INTRODUCTION — Atrial fibrillation (AF) can cause significant symptoms; impair functional status, hemodynamics, and quality of life; and increase the risk of stroke and death. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)
Diagnosis of AF has important implications for acute and long-term management. A missed diagnosis of AF may result in a failure to appropriately anticoagulate for stroke prophylaxis or effectively treat symptoms due to AF, while overdiagnosis of AF may lead to inappropriate testing and therapy including unwarranted anticoagulation with associated risk of major bleeding. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)
This topic will review the electrocardiographic (ECG) features of AF. The mechanisms of AF are presented separately. (See "Mechanisms of atrial fibrillation".)
DIAGNOSIS OF ATRIAL FIBRILLATION — AF is diagnosed by interpretation of the 12-lead ECG. In most patients, a single 12-lead ECG, recorded while the patient is in AF, is sufficient to secure the diagnosis. Examination of prior ECGs may be helpful, but prior diagnosis (or misdiagnosis) of AF should not influence interpretation of a current ECG. In some patients, AF is detected on ECG recordings from cardiac telemetry, ambulatory ECG monitor (eg, Holter monitor or loop recorder), or cardiac implantable electronic device (permanent pacemaker [PPM] or implantable cardioverter-defibrillator [ICD]). (See "Ambulatory ECG monitoring" and "Permanent cardiac pacing: Overview of devices and indications" and "Implantable cardioverter-defibrillators: Overview of indications, components, and functions".)
Our approach — While the ECG diagnosis of AF with typical features can be straightforward in patients with characteristic features of AF (see 'Key features of atrial fibrillation' below), misdiagnosis of AF is common, as there are a significant number of AF mimics that should be excluded. (See 'Differential diagnosis' below.)
The following is our approach to ECG identification of the cause of an irregularly irregular ventricular rhythm (or regular rhythm with fibrillatory or absent P waves) (algorithm 1):
●Exclude artifact – If artifact may be present, examine all 12 leads and examine atrial activity in the leads with the least amount of artifact-related oscillations (waveform 1 and waveform 2). If atrial activity cannot be adequately assessed, address the cause of the artifact to the extent possible and repeat the ECG. (See 'Differential diagnosis' below.)
●Identify atrial activity – Examine all 12 leads of the ECG closely for the presence of atrial activity, particularly the inferior leads and lead V1. Focus on areas with longer R-R intervals that display longer periods of isoelectric baseline.
●Increase amplitude, if needed – If no atrial activity is detected or the morphology of atrial activity is not well visualized, use ECG amplification (either digital magnification or an increase in gain for the entire ECG signal) (waveform 3).
●Examine atrial activity – The morphology, frequency, and timing of atrial activity in relationship to QRS complexes should be assessed.
●Exclude AF mimics. (See 'Differential diagnosis' below.)
●If AF mimics are excluded, and there are fibrillatory waves or no P waves (despite ECG amplification), AF is diagnosed. Common and uncommon ECG characteristics of AF are described below. (See 'Key features of atrial fibrillation' below.)
Key features of atrial fibrillation
Common findings — The following findings are commonly seen with AF:
●Atrial activity (see 'Atrial activity' below):
•Lack of discrete P waves (waveform 4).
•Rapid, low-amplitude fibrillatory (or f) waves vary continuously in amplitude, morphology, and rate. The rate may be between 350 to 600 beats per minute (bpm) or unmeasurable. If present, f waves usually are best seen in the inferior leads and in V1. The f waves may be identified between QRS complexes and are sometimes visible superimposed on the ST segment and T waves.
●Ventricular activity (see 'Ventricular activation' below):
•The ventricular rhythm is described as "irregularly irregular," meaning lacking a repetitive, predictable pattern. (See 'General features' below.)
•The ventricular rate (especially in absence of atrioventricular [AV] nodal blocking drugs or intrinsic conduction disease) is usually 90 to 170 bpm, with higher rates seen in younger individuals (see 'General features' below). Based on the ventricular rate, AF is often characterized as having "slow" (<60 bpm), "moderate" (60 to 100 bpm), or "rapid" (>100 bpm) ventricular response (waveform 5).
•The QRS complexes are narrow unless conduction through the His-Purkinje system is abnormal due to preexisting right or left bundle branch (waveform 6), fascicular block, functional (rate-related) aberration, or ventricular preexcitation with anterograde conduction via an AV accessory pathway. (See 'With aberrant conduction' below and 'With Wolff-Parkinson-White syndrome' below.)
Uncommon findings — The following findings are less commonly identified in patients with AF:
●A regular (rather than an irregularly irregular) ventricular rhythm:
•Regular ventricular escape complexes in patients with complete or high-grade AV block are referred to as "regularization of AF." Complete or high-grade AV block may be caused by conduction system disease, AV node ablation, or drugs (including digoxin toxicity). (See "Etiology of atrioventricular block" and "Atrial fibrillation: Atrioventricular node ablation" and "Third-degree (complete) atrioventricular block" and "Cardiac arrhythmias due to digoxin toxicity", section on 'Digoxin-induced arrhythmias'.)
-Junctional escape – Most commonly, the escape pacemaker is located in the AV junction above the bifurcation of the bundle branches, leading to a QRS complex that has the same morphology as if it had conducted from the atria through the AV node (waveform 7). This pacemaker generally has a characteristic rate of approximately 60 bpm, unless it is accelerated or depressed due to pathology, ischemia, or drugs (eg, digoxin).
-Ventricular escape – With less commonly seen ventricular (subjunctional or fascicular) escape rhythms, the QRS is wide and, unless accelerated, the ventricular rate is generally 30 to 50 bpm (waveform 7).
•Ventricular pacing produces a regular paced ventricular rhythm with wide QRS. (See "Permanent cardiac pacing: Overview of devices and indications" and "Modes of cardiac pacing: Nomenclature and selection".)
•The ventricular rhythm is typically regular when there is ventricular tachycardia in the presence of AF.
•With very fast rates of AV conduction, the ventricular rate may appear regular.
•If there is conversion between AF and atrial flutter with a fixed ratio of conduction, the ventricular rate will be regular during periods of atrial flutter.
●Variable (rather than consistent) QRS morphology may result from varying combinations of AV conduction and native or paced ventricular beats (waveform 8). In these unusual cases, there may be AV conduction and fusion beats (hybrid complexes produced by coincident AV conduction and ventricular or paced beats) or pseudofusion beats (QRS complexes with morphology of AV conducted beats but with superimposed pacemaker stimuli). An example is the occurrence of AF with rapid ventricular response in concert with a "competing" tachycardia (eg, ventricular tachycardia) (waveform 9). (See "ECG tutorial: Miscellaneous diagnoses", section on 'Fusion and capture beats' and "ECG tutorial: Pacemakers", section on 'Ventricular pacing only'.)
Differential diagnosis — When there are no recognizable atrial deflections in any ECG lead, turning up the gain on the ECG may enable identification of f or P waves and thus help distinguish fine AF from sinus rhythm with irregularity (due to ectopy or sinus arrhythmia) (waveform 3).
AF can be confused with a number of other supraventricular arrhythmias that exhibit atrial activity (ie, sinus P waves, ectopic P waves, or flutter waves). "Coarse" AF (large-amplitude f waves, especially in lead V1) should be distinguished from atrial flutter and multifocal atrial tachycardia, as discussed below.
Specific AF mimics can be subdivided based on the type of atrial activity present. One or more of the following types of rhythms may be present:
●Atrial flutter – Atrial flutter is characterized by flutter waves on the isoelectric baseline between longer R-R intervals and on the ST segments and/or T waves, usually best seen in inferior leads or V1 (waveform 10). Both typical and atypical atrial flutter can mimic AF. In atrial flutter, atrial rates are generally 250 to 350 bpm (but are sometimes as low as 190 to 200 bpm). While atrial flutter with a constant degree of AV block (2:1, 3:1, 4:1) typically results in regular rhythms, atrial flutter with variable AV conduction is irregular. Some patients with AF also have episodes of atrial flutter. (See "Overview of atrial flutter", section on 'Electrocardiogram'.)
We avoid use of the term "atrial fibrillation/flutter," which is commonly used when the precise type of atrial activity is unclear. The term is inaccurate and may impact care as there are differences in the short- and long-term management for AF and atrial flutter. When it is difficult to distinguish these conditions, we use alternate language such as "The atrial activity is unclear and coarse, but the likely diagnosis is AF. However, atrial flutter with variable conduction cannot be excluded." Some patients have both of these conditions. If an ECG catches a transition between AF and atrial flutter, this transition should be noted and not labeled as "atrial fibrillation/flutter."
●The presence of sinus P waves (upright in II, inverted in aVR, and biphasic in V1) suggests an underlying sinus rhythm.
•Sinus arrhythmia – If all P waves are sinus, variation in PP (by >0.16 seconds) with a relatively constant PR suggests sinus arrhythmia (waveform 11). There is progressive increase and decrease in the P-P interval (See "ECG tutorial: Rhythms and arrhythmias of the sinus node", section on 'Sinus arrhythmia' and "Normal sinus rhythm and sinus arrhythmia", section on 'Sinus arrhythmia'.)
•Sinus arrhythmia with competing junctional escape rhythm – If there is variation in PP and there is one or more QRS complex without a preceding P wave or preceded by a shorter than normal PR interval, consider sinus arrhythmia with a competing junctional escape rhythm (also known as isorhythmic AV dissociation) (waveform 12). This occurs when the sinus rate intermittently drops below that of the junctional escape rhythm. The inconsistent P-QRS relationship is more challenging for the standard AF algorithms of ECG machines, and the rhythm is often misinterpreted as AF. (See "ECG tutorial: Rhythms and arrhythmias of the sinus node", section on 'Types' and "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Junctional escape beats'.)
•Sinus rhythm with second-degree AV block – Sinus rhythm with second-degree AV block can result in an irregular rhythm with occasional dropped beats (nonconducted P waves) which may (Mobitz I) or may not (Mobitz II) be preceded by progressive PR prolongation (waveform 13). (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)" and "Second-degree atrioventricular block: Mobitz type II" and "ECG tutorial: Atrioventricular block".)
•Sinus rhythm with premature ventricular complexes (PVCs) – Sinus rhythm with PVCs can result in an irregular rhythm that may be mistaken as AF when P wave amplitude is diminished or in the setting of artifact.
●One morphology of nonsinus P waves (along with sinus P waves):
•Sinus rhythm with premature atrial complexes (PACs) – The combination of sinus rhythm and PACs results in an irregular rhythm that can resemble AF, especially when the P waves of sinus beats and/or PACs are superimposed on the ST segment or T waves of preceding beats . To distinguish this rhythm from AF, magnification of digitized ECG tracings may facilitate recognition of sinus and ectopic P waves and demonstrate a consistent one-to-one relationship between P waves and QRS complexes (waveform 3). (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Premature atrial complex'.)
•Runs of nonsinus P waves – A shift in atrial activation arising from the sinus node to that from an ectopic atrial site (or vice versa) can lead to a sudden change in P wave morphology and, often, some irregularity that could mimic AF.
-Ectopic atrial rhythm – Atrial rate is ≤100; generally, 30 to 60 bpm (waveform 14). (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Ectopic atrial rhythm'.)
-Focal atrial tachycardia – Atrial tachycardia (AT) is characterized by atrial rates in the 140 to 180 bpm range (waveform 15). In the presence of AV block, the ventricular response can be irregular and mimic AF. While AT with block has been commonly described with digoxin toxicity, it can occur in the absence of digoxin. (See "Cardiac arrhythmias due to digoxin toxicity", section on 'Digoxin-induced arrhythmias'.)
●Three or more P wave morphologies:
•Wandering atrial pacemaker or multifocal atrial rhythm is an irregular rhythm that is also characterized by P waves of at least three morphologies and is characterized by ventricular rates <100 bpm (waveform 16). (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias" and "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Wandering atrial pacemaker'.)
•Multifocal atrial tachycardia (MAT) – MAT is a rapid irregularly irregular rhythm (ventricular rate ≥100 bpm) characterized by P waves of at least three different morphologies and with a one-to-one correspondence of P waves to QRS complexes (waveform 17). (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Multifocal atrial tachycardia' and "Multifocal atrial tachycardia", section on 'Clinical manifestations and diagnosis'.)
●Ventricular tachycardia – AF with aberrant conduction may include consecutive runs of aberrantly conducted beats with wide QRS complexes, which may appear similar to ventricular tachycardia. The ventricular rate with AF is generally irregular. (See 'With aberrant conduction' below.)
EXPLANATION OF ECG FEATURES
Atrial activity — In AF, there is no regular or organized atrial activity (waveform 4). Numerous apparent microreentrant circuits within the atria may generate multiple waves of impulses that compete with or extinguish each other in what is termed "fibrillatory conduction." The sinus node is suppressed and cannot activate the atrium. Mechanisms causing this abnormal pattern of atrial electrical activity are discussed elsewhere. (See "Mechanisms of atrial fibrillation".)
Rapid, irregular, and variable fibrillatory (f) waves may be coarse (amplitude ≥1 mm) or fine (<1 mm) and may not be identified. Some studies have found that fine AF is associated with older age, but age ranges for coarse and fine AF overlap widely [1,2]. The amplitude of f waves does not correlate with left atrial size [1,3].
The differential diagnosis for AF is discussed above. (See 'Differential diagnosis' above.)
General features — In AF, the ventricular response rate is dependent on properties of the AV conduction system. As rapid and irregular atrial impulses bombard the AV node, some impulses occur in such rapid succession that they are blocked due to the refractoriness of the AV node, resulting in irregular impulse conduction through the AV node to the ventricular myocardium via the His-Purkinje system. High frequency of atrial stimuli reaching the AV node does not lead to high frequency of AV conduction, as frequent impulses may cause "concealed" depolarization (ie, not evident on the surface ECG) impairing AV conduction. The large number of atrial impulses arriving at the AV node compete with each other, interfering with their penetration into and through the node, leaving this tissue variably refractory.
While the ventricular rate in adults with AF is usually 90 to 170 bpm, in young, untreated individuals, rates are 160 to 200 bpm, reflecting the maximal rate at which the AV node can conduct (as determined by its refractory period in lieu of concealed conduction). Increases in the ventricular response rate to over 200 bpm may occur if the refractory period of the AV node is shortened, as with an increase in circulating catecholamines (eg, sympathetic stimulation or pheochromocytoma, hyperthyroidism, or conduction down a manifest accessory pathway). A decrease in the ventricular response rate occurs when the refractory period of the AV node is increased (eg, with aging, conduction system disease, drugs, or enhanced vagal tone) or AV conduction otherwise slows.
With aberrant conduction — A common cause for QRS widening during AF is aberrant conduction, which is a rate-related change in conduction. Most aberrancy is tachycardia-dependent, although bradycardia-dependent aberrancy does occur . The aberrant conduction in AF involves a rate-related (tachycardia-induced) change in conduction, typically a functional bundle branch block; right bundle branch block (RBBB) is more common than left bundle branch block (LBBB), as the RBBB has a longer refractory period than the LBBB.
An important property of the conducting system and myocardium is that refractoriness is longer at slow rates and shorter at faster rates. The refractoriness of the conducting system varies on a beat-by-beat basis and is related to the coupling interval of the preceding beat. As such, a long coupling interval leads to prolongation of bundle branch refractoriness (typically R>L), and if the next beat comes in early (ie, a long-short cycle), the refractoriness of the RBBB leads to a RBBB configuration and QRS widening that resembles a premature ventricular complex (PVC). This pattern of long-short cycle typically leads to RBBB morphology (known as Ashman phenomenon ) and can occur during sinus rhythm with appropriately timed premature atrial complexes (PACs) (waveform 18) as well as during AF (waveform 19). Aberrancy with LBBB morphology is less common but can occur. The QRS of aberrant beats typically exhibits an upstroke similar to those of other native supraventricular beats in leads other than V1 to V2, while PVCs typically exhibit markedly different morphology from supraventricular beats in multiple leads, as shown for sinus rhythm (waveform 18). The approach to evaluating wide QRS complex tachycardia to distinguish supraventricular tachycardia from ventricular tachycardia is discussed separately. (See "Wide QRS complex tachycardias: Approach to the diagnosis".)
During AF, Ashman phenomenon is associated with frequent isolated wide-complex aberrantly conducted beats. However, aberrantly conducted beats can also occur in couplets or longer nonsustained runs that can resemble ventricular tachycardia (waveform 19). In these situations, there is no longer a long-short cycle but rather short-short cycles of rapid AF. In this case, the functional RBBB and activation down the LBBB is followed by partial penetration up the right bundle, leading to RBBB of the subsequent beat. This represents "concealed conduction" up the right bundle (ie, not evident on the surface ECG, which solely reflects atrial and ventricular activity). This can continue for a number of consecutive beats until functional BBB resolves either despite continued short cycle length or when the cycle length lengthens. As such, AF with aberrant conduction can resemble ventricular tachycardia, and it is critical to distinguish between ventricular tachycardia and sustained aberrancy . (See 'Differential diagnosis' above.)
With Wolff-Parkinson-White syndrome — When AF is associated with ventricular preexcitation due to anterograde conduction down an accessory pathway in patients with Wolff-Parkinson-White syndrome (WPW), the ventricular response rate may be very rapid and may exceed 280 to 300 bpm (waveform 20), since impulse activation bypasses the AV node. Preexcited AF is facilitated when the refractory period of the accessory pathway is very short. Accessory pathway tissue differs from that of the AV node. Specifically, the accessory pathway does not exhibit postrepolarization refractoriness but rather conducts rapidly as the tissue is dependent on sodium (rather than calcium) channel activity.
Conduction down the accessory pathway typically results in a slurred QRS upstroke (ie, "delta" wave), and the QRS morphology depends on the location of the pathway and its insertion into the ventricular myocardium. The QRS complex is usually wide, with rapid activation down the accessory pathway into ventricular muscle, often in concert with some conduction down the AV node and His-Purkinje system. The more conduction proceeds through the accessory pathway, the wider and more slurred the QRS complex. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Electrocardiographic findings'.)
A distinguishing feature of AF with preexcitation is the relationship between heart rate and QRS duration; the faster the rate, the wider the QRS. At times, it can resemble ventricular tachycardia (based on its appearance and, often, the presence of precordial concordance). While the rhythm is irregularly irregular, variations may be difficult to measure at extremely fast rates. The clinical significance of AF with rapid ventricular response in patients with WPW is discussed separately. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Ventricular fibrillation and sudden death'.)
ROLE OF COMPUTER TECHNOLOGY
Computer interpretation — Each ECG computer interpretation should be overread by a trained clinician as an essential requirement for patient care and safety. Automatic computer interpretation of the ECG is common practice, with over 100 million automatic ECG interpretations yearly. Limited data are available on the accuracy of automatic computer interpretation for AF, but an estimated 10 to 30 percent of the computer ECG interpretations may misdiagnose AF, and such misdiagnosis may be frequently missed by clinicians [6,7]. Such misdiagnosis can lead to inappropriate interventions and therapies. The methodological approaches that computers utilize to determine whether or not AF is present are not well clarified. Insufficient overreading may be a growing problem as formal ECG interpretation becomes less of a focus in many training programs.
Wearable consumer devices — While ambulatory ECG monitoring (Holter, event, or patch-based monitors, and implantable loop recorders) is a commonly employed clinical method to detect occult AF (see "Ambulatory ECG monitoring"), there has been growing use of wearable consumer devices such as smart watches and other devices that can connect to smart phones [8,9] to monitor heart rate and rhythm [10,11]. While these widely used electronic devices have potential capabilities for detecting AF, and algorithms are improving, they are subject to limitations. Generally, the methodology (often proprietary) monitors the irregularity in ventricular response rates but does not monitor the presence and type of atrial activation. Also, some devices may require a threshold episode duration (eg, 30 seconds) to detect an arrhythmia. These limitations are likely to limit the sensitivity and specificity of these devices in detecting and diagnosing AF. Thus, all patients with suspected AF require clinician review of recordings on clinically approved ECG equipment, as described above . (See 'Our approach' above.)
SUMMARY AND RECOMMENDATIONS
●Atrial fibrillation (AF) is diagnosed by interpretation of the 12-lead electrocardiogram (ECG). AF should be considered in patients with an irregularly irregular ventricular rhythm (or regular rhythm with fibrillatory or absent P waves). (See 'Diagnosis of atrial fibrillation' above and 'Differential diagnosis' above.)
In some patients, AF is detected on ECG recordings from cardiac telemetry, ambulatory ECG monitor (eg, Holter monitor or loop recorder), or cardiac implantable electronic device (permanent pacemaker [PPM] or implantable cardioverter-defibrillator [ICD]). (See "Ambulatory ECG monitoring" and "Permanent cardiac pacing: Overview of devices and indications" and "Implantable cardioverter-defibrillators: Overview of indications, components, and functions".)
●Our approach to diagnosis of AF involves exclusion of artifact, ECG amplification (if no atrial activity is detected or the morphology of atrial activity is not well-visualized), and exclusion of AF mimics (algorithm 1). (See 'Our approach' above and 'Differential diagnosis' above.)
●Common features of AF include lack of discrete P waves, presence of fibrillatory (f) waves, and irregularly irregular ventricular rhythm. QRS complexes are narrow unless there is a right or left bundle branch block, fascicular block, functional (rate-related) aberration, or antegrade conduction via an AV accessory pathway. (See 'Common findings' above.)
●ECG features that are uncommonly associated with AF include a regular ventricular rhythm and variable QRS morphology. (See 'Uncommon findings' above.)
●The differential diagnosis of AF includes artifact, atrial flutter, sinus rhythm (with sinus arrhythmia, second-degree AV block, or premature atrial complexes [PACs]), ectopic atrial rhythm, multifocal atrial tachycardia (MAT), wandering atrial pacemaker, focal atrial tachycardia with block, sinus rhythm with competing junctional rhythm, and ventricular tachycardia. (See 'Differential diagnosis' above.)
●Each ECG computer interpretation should be overread by a trained clinician as an essential requirement for patient care and safety. Limited data on the accuracy of automatic computer interpretation for AF suggest that 10 to 30 percent of the computer ECG interpretations may misdiagnose AF. (See 'Computer interpretation' above.)
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