Version May 2024
INTRODUCTION — Supraventricular rhythms appear on an electrocardiogram (ECG) as narrow complex rhythms, which may be regular or irregular. They may have a normal rate, be tachycardic, or be bradycardic depending on the underlying arrhythmia mechanism and presence of atrioventricular (AV) nodal block. Bundle branch blocks may be present either at baseline or due to rate-related aberrancy, which can make the QRS complex wide, though these rhythms are more commonly narrow complex. When evaluating the rhythm, the most important steps are to evaluate for the presence of P waves and determine if the morphology, axis, and duration match the normal sinus rhythm P wave.
ESCAPE ATRIAL BEATS — Escape atrial beats may occur after a long sinus pause, usually resulting from sinus node exit block or sinus node arrest (waveform 1) (see "Sinoatrial nodal pause, arrest, and exit block"). 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 ectopic atrial rhythm due to an ectopic site. (See 'Ectopic atrial rhythm' below.)
The rate of the escape atrial beats is slower than that of the sinus node (since it is an escape rhythm) and the P wave morphology differs from that of the sinus P wave, depending upon the location of the ectopic atrial focus. (See 'Ectopic atrial rhythm' below.)
ECTOPIC ATRIAL RHYTHM — Ectopic atrial rhythm occurs when the dominant pacemaker is an ectopic focus in the atrium and not the sinus node (waveform 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 [bpm]) or the acceleration of an ectopic atrial focus faster than the rate of the sinus node. 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 outside the sinus node. The P wave morphology, axis, and duration vary based on the site of origin within the atrium. The QRS complexes of an ectopic atrial rhythm resemble those seen during sinus rhythm since myocardial activation is still via the His Purkinje system. However, since atrial activation is abnormal and no longer via the normal intra-atrial pathways, right and left atrial abnormalities (hypertrophy or conduction abnormality) cannot be reliably diagnosed.
ATRIAL TACHYCARDIA — When the ectopic atrial rhythm is at a rate >100 bpm, it is termed "atrial tachycardia." (See "Focal atrial tachycardia".)
Atrial tachycardia with 1:1 conduction is a supraventricular tachyarrhythmia that typically has a rate of 140 to 220 bpm (waveform 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 (if AV block is present) is flat and isoelectric on the ECG. 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 PP cycle length between the first several beats occurs. There may also be a cool-down phase at the end of the tachycardia, during which the rate gradually decelerates, with progressive lengthening of the PP cycle length.
Although all of the P waves are the same, they have a different morphology than the sinus P wave, depending on the site of origin. The best lead for determining whether the location is from the left or right atrium is V1. A negative or biphasic positive/negative P wave in V1 was 100 percent specific in one study for predicting a right atrial location (see "Focal atrial tachycardia", section on 'Localization of AT focus'). Similarly, a positive or biphasic negative/positive P wave in V1 was 100 percent sensitive for a left atrial location.
In general, there is prolongation of the PR interval as a result of decremental conduction through the AV node. In other words, there is a progressive slowing of the rate of impulse conduction through the AV node as the atrial rate increases. Therefore, the PR interval is usually longer than in sinus rhythm. On occasion, the PR interval may be shorter than that seen during sinus rhythm if the ectopic atrial focus is close to the AV node and bypasses intra-atrial conduction, or if there is significant sympathetic tone.
Since the ectopic focus is within the atrial myocardium and not affected by the vagus nerve, 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 (or adenosine) may block the AV node and result in slowing of the ventricular rate, unmasking the atrial activity (waveform 4). In this situation, sequential, discrete, non-conducted P waves are seen, and there is an isoelectric baseline between the P waves. An increase in circulating catecholamines may increase the atrial rate by directly enhancing the automaticity of the ectopic atrial focus.
Atrial tachycardia with atrioventricular block — If the atrial rate is faster than the capability of the AV node to conduct each impulse, some of the impulses do not traverse through the node, resulting in a form of AV block (waveform 4). The ventricular rate may be variable or occur in a repeating pattern, such as 2:1, 3:1, 4:1, or Wenckebach. AV nodal block may occur because of:
●Normal AV nodal decremental properties
●Increased vagal tone to the AV node (such as with digitalis or carotid sinus pressure)
●Intrinsic AV nodal disease
●Drugs that depress nodal function (such as calcium channel blockers and beta blockers)
WANDERING ATRIAL PACEMAKER — A wandering atrial pacemaker (also termed "multifocal atrial rhythm") is present when there are three or more ectopic foci within the atrial myocardium that serve as the source of the P wave (waveform 5). Since they discharge in random fashion, the site of atrial origin is continuously shifting and may be located anywhere in the atrial myocardium. As a result, there is a changing vector of atrial activation that causes a changing P wave morphology and PR interval duration. A dominant P wave (sinus or atrial) cannot be identified. The rate is ≤100 bpm.
The QRS intervals have variable cycle lengths since the ectopic foci exhibit differences in automaticity and rates of impulse generation. The rhythm is therefore irregularly irregular, and it can be confused with atrial fibrillation. However, in contrast to atrial fibrillation, distinct P waves of multiple morphologies are present. Sinus arrhythmia may also be irregularly irregular; however, one P wave morphology is seen in this situation. This arrhythmia may also be confused with sinus rhythm with multifocal premature atrial complexes, although in this situation, a dominant sinus P wave can be identified and there are periods of RR interval regularity.
MULTIFOCAL ATRIAL TACHYCARDIA — Multifocal atrial tachycardia is similar to a wandering atrial pacemaker in that there are three or more independent ectopic foci, except that the heart rate is greater than 100 bpm (waveform 6). (See "Multifocal atrial tachycardia".)
This arrhythmia usually occurs when there is damage to or distension of the atrial myocardium. Within such a myocardium, there is the potential for multiple independent ectopic foci that generate impulses at variable rates. If there is sympathetic nervous system activation, there can be 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 morphology is unchanged and is similar to sinus rhythm since ventricular activation is normal.
Since the rhythm is rapid and irregularly irregular, it is often confused with atrial fibrillation. With atrial fibrillation, however, there are no distinct P waves seen.
PREMATURE ATRIAL COMPLEX — Premature atrial complex (PAC; also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) occurs when there is 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 (waveform 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). (See "Supraventricular premature beats".)
PACs can be unifocal or multifocal. The P waves of the premature complexes exhibit identical morphology in unifocal PACs and variable morphology in multifocal PACs. Atrial bigeminy and trigeminy refer to rhythms in which every other beat (bigeminy) or every third beat (trigeminy) is a PAC. Apart from the repeating pattern and amount of ectopy, there is no clinical significance to this finding.
The P wave morphology differs from that of sinus rhythm and its axis and morphology depend upon the atrial location of the ectopic focus. The PR interval is often longer than that of the sinus beat, a result of decremental conduction, though this finding may be subtle. However, the PR interval may be shorter if the ectopic focus is near the AV node and does not occur too prematurely. 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 effect on sinus nodal function and impulse generation. These findings can be reproduced in the electrophysiology lab during testing of the sinoatrial conduction time (see "Invasive diagnostic cardiac electrophysiology studies", section on 'Electrocardiographic and electrophysiologic recordings'):
●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 P wave before and the first P wave after the premature beat is less than twice the cycle length of two sinus P waves.
●If the premature beat collides with the sinus node impulse in the sinoatrial junction, the sinus node activity is not suppressed and there is a true compensatory pause seen. 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 PAC is appropriately timed such that it only results in a slowing of impulse conduction through the sinoatrial junction, as opposed to block, there is a delay in atrial activation of the next sinus beat, and the compensatory pause will have a cycle length greater than two sinus beat cycle lengths.
●If there is sinus node dysfunction present, the PAC may depress the sinus node and there may be a long delay before sinus node automaticity recovers. In this situation, the pause is much longer than a full compensatory pause.
●The PAC is said to be interpolated when it does not affect the sinus node and sinus rhythm is not altered.
Nonconducted or blocked PACs occur when there is premature activation of the atrial myocardium from an ectopic atrial focus at a time when the AV node is still refractory due to the previous sinus beat (waveform 8). Since the block is in the AV node, there is an isolated P wave with no QRS. The P wave may be difficult to see if it is located within the ST segment or T wave of the prior beat.
Aberrant conduction of a PAC generally occurs when there is conduction delay or block within the right or left bundle branches, although abnormal conduction along an accessory pathway can also be a cause (waveform 9). The PAC is conducted through the AV junction but reaches one of the bundles or its fascicles at a time when it has not yet recovered and is still relatively refractory. Impulse conduction via this pathway is therefore blocked, although conduction will occur normally through the other parts of the His-Purkinje system. This results in a right or left bundle branch block pattern, depending on which bundle or fascicle is involved. The mechanism is similar to the Ashman phenomenon. (See "ECG tutorial: Intraventricular block", section on 'Ashman phenomenon'.)
ATRIAL FIBRILLATION AND ATRIAL FLUTTER — These topics are discussed in detail elsewhere. (See "The electrocardiogram in atrial fibrillation" and "Electrocardiographic and electrophysiologic features of atrial flutter".)
ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA — Atrioventricular nodal reentrant tachycardia (AVNRT, also called "junctional reciprocating tachycardia") is a supraventricular tachyarrhythmia that originates within the AV node and adjacent atrial myocardium and is the result of dual pathways entering the compact AV node (waveform 10). (See "Atrioventricular nodal reentrant tachycardia" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)
The rate is generally between 140 to 220 bpm, and there is usually 1:1 AV association; as a result, every QRS complex has an associated P wave. Rarely is there 2:1 AV block (due to lower common pathway, infra-nodal or infra-Hisian block) with two P waves and one QRS, or 2:1 ventriculoatrial (VA) block (due to upper common pathway block) with two QRS complexes for every P wave.
Atrial and ventricular activation are usually 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 (figure 1). This is referred to as "typical" or "slow-fast" tachycardia since the antegrade limb to the ventricles is a slow pathway while the retrograde limb back to the atrium is a fast pathway. Less frequently, AVNRT will be associated with a long RP interval, also called "atypical AVNRT" (figure 2). This occurs when there are two slow pathways and no fast pathway (termed "slow-slow") or there is antegrade conduction via the fast pathway and retrograde conduction to the atrium via the slow pathway (called "fast-slow").
In contrast to an atrial tachycardia, AVNRT usually starts and stops abruptly and does not usually manifest a warm-up or cool-down period. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)
Since this arrhythmia is usually initiated by a PAC, there is an initial ectopic atrial P wave and prolonged PR interval. Infrequently, a premature ventricular complex/contraction (PVC; also referred to as premature ventricular beats or premature ventricular depolarizations) initiates AVNRT as a result of retrograde conduction through the AV node.
ATRIOVENTRICULAR REENTRANT TACHYCARDIA — Atrioventricular reentrant tachycardia (AVRT), or atrioventricular reciprocating tachycardia, is a supraventricular tachycardia that utilizes an accessory pathway between the atria and ventricles. It is frequently, but not exclusively, associated with a preexcitation syndrome (ie, the Wolff-Parkinson-White syndrome) (waveform 11), since pathways may conduct antegrade only, retrograde only, or antegrade and retrograde. Retrograde only pathways cannot be seen on the ECG. The circuit involved in this reentrant arrhythmia includes the accessory bypass tract, AV node, and His Purkinje system, as well as the atria and ventricles. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome".)
The most common type of AVRT uses the AV 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 AVRT," QRS complexes are narrow (figure 3 and waveform 12). There is always 1:1 conduction of the impulse between the atria and ventricles since both structures, along with the AV node and accessory pathway, are a necessary part of the circuit. Since there is retrograde activation of the atrium during orthodromic AVRT, a negative P wave may be seen in the inferior leads with a short RP interval.
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 AV node (figure 4). In this tachycardia, called "antidromic AVRT," the QRS complexes are maximally pre-excited and very wide, and there is a retrograde (and negative) P wave in lead II (waveform 13). This form of AVRT may be difficult to distinguish from ventricular tachycardia. (See "Wide QRS complex tachycardias: Approach to the diagnosis".)
ATRIOFASCICULAR AND MAHAIM FIBER TACHYCARDIAS — Atriofascicular pathways are rare types of bypass tracts. In contrast to AV bypass pathways in the classic Wolff-Parkinson-White syndrome, atriofascicular pathways are typically found along the tricuspid annulus and connect directly into the right bundle branch system. Conduction is decremental, like that in the AV node, such that faster heart rates (eg, with atrial pacing) or spontaneous premature atrial complexes can lead to a prolongation of the PR interval. Since the supraventricular tachycardia circuit only conducts down the atriofascicular pathway and then up the AV node (antidromic pathway), clinicians usually observe a wide QRS with a left bundle branch block morphology, an R wave in lead I, and a QRS transition zone usually at or to the left of lead V4. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome" and "General principles of asynchronous activation and preexcitation".)
Mahaim fibers, which include nodoventricular or nodofascicular pathways, may also be an unusual cause of supraventricular tachycardia. (See "Atriofascicular ("Mahaim") pathway tachycardia".)
JUNCTIONAL ECTOPIC RHYTHM — Junctional ectopic rhythm is most often the result of an acceleration of impulse generation from the AV junction, which, if more rapid than the sinus node rate, assumes control as the dominant pacemaker of the heart (figure 5). In such cases, there are no P waves seen before the QRS complexes; instead, they occur either simultaneously with the QRS complexes or more commonly are retrograde (seen after the QRS complex located in the ST segment or T wave). Sinus node activity is suppressed by the retrograde atrial activation. If there is retrograde AV block of the impulse to the atrium, sinus node activity is not suppressed by the junctional rhythm, and sinus P waves can be seen occurring independently at a slower rate than the QRS complexes. This is a type of AV dissociation. When the junctional rhythm is faster than 100 beats/min, it is called junctional tachycardia. In some cases, the junctional ectopic rhythm develops because there is failure of the sinus node. Since the rate is slower than the expected sinus rate, it is known as a junctional escape rhythm.
JUNCTIONAL PREMATURE BEATS — Junctional premature beats are early ectopic beats that originate in or near the AV junction and have a QRS morphology that resembles the sinus complex (waveform 14). Although their timing and morphology are similar to that of a premature atrial complexes, there is no P wave present before the QRS complex, though a P wave may be noted after the QRS complex if there is retrograde conduction through the AV node.
As with atrial premature beats, junctional premature beats may occasionally be conducted with a bundle branch block pattern. In addition, junctional premature beats may occur with a bigeminal or trigeminal pattern.
JUNCTIONAL ESCAPE BEATS — Junctional escape beats or rhythm occur when there is failure of upper pacemaker tissue (in other words, the absence of impulse generation from the sinus node or atrial myocardium or with complete AV block). These beats occur after a variable pause that is longer than the underlying sinus cycle length (waveform 15).
In this arrhythmia, there are one or more normal QRS complexes that are not preceded by a P wave. If there is retrograde conduction through the AV node, retrograde P waves may be seen after each QRS complex, in the ST segment, or in the T wave.
The rate is slower than that of the underlying sinus rate. An escape junctional rhythm may occur during sinus arrest or when there is a complete AV block, preventing the sinus impulse from reaching the ventricles. In this case, there are P waves that are disassociated 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 AV dissociation.
SUMMARY
●Atrial tachycardia – Atrial tachycardia occurs at 140 to 220 beats per minute and usually has 1:1 atrioventricular (AV) conduction (waveform 3). In some situations, there may be block within the AV node, leading to variable or repetitive block patterns (waveform 4). P-wave morphology can be used to determine the atrial tachycardia site of origin. (See 'Atrial tachycardia' above.)
●Wandering atrial pacemaker and multifocal atrial tachycardia – Wandering atrial pacemaker (rate ≤100 beats per minute [bpm]) (waveform 5) and multifocal atrial tachycardia (rate >100 bpm) (waveform 6) demonstrate three or more different P-wave morphologies with no dominant P wave. (See 'Wandering atrial pacemaker' above and 'Multifocal atrial tachycardia' above.)
●AVNRT – Atrioventricular nodal reentrant tachycardia (AVNRT) originates within the AV node and adjacent atrial myocardium and is the result of dual pathways entering the compact AV node. Atrial and ventricular activation are commonly simultaneous; as a result, the P wave is superimposed upon the QRS complex and therefore not obvious on the surface ECG (waveform 10). Less frequently, AVNRT will be associated with a long RP interval, also called "atypical AVNRT" (figure 2). (See 'Atrioventricular nodal reentrant tachycardia' above.)
●AVRT – Atrioventricular reentrant tachycardia (AVRT) utilizes an accessory pathway between the atria and ventricles. It is frequently, but not exclusively, associated with a preexcitation syndrome (ie, the Wolff-Parkinson-White syndrome) (waveform 11). Atrial and ventricular activation are usually simultaneous; as a result, a P wave is superimposed upon the QRS complex and therefore not obvious on the surface ECG. AVRT must have 1:1 atrial and ventricular conduction, and, therefore, a P wave follows every QRS, even if not well seen. (See 'Atrioventricular reentrant tachycardia' above.)
●Junctional beats – Junctional beats have a QRS morphology similar to a natively conducted QRS, but have no P wave preceding it (waveform 14). Junctional escape beats or rhythm can occur with sinus arrest or complete AV block (waveform 15). (See 'Junctional ectopic rhythm' above and 'Junctional premature beats' above and 'Junctional escape beats' above.)
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