ESCAPE ATRIAL BEATS – Escape atrial beats or rhythm may occur after a long sinus pause, resulting (most commonly) from sinus node exit block or sinus node arrest (show ECG 1).  If the pause is long enough, there will be an escape atrial rhythm at a rate correlating with the intrinsic automaticity of the atrial focus. This may be a single atrial beat, multiple atrial complexes, or a sustained atrial rhythm due to an accelerated or ectopic pacemaker.

The rate of the atrial rhythm is slower than that of the sinus node and the P wave morphology differs from that of the sinus P wave. Since the atrial focus is often within the atrial myocardium and therefore closer to the atrioventricular node, the time for atrial conduction to the atrioventricular node is decreased and the PR interval is shorter than that seen during sinus rhythm. The P wave morphology depends upon the location of the ectopic atrial focus.

ECTOPIC ATRIAL RHYTHM – Ectopic atrial rhythm occurs when the dominant pacemaker is an ectopic focus in the atrium (show ECG 2). This may result from sinus node failure and the development of an escape atrial rhythm (generally at a rate of 30 to 60 beats per minute). Another cause is the acceleration of an ectopic atrial focus, as with sympathetic nervous system activation. If the rate of this focus exceeds that of the sinus node, an atrial rhythm will be present at a rate faster than the intrinsic sinus rate. In such cases, sinus node impulse generation is suppressed.

The direction of atrial activation may be altered when an atrial rhythm is present since the pacemaker focus is within the atrial myocardium. The P wave is often small in duration and amplitude. The P wave axis depends upon the location of the ectopic pacemaker and the vector resulting from the direction of atrial activation. The P wave is inverted due to retrograde atrial activation when the pacemaker focus is in the low atrium, the area of the coronary sinus or the left atrium. This is often referred to as a "coronary sinus rhythm." The QRS complexes of an atrial tachycardia resemble those seen during sinus rhythm since myocardial activation is via the His Purkinje system.

ATRIAL TACHYCARDIA – Atrial tachycardia with 1:1 conduction is a supraventricular tachyarrhythmia that has a rate of 140 to 220 beats per minute (show ECG 3).  The QRS complexes occur at regular intervals (there is constant RR cycle length), and there is a P wave with a uniform morphology and the same PR interval. The baseline between successive P waves is flat and isoelectric on the electrocardiogram. The QRS complexes are similar to those seen during sinus rhythm since activation of the ventricular myocardium is unaltered and is via the His Purkinje system. Commonly, there is a warm up phase at the onset of the tachycardia, during which gradual rate acceleration or progressive shortening of the RR cycle length between the first several beats occurs.

Although all of the P waves are the same, they usually have a reduced amplitude and duration when compared to the sinus P wave. An atrial premature beat will reset, but not terminate the tachycardia. In general, there is prolongation of the PR interval as a result of decremental conduction through the atrioventricular node. In other words, there is a progressive slowing of the rate of impulse conduction through the atrioventricular node as it is stimulated at increasing rates. This is seen when the rate increase is not the result of sympathetic stimulation as is present in sinus tachycardia during which the PR interval shortens.

Since the ectopic focus is within the atrial myocardium and not affected by the vagus nerve (which only sparsely innervates the atria), activation of the parasympathetic nervous system (as produced by carotid sinus pressure) does not alter the atrial rate of the tachycardia. However, increased parasympathetic nervous activity may block the atrioventricular node and result in slowing of the ventricular rate (show ECG 4). An increase in circulating catecholamines will cause an acceleration of the atrial rate by directly enhancing the automaticity of the ectopic atrial focus.

WANDERING ATRIAL PACEMAKER – A wandering atrial pacemaker is present when there are multiple ectopic foci within the atrial myocardium which serve as the dominant pacemaker (show ECG 5). Since they discharge in random fashion, the pacemaker location is continuously shifting and may be located anywhere in the atrial myocardium. As a result, there is a changing vector of atrial activation which causes a changing P wave morphology and PR interval duration.

The QRS intervals have very variable cycle lengths since the ectopic foci have differences of automaticity and rates of impulse generation. The rhythm is therefore irregularly irregular and can be confused with atrial fibrillation. However, in contrast to atrial fibrillation, distinct P waves are present. QRS morphology is not altered from that seen during sinus rhythm, since activation of the ventricular myocardium occurs normally via the His-Purkinje system. This arrhythmia may be similar to sinus rhythm with multifocal atrial premature beats.

MULTIFOCAL ATRIAL TACHYCARDIA – Multifocal atrial tachycardia is similar to a wandering atrial pacemaker, except that the heart rate is rapid (greater than 100 beats per minute) (show ECG 6).

This arrhythmia usually occurs when there is damage to and distension of the atrial myocardium. Within such a myocardium, there is the potential for multiple independent ectopic foci which generate impulses at variable rates. If the automaticity of these foci is increased, as with sympathetic nervous system activation, the rate at which these foci generate an action potential increases, resulting in an increase in the heart rate.

Since these foci are located in multiple areas of the atrial myocardium, there is great variability of the P wave morphology and axis, the PR intervals, and the cycle lengths of the QRS complexes. The QRS complexes are unchanged and are similar to sinus rhythm since ventricular activation is normal.

Since the rhythm is rapid and irregularly irregular, it is often confused with atrial fibrillation.

ATRIAL PREMATURE BEATS NORMALLY CONDUCTED – Atrial premature beats occur when there is the premature or early activation of the atrial myocardium as a result of an impulse generated by an ectopic focus within the atrial myocardium rather than the sinus node (show ECG 7). The interval between the last sinus beat and the ectopic beat is shorter than the interval between two sinus beats (ie, it is premature).

The P wave morphology differs from that of sinus rhythm and its axis and amplitude depend upon the atrial location of the ectopic focus. Since the RR cycle length is shorter, there is a decrease in the rate of conduction of the ectopic beat through the atrioventricular node, a result of decremental conduction. The PR interval is therefore often longer than that of the sinus beat. Since activation of the ventricular myocardium occurs in a normal fashion, the QRS complex is unchanged from that of sinus rhythm.

Premature activation of the atrial myocardium by an ectopic focus results in a transient and variable affect on sinus nodal function and impulse generation.

• If the sinus node is depressed and reset, it activates the atrium after an interval identical to the usual sinus cycle length. In this setting, there is less than a full compensatory pause. In other words, the cycle length measured between the last beat before and the first beat after the premature beat is less than twice the cycle length of two sinus beats.

• If the premature beat fails to depress the sinus node, it generates an appropriately timed impulse which fails to activate the atrial myocardium since it is still refractory due to the premature beat. In this case, there is a true compensatory pause; the cycle length between the sinus beat just prior to and the first beat after the ectopic beat is twice the cycle length of two successive sinus beats.

• If the atrial premature beat is appropriately timed such that it results in a slowing of impulse conduction through the sinoatrial junction and hence a delay in atrial activation by the next sinus beat, the compensatory pause may have a cycle length greater than two sinus beat cycle lengths.

• The atrial premature beat is said to be interpolated when the atrial premature beat does not affect the sinus node and sinus rhythm is not altered.

NONCONDUCTED ATRIAL PREMATURE BEATS – Nonconducted or blocked atrial premature beats occur when there is premature activation of the atrial myocardium from an ectopic atrial focus at a time when the atrioventricular node is still refractory due to the previous sinus beat (show ECG 8). Since the block is in the atrioventricular node, there is an isolated or nonconducted P wave seen on the ECG. In some cases, however, it may be located within the ST segment or T wave of some leads and is obvious in other leads. In such cases, the P wave morphology is different from that of the sinus beat and the pause may be less than, identical to, or greater than a full compensatory pause depending upon the effect of the premature beat on the sinus node.

ABERRANTLY CONDUCTED ATRIAL PREMATURE BEATS – Although abnormal conduction along an accessory pathway may be the etiology, atrial premature beats with aberrant conduction generally occur when there is conduction delay or block within the right or left bundle branches (show ECG 9).

The atrial premature beat is conducted through the atrioventricular junction but reaches one of the bundles or its fascicles at a time when it has not yet recovered and is still relatively refractory. The velocity of impulse conduction via this pathway is therefore slowed. This results in a prolongation in the activation time of either the right or left ventricle, causing a widened or aberrant QRS complex.

An aberrantly conducted atrial premature beat is preceded by an ectopic P wave and a normal or prolonged PR interval; by comparison, there is usually no P wave before a ventricular premature beat. If the ventricular premature beat is late, there may be a P wave preceding, but it is non conducted and the PR interval is abnormally short. The morphology of the aberrant QRS complex depends upon which bundle or fascicle is involved. It is important to distinguish this from a ventricular premature beat.

ATRIAL TACHYCARDIA WITH ATRIOVENTRICULAR BLOCK – Atrial tachycardia with block is seen when there is failure of the atrioventricular (AV) node to conduct some of the atrial impulses to the ventricle (show ECG 4).

In this arrhythmia, an ectopic atrial focus is the dominant pacemaker and activates the atrial myocardium at a rate of 140 to 220 beats per minute. Due to changes in the electrophysiologic properties of the atrioventricular node, however, there is a slowing of impulse conduction through and prolongation of the refractory period of the AV node resulting in failure of the node to conduct some of the atrial impulses. This failure to conduct may be variable or may occur in a repeating pattern, such as 2:1, 3:1, 4:1 or Wenckebach.

The P wave differs from the P wave in sinus rhythm; it is usually diminutive, narrow, and often bizarre, but generally upright in the inferior leads. The PR interval is prolonged in relation to the rate due to decremental atrioventricular nodal conduction.

If the atrial rate is faster than the capability of the atrioventricular node to conduct each impulse, some of the impulses do not traverse through the node and are thus nonconducted to the ventricle, resulting in block. In this setting, AV nodal block may also occur because of:

• Increased vagal tone to the atrioventricular node (such as with digitalis or carotid sinus pressure)

• Intrinsic nodal disease

• Drugs that depress nodal function (such as calcium channel blockers)

• Prevention of sympathetically mediated actions due to beta blockers.

The potential for atrial tachycardia with block may be exposed with carotid sinus pressure which, by activating the vagus, will cause a delay or blockade of impulse transmission through the atrioventricular node without altering the atrial rate.

ATRIAL FLUTTER – Atrial flutter results from reentry within the right atrium, creating a macroreentrant circuit. 

The atrial rate in atrial flutter is generally 260 to 320 when no cardiac drug therapy is being administered. Since there is usually 2:1 block within the atrioventricular node, the ventricular response rate is 130 to 150 beats per minute (show ECG 10). The most frequent atrial rate in flutter is 300 with a ventricular rate of 150. Atrial rates may be slower if a drug which slows impulse conduction within the atrium, such as a IA or IC antiarrhythmic agent, is being administered.

The ventricular response rate depends upon the effect of the drug on the atrioventricular node and its conduction properties. In most cases, there is a concomitant decrease in the ventricular rate; however, in others, a slowing of the atrial rate without a change in nodal conduction properties may result in an increase in the number of impulses going through and reaching the ventricles.The rhythm is usually regular, although a regularly irregular rhythm may be present due to variable atrioventricular nodal conduction and block.

The flutter waves usually have a monotonously repeating saw tooth pattern due to a constantly undulating or zigzag baseline. This pattern either represents continuous depolarization and repolarization of the atria, or right followed by left atrial depolarization. There is no isoelectric period between successive flutter waves and all of the flutter waves are identical. These flutter waves are best seen in the inferior leads (2,3,aVF) or in lead V1. However, the flutter waves may not be obvious in some cases, especially if there are abnormalities of the ST segment and T waves. In this setting, they may be exposed with a reduction of the ventricular rate resulting from a slowing or blockade of impulse transmission to the ventricle via the atrioventricular node. Dampening of impulse transmission may occur when the vagal innervation to the node is activated by carotid sinus pressure or the Valsalva maneuver.

Two forms of atrial flutter have been identified based upon the contour of the flutter wave. In the common form, type 1, the flutter wave has a prominent negative component in the inferior leads and a positive deflection in leads aVR and aVL, indicating that the impulse originates in the low part of the atria. In the uncommon form, type II, the flutter deflections are positive in the inferior leads since the origin is in the proximal part of the atrium. 

Varying degrees of conduction between the atrium and ventricle may be observed based upon conduction delay, vagal tone, and other factors. Most commonly, there is 2:1 conduction between the atrium and the ventricle; however, there may be 4:1 or 6:1 conduction when there is conduction delay or block within the atrioventricular node such as with drugs or enhanced vagal tone. Odd numbered conduction ratios, such as 3:1 or 5:1, are rarely seen. However, when this occurs, it is often due to dual atrioventricular nodal pathways and two levels of nodal blockade.

There may also be other combinations of atrioventricular conduction resulting from the electrophysiologic properties of the node. Not infrequently seen is atrioventricular nodal Wenckebach which results from progressive slowing of conduction through the node and ultimate blockade, resulting in a repeating pattern such as 3:2. As a result of variable concealed conduction within the atrioventricular node, there may also be some variation in the interval between the flutter wave and the QRS complex. In this situation, a preceding flutter wave may be blocked in the atrioventricular node and alter the conduction of the next flutter wave. Depending upon the timing of these impulses, the conduction time and hence the intervals between the flutter wave and QRS complexes are variable. This may be mistaken for complete heart block.

ATRIAL FIBRILLATION – Atrial fibrillation is an irregularly irregular rhythm without regular or organized atrial activity (show ECG 11). Multiple reentrant circuits within the atrial myocardium generate multiple waves of impulses which often compete with or even extinguish each other. As a result, no uniform activation of the atrial tissue and no distinctive P waves are generated or recognized on the surface ECG. Since these multiple wavelets generate rapid and localized impulses, the sinus node is suppressed or not able to be expressed as it cannot activate the atrium.

Atrial activation is rapid (generally greater than 320 beats per minute) and of various amplitudes, and occurs with irregularly irregular intervals. No discrete P waves are seen on the electrocardiogram. Instead, rapid, irregular, variable and low amplitude oscillating fibrillatory waves are observed between the QRS complexes. When the atrial fibrillation is of recent onset, the fibrillatory waves are often coarse (>2 mm); by comparison, the fibrillatory waves are usually fine (<1 mm) with atrial fibrillation of greater duration.

The fibrillatory waves are of greater amplitude when there is hypertrophy of left atrial myocardium and become smaller with increasing atrial scarring and fibrosis. The amplitude of the fibrillatory waves do not correlate with the actual atrial size.

In some cases, there are no recognizable deflections of the baseline in any ECG lead and atrial fibrillation is inferred because of the absence of P waves and the irregularly irregular ventricular response. If present, the fibrillatory waves are best seen in the inferior leads and in V1.

While the atrial rate is very rapid and depends upon the electrophysiologic characteristics of the atrial myocardium, the ventricular response rate is dependent upon the properties of the atrioventricular node. The irregularity of the ventricular response is the result of the irregular and rapid atrial rate and the degree of concealed conduction within the atrioventricular node. The large number of atrial impulses bombarding the node compete with each other, interfering with their penetration into and through the node, leaving this tissue variably refractory. Irregular impulse conduction through the node to the ventricular myocardium therefore results.

A regular ventricular rate (regularization of atrial fibrillation), however, may infrequently occur despite a fibrillating atrium due to the complete blockade of atrioventricular nodal conduction and the subsequent development of an junctional escape rhythm. Drugs that impair nodal conduction (such as digoxin, beta blockers or calcium channel blockers) or AV nodal disease (which becomes obvious when the atrial rate is this rapid) may result in the development of this rhythm disturbance. 

The ventricular rate is generally 160 to 180 beats per minute, reflecting the maximal rate at which the atrioventricular node can conduct (as determined by its refractory period). Increases in the ventricular response rate to over 180 beats per minute may occur if the refractory period of the atrioventricular node is shortened, as with sympathetic stimulation or an increase in circulating catecholamines. In comparison, a decrease in the ventricular response rate occurs when the refractory period of the node is increased due to intrinsic atrioventricular nodal disease in combination with sympathetic blockade or direct depression of the atrioventricular node, or enhanced vagal tone from digoxin

When atrial fibrillation is associated with a preexcitation syndrome, the ventricular response rate may be very rapid, often in excess of 280 to 300 beats per minute. This is because impulse conduction bypasses the atrioventricular node, as conduction from the atria to the ventricles is via an accessory or intranodal pathway. If the refractory period of this pathway is very short, it is capable of conducting impulses at a very rapid rate. In such cases, the QRS complex is usually aberrant and may be confused with ventricular tachycardia, although the rhythm is still irregularly irregular. 

ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA – Atrioventricular nodal reentrant tachycardia (AVNRT, also called junctional reciprocating tachycardia) is a supraventricular tachyarrhythmia that originates within the atrioventricular node; this tachyarrhythmia may be the result of dual pathways within the node, a concealed bypass tract capable only of retrograde ventriculoatrial (VA) conduction, or intrinsic abnormalities of the node (show ECG 12). 

The rate is generally between 140 to 220 beats per minute in AVNRT and there is usually a 1:1 atrial-ventricular association; as a result, every QRS complex has an associated P wave. Infrequent findings include AV dissociation (due to impaired retrograde or only intermittent VA conduction through the AV node) and 2:1 AV block (due to infra-nodal or intra-Hisian block).

Atrial and ventricular activation may be simultaneous; as a result, a P wave is superimposed upon the QRS complex and therefore not obvious on the surface ECG. In some cases, the P wave may fuse with the terminal portion of the QRS complex producing a pseudo-r' in lead V1 and/or a pseudo-S in the inferior leads (show ECG 13). When the etiology is a concealed bypass tract or when there is delayed retrograde conduction through the atrioventricular node, a retrograde P wave will follow the QRS complex. Although the RP interval is generally short in this setting, it will infrequently be long (long RP syndrome) due commonly to a bypass tract or intranodal tract that conducts slowly in the retrograde direction (uncommon form of AVNRT) (show ECG 14). In contrast to an atrial tachycardia, a junctional tachycardia does not manifest a warm up period. In other words, no progressive acceleration of rate or shortening of the RR cycle length of the first few beats is observed.

Since this arrhythmia is usually initiated by an atrial premature beat, there is an initial ectopic atrial P wave and prolonged PR interval which differs from the retrograde P waves which are associated with each subsequent QRS complex. Infrequently a ventricular premature beat initiates the junctional tachycardia as a result of retrograde conduction through the atrioventricular node. In contrast to an atrial tachycardia, junctional tachycardia is not reset by a premature stimulus but may be terminated by it.

ATRIOVENTRICULAR NODAL (JUNCTIONAL) ECTOPIC RHYTHM – Junctional ectopic rhythm is most often the result of an acceleration of impulse generation from the atrioventricular junction which, if more rapid than the sinus node rate, assumes control as the dominant pacemaker of the heart (show ECG 15). In such cases, there are no P waves seen before the QRS complexes; instead, they occur either simultaneously with the QRS complexes or are retrograde (seen after the QRS complex located in the ST segment or T wave). Sinus node activity is suppressed since there is usually retrograde atrial activation. If there is retrograde VA block of the impulse to the atrium, sinus node activity is not suppressed by the accelerated junctional rhythm, and sinus P waves can be seen occurring independently at a slower rate than the QRS complexes. This is known as atrioventricular dissociation. In some cases, the junctional ectopic rhythm develops because there is failure of the sinus node and of an atrial focus to assume pacemaker function which is therefore assumed by the atrioventricular junction. This is known as a junctional escape rhythm.

ATRIOVENTRICULAR REENTRANT TACHYCARDIA – Atrioventricular reentrant tachycardia (AVRT) is a supraventricular tachycardia associated with a preexcitation syndrome (particularly the Wolff-Parkinson-White syndrome) which results due to the presence of an accessory pathway (show ECG 16). The circuit involved in this reentrant arrhythmia includes the accessory bypass tract, atrioventricular node and His Purkinje system as well as the atria and ventricles which serve as the proximal and distal limbs between the two pathways. 

In this arrhythmia, there is always 1:1 conduction of the impulse between the atria and ventricles since both structures, along with the atrioventricular node and accessory pathway, are a necessary part of the circuit. The bypass tract and the atrioventricular node-His Purkinje pathway may conduct the impulses in either an antegrade or retrograde direction. The direction of travel depends upon the refractory periods of these two pathways and the relationship between them.

The most common type of supraventricular tachycardia uses the atrioventricular node and His Purkinje system (which has a relatively short refractory period) for antegrade conduction to the ventricles and the accessory pathway (which in these patients has a relatively long antegrade refractory period when compared to the node) for retrograde conduction. During this type of arrhythmia, called orthodromic tachycardia, QRS complexes are narrow (show figure 1 and show ECG 17). During sinus rhythm, however, wide and bizarre QRS complexes (indicative of the WPW pattern) are caused by conduction over both the accessory and normal pathways, resulting in a fusion beat. Since during the AVRT there is 1:1 retrograde activation of the atrium, a negative P wave may be present following the QRS complex.

Less commonly, particularly when the refractory period of the accessory pathway is shorter than that of the AV node and the His Purkinje system, the antegrade limb of the circuit, activating the ventricle, is the accessory pathway and the impulse is conducted retrogradely to the atrium via the His-Purkinje and atrioventricular node (show figure 2). In this tachycardia, called antidromic tachycardia, the QRS complexes are wide or aberrant resembling the QRS complexes seen during sinus rhythm and there is a retrograde or negative P wave (show ECG 18). 

ATRIOVENTRICULAR NODAL (JUNCTIONAL) PREMATURE BEATS – Junctional premature beats are early ectopic beats which originate in or near the atrioventricular junction and have a QRS morphology which resembles the sinus complex (show ECG 19). Although their timing and morphology are similar to that of an atrial premature beat, there is no P wave present before the QRS complex. Although no P wave is usually seen, a retrograde P wave may be obvious if there is retrograde conduction through the atrioventricular node.

As with atrial premature beats, junctional premature beats may be conducted with aberration if they originate near a perinodal accessory pathway (such as Mahaim or James fiber) or if there is conduction system disease and the development of a bundle branch block when the RR cycle length is short.

ATRIOVENTRICULAR NODAL (JUNCTIONAL) ESCAPE BEATS – Escape junctional beat or rhythm occurs when there is failure of upper pacemaker tissue. In other words, the absence of impulse generation from the sinus node or atrial myocardium. This rhythm occurs after a variable pause which is longer than the underlying sinus cycle length (show ECG 20).

In this arrhythmia, there are one or more normal QRS complexes that are not preceded by a P wave. In addition, there may be continuous normal supraventricular QRS complexes which occur at regular intervals but which are without P wave activity preceding each complex. If there is retrograde conduction through the atrioventricular node, inverted or retrograde P waves may be seen after each QRS complex, in the ST segment or on the T waves.

The rate is slower than that of the underlying sinus rate. An escape junctional rhythm may also occur when there is a complete block of atrioventricular nodal conduction, preventing the sinus impulse from reaching the ventricles. In this case, there are observed P waves which are unassociated with the QRS complexes, and the PR intervals are variable. Such P waves occur at a rate that is more rapid than the ventricular rate, resulting in atrioventricular dissociation.