm Society Task Force, 2014). Loss of atrial coordination will decrease cardiac output and cause contractions to be ineffective. This leads to a disruption in the flow of the blood through the ventricular chambers of the heart. As a result, blood often pools in the ventricles leading to the formation of clots. It is these clots that create the highest risk for an AF patient, peripheral thromboembolism or thromboembolic stroke.
There are several classifications of AF based on the cause and frequency or duration of the arrhythmia. AF can be classified as Paroxysmal, Persistent, Longstanding Persistent, Permanent. It is further classified as Valvular or Nonvalvular. Paroxysmal AF is self-limiting, in that it lasts less than 7 days and it stops on its own without intervention, however, it can return periodically. Persistent AF is continuous and lasts great then 7 days. Longstanding Persistent AF is diagnosed when the AF lasts greater than 1 year. Permanent AF is a designation given when the patient and their provider decide that they accept that the patient cannot achieve a sinus rhythm. Despite the term permanent, the patient and provider may decide that new treatments or changes in the patient’s condition warrant additional attempts at returning the patient to a sinus rhythm. Valvular AF are those patients with AF who have a form of mitral valve stenosis or a mitral valve repair, whereas Nonvalvular patients do not (AHA/ACC/HRS, 2014). Classification of a patient’s AF can be a fluid state, as over the course of a lifetime this can change. What was initially diagnosed as Paroxysmal AF may later be changed to Persistent or Permanent AF.
The causes of AF can be multifaceted, which makes it difficult to manage at times. It can result from a combination of less than optimal heart rate control, loss of coordinated atrial contractions, variations in ventricular filling, or activation of the sympathetic nervous system. It is often a co-morbidity with hypertension, hyperlipidemia, congestive heart failure, diabetes mellitus, chronic kidney disease, COPD, arthritis, anemia, and ischemic heart disease (Centers for Disease Control and Prevention, 2015).
Symptoms of AF vary greatly depending on the patient. Patients can be asymptomatic, but are more likely to experience fatigue, palpitations, hypotension, syncope, heart failure, and dyspnea, with fatigue being the most common. The diagnosis of AF is usually associated with an exacerbation of another heart disease, either because AF was a causative factor, or because it contributed to the exacerbation. Diagnosis is determined by an electrocardiogram (ECG), Holter monitoring, telemetry monitoring, implanted loop recorders, pacemakers, or electrophysiological study (AHA/ACC/HRS, 2014).
Literature Review
According to the National Institute for Health and Care Excellence [NICE], evidence-based practice for the diagnosis of AF calls for manual palpation of pulse for any person presenting with dyspnea, palpitations, dizziness, chest pain, or stroke (2014). An electrocardiogram (ECG) should be performed on all persons who have an irregular pulse if AF is suspected. In those people for whom electrocardiogram fails to show AF, but it is still suspected, a Holter monitor is recommended. Further diagnostic testing using transthoracic echocardiogram (TTE) is recommended in those patients suspected of having an underlying heart defect. Finally, if TTE is not possible, transoesophageal echocardiography (TOE) can be used to evaluate possible heart defects (NICE, 2014).
Rate control is the first and best treatment for AF, and should be used unless a reversible cause is found or if rhythm control is thought to be more appropriate. Rate control is usually achieved through a standard betablocker, such as metoprolol, or a ratelimiting calciumchannel blocker, such as amlodipine. Digoxin should be prescribed only for people with nonparoxysmal atrial fibrillation and only if they get are relatively inactive (NICE, 2014).
Rhythm control is used only if patients are still symptomatic after rate control is achieved, or if rate control medications have failed. Rhythm control is usually achieved with sodium channel blockers or potassium channel blockers.
Cardioversion is another treatment strategy for patients with AF. This can be achieved pharmacologically with one or several anti-arrhythmia medications, such as amiodarone, usually administered in a hospital setting. Electrical cardioversion is another option. It is also done in the hospital setting and involves giving the patient a low voltage shock to reset the heart rhythm. It is usually only recommended for those patients with AF that has persisted longer than 48 hours, or for those patients with a condition known as AF with Rapid Ventricular Rate (RVR), or a heart beat over 100 beats per minute (AHA/ACC/HRS, 2014).
Cardiac ablation of the AV node with subsequent pacemaker implantation is another possible treatment for patients with AF. It can he helpful for those with paroxysmal, persistent, or longstanding persistent AF, but since anti-coagulation therapy is necessary after ablation, it is not recommended on those patients for whom anti-coagulation therapy is contraindicated (AHA/ACC/HRS, 2014).
Atrial Fibrillation can be prevented only in some cases. Maintaining a healthy lifestyle and managing other cardiac diseases, such as hypertension and high cholesterol, can reduce your risk of AF (NICE, 2014). For those patients who already have AF, thromboembolism prevention is the priority in care. Peripheral thromboembolism or thromboembolic ischemic stroke are associated with increased risk of recurrent thromboemboli, severe disability, and death. Thromboembolic stroke risk increases 5 times for those patients with nonvalvular AF, and it increases 20 times for those patients with AF secondary to mitral stenosis (AHA/ACC/HRS, 2014). Anti-coagulation and anti-platelet drugs, along with controlling other risk factors for stroke such as hypertension and high cholesterol, are the most common preventative measure used in AF patients. Older drug therapies, such as warfarin and clopidogrel, have greater bleeding risks associated with them, entail dietary restrictions, and require frequent monitoring by providers, however, they are inexpensive and anecdotes are readily available in the case of supratherapeutic levels in the blood. The newer drug therapies, such as dabigatran and rivaroxaban, have shown promise in the prevention of thromboembolic stroke. They require less monitoring, less dietary restrictions, and less bleeding risks, however they are considerably more expensive and no anecdote has been developed in the case of overdose (AHA/ACC/HRS, 2014). Choosing the proper anti-thrombotic therapy involves many clinical factors, as well as the preferences of the patient and the provider, and it too can be a fluid process that evolves over time.
Summary of Interview
My interview of my father and his experiences with AF revealed a great deal about the disease and its effect on patients. My father reported that his primary symptom of AF at the time of diagnosis was palpitations, but an ECG failed to capture AF, so he was initially diagnosed as having angina, when in fact he likely had paroxysmal AF. Subsequent episodes of palpitations over several months led to a diagnosis of persistent AF. He was 55 years old at the time. For 2 months, attempts were made to control his rate and rhythm with medications, and when that failed, electrical cardioversion was attempted. Unfortunately, this failed to convert him to a normal sinus rhythm, and his diagnosis was changed to longstanding persistent AF. My father has had AF for 19 years now, and has been on a beta-blocker, a calcium channel blocker, and anti-coagulation therapy the entire time. There have been several attempts to remove one medication or the other over the years, but ultimately his course of treatment returns to those three medications. Unlike some patients, there has never been a discussion between my father and his provider about ablation surgery being a potential treatment for his AF. At the age of 74, it seems unlikely that he is a good candidate for this procedure. My father has never been told a cause for his AF. He does not have hypertension or high cholesterol, but he does have congestive heart failure (CHF). Like many so many AF patients, it is unclear if the CHF was a result of the AF, or vice versa. My father indicated that AF has not had a major impact on his way-of-life, other than the frequent monitoring. When he was younger and frequently travelled for his work, he had to be monitored more often, and while this was an inconvenience, it did not effect his ability to do his job. He also mentioned that he has had to postpone surgical procedures in the past, because his PT/INR levels were elevated, but this was also only a minor inconvenience (P. Olmstead, personal communication, March 5, 2016). In general, my father’s experience with AF seemed to fall along the same lines as described in my literature review.
Conclusion
Atrial Fibrillation is a disorder effecting the rhythm of the heart. It grows in frequency with aging, and can be a result of other cardiac related diseases. It can also exacerbate these same diseases once it is present. Patients presenting with new onset AF usually exhibit fatigue, dyspnea, palpitations, hypotension, heart failure, and/or syncope. Not all symptoms will be present in every patient. Patients are initially treated with beta-blockers or calcium channel blockers, though rhythm control medications may be prescribed as well. Some patients are cardioverted, either chemically or electrically, in an effort to return them to normal sinus rhythm. Other patients have cardiac ablation of their AV node followed by pacemaker implantation in an effort to modulate the rhythm of their heart. AF is categorized based on the frequency and duration of the arrthymia, and further categorized based on the cause of the AF. Patients who do not control their AF will most likely develop some type of tachycardia related ventricular dysfunction and/or heart failure, and are increased risk of thromboembolism. Interviewing my father, I found that he is a typical AF patient in his symptoms, treatment, and progression of the disease. His experience with AF was similar to what was found in the literature review.

References
American College of Cardiology/American Heart Association/Heart Rhythm Society Task Force. (2014). Guideline for the management of patients with atrial fibrillation. American College of Cardiology, 64(21). http://dx.doi.org/10.1161/CIR.0000000000000041
Centers for Disease Control and Prevention. (2015). Atrial fibrillation fact sheet. Retrieved from http://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_atrial_fibrillation.htm
National Institute for Health and Care Excellence. (2014). Atrial fibrillation: Management (CG180). Retrieved from https://www.nice.org.uk/Guidance/CG180