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Official reprint from UpToDate www.uptodate.com ©2015 UpToDate

AuthorBrian Olshansky, MD

Section EditorsAry L Goldberger, MDBradley P Knight, MD,FACC

Deputy EditorGordon M Saperia, MD,FACC

The electrocardiogram in atrial fibrillation

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Jun 2015. | This topic last updated: May 01, 2015.

INTRODUCTION — Atrial fibrillation (AF) can cause significant symptoms and impair functional status andquality of life, and can increase the risk of stroke and death. (See "Overview of atrial fibrillation".)

The diagnosis of AF is often based on a 12 lead electrocardiogram (ECG) characterized by absence ofdiscrete P waves and an irregularly irregular ventricular rate. In most patients, a single ECG is sufficient tosecure the diagnosis, assuming the patient is in AF at the time of the ECG. In some patients it is alsodiagnosed using a heart rhythm recording such as a telemetry strip, Holter monitor, or an event monitor.

Occasionally, the electrocardiographic diagnosis of AF may be difficult. (See 'Difficulties in diagnosis' below.)Further, other rhythm disturbances may be confused with AF.

This topic will review the electrocardiographic features of AF. The mechanisms of AF are presentedseparately. (See "Mechanisms of atrial fibrillation".)

COMMON FINDINGS — AF is associated with the following changes on ECG (waveform 1 and waveform 2and waveform 3):

ATRIAL ACTIVITY — In AF there is no regular or organized atrial activity (waveform 2 and waveform 1).Numerous micro­reentrant circuits within the atria generate multiple waves of impulses which often competewith or even extinguish each other. As a result, no uniform activation of the atrial tissue and no distinctive Pwaves are generated or recognized on the surface ECG. Since these multiple wavelets generate rapid andlocalized impulses, the sinus node is suppressed or not able to be expressed as it cannot activate theatrium. The mechanisms causing this pattern of electrical activity in the atria are discussed in detailelsewhere. (See "Mechanisms of atrial fibrillation".)

Atrial electrical activation is rapid (generally greater than 350 to 360 beats per minute) and of variousamplitudes, and occurs with irregularly irregular intervals. No discrete P waves are seen on theelectrocardiogram. Instead, rapid, irregular, variable, and low amplitude oscillating fibrillatory (f) waves areobserved between the QRS complexes. When the AF is of recent onset, the f waves are often coarse (>2mm); by comparison, the f waves are usually fine (<1 mm) with AF of greater duration.

The f waves are of greater amplitude when there is hypertrophy of left atrial myocardium and becomesmaller with increasing atrial scarring and fibrosis. The amplitude of the fibrillatory waves does not correlate

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Lack of discrete P waves.

Fibrillatory or f waves are present at a rate that is generally between 350 and 600 beats/minute; the fwaves vary continuously in amplitude, morphology, and intervals.

Ventricular response follows no repetitive pattern; the variability in the intervals between QRScomplexes is often termed “irregularly irregular.”

The ventricular rate (especially in the absence of AV nodal blocking agents or intrinsic conductiondisease) usually ranges between 90 to 170 beats/min. (See 'Ventricular rate' below.)

The QRS complexes are narrow unless AV conduction through the His Purkinje system is abnormaldue to functional (rate­related) aberration, pre­existing bundle branch or fascicular block, or ventricularpreexcitation with conduction down the accessory pathway.

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with the actual atrial size. “Coarse” AF in which the amplitude of the f waves is large (especially in lead V1)is more common in recent onset AF and can be confused with atrial flutter or multifocal atrial tachycardia.(See "Electrocardiographic and electrophysiologic features of type I atrial flutter", section on'Electrocardiographic features' and "Multifocal atrial tachycardia", section on 'Definition, pathogenesis, andprevalence'.)

In some cases, there are no recognizable deflections of the baseline in any ECG lead (more common inlongstanding AF) and AF is inferred because of the absence of P waves and the irregularly irregularventricular rate. If present, f waves are best seen in the inferior leads and in V1.

VENTRICULAR RATE — The ventricular rate (especially in the absence of nodal blockade) usually rangesfrom 90 to 170 beats/min. However, many factors determine the rate at any moment in any individual.

While the atrial rate is very rapid and depends upon the electrophysiologic characteristics of the atrialmyocardium, the ventricular response rate is dependent upon the properties of the atrioventricular node (AV)and His Purkinje system. The irregularity of the ventricular response is the result of the irregular and rapidatrial rate and the degree of bombardment of the AV node with impulses, some of which occur in such rapidsuccession that they cannot conduct through the AV node due to refractoriness. The frequency ofbombardment of the AV node can lengthen conduction time, and these impulses that reach the AV node butdo not conduct are said to lead to concealed conduction within the AV node. The large number of atrialimpulses arriving at the node compete with each other, interfering with their penetration into and through thenode, leaving this tissue variably refractory. Irregular impulse conduction through the AV node to theventricular myocardium via the His Purkinje system therefore results.

The ventricular rate in young individuals with untreated AF is generally 160 to 200 beats per minute,reflecting the maximal rate at which the AV node can conduct (as determined by its refractory period in lieuof concealed conduction). Increases in the ventricular response rate to over 200 beats per minute may occurif the refractory period of the AV node is shortened, as with sympathetic stimulation or an increase incirculating catecholamines or conduction down an accessory pathway if present. A decrease in theventricular response rate occurs when the refractory period of the node is increased, as happens with aging.Other causes of a slower ventricular rate include intrinsic AV nodal disease in combination with sympatheticblockade, direct depression of the AV node with some drugs, or enhanced vagal tone.

A regular ventricular rate, often referred to as “regularization of atrial fibrillation,” may infrequently occurdespite a fibrillating atrium due to the complete blockade of AV nodal conduction and the subsequentdevelopment of a junctional (narrow QRS) or ventricular (wide QRS) escape rhythm.

Also, at very fast rates of conduction, the ventricular response rate can appear to be regular. In some cases,regularization in rate is due to conversion of AF into atrial flutter with a fixed ratio of conduction. Drugs thatimpair nodal conduction (such as digoxin, beta or calcium channel blockers) or AV nodal disease may resultin the development of slowing and regularization of the ventricular response. Digoxin is the most likely to doso. (See "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy" and "Cardiac arrhythmiasdue to digoxin toxicity".) Atrial flutter and fibrillation can coexist.

When AF is associated with a preexcitation syndrome (ie, the presence of an antegrade conductionaccessory pathway), the ventricular response rate may be very rapid, often in excess of 280 to 300 beatsper minute. This is because impulse conduction bypasses the atrioventricular node, as conduction from theatria to the ventricles occurs by an accessory or intranodal pathway. If the refractory period of this pathwayis very short, impulse conduction can be very rapid. The tissue of accessory pathways does not have thesame characteristics as the AV node and does not exhibit postrepolarization refractoriness and conductsrapidly as the tissue is not dependent on calcium conduction, but rather sodium conduction similar to atrialand ventricular muscle. In such cases, the QRS complex is usually aberrant (and wide) and may beconfused with ventricular tachycardia, although the rhythm is still irregularly irregular. This rhythm may alsobe confused with AF with aberrancy; but with standard aberration, the morphology is more typical of a left orright bundle branch block. Conduction via an accessory pathway often shows a slurred QRS upstroke (see“Delta” wave), and this morphology depends on the location of the pathway and wherein inserts into theventricular myocardium. During so­called preexcitation syndromes, conduction can proceed through the AV

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node and/or the accessory pathway. The more conduction proceeds through the accessory pathway, themore QRS appearance is “aberrant.” A distinguishing feature of this entity of AF with preexcitation is therelationship between heart rate and QRS duration; the faster the rate, the wider the QRS width. (See"Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway" and "Approach to thediagnosis of wide QRS complex tachycardias".)

DIFFICULTIES IN DIAGNOSIS — Although the above findings usually allow the diagnosis of AF to be madeeasily, there are several pitfalls in correct identification of the rhythm. Errors in the diagnosis of AF are notuncommon, especially with computerized ECG interpretation [1].

Morphology of the QRS complex — The QRS complex usually maintains its normal narrow configurationin AF, since activation through the infranodal conduction system is intact. There are, however, settings inwhich widening of the QRS complex occurs. These include: a pre­existing conduction defect (left or rightbundle branch block); functional (generally rate­related) block in a portion of the infranodal conductionsystem that results in asynchronous or aberrant activation and, for example, a right bundle branch block

The f waves may be inapparent on the standard and precordial leads (waveform 3). This is most likelyto occur when AF is of long duration.

The f and u waves may have sufficient amplitude to look like P waves.

Extracardiac artifacts, such as those seen in patients with Parkinson disease and tremors, maysimulate f waves.

AF should be distinguished from other rhythms in which the R­R intervals are irregularly irregular.These include multifocal atrial tachycardia (MAT), wandering atrial pacemaker (WAP), multifocal atrialpremature beats, and atrial tachycardia or atrial flutter with varying AV block. In general, distinct(although often abnormal and in, the case of MAT and WAP, variable) P (or flutter) waves are presentin contrast to AF. (See "Clinical manifestations, diagnosis, and evaluation of narrow QRS complextachycardias".)

The R­R interval may be regular with AV dissociation or block, a setting in which a lower junctional,subjunctional, or ventricular pacemaker assumes control of the ventricles. This and the followingproblem may be seen, for example, with advancing digitalis toxicity. (See 'Effect of high degrees of AVnodal block and exit block on ventricular response' below.)

The R­R interval may be regularly irregular and show group beating with the combination of completeheart block and a lower nodal pacemaker with a Wenckebach type of exit block. (See "Second degreeatrioventricular block: Mobitz type I (Wenckebach block)".)

AF is frequently unrecognized in patients who are continuously or intermittently paced; the ECGs inthese patients should be closely examined for the presence of AF [2]. On the electrocardiogram, thereare no apparent P waves. Further, for some patients who have ventricular pacing, an atrial lead may bepresent so that intracardiac electrograms can be used to determine the presence of atrial fibrillation.

Atrial flutter can present with a variable response rate and the ventricular response can be irregularlyirregular. Additionally, frequent multiform PACs may present as an irregular response and appear to beatrial fibrillation. In some instances, short runs of atrial tachycardia can present as an irregularventricular response rate similar to AF and the P waves may be absent.

Patients who have no obvious P waves and a slow ventricular rate, whether it is regular or irregular,may have complete heart block.

Atrial fibrillation with rapid ventricular rates may be misdiagnosed as paroxysmal supraventriculartachycardia. In such cases, patients are commonly treated with adenosine, which will not convertpatients with AF [3].

AF with a wide QRS complex, as occurs in patients with either preexcitation or aberrancy, may make itdifficult to determine if the rhythm is AF or ventricular tachycardia. (See 'Morphology of the QRScomplex' below.)

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(RBBB) pattern; or preexcitation through an atrioventricular (AV) bypass tract which is capable of antegradeconduction. (See 'AF with an AV bypass tract' below.)

The diagnosis of aberrant conduction is a challenge. An aberrantly conducted beat due to a bundle branchblock generally has the pattern of a classical bundle branch or fascicular block. The cycle length of theaberrant beat must be sufficiently short so that it finds one of the pathways refractory, usually the rightbundle branch. In AF, however, some beats with identical cycle lengths may aberrate while others do not.

To understand why this might occur, it must be appreciated that the refractory period of the Purkinje cells ofthe bundle branches and fascicles is importantly determined by the preceding cycle length: A long precedingcycle lengthens and a short preceding cycle shortens the refractory period in these structures. A long­shortcycle, then, predisposes to aberration. Using functional RBBB as an example, a long preceding cyclelengthens the refractory period in the right bundle branch, and the following short cycle introduces a beatthat can traverse the left bundle branch but finds the right bundle refractory; the net effect is an ECG patternof RBBB (waveform 4). (See "ECG tutorial: Intraventricular block", section on 'Right bundle branch block'.)

Aberration following a long­short cycle in AF is often called the Ashman or Gouaux­Ashman phenomenon[4]. If, on the other hand, there were a short preceding cycle, then the right bundle would not be refractoryand normal conduction would occur. The initiation of aberration occurs with a long­short or more likely ashort­long­short interval that leads to conduction block in one of the bundle branches, usually the rightbundle, due to alterations of variations and refractoriness between the two bundles. Aberration can be inboth bundles so that there is alternating bundle branch block and there can also be something called“concealed perpetuated aberration.” In this instance, the abnormal bundle branch block activation continuesdespite irregularity, even slowing in the ventricular response rate due to the fact that there is concealedretrograde penetration in the other bundle

This type of functional bundle branch block occurs most commonly in the right bundle branch. The leftanterior fascicle is also frequently involved, often in combination with RBBB. In contrast, functionalaberration is uncommon in the His bundle, the left posterior fascicle, or the main left bundle. Rarely, thefunctional aberration can be sustained by concealed conduction within the AV node. In this setting, atrialfibrillatory waves may not be seen and the ECG may have the appearance of a ventricular tachycardia.

Although functional bundle branch block is common in AF, premature ventricular beats are even morefrequent. These beats generally do not have the morphology of a classic bundle branch or fascicular blockand do not necessarily follow a pattern of a preceding long­short cycle.

AF with an AV bypass tract — AF may develop in patients with an AV bypass tract that is capable ofantegrade or atrioventricular conduction. In this situation, the QRS complex is a fusion beat between thearea that is preexcited through the fast response bypass tract and the normal sequence of activation throughthe AV node. (See "General principles of asynchronous activation and preexcitation".)

The electrophysiologic properties of activation and reactivation are such that very rapid atrioventriculartransmission is possible, including the development of ventricular fibrillation [5,6]. This may occur whennormal conduction through the AV node and His­Purkinje system is blocked (such as occurs with an AVnodal blocking drug) and ventricular activation occurs only via the rapidly conducting accessory pathway,resulting in extremely rapid ventricular rates (that may be greater than 300 beats/min).

Effect of high degrees of AV nodal block and exit block on ventricular response — In patients withhigh grade or third­degree block in the AV node (as may occur with digitalis toxicity or progressive AV nodaldisease), impulses from the fibrillating atria fail to reach the infranodal conduction system. As a result, apacemaker below the level of the block assumes control of the ventricles. The pacemaker is usually locatedin the AV junction above the bifurcation of the bundle branches, leading to a QRS complex that has thesame morphology as if it had been conducted from the atria through the AV node. This pacemaker has acharacteristic rate of about 60 beats/min, unless it is accelerated or depressed due to pathology, ischemia,or drugs.

Less commonly, the pacemaker is subjunctional or ventricular. In this setting, the QRS complex will be wideand, unless accelerated, the ventricular rate will be relatively slow at 30 to 50 beats/min.

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The ECG findings vary with the severity of AV block and with the possible presence of exit block below thepacemaker. As an example, the following sequence can be seen with increasing degrees of digitalis toxicity(waveform 5A­D) [7,8].

SUMMARY — The electrocardiogram (ECG) in a patient with atrial fibrillation (AF) often has the followingcharacteristics (waveform 1 and waveform 2 and waveform 3):

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REFERENCES

1. Bogun F, Anh D, Kalahasty G, et al. Misdiagnosis of atrial fibrillation and its clinical consequences. AmJ Med 2004; 117:636.

2. Patel AM, Westveer DC, Man KC, et al. Treatment of underlying atrial fibrillation: paced rhythmobscures recognition. J Am Coll Cardiol 2000; 36:784.

3. Knight BP, Zivin A, Souza J, et al. Use of adenosine in patients hospitalized in a university medicalcenter. Am J Med 1998; 105:275.

4. GOUAUX JL, ASHMAN R. Auricular fibrillation with aberration simulating ventricular paroxysmaltachycardia. Am Heart J 1947; 34:366.

5. Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in the Wolff­Parkinson­White syndrome.N Engl J Med 1979; 301:1080.

A high but not complete degree of AV block in AF will initially lead to single junctional, subjunctional, orventricular escape beats with a cycle length characteristic of that pacemaker. These escape beatsrecur episodically during a rhythm strip; they can be diagnosed by the demonstration that the recurringlongest R­R intervals have a constant cycle length.

A higher degree of AV or third­degree block results in so few atrial impulses being conducted that thelower pacemaker takes over, leading to an escape junctional, subjunctional, or ventricular rhythm witha regular R­R interval for two or more cycles.

Rarely, the lower pacemaker may be regular but there is a Wenckebach type of exit block, resulting indecreasing R­R intervals with group beating characteristic of the Wenckebach phenomenon. (See"Second degree atrioventricular block: Mobitz type I (Wenckebach block)".)

Even less commonly, impulses from the lower pacemaker travel alternately down the right and leftbundle branches, resulting in a "bidirectional tachycardia" (waveform 6). This arrhythmia, which is alsofrequently a reflection of marked digitalis toxicity, may be considered to be ventricular bigeminy. In truebigeminy, however, the ventricular beat in the bigeminal pattern is premature. In comparison, the R­Rinterval is regular with a bidirectional tachycardia, since all of the beats arise from a single pacemaker.

Absence of discrete P waves.

Fibrillatory or f waves are present at a rate that is generally between 350 and 600 beats/minute; the fwaves vary in amplitude, morphology, and intervals. (See 'Atrial activity' above.)

The RR intervals follow no repetitive pattern; they have been labeled as “irregularly irregular.” (See'Ventricular rate' above.)

The ventricular rate usually ranges from 90 to 170 beats/min. (See 'Ventricular rate' above.)

The QRS complexes are narrow unless AV conduction is abnormal due to functional (rate­related)aberration, pre­existing bundle branch or fascicular block, or ventricular preexcitation. (See 'Ventricularrate' above.)

Although ECG findings described above usually allow the diagnosis of AF to be made easily, there areseveral pitfalls in correct identification of the rhythm. Errors in the diagnosis of AF are especiallycommon with computerized ECG interpretation. (See 'Difficulties in diagnosis' above.).

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6. Wellens HJ, Durrer D. Wolff­Parkinson­White syndrome and atrial fibrillation. Relation betweenrefractory period of accessory pathway and ventricular rate during atrial fibrillation. Am J Cardiol 1974;34:777.

7. Kastor JA, Yurchak PM. Recognition of digitalis intoxication in the presence of atrial fibrillation. AnnIntern Med 1967; 67:1045.

8. Childers R. Classification of cardiac dysrhythmias. Med Clin North Am 1976; 60:3.

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GRAPHICS

Atrial fibrillation

Lead V1 showing coarse atrial fibrillation with moderate ventricular response. Thetwo characteristic findings in AF are present: the very rapid atrial fibrillatory waves(f waves) which are variable in appearance; and the irregularly irregular ventricularresponse as the R­R interval between beats is unpredictable. Coarse atrial fibrillationmay appear similar to atrial flutter. However, the variable height and duration of thef waves differentiate them from atrial flutter (F) waves which are identical inappearance and occur at a constant rate of about 250 to 350 beats/min.

Courtesy of Ary Goldberger, MD.

Graphic 73958 Version 2.0

Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Atrial fibrillation

Atrial fibrillation is an irregularly irregular rhythm without regular ororganized atrial activity. Atrial activation is rapid (generally greater than320 beats per minute) and of various amplitudes. No discrete P wavesare seen on this tracing. Instead, rapid, irregular, variable and lowamplitude oscillating fibrillatory waves are observed between the QRScomplexes. When the arrhythmia is of long duration, the fibrillatorywaves may be inapparent.

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Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.

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Lead V5 from the same patient with atrial fibrillation

F waves are not apparent in this lead, as the only finding suggestive of AF is theirregularly irrregular ventricular response.

Courtesy of Morton Arnsdorf, MD.

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Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Functional right bundle branch block (RBBB) in atrialfibrillation occurring in the short cycle following a precedinglong cycle that lengthened the refractory period in the rightbundle branch (the ashman phenomenon)

Courtesy of Morton Arnsdorf, MD.

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Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Single­lead electrocardiogram (ECG) showing atrialfibrillation (AF) with junctional escape beats suggestingdigoxin toxicity

The 4 electrocardiograms in this sequence demonstrate increasing severity of digoxintoxicity in a patient with atrial fibrillation.This ECG shows atrial fibrillation with an irregularly irregular ventricular response.However, the longest recurring R­R intervals are constant, suggesting junctionalescape beats due to AV nodal block. The escape interval of 680 msec indicates anaccelerated automatic pacemaker with a rate of 88 beats/min.

The four electrocardiograms are adapted from: Childers R, Med Clin North Am 1976; 60:3.

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Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Single­lead electrocardiogram (ECG) showing atrialfibrillation with an accelerated junctional pacemaker

The 4 electrocardiograms in this sequence demonstrate increasing severity of digoxintoxicity in a patient with atrial fibrillation.In this strip, the R­R intervals are constant, as the ventricles are controlled by anaccelerated junctional pacemaker, resulting in a regular tachycardia at 115 beats perminute. Physical examination at this time might lead to the erroneous diagnosis of aregular sinus mechanism.

The four electrocardiograms are adapted from: Childers R, Med Clin North Am 1976; 60:3.

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Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0

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Single­lead electrocardiogram (ECG) showing atrialfibrillation with further accelerated junctional pacemaker

The 4 electrocardiograms in this sequence demonstrate increasing severity of digoxintoxicity in a patient with atrial fibrillation.In this strip, the R­R intervals remain constant with further acceleration of thejunctional pacemaker to a rate of 142 beats per minute.

The four electrocardiograms are adapted from: Childers R, Med Clin North Am 1976; 60:3.

Graphic 55119 Version 7.0

Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

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Single­lead electrocardiogram (ECG) showing atrialfibrillation and a junctional pacemaker with a 4:3Wenckebach exit block

The 4 electrocardiograms in this sequence demonstrate increasing severity of digoxintoxicity in a patient with atrial fibrillation.In this strip, the result is group beating characterized by three beats with decreasingR­R intervals. On physical examination, this seemingly irregular rhythm might lead tothe mistaken diagnosis of an irregularly irregular response to atrial fibrillation, ratherthan arrhythmia associated with severe digoxin toxicity. This patient presented withthis ECG; the preceding electrocardiograms reflected (in reverse order) the sequenceof recovery as the effect of digoxin wore off.

The four electrocardiograms are adapted from: Childers R, Med Clin North Am 1976; 60:3.

Graphic 66940 Version 7.0

Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0

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Single­lead electrocardiogram (ECG) showingbidirectional ventricular tachycardia (VT)

Rhythm strip showing bidirectional ventricular tachycardia (VT) which maybe a manifestation of digoxin toxicity. This rare, life­threateningtachyarrhythmia is characterized by beat­to­beat changes in the polarityof consecutive premature ventricular complexes.

Courtesy of Ary Goldberger, MD.

Graphic 71796 Version 3.0

Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0

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Disclosures: Brian Olshansky, MD Speaker's Bureau: Daiichi Sankyo [Anticoagulation (Edoxaban)].Consultant/Advisory Boards: BioControl [Vagal stimulation]; Boehringer Ingelheim [Anticoagulation(Dabigatran)]; Medtronic [ICDs]; Boston Scientific [ICDs, pacemakers]; Cardionomic [Autonomics];Lundbeck [Blood pressure (Droxidopa)]; Biotronick [ICDs]. Employment: Executive Health Resources[ICD implants]. Ary L Goldberger, MD Nothing to disclose. Bradley P Knight, MD, FACCGrant/Research/Clinical Trial Support: BSCI; MDT; SJM; Biotronik; Biosense Webster [EP (implantabledevices and ablation tools)]. Speaker's Bureau: BSCI; MDT; SJM; Biotronik; Biosense Webster [EP(implantable devices and ablation tools)]. Consultant/Advisory Boards: BSCI; MDT; SJM; Biotronik;Biosense Webster; Apama Medical [EP (implantable devices and ablation tools)]. Gordon M Saperia,MD, FACC Nothing to disclose.Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these areaddressed by vetting through a multi­level review process, and through requirements for references to beprovided to support the content. Appropriately referenced content is required of all authors and mustconform to UpToDate standards of evidence.Conflict of interest policy

Disclosures