Premature supraventricular complexes are premature complexes of supraventricular origin. These include those of atrial (A‐PSVC) and atrioventricular junctional origin (J‐PSVC). Most PSVCs have a fixed or nearly fixed coupling interval (distance from the beginning of the previous sinus P wave to the beginning of the premature ectopic P′), because their origin is dependent on the baseline heart rhythm. They are commonly called extrasystoles. The most frequent mechanism causing PSVC is micro‐reentry in the atrial muscle. Premature supraventricular complexes that have an extremely variable coupling interval are called parasystoles, and the most common mechanism is increased automatism. The automatic focus is protected from the basic rhythm (entry and exit block), and is therefore independent of it. In the ECG, a premature ectopic P (P′) wave is observed, which is followed, if not blocked in the atrioventricular (AV) junction, by a QRS complex, which is also premature. The P′ wave is usually hidden in the previous T wave, which is usually modified by the P′ wave, resulting in a masked P′ morphology (Figure 15.1). If the origin of a PSVC is the AV junction (J‐PSVC), then the premature P wave is always negative in II, III, and aVF due to retrograde activation of the atrium from the junction region. PSVCs may be isolated or occur in runs (Figure 15.2). They rarely comply with the ECG criteria for atrial parasystole (see Figure 14.5D). PSVCs may be conducted to the ventricles in three different ways: normal conduction, aberrant conduction, or blocking in the AV junction (non‐conducting), leading to a pause (Figure 15.1). When supraventricular tachyarrhythmia runs occur, sometimes the first complex of the run shows an aberrant morphology which is a result of the Gouaux–Ashman phenomenon (Figure 15.3B) (Longo and Baranchuk 2017). The differential diagnosis between aberrant PSVCs and ventricular complexes is shown in Table 15.1. From a clinical point of view, PSVCs are generally benign. It is important to determine: (i) their frequency; (ii) if they are associated with paroxysmal arrhythmias, (iii) if they disappear with exercise; and (iv) any etiological factors. PSVCs may be associated with heart disease (i.e. ischemic heart disease (IHD), cor pulmonale, thyroid dysfunction, pericardial diseases, psychologic factors, drugs, digitalis intoxication, etc.) or may be due to functional disturbances. In healthy individuals, they are usually related to digestive problems (aerophagia, etc.), coffee consumption, alcohol, and stress. More recently, the number (burden) of PSVCs in 24 hours has been associated with an increased risk of atrial fibrillation (Prasitlumkum et al. 2018). Sinus tachycardia is defined as sinus rhythm with a rate greater than 100 bpm. Most cases of sinus tachycardia are caused by an increase of sinus automaticity as a response to different physiologic sympathetic stimuli (exercise, emotions, etc.) (Figure 15.4), or other specific causes such as fever, hyperthyroidism, pulmonary embolism, acute myocardial infarction, heart failure, etc. Occasionally, orthostatism leads to an exaggerated sinus tachycardia (postural orthostatic tachycardia syndrome (POTS)). Figure 15.1 Sinus rhythm alternating with paroxysmal atrial fibrillation (AF) episodes and frequent premature supraventricular complexes (PSVCs). (A) A PSVC is conducted normally. (B) A PSVC is conducted with aberrancy because it occurs earlier. (C) A PSVC is blocked, because it occurs earlier in the cycle and the preceding diastole is a little longer. The pause is due to an active, not to a passive arrhythmia. There have been cases caused by an inappropriate increase of sinus automaticity, probably due to a lack of autonomic modulation of the sinus node or a sinoatrial reentrant tachycardia (Gomes et al. 1985; Femenía et al. 2012) (Figure 15.5). In the ECG, sinus tachycardia presents as an increase in heart rate that occurs progressively in the majority of cases, and persists over a certain amount of time, with certain changes, until the triggering stimulus disappears. Heart rate during exercise, especially in young people with sympathetic overdrive, may reach 180–200 bpm. If the P wave falls in the refractory period of the AV junction, it may conduct with a long PR interval, resulting in a PR > RP. In such cases, in order to better visualize the P wave, some maneuvers (Figure 15.5) or an amplifying technique, a filtering T wave technique, or special leads (Lewis leads) are useful. In patients with sinus tachycardia due to physiologic sympathetic overdrive (exercise, emotions, etc.), it is frequently observed that the PR and ST segments form part of a circumference, as the PR segment descends whereas the ST segment ascends (Figure 15.4). Figure 15.2 Examples of supraventricular premature complexes: (A) isolated; (B) in pairs; (C) in runs. Figure 15.3 (A) A healthy 8‐year‐old girl with atrial trigeminy, at times normally conducted and at other times blocked (see change in T wave morphology in the AV‐pause, arrow (compare AB = CD)). Sometimes, it was conducted with right bundle branch (RBB) and other times with left bundle branch (LBB) morphology. (B) A short run of supraventricular tachycardia. Only the first complex of the run is aberrant due to the Gouax–Ashman phenomenon. Table 15.1 ECG evidence indicative of the presence of ectopy or aberrancy when early wide isolated QRS complexes are observed in the presence of sinus rhythma a Specificity ≥90%. The appearance of abrupt sinus tachycardia suggests sino‐reentrant mechanisms (Figure 15.6). Sinus tachycardia caused by a large sympathetic overdrive decreases at night or at rest because of vagal prevalence. This helps to distinguish it from sinus tachycardia due to pathologic causes such as pulmonary embolism, hyperthyroidism, or heart failure, in which sinus tachycardia is more persistent. Treatment for sinus tachycardia consists of suppression of the underlying triggering cause, if feasible (i.e. stimulant intake), or treating the underlying disease (heart failure, hyperthyroidism, fever, etc.) and usually prescribing beta blockers and/or ivabradine (Femenía et al. 2012). Physiologic tachycardia will disappear when the triggering factor is removed, as previously discussed. Figure 15.4 Sinus tachycardia in a 32‐year‐old man at different moments during a parachute jump: control jump (C), with placebo (P), and after taking a beta blocker (BB). Beta blocker (propanolol) administration leads to a less accelerated heart rate. During the control and placebo jumps, a typical ECG sympathetic overdrive pattern is observed (140 bpm), where PR and ST are part of an arch circumference (drawing). Table 15.2 Supraventricular active rhythms Table 15.3 Classification of supraventricular tachyarrhythmias according to RR (regular or irregular) Monomorphic atrial tachycardia includes all types of atrial tachycardias that display non‐sinus monomorphic P waves (P′) on the surface ECG. Both the initial P′ waves, which initiate the tachycardia, and the subsequent waves have the same morphology (Figure 15.7). The high atrial tachycardias close to the sinus node (parasinus origin) usually produce a P′ wave that may be identical to a sinus P wave. There are two well‐defined types of monomorphic atrial tachycardia (MAT): Figure 15.5 Above: Tachycardia at 110 bpm with barely visible atrial activity (a notch following the QRS complex is observed in V3). Breathing (II, continuous trace) results in a slowed down tachycardia, allowing us to see the atrial wave, which is close to the end of the T wave and shows sinus polarity (arrow). Figure 15.6 Sudden onset of supraventricular tachycardia at a rate of 110 bpm with P wave identical to the sinus wave. This may correspond to reentrant sinoatrial tachycardia. Table 15.4 Clinical, electrophysiological, and pharmacological differences between the different types of monomorphic atrial tachycardia with ectopic focus (MAT‐EF), depending on their triggering mechanism (micro‐reentry, increase of automatism, or triggered activity) a This group includes the micro‐reentry originating in an ectopic focus and also the macro‐reentry originating in the area surrounding an atrial postsurgical scar. The P wave usually shows, in the case of MAT‐EF of the left atrium, the majority originating from the pulmonary veins, a prolongation of P wave that is often notched. Figure 15.10 summarizes the sites of origin and an algorithm allowing their identification by ECG (Kistler et al. 2006). Table 15.5 Characteristics of atrial activity in monomorphic supraventricular tachyarrhythmiasa a Monomorphic atrial tachycardias generated in the areas surrounding a postsurgical scar in patients operated for congenital heart disease or subjected to atrial ablation procedures (atrial macro‐reentry) may feature different ECG morphologies: the most characteristic ones are identical to those observed in the reverse flutter, although sometimes they may show the same morphologies as the common or atypical flutter (see Atypical flutter), or even MAT‐EF. b It is usually considered that its morphology cannot be distinguished from that of fast macro‐reentrant atrial tachycardias, and that both mechanisms are the same (generally left atrial macro‐reentry). An atypical flutter is named when the arrhythmia rate >220 bpm, and MAT‐MR when the arrhythmia rate is lower. Figure 15.7 Upper tracing: A 20‐year‐old patient with dilated cardiomyopathy and incessant atrial tachycardia due to an ectopic focus (AB = 0.64 sec and CD = 0.52 sec). Lower tracing: After amiodarone administration, the focus activity is slowed down, with a progressive reduction of rate discharge. All of this suggests that the cause is increased automaticity (see Table 15.4). Table 15.6 ECG characteristics of the different types of paroxysmal supraventricular tachyarrhythmias with regular RR and narrow QRS complexesa (onset during tachycardia) a Basal ECG with or without WPW‐type pre‐excitation. b MAT may be due to an ectopic focus (MAT‐EF) or an atrial macro‐reentry (MAT‐MR). c AVNRT: tachycardia exclusively involving the AV junction; AVRT: tachycardia with a circuit also involving an anomalous pathway. d JT‐EF: junctional tachycardia due to an ectopic focus; MAT: monomorphic atrial tachycardia. The AV conduction is often 1 : 1. When the rate of tachycardia is high, sometimes due to the effect of different drugs (digitalis), various degrees of AV block and even AV dissociation may be seen (Figure 15.9). The P′R usually is less than the RP′ (P“R < RP′) (Figures 15.7 and 15.13D). However, in cases of first‐degree AV block, it may be P′R ≥ RP′. In this case, it may be difficult to make the differential diagnosis with other paroxysmal tachycardias, especially atrioventricular reentrant tachycardias (AVNR) with accessory pathway (see Tables 15.5, 15.6, and 12.1) once the tachycardia is established. Table 15.7 Differential diagnosis between incessant AV junctional reentrant tachycardia (I‐JRT) and incessant tachycardia due to an atrial ectopic focus (I‐MAT‐EF) Figure 15.8 The P wave polarity is clearly indicative of the ectopic origin in the low right atrium around the tricuspid ring (negative P′ wave in V1, III, aVF and −+ in II). Therefore, this is a clear case of monomorphic atrial tachycardia at a low rate (110 bpm) misdiagnosed as a sinus tachycardia by the computerized interpretation as a result of the erroneous assessment of the polarity in lead II (−+), which cannot be a sinus polarity. A stress test showed that the tachycardia disappeared when the sinus rhythm accelerated to a higher rate. The QRS complex is usually equal to the baseline rhythm. Occasionally, it is wide due to an aberrant ventricular conduction. This has a variable effect (Table 15.4). MAT‐MR is not characterized by a specific ECG morphology. The atrial wave morphology varies from the typical to the reverse or atypical atrial flutter. It may even be similar to MAT‐EF morphology. In incessant monomorphic atrial tachycardia due to an ectopic focus (I‐MAT‐EF), the heart rate typically varies between 90 and 150 and P′R < RP′ (Figure 15.7). All the aspects related to the morphology of ectopic P′ have been previously explained. Figure 15.9 A digitalis‐intoxicated patient with atrial tachycardia due to an ectopic focus at 175 bpm, with P waves that are different from the preceding sinus waves but not narrow. The atrial waves have some variable cadence and different degrees of AV block. Figure 15.10 (A) Most frequent locations of atrial tachycardias of focal origin. (B) Algorithm to localize the most frequent sites of origin of tachycardias based on P′ wave morphology in V1 (see location inside the figure) (Adapted from Kistler et al. 2006). The main differential diagnosis of I‐MAT‐EF is with incessant junctional reentrant tachycardia (I‐JRT), which once established, also features a P′R < RP′ interval (Figure 15.15) (see Table 15.7). The prognosis depends on the heart rate, the underlying pathology, and the impact over LV function and whether the tachycardias are paroxysmal or incessant. The prognosis and treatment depend particularly on the tachycardia rate and the patient′s clinical condition. In the case of a stable patient, a paroxysmal episode may be treated, if vagal maneuvers fail, with adenosine, beta blockers, or amiodarone (class I aC). However, pharmacologic treatment is often not useful. If the tachycardia rate is high and not well‐tolerated, electrical cardioversion (CV) may be required (class IB). Later, ablation techniques should be considered to resolve the arrhythmia (class IB), usually with a high success rate. No consensus has been reached with regard to the most appropriate name for tachycardias due to a reentrant mechanism, whose circuits are exclusively located in the AV junction or involve an accessory pathway (see Chapter 14). However, the most accepted names according to the guidelines are junctional AV reentrant (reciprocating) tachycardia with a circuit exclusively involving the AV junction (AV node) (AVNRT) and junctional reentrant (reciprocating) tachycardia with circuits involving an accessory pathway (AVRT). The tachycardias may be paroxysmal (slow–fast type) (Figures 15.11 and 15.12), which are much more frequent and often have characteristic clinical features (sudden onset, polyuria, etc.) (Josephson 1978; Wu et al. 1978; Bar et al. 1984; Inoue and Becker 1998; Katritsis and Becker 2007), or incessant (fast–slow type) (Figure 15.15), which are much less frequent and often seen in the pediatric population (Coumel et al. 1974). The circuit may be located just in the AV junction (AVNRT) or may include an accessory pathway in the circuit (AVRT) (see Chapter 14). In all cases, tachycardia is initiated when there is a unidirectional block (anterograde) in some part of the circuit. When the circuit exclusively involves the AV junction (AVNRT tachycardia) (Figure 15.11), the block takes place in the AV junction where the β pathway is located (see Figure ). The same β pathway is used by the stimulus to reenter. This slow–fast tachycardia is thus characterized by a long AH (atrial–His) interval and a short HA interval (His–atrial) as shown in Figure 15.11C. When a Kent bundle‐type accessory pathway is involved in the circuit (Figure 15.12A), the block generally occurs antregradely in the accessory pathway and the stimulus reaches the ventricles through the normal AV conduction. The stimulus reenters retrogradely over an accessory pathway (see Figure 14.11). The retrograde atrial activation shows a longer HA interval than when the circuit exclusively involves the AV junction, as the circuit is larger (compare Figures 15.11C and 15.12B). Because the anterograde conduction is through the normal AV junction, paroxysmal tachycardias with the involvement of an accessory pathway have a narrow QRS complex, although very often a pre‐excitation delta wave is observed in the ECG without tachycardia (Wolff–Parkinson–White (WPW) syndrome). In just a very few cases showing anterograde conduction through the accessory pathway, a wide QRS tachycardia can be seen (differential diagnosis with ventricular tachycardia) (see Figure 16.18) (Nadeau‐Routhier and Baranchuk 2016). The onset of paroxysmal junctional reentrant tachycardia (Figures 14.13 and 15.11D) is triggered by a premature impulse. The termination of the tachycardia also helps in establishing the mechanism, thus, the differential diagnosis (Chiale et al. 2015). Incessant tachycardias usually start as a result of a critical shortening of the sinus RR interval (Figure 15.15). In incessant or permanent tachycardias, the anterograde block occurs in the AV junction (α pathway). The stimulus reaches the ventricles by the β pathway and reentry occurs over an anomalous bundle with a slow retrograde conduction (Figures 14.14 and 15.15). The baseline ECG of patients with AVNRT and AVRT are usually normal. In nearly 40% of cases, a usually non‐ischemic negative T wave is present at the end of the episode (Paparella et al. 2000). In AVRT the WPW pattern could be present if there is anterograde pre‐excitation in sinus rhythm; however, in cases of accessory pathway with retrograde conduction only (concealed pre‐excitation), the short PR and delta wave will not be seen (see Table 12.1). The heart rate generally varies between 130 and 200 bpm. The QRS complex morphology is the same as or very similar (see later) to the baseline rhythm when the circuit exclusively involves the AV junction (AVNRT). If the baseline ECG shows WPW‐type pre‐excitation (AVRT), this pattern disappears during the tachycardia (narrow QRS complex). To determine which type of circuit is involved in the paroxysmal junctional reentrant tachycardia, it is essential to determine the relationship between the P′ wave and the QRS complex (Figure 15.13). If the circuit includes the AV junction exclusively (AVNRT), then the P′ wave will be within the QRS in 60% of cases, or will appear immediately afterward (30–40%). It simulates an “r” in lead V1, a slurred “s” in inferior leads, or a notch in aVL (Di Toro et al. 2009; Nadeau‐Routhier and Baranchuk 2016) (Figures 15.11 and 15.13A,B). If an accessory pathway is involved in the circuit that forms its retrograde arm, the path from the ventricles to the atria is longer, resulting in a P′ wave that is always slightly behind the QRS complex (Figures 15.13C and 15.12B). If the accessory pathway is found on the left side, the P′ wave is frequently negative in lead I, because the atrial activation occurs from left to right. Figure 15.11 (A) ECG of a patient with no heart disease and episodes of paroxysmal supraventricular tachycardia (AVNRT). The tracing is normal. (B) ECG during one episode: “s” wave appears in II and aVF, whereas a minimal r′ is observed in V1. Apart from this, no other modifications are observed in the ECG. (C) The same patient with extra stimulation (S1 S2 at 380 ms): a significant AH lengthening is reported (180 ms) but no paroxysmal tachycardia (PT) is initiated. When extra stimulation is coupled at 370 ms, a critical AH lengthening (330 ms) is reached, initiating the junctional reentrant tachycardia with synchronic atrial and ventricular activation (AV junctional exclusive circuit). HB: His bundle; CS: coronary sinus. (D) Onset and termination of a AVNRT episode. We can observe the initial P′R lengthening and the small QRS changes during the episode due to the P′ overlapping (r′ in V1 and s in II and aVF (compare with A and B). Relatively often (≈40% of cases) during tachycardia, ST segment depression appears, but this does not necessarily represent ischemia. If during the tachycardia, the AV conduction is over one accessory pathway (Kent bundle) or a long atriofascicular tract (see Chapter 12), the QRS is wide (antidromic tachycardia) (Figure 15.16). In this case, the retrograde arm of the circuit may be the His–Purkinje system or another accessory pathways. These types of tachycardias must be included in the differential diagnosis of wide QRS tachycardias, along with supraventricular tachycardias with bundle branch block (aberrancy) and ventricular tachycardias (see Chapter 16). When bundle branch block morphology appears during paroxysmal AVRT reentrant tachycardia, the RR lengthens if the accessory pathway is on the same side as the blocked branch. This happens because the stimulus descending through SCS will have to cross the septum (a longer distance) to complete the reentry circuit. Junctional reentrant tachycardias usually have a narrow QRS complex, either when the circuit exclusively involves the AV junction (AVNRT) (Figure 15.11), or when it also involves an accessory pathway (AVRT) (Figure 15.12), because the stimulus reaches the ventricles through the AV junction usually with a normal intraventricular conduction. The ECG characteristics of I‐JRT are the following (Figure 15.15) (Table 15.7): Figure 15.12 (A) Example of junctional paroxysmal tachycardia with left accessory pathway (Kent bundle) in the reentrant circuit (AVRT type). The QRS complex is narrow and the ectopic P is negative in I, II, III, aVF, and V6 (after QRS), with RP′ < P’R. In V3 a QRS complex alternans is presumed (see C left). (B) Electrophysiologic study showing an atrial retrograde activation in which the left atrium is the area first depolarized. As seen in the CS lead (distal), this is where the retrograde atrial activation (A) is first recorded. This may be suggested by surface ECG because in I and V6, the retrograde p′ is clearly negative (leads I and V6 are facing the tail of the atrial activation vector). HRA: high right atrium; HB: His bundle; CS: coronary sinus. (C) AVRT. Left: V3, where alternans of QRS complexes are observed. Right: V6, where the termination of the episode with anterograde block in the AV junction is observed, with an onset of pre‐excitation in the second sinus complex. Figure 15.13 Location of P′ waves in paroxysmal supraventricular tachycardias. (A) Non‐visible P′ wave, hidden within the QRS (circuit exclusively involving the AV junction). (B) P′ wave that distorts the end of the QRS (simulating that it ends with an S wave) (circuit exclusively involving the junction as well). (C) P′ wave separated from the QRS, but with RP′ < P′R (reentrant) (circuit involving an accessory pathway). (D) P’ wave preceding the QRS with P′R < RP′ (atrial circuit or atrial ectopic focus). The differential diagnosis of paroxysmal AV reentrant tachycardias is shown in Tables 15.5 and 15.6 and has already been discussed. Regarding the incessant reentrant AV tachycardias, it is important to differentiate I‐JRT from I‐MAT‐EF. The most relevant data have also already been mentioned (see Table 15.7). Figure 15.14 (A) aVF and V1 in a patient with heart failure and fixed ventricular rate throughout a 24 h examination. This led us to suspect that the rhythm was not sinus, although a possible sinus P wave around 120 bpm might be inferred in V1. The compression of the carotid sinus blocked the AV node temporarily, which allowed for the identification of “f” waves from an atypical flutter (aVF, B top). The cardioversion successfully restored sinus rhythm. Note the P ± waves in II, III, and aVF corresponding to an advanced interatrial block with retrograde conduction to the left atrium (VF, B bottom). The diagnosis of paroxysmal reentrant tachycardias has to be suspected by history taking, especially when the onset and offset are sudden, and because polyuria is observed especially in long‐lasting episodes. Diagnosis of AVNRT‐type is supported by the presence of pounding in the neck, and is more common in female patients whose first episode appears after childhood (González‐Torrecilla et al. 2009). In general, paroxysmal AV reentrant tachycardias are not life threatening, although they can be very troublesome, because of fast heart rate, the duration of the tachycardia, and the underlying illness, if present. Cases with an accessory pathway involved in the circuit (AVRT) may be potentially dangerous because in rare cases, a rapid atrial fibrillation may be triggered (see later). To terminate an episode due to a paroxysmal junctional reentrant tachycardia immediately after it starts, it is important to block the circuit at any level, usually at the AV junction. This may be achieved by: (i) hard coughing; (ii) performing a carotid sinus massage (CSM), if feasible; and (iii) administering drugs immediately, if the episode persists, to terminate it as soon as possible. A treatment, known as the “pill‐in‐the‐pocket” approach (recommendation class IIa), was proposed by Lown more than 30 years ago (Alboni et al. 2004). Figure 15.15 Holter continuous recording. Incessant junctional reentrant tachycardia with the fast–slow circuit type AVRT. The accessory bundle with slow conduction constitutes the retrograde arm of the circuit (see Figure 14.13). Bottom: Lewis diagram corresponding to the onset of one episode. If the crisis does not cease, after some time (from minutes to hours depending on the tolerance), the patient should be hospitalized, and if the tachycardia is of AVNRT‐type (this diagnosis may be suggested by ECG non‐visible P′ or a slight change at the end of QRS (Figure 15.11), intravenous adenosine (treatment of choice) or other antiarrhythmic drug such as amiodarone should be administered. Ablation of the slow pathway (AVNRT) or accessory pathway (AVRT) is now considered first line of treatment. In cases of WPW pattern, even without crisis of AVRT, after discussing the situation with the patient, especially in the case of young people practicing sports, we advise ablation in a well‐experienced center after examining the results of the exercise testing, Holter monitoring, and electrophysiologic studies (Bayés de Luna and Baranchuk 2017). This is based on the infrequent but real risk that the first episode could lead to a fast atrial fibrillation that, in very rare cases, may trigger ventricular fibrillation. Exercise testing has limitations to determine the risk of sudden death in patients with anterograde conduction over a pathway, and ablation can be curative (Jastrzębski et al. 2017) In the majority of cases of repetitive crisis, ablation techniques solve the problem. Therefore, ablation is the best solution for patients who do not tolerate junctional reentrant tachycardias or experience them frequently.
Chapter 15
Active Supraventricular Arrhythmias
Premature supraventricular complexes
Concept and mechanisms
ECG findings
Morphology
Conduction to the ventricles
Clinical implications
Sinus tachycardia (Tables 15.2 and 15.3)
Concept
Mechanisms
ECG findings
Indicative of ectopy: ventricular extrasystoles
and QRS morphology in V6: 
Indicative of aberrancy: supraventricular extrasystoles
, particularly if QRS morphology in V6 is 
Clinical implications
Regular RR (Figure 15.20)
Irregular RR
Monomorphic atrial tachycardia (Tables 15.4–15.7)
Concept
Mechanisms
Micro‐reentrya
Increase of automatism
Triggered activity
No
Yes
Sometimes
Yes
No
Yes
Yes
No
No
Generally, they have no effect, although it may cause an AV block
Transient suppression
Termination
No effect
Transient suppression
Termination
Contradictory results. Most of the times, it has no effect
Transient suppression
Termination
Paroxysmal form is more frequently observed
Generally incessant type
Paroxysmal or incessant
ECG findings (Tables 15.5 and 15.6)
Paroxysmal monomorphic atrial tachycardia due to an ectopic focus
P wave morphology in sinus rhythm
The ECG during the tachycardia (Figures 15.7–15.10)
ECG diagnosis
Atrial activation
Morphology (II, III, aVF)
Morphology V1
Atrial activity frequency
AV block
Sinus tachycardia (Figures 15.4–15.6)
Sinus
Generally, positive or ± in III. It rarely may be ± in II, III, and aVF
Positive or ±
100–180 bpm Sometimes, (mainly in young people) it may even be >200 bpm
Rarely present, even in the fastest types
Monomorphic atrial tachycardia (Figures 15.7–15.10)
Focal origin (MAT‐EF) or due to an atrial macro‐reentrya (MAT‐MR)
Depends on the focus location in case of ectopic origin (Figure 15.10) macro‐reentrant tachyarrhythmias may feature different morphologies
Depends on the focus location. Macro‐reentrant tachyarrhythmias may feature different morphologies (see text)
Generally <150 bpm. It may reach 240 bpm (see text).
Sometimes, in the fastest types
Common flutter (Figures 15.32 and 15.33)
Permanently counterclockwise. This explains the lack of isoelectric baseline in some derivations
Sawtooth F predominantly negative waves. No isoelectric baseline
Generally positive and not very narrow F waves, except in the presence of significant atrial disease
200–300 bpm′
Generally present
Reverse flutter (Figure 15.34)
Clockwise. Generally permanent
Positive F waves in II, III, and aVF generally without isoelectric baseline
F waves generally wide and negative in V1, with no isoelectric baseline
200–300 bpm
Generally present
Atypical flutterb (Figure 15.35)
Probably a left atrial macro‐reentry. Often unknown
Generally positive waves in II, III, and aVF Frequently a slight undulation is observed
Usually positive
220–280 bpm
Very frequently
Junctional reciprocant tachycardia (JRT) (Figures 15.11 and 15.12)
Retrograde, either in the AV junction or in an anomalous pathway
Concealed in the QRS complex or stuck at its end (AVNRT) or following the QRS complex (AVRT)
If the circuit exclusively comprises only the AV junction, it frequently simulates an r’
Generally 130–200 bpm
Not present
Junctional tachycardia due to an ectopic focus (Figure 15.17)
Retrograde, except in the case of AV dissociation
A negative retrograde activation is observed
Variable
100–200 bpm
AV dissociation due to interference is frequently observed (Figure 15.17)
Atrial flutter
Junctional reciprocant tachycardiaa
Sinus tachycardia
Monomorphic atrial tachycardiab
Junctional tachycardia due to an ectopic focus
AVNRTc
AVRTc
Beginning of tachycardia
Usually initiated with a premature supraventricular impulse
P′ wave initiating the tachycardia shows a different morphology, compared with the subsequent P′ waves
P′ initiating the tachycardia is generally different to subsequent P’ waves
Progressive initiation. P wave does not feature significant changes
Initial P′ wave is identical to the subsequent P′ waves
Initiation and termination may be either abrupt or gradual. Initial P′ wave is identical to the following P′ waves
Status of the atrial activity wave (P, P′, or F) during tachyarrhythmia
Flutter waves, generally two waves per each QRS complex. Almost never 1 × 1
P′ within the QRS complex = 65%. P′ following the QRS complex = 30% (very close to it). P′ preceding the QRS complex = 5% (Figure 15.13)
P′ following the QRS complex in 100% of the cases, but with RP′ < P’R
P preceding the QRS complex shows a sinus polarity. Almost always P‐QRS < QRS‐P
P′ wave precedes the QRS complex, usually with P′‐QRS < QRS‐P′
It is generally concealed in the QRS complex or, more frequently, an AV dissociation is observed
Presence of ventricular block
Depends on the underlying disease and the heart rate
Rarely seen. Almost always features a RBBB morphology
Sometimes observed
Depends on the underlying disease and the heart rate
Depends on the underlying disease and the heart rate
Depends on the underlying disease and the heart rate
QRS alternans (voltage difference >1 mm)
No
No
20% of the cases
No
No
No
AV dissociation
Usually a 2 × 1 AV block is present
Never, unlike what is observed in JT‐EFd
Never. If AV dissociation is observed, Kent bundle involvement in the circuit is excluded
Generally not present
2 × 1 AV block may be present
Frequently AV dissociation due to interference is observed (ventricular rhythm faster than atrial rhythm, if this is of sinus origin)
Mechanism and clinical presentation
Atrial macro‐reentry, usually in heart disease patients. It may be a paroxysmal or chronic flutter
Reentry exclusively in the junction. Almost always in healthy patients. The incessant type rarely occurs
Reentry through an anomalous pathway. Almost always in healthy patients. The incessant type rarely occurs
Generally, it is due to a physiological increase of automatism.
On some rare occasions, sinus reentry may be involved
It may be to an ectopic focus (EF) or because of an atrial macro‐reentry (AM). Those due to an EF may be paroxysmal or incessant. Those due to a macro‐reentry are paroxysmal tachycardias
In many cases, it is observed in heart disease patients. Initiation and termination sometimes are not abrupt. Incessant types may be observed
The AV conduction
Heart rate is increased previously to tachycardia initiation
Polarity of the P waves following the P–P′ triggering the tachycardia
Presence of fusion complexes at the beginning or at the end
Progressive acceleration and desacceleration, both at the beginning (warming‐up) and at the end (cooling‐down) of the tachycardia
Incessant tachycardia due to an atrial ectopic focus
Heart rate is not accelerated prior to tachycardia initiation
Polarity of the P′ wave triggering the tachycardia is the same as that from the successive waves
They may be present
Yes
Incessant AV junctional reentrant tachycardia
Heart rate is accelerated prior to tachycardia initiation
Polarity of the P–P′ wave triggering the tachycardia is not the same as that from the successive P′ waves
Not present
No 
The QRS complex
The carotid sinus massage
Monomorphic atrial tachycardia due to macro‐reentry
Incessant monomorphic atrial tachycardia due to an ectopic focus
Clinical implications
Junctional reentrant (reciprocating) tachycardia
Concept
Mechanism
Paroxysmal tachycardias (slow–fast circuit)
Incessant tachycardias (fast–slow circuit)
ECG findings
Paroxysmal junctional reentrant tachycardia(slow–fast type circuit)
Sinus rhythm
During tachycardia
Incessant junctional reentrant tachycardia (fast–slow type of circuit)
Differential diagnosis
Clinical implications
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