By Jamie Lintgen
October 7, 2026
Atrial fibrillation, often referred to as a-fib or abbreviated to AF, is the most common heart arrhythmia, consisting primarily of irregular atrial electrical activity with no clear moment of contraction. It is easily recognizable on electrocardiogram (ECG) for the chaotic, low amplitude waves that are persistent throughout the cardiac cycle, with no clear P waves and inconsistent intervals between QRS complexes. The formation of clots in turbulent atria in AF is the most common cardiac cause of stroke, so diagnosis and treatment is essential. AF is generally caused by either one or multiple reentrant conduction currents in the atria, or one or more abnormal sources of the initial electrical impulse of the heart beat. Cardiac muscle cells conduct through each other in the branching pattern in which they are connected, and it isn’t uncommon for electrical impulses to split when traveling through a branching cell, this is after all how the impulse is propagated throughout the myocardium. Reentrant circuits can occur when the bifurcation leads to two cells which themselves are connected. If one of those cells were to be blocked from electrical conduction entering it and the other conducts the impulse slowly the impulse may be able to travel in retrograde from the standard direction of current. If conduction through the slowed conduction cell is slow enough, the current may reach the original cell after it has already repolarized and create a complete circuit. The block from electrical conduction which is atypical may occur from the cell in question being in electrical refractory, or from it having some sort of local disease (ischemia, etc). It is easily visible from this how a-fib is associated strongly with other electrical or structural defects of the heart, particularly when parts of the atria are ischemic, dilated, or hypertrophied. The other primary morphology of AF is one where standard cardiac muscle cells become capable of themselves producing spontaneous action potentials. This typically only occurs in the sinoatrial (SA) node, where the impulse for the non-pathological heart rhythm is generated. Standard myocytes not in the SA node maintain their resting potential at -75-80mV (in atrial cells) because of membrane permeability to potassium. The combination of the concentration difference between extracellular potassium and intracellular potassium and the membrane potential difference creates an electrochemical equilibrium point at ~-80mV. This equilibrium prevents standard myocytes from reaching the ~-60mV threshold for voltage gated Na+ gates to open and cause depolarization. Atrial cells can become capable of producing spontaneous action potentials, (these spots are often called “ectopic foci”), when this equilibrium is jeopardized, and membrane potential can reach the activation threshold spontaneously. This can happen through ischemia, potassium level irregularities, necrosis causing other electrolyte imbalances (Ca, Mg, etc), or other pathological situations. Typically, the rhythm of the heart is controlled by a small bundle of cardiac cells near the top of the right atrium called the sinoatrial (SA) node. In sinus rhythm (the standard rhythm of the heart), these cells create the initial action potential of each cardiac cycle, which is then propagated throughout the atrium in an orderly fashion, causing atrial contraction (P wave on ECG), before reaching the atrioventricular (AV) node. The AV node essentially holds the action potential for a brief delay (PR interval on ECG) to allow the ventricles to fully fill before dispatching the electrical impulse through the ventricles (QRS complex on ECG). In AF, the atria are in a state of constant electrical depolarization and repolarization through either reentrant circuits or alternative ectopic foci. In these cases, the AV node’s electrical refractory period is what controls heart rate as opposed to the natural, consistent cycle of the SA node. This leads to inconsistent and often high heart rates, since the ventricles essentially contract whenever the AV node is depolarized and a random action potential happens to reach it from the atrium. Key risk factors for AF include advanced age, hypertension, unrelated hypertrophic, ischemic, valvular or other cardiovascular disease. These are all the most major risk factors due to all generally causes structural or electrical remodeling of the heart, which, as previously mentioned, predisposes a patient to AF. Other risk factors include smoking, illicit drug use, excessive alcohol consumption, obstructive sleep apnea, history of rheumatic fever or pericarditis, and hyperlipidemia. AF can be paroxysmal, lasting for hours to days, persistent, lasting for more than seven days, long-standing persistent, lasting for years, or permanent, if long-standing persistent AF recurs following attempts to reset. AF often starts in recurrent paroxysmal incidents, before developing into persistence. This happens because AF promotes remodeling of the heart, including dilation of the atria, which in turn makes one more susceptible to AF. This is one reason why cardioversion of long standing AF is often unsuccessful. The most major issues to worry about with AF include high acuity cases in which patients are hemodynamically unstable and persistent cases where thrombosis (blood clot formation) can occur in the left atrium and travel to the brain, causing a stroke. In cases of hemodynamic instability (defined by indication of poor perfusion –altered mental status, ischemic chest pain, diaphoresis, weak pulse– drop in blood pressure from baseline, dangerous tachycardia, etc), immediate DC cardioversion is indicated. Extreme ventricular rates can cause hypoperfusion because the ventricles become unable to fully relax in between contractions, which reduces filling. In cases of Wolff-Parkinson-White (WPW) syndrome, AF is a much more dangerous arrhythmia, since reentrant circuits are not limited by the AV node and can travel in the ventricles, learning to fibrillatory electrical rhythms in the ventricles. From the more clinical perspective, AF can present anywhere from completely asymptomatic to cardiogenic shock. On the more mild end, common complaints include dyspnea, fatigue and low exercise tolerance, syncope, or palpitations. History should include assessment of initial occurrence and frequency of symptoms as well as documentation of risk factors, particularly other forms of cardiac disease. In cases of hemodynamic instability, such as hypotension, or angina, immediate DC cardioversion is indicated, and Advanced Cardiac Life Support guidelines should be followed. Diagnosis is simple with an ECG, where no P waves will be seen, although low amplitude, high frequency fibrillatory waves may be seen; RR intervals are also often inconsistent and tachy, ranging from 80-180 per minute. More recent recommendations guidelines consider discussing modifiable risk factors with patients when many are present, using the HEAD-TOES (heart failure, exercise, arterial hypertension, diabetes, tobacco, obesity, ethanol, sleep) acronym. AF treatment is generally divided into three pillars: stroke risk management, rate control, and rhythm control, as well as lifestyle and risk factor management (LRFM). LRFM includes providing comprehensive guidance on losing weight if overweight, becoming physically active, moderating alcohol consumption, smoking and tobacco cessation, controlling diabetes, and mitigating hypertension to the degree possible. As previously discussed, AF comes with an increased risk of stroke, and management of this risk is key to improving survival of patients with AF. All patients with AF should be evaluated for stroke risk with a scoring system such as CHA2DS2-VAS (Congestive heart failure, hypertension, age > 75 (2 points), diabetes, past stroke (2 points), vascular disease, age 65-75, female sex). Anticoagulants also increase risk of bleeding, so the risks of stroke generally need to be weighed against the patient's risk of hemorrhagic pathologies. Additional evaluation methods exist for bleeding risk, but they generally include many of the same factors as stroke risk evaluation methods, so they may unnecessarily dissuade the usage of anticoagulants when indeed the reduced risk of stroke is worth the increased risk of bleeding. Usage of anticoagulants to reduce stroke risk should be purely based on determined risk of a thromboembolic event, without regard for the duration of the AF. Reevaluation of stroke risk is also periodically needed to reconsider choice of stroke prevention method. Anticoagulant usage is recommended regardless of rate/rhythm control strategy. Rhythm control encompasses a broad array of strategies that can be implemented with the goal of reducing, and if possible, eliminating arrhythmia and restoring a sinus rhythm. Historically, this was the first line option for addressing atrial fibrillation, and involves cardioversion with anti-arrhythmatic drugs. There has been a shift towards the effectiveness of rate control measures, but emerging research suggests that early rhythm control preventing atrial remodeling can have better results. This has come with the development of more advanced options such as catheter ablation, an operation where areas of the myocardial tissue perpetuating the AF rhythm are strategically scarred to prevent electrical conduction. Rate control attempts to reduce the adverse effects of longstanding AF by controlling ventricular rhythm through the prescription of AV node blocking drugs or the ablation of the AV node intersection. Recent research generally suggests that these methods are not as effective of a measure for treating AF in its onset, but for longstanding cases where rhythm control is deemed to be hopeless, it still can be effective. Many of the most detrimental effects of AF, other than stroke risk, such as hypertension, high ventricular rates, and eventual ventricular remodeling and hypertrophy can be mitigated with the control of ventricular rates. Thus, maintaining a reasonable ventricular rate can be the best available option to treat AF if rhythm control is impossible. Bibliography Boehmer AA, Ninni S, Heijman J, Dobrev D, Nattel S. The clinical pathophysiology of atrial fibrillation: outstanding questions from bedside to bench and back. Physiol Rev. 2026;106(3):1055-1121. doi:10.1152/physrev.00020.2025 Nesheiwat Z, Goyal A, Jagtap M. AF. [Updated 2023 Apr 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526072/ Li J, Gao M, Zhang M, Liu D, Li Z, Du J, Hou Y. Treatment of atrial fibrillation: a comprehensive review and practice guide. Cardiovasc J Afr. 2020 May/Jun 23;31(3):153-158. doi: 10.5830/CVJA-2019-064. Epub 2020 Mar 18. PMID: 32186324; PMCID: PMC8762786. Wigginton JG, Agarwal S, Bartos JA, et al. Part 9: Adult Advanced Life Support: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(16_suppl_2). doi:https://doi.org/10.1161/cir.0000000000001376 Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. New England Journal of Medicine, 347(23), 1825-1833. Camm, A, Naccarelli, G, Mittal, S. et al. The Increasing Role of Rhythm Control in Patients With Atrial Fibrillation: JACC State-of-the-Art Review. JACC. 2022 May, 79 (19) 1932–1948. https://doi.org/10.1016/j.jacc.2022.03.337