Atrial fibrillation (AF) is an abnormal rhythm caused by the rapid firing of multiple cells in the atria, the upper chambers of the heart, which cause the atria to quiver ineffectively. Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia encountered in clinical practice and is associated with increased risk of stroke, dementia, falls, and death, among other outcomes.1 A report based on the Framingham study suggests that from the age of 40 years there is a lifetime risk of developing AF of one in four, independent of gender, and of one in six in the absence of congestive heart failure or myocardial infarction.3
Normally, the SA note in the right atrium initiates the electrical signal that induces the atria to contract, forcing blood through the upper chambers to the ventricles. The electrical signal is propagated through the atria to the AV node. At the AV node and beyond into the ventricles, the electrical impulse signals the ventricles to contract, and blood is pumped out of the ventricles to the body. In atrial fibrillation, the rapid and chaotic firing of multiple cells in the atria bombards the AV node with impulses, only some of which get through to signal the ventricles to contract. Thus the atrial rate is much faster than the ventricular rate.
AF can be maintained by reentry and/or rapid focal ectopic firing.8 The irregular atrial discharge typical of AF may result from an irregular atrial response to a rapidly discharging regularly firing driver (mechanism causing AF) resulting from either local ectopic firing or a single localized reentry circuit.5
AF is a progressive disease with many patients experiencing initial short and infrequent episodes to longer and more frequent ones while some may remain in permanent or chronic AF.7 Most patients remain conscious when they go into AF, and many do not even know they are in an abnormal rhythm. Some patients are in AF for a long time before the rhythm is discovered.
Assessment and Monitoring
AF often initially presents in a paroxysmal (PAF) form, defined by self-termination within 7 days, while persistent AF requires termination by pharmacological or direct-current electric cardioversion.5 It is believed that in many cases the natural history of AF involves evolution from paroxysmal to persistent (PersAF) to permanent forms through the influence of atrial remodeling caused by the arrhythmia itself and/or progression of underlying heart disease.4 However, AF will remain paroxysmal in a small proportion of patients (2–3%) or spontaneously regress from persistent to paroxysmal AF in some.6
Current classification includes: newly diagnosed AF, PAF, PersAF, long-standing PersAF, and permanent AF.7
Upon assessment of a stable patient, auscultation will reveal irregularly irregular heart sounds. The patient may complain of palpitations, dizziness, lightheadedness, or feeling faint, especially upon exertion. Patients with this rhythm should have constant cardiac monitoring, whether hardwired or telemetry. Assessment of the rate and rhythm, observing for changes in either, is important due to different morphology that can increase the patient’s symptoms. Chest pain, shortness of breath, and/or signs of poor perfusion should be viewed as signs that the patient is becoming unstable and may require acute intervention.
The monitor will also present irregularly irregular QRS complexes. The baseline will appear wavy and chaotic, representing fibrillating atrial activity that are far greater than the number of QRS complexes. When the heart rate is greater than 100 beats per minute, it is referred to as an uncontrolled ventricular response. Patients will often experience untoward symptoms at 150 beats per minute and higher, but some patients may experience symptoms at a lower rate. In addition to continuous cardiac monitoring, these patients should have intravenous access in case rapid treatment is needed.
The goal of treatment in AF is three-fold: to control the rate, to control the rhythm and to prevent stroke.
Medications that are used in the treatment of new onset stable atrial fibrillation include diltiazem (calcium channel blocker) or metoprolol (beta-blocker). These medications are given to control rate. Depending on the severity of the patient’s symptoms, these medications can be given intravenously or orally. Digoxin is sometimes used, but it is not as effective as calcium channel blockers or beta-blockers for active patients.
Pluymaekers et. al reported that among patients who presented to the emergency department with recent-onset, symptomatic atrial fibrillation, a wait-and-see strategy was non-inferior to early cardioversion in obtaining sinus rhythm at 4 weeks after the index visit. They stated four benefits to the wait-and-see strategy, with delayed cardioversion if needed within 48 hours after symptom onset:
- Cardioversion (along with its potential complications) may be avoided.
- The time spent in the emergency department during the initial presentation may be reduced.
- Spontaneous conversions of atrial fibrillation may be observed, leading to fewer misclassifications of persistent atrial fibrillation.
- Patients may have the experience that their arrhythmia terminated by itself, which may broaden their insight into treatment options.
Another classification of medication used in the treatment of AF is an anticoagulant, usually in the form of a heparin drip for new onset atrial fibrillation. This is due to the potential for clotting in the atria when they do not eject blood adequately, which can lead to both heart attacks and strokes. Close monitoring is needed to ensure the heparin remains within therapeutic range, through serial blood tests. Conversion from heparin to warfarin is usually begun almost immediately, but it can take several days before oral anticoagulants can maintain the blood within the target range. It is mandatory to manage stroke risk appropriately in patients presenting to the emergency department with acute atrial fibrillation, independent of cardioversion strategy.2
Conversion and Long-Term Treatment
Besides medication, other measures can be taken to convert AF. One of these methods is synchronized cardioversion. By administering a shock, the hope is that the SA node will reassert itself and the patient will convert into a normal sinus rhythm. Patients will require sedation, as cardioversion is quite painful. Patients who have been in atrial fibrillation for longer than 48 hours should be anticoagulated before being cardioverted to prevent clots from the atria from traveling through the bloodstream, where they may cause a heart attack, stroke, or pulmonary embolism. Sometimes the effects of cardioversion are short-lived, in which case ablation may be an option.
Ablations are performed the same way as cardiac catheterizations. A catheter is inserted into the femoral artery, and the catheter is then threaded into the right atrium. Using angiography, the cardiologist attempts to find the cells in the atrium that are firing erratically. Once these cells are identified, the catheter is used to burn or destroy those cells. When those cells are no longer interfering with the SA node, the patient usually converts to a sinus rhythm. Ablation is often more successful than cardioversion.
(This article barely reviews the basics of AF and its causes and treatments. For a thorough study of AF and current treatment modalities, obtain a copy of the “2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS.”)
- Cerasuolo JO, Montero-Odasso M, Ibañez A, et al. Decision-making interventions to stop the global atrial fibrillation-related stroke tsunami. Int J Stroke. 2017;12:222-228.
- Coll-Vinent B, Martin A, Sanchez J, et al. Benefits of emergency departments’ contribution to stroke prophylaxis in atrial fibrillation: the EMERG-AF Study (Emergency Department Stroke Prophylaxis and Guidelines Implementation in Atrial Fibrillation). Stroke. 2017; 48: 1344-52.
- Cottrell C. Atrial fibrillation part I: pathophysiology. Practice Nursing. 2012;23:16-21.
- de Vos CB, Pisters R, Nieuwlaat R, Prins MH, Tieleman RG, Coelen RJ, van den Heijkant AC, Allessie MA, Crijns HJ. Progression from paroxysmal to persistent atrial fibrillation clinical correlates and prognosis. J Am Coll Cardiol. 2010;55:725–731.
- Iwasaki Y, Nishida K, Kato T, Nattel S. Atrial fibrillation pathophysiology. Circualtion. 2011;2264-2274.
- Jahangir A, Lee V, Friedman PA, Trusty JM, Hodge DO, Kopecky SL, et al. Long-term progression and outcomes with aging in patients with lone atrial fibrillation: a 30-year follow-up study. Circulation. 2007;115:3050–6.
- Lau DH, Linz D, Schotten U, Mahajan R, Sanders P, Kalman JM. Pathophysiology of paroxysmal persistent atrial fibrillation: Rotors, foci, and fibrosis. Heart and Lung Circulation. 2017;26:887-893.
- Nattel S. New ideas about atrial fibrillation 50 years on. Nature. 2002;415:219 –226.
- Pluymaekers NAHA, Dudink EAMP, Luermans JGLM, Meeded JG, Lenderink T, Widdershoven J, Bucx JJJ, Rienstra M, Kamp O, Van Opstal JM, Alings M, Oomen A, Kirchof CJ, Van Dijk VF, Ramanna H, Liem A, Dekker LR, Essers BAB, Tijssen JGP, Van Gelder IC, Crijns HJGM. Early or delayed cardioversion in recent-onset atrial fibrillation. N Engl J Med. 2019;380:1499-1508.
Dan Bunker DNAP, MSNA, CRNA—Dan has worked in the healthcare industry for nearly 30 years. He worked as a registered nurse in the coronary care ICU for 7 years and was a flight nurse with Intermountain’s Life Flight for nearly 10 years. He has been a certified registered nurse anesthetist (CRNA) for 11 years, working in the hospital setting as well as maintaining his own private practice. In addition, he is a professor in the nurse anesthesia program at Westminster College in Salt Lake City, Utah. He has served in various leadership roles within the Utah Association of Nurse Anesthetists (UANA) and is currently the president-elect.