2019 ESC - supraventricular tachycardia

tend to last longer than AT episodes, which may occur in a series of repetitive runs.32 Clear descriptions of pounding in the neck (the socalled ‘frog sign’) or ‘shirt flapping’ would point to the possible competing influences of atrial and ventricular contraction on the tricuspid valve, and to AVNRT as a likely cause.15,38,39

SVT may be unrecognized at initial medical evaluation and the clinical characteristics can mimic panic disorder.40 In patients with possible sinus tachycardia in association with anxiety and postural orthostatic tachycardia syndrome (POTS), it is important to rule out the possibility of a re-entrant tachycardia.

8 Initial evaluation of patients with supraventricular tachycardia

Complete history taking, including family history, and physical examination are essential. As discussed, clinical history is especially relevant in cases of palpitations without ECG documentation of the tachycardia. Initial evaluation points to a re-entrant arrhythmia when the mode of onset/termination is sudden, is often associated with a change of position, and the tachycardia is perceived as regular. Initiation of the episode(s), frequency, and conditions of triggering the arrhythmia are important clues for a specific diagnosis.3 There may be evidence that specific actions lead to arrhythmia termination. These could include standard vagal manoeuvres,41 but also abortive measures such as drinking a glass of iced water. Also, responses to the administration of drugs (e.g. adenosine or verapamil), where termination has been observed but ECGs are missing, may provide diagnostic help.

Full blood counts and a biochemistry profile—including renal function, electrolytes, and thyroid function tests—can be useful in specific cases (Table 7). An ECG recorded during tachycardia is ideal, and patients should be encouraged to seek medical assistance and recording of their ECG during episodes. A 12 lead resting ECG and baseline echocardiographic assessment are necessary. It may be useful to do 24 h ECG recordings, but tachycardia episodes are usually sporadic and may not be frequent enough to be recorded on ambulatory monitoring. Transtelephonic monitoring, mobile recording devices, or, very rarely, an implantable loop recorder may be required. Wrist-worn, optically based heart rate monitors are user-friendly, but appropriate validation of the device used is imperative.42 A tolerance exercise test may also be useful in patients with apparent preexcitation and in cases of catecholamine-dependent arrhythmias. Myocardial ischaemia testing is also needed in patients with angina or significant risk factors for coronary artery disease.43 An electrophysiology study (EPS) is usually necessary to establish the diagnosis, particularly when catheter ablation is anticipated.

9 Differential diagnosis of tachycardias

9.1 Narrow QRS ( 120 ms) tachycardias

Narrow QRS complexes are due to rapid activation of the ventricles via the His Purkinje system (HPS), which suggests that the origin of the arrhythmia is above or within the His bundle. However, early

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activation of the His bundle can also occur in high septal VTs, thus resulting in relatively narrow QRS complexes (110 140 ms).44

9.1.1 Electrocardiographic differential diagnosis

In the absence of an ECG recorded during the tachycardia, a 12 lead ECG in sinus rhythm may provide clues for the diagnosis of SVT and should be scrutinized for any abnormality. The presence of preexcitation in a patient with a history of regular paroxysmal palpitations is generally suggestive of AVRT. The absence of apparent pre-excitation does not rule out the diagnosis of AVRT, as it may be due to a concealed accessory pathway (AP) that conducts only retrogradely or to an atypical (Mahaim) pathway, which is latent at sinus rhythm.

An ECG taken during tachycardia is very useful in the efficient diagnosis of SVT, although it may fail to lead to a specific diagnosis.45 It may not be available in patients with very short or infrequent periods of palpitations.

9.1.1.1 Initiation and termination of the tachycardia

Sudden prolongation of the PR interval occurs in typical AVNRT after an atrial ectopic beat. An AT may also be initiated by an atrial ectopic beat, but is not dependent on marked PR prolongation. Automatic, focal ATs are characterized by gradual acceleration (warm-up phenomenon) followed by deceleration (cool-down phenomenon),46 and may also be incessant with short interruption by sinus beats. Premature atrial or ventricular beats may trigger AVRT. Premature ventricular complexes are a common trigger of atypical AVNRT, but rarely induce typical AVNRT, and only exceptionally AT.

9.1.1.2 Regularity of tachycardia cycle length

The regularity of the RR interval should be assessed (Figure 1). Irregular tachycardias may represent focal or multifocal AT, focal AF, and atrial flutter with varying AV conduction. Patterns of irregularity can sometimes be found, such as in atrial flutter conducted with Wenckebach periodicity. Irregular arrhythmias, such as multifocal AT, typically display variable P-wave morphologies, and varying PP, RR, and PR intervals. Atrial flutter can have fixed AV conduction and present as a regular tachycardia, and even AF may appear almost regular when very fast. Re-entrant tachycardias, whether micro or macro-re-entries, are usually regular. Incessant tachycardias may be the so-called permanent junctional reciprocating tachycardia (PJRT), focal AT, or, rarely, atypical AVNRT. Cycle length (CL) alternans (also called RR alternans) may be seen in AVNRT, but these changes are <15% of the tachycardia CL.47 If the irregularity exceeds 15% of the CL, a focal arrhythmia is much more likely.48 QRS alternans is a rare phenomenon in slow SVTs, which may not be related to CL alternans, and has been initially described with AVRT.49,50 However, this may be seen in any fast SVT.51

A change in ventricular CL preceded by a change in atrial CL is seen in AT or atypical AVNRT. A change in ventricular CL preceding a change in subsequent atrial CL favours typical AVNRT or AVRT.47,52 A fixed ventriculoatrial (VA) interval in the presence of variable RR intervals excludes AT.45

9.1.1.3 P/QRS relationship

According to their P/QRS relationships, SVTs are classified as having short or long RP intervals. Short-RP SVTs are those with RP intervals

shorter than one-half the tachycardia RR interval, whereas long-RP SVTs display RP>PR (Figure 1). Rarely, recording of U waves during

typical AVNRT may simulate a long-RP tachycardia.53

On EPS, a very short VA interval (<70 ms) usually indicates typical AVNRT, or less commonly focal AT, but has also been reported in AVRT.54 For surface ECG measurements, a cut-off interval of 90 ms has been shown to be useful and can be used if P waves are visible,55 but data on actual RP measurements during various types of SVT are scarce.

P waves similar to those in normal sinus rhythm suggest appropriate or inappropriate sinus nodal tachycardia, sinus nodal re-entrant tachycardia, or focal AT arising close to the sinus node. P waves different from those in sinus rhythm, and conducted with a PR interval equal to or longer than the PR in sinus rhythm, are typically seen in focal AT. In AT, the conduction to the ventricles may be fast (1:1) or slow (3:1 or 4:1). The possibility of atrial flutter with 2:1 conduction should also be considered if the ventricular rate during SVT is 150 b.p.m., as the atrial activity is usually 250 - 330 b.p.m. In the presence of antiarrhythmic medication in this setting, lowering the atrial rate may result in a higher ventricular rate in the absence of AV nodal blockade.

In the case of relatively delayed retrograde conduction that allows the identification of retrograde P waves, a pseudo r deflection in lead V1 and a pseudo S wave in the inferior leads are more common in typical AVNRT than in AVRT or AT.56,57 These criteria are specific (91 100%) but modestly sensitive (58 and 14%, respectively).56 A difference in RP intervals in leads V1 and III >20 ms is also indicative of AVNRT rather than AVRT due to a posteroseptal pathway.57 The presence of a QRS notch in lead aVL has also been found to be a reliable criterion suggesting AVNRT,58 while a pseudo r in aVR has been shown to have greater sensitivity and specificity than a pseudo r in V1 for the diagnosis of typical AVNRT.59 However, in all referenced studies, cases of AT or atypical AVNRT were limited or entirely absent.

AV block or dissociation during narrow QRS tachycardia is not often seen, but it rules out AVRT as both atria and ventricles are parts of the circuit. The development of bundle branch block (BBB) during SVT may also be helpful in the diagnosis of AVRT. BBB ipsilateral to the AP can result in CL prolongation due to VA prolongation, as the ventricular arm of the circuit is prolonged by conduction through the interventricular septum from the conducting bundle branch.60 However, it should be noted that lengthening of the VA interval may not necessarily result in CL prolongation, due to a potential switch of antegrade conduction from the slow to the fast AV nodal pathway.

9.1.2 Vagal manoeuvres and adenosine

Vagal manoeuvres (such as carotid sinus massage) and adenosine injection may help in clinical diagnosis, particularly in situations in which the ECG during tachycardia is unclear. Possible responses to vagal manoeuvres and adenosine are shown in Table 8 and Figure 2.

Termination of the arrhythmia with a P wave after the last QRS complex is very unlikely in AT, and most common in AVRT and typical AVNRT. Termination with a QRS complex is often seen in AT, and possibly in atypical AVNRT. Adenosine does not interrupt mac- ro-re-entrant ATs (MRATs).61 Fascicular VTs, in particular, are

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. verapamilbut not adenosine-sensitive. Most VTs, as opposed to

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. SVTs, do not respond to carotid sinus massage, but a narrow QRS

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. VT originating at the left bundle branch and terminated with carotid

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. 62

. sinus massage has been reported.

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Table 8 Possible responses of narrow QRS tachycardia to vagal manoeuvres and adenosine

(1)Slowing of AVN conduction and induction of intermittent AV block. Atrial electrical activity can thus be unmasked, revealing dissociated P waves (focal AT, atrial flutter, or AF waves).

(2)Temporary decrease in the atrial rate of automatic tachycardias (focal AT, sinus tachycardia, and JET).

(3)Tachycardia termination. This can happen by interrupting the re-entry circuit in AVNRT and AVRT by acting on the AVN that is part of the circuit. More rarely, sinus nodal re-entry and ATs due to triggered activity can slow down and terminate.

(4)No effect is observed in some cases.

AF = atrial fibrillation; AT = atrial tachycardia; AV = atrioventricular; AVN = atrioventricular node; AVNRT = atrioventricular nodal re-entrant tachycardia; AVRT = atrioventricular re-entrant tachycardia; JET = junctional ectopic tachycardia.

		Adenosine
	in regular, narrow QRS tachycardia
	Response	Diagnosis
		Inadequate dose/
	No effect	delivery
		High septal VT
		Sinus tachycardia
	Gradual slowing	Automatic focal AT
	then reacceleration	Junctional ectopic
		tachycardia
		AVNRT
		AVRT
	Sudden termination	Sinus nodal re-entry
		Triggered focal AT
		(DADs)
	Persisting atrial	Atrial flutter	2019
	tachycardia with
		Micro-re-entrant
	transient high-grade
		focal AT
			©ESC
	AV block

Figure 2 Responses of narrow-complex tachycardias to adenosine. AT = atrial tachycardia; AV = atrioventricular; AVNRT = atrioventricular nodal re-entrant tachycardia; AVRT = atrioventricular re-entrant tachycardia; DADs = delayed after-depolarizations; VT = ventricular tachycardia.

9.1.3 Electrophysiology study

Several electrophysiological techniques and manoeuvres can be employed in the electrophysiology laboratory for differential diagnosis of regular narrow QRS tachycardia.45 A detailed discussion is beyond the scope of these Guidelines.

9.2 Wide QRS (>120 ms) tachycardias

Wide QRS tachycardias can be VT, SVT conducting with BBB aberration, or antegrade conduction over an AP, with reported proportions of 80, 15, and 5%, respectively.63 The correct diagnosis of a VT is critical to management, as misdiagnosis and administration of drugs usually utilized for SVT can be harmful for patients in VT.64 Therefore, the default diagnosis should be VT until proven otherwise. The differential diagnosis includes:65

(1)SVT with BBB. This may arise due to pre-existing BBB or the development of aberrancy during tachycardia (so-called phase 3 block), which is more commonly, although not invariably, a right BBB (RBBB) pattern due to the longer RP of the right bundle branch.

(2)SVT with antegrade conduction over an AP, ‘pre-excited SVT’, which participates in the circuit (antidromic AVRT) or is a bystander during AF, focal AT/atrial flutter, or AVNRT.

(3)SVT with widening of QRS interval induced by drugs or electrolyte disturbances. Class IA and IC drugs cause use-dependent slowing of conduction, and class III drugs prolong refractoriness at His Purkinje tissue more than in the ventricular myocardium. They can both result in atypical BBB morphologies during SVT that mimics VT.

(4)Pacemaker-related endless loop tachycardia and artefacts, which can also mimic VT.

Table 9 Summary of key electrocardiographic criteria that suggest ventricular tachycardia rather than supraventricular tachycardia in wide complex tachycardia

AV dissociation	Ventricular rate > atrial rate
Fusion/capture beats	Different QRS morphology from that
	of tachycardia
Chest lead negative	All precordial chest leads
concordance	negative
RS in precordial leads	- Absence of RS in precordial leads
	- RS >100 ms in any leada
QRS complex in aVR	• Initial R wave
	• Initial R or Q wave >40 ms
	• Presence of a notch of a predomi-
	nantly negative complex
QRS axis 290 to 6180	Both in the presence of RBBB and
	LBBB morphology
R wave peak time	R wave peak time >50 ms
in lead II
RBBB morphology	Lead V1: Monophasic R, Rsr’, biphasic
	qR complex, broad R (>40 ms), and a
	double-peaked R wave with the left
	peak taller than the right (the so-called
	‘rabbit ear’ sign)
	Lead V6: R:S ratio <1 (rS, QS patterns)
LBBB morphology	Lead V1: Broad R wave, slurred or
	notched-down stroke of the S wave,
	and delayed nadir of S wave
	Lead V6: Q or QS wave

AV = atrioventricular; LBBB = left bundle branch block; RBBB = right bundle branch block.

aRS: beginning of R to deepest part of S.

9.2.1 Electrocardiographic differential diagnosis

If the 12 lead ECG is available in sinus rhythm, it can provide useful diagnostic information. Specifically, if the QRS morphology is identical during sinus rhythm and tachycardia, the arrhythmia is most likely not a VT. However, bundle branch re-entrant VTs and high septal VTs exiting close to the conduction system can have similar morphologies to sinus rhythm. The presence of a contralateral BBB pattern in sinus rhythm is more indicative of VT.

9.2.1.1 Atrioventricular dissociation

The presence of either AV dissociation or capture/fusion beats in the 12 lead ECG during tachycardia are key diagnostic features of VT. AV dissociation may be difficult to recognize because P waves are often hidden by wide QRS and T waves during a wide QRS tachycardia. P waves are usually more prominent in inferior leads and in modified chest lead placement (Lewis lead).63

The relationship between atrial and ventricular events is 1:1 or greater (more atrial than ventricular beats) in most SVTs (Table 9). AVNRT can be associated with 2:1 conduction,66 but this is rare. Although VA conduction can be found in <50% of patients with VT and a 1:1 relationship is possible, most VTs have a relationship <1:1 (more QRS complexes than P waves).

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9.2.1.2 QRS duration

A QRS duration >140 ms with RBBB or >160 ms with left BBB (LBBB) pattern suggests VT. These criteria are not helpful for differentiating VT from SVT in specific settings, such as pre-excited SVT, or when class IC or class IA antiarrhythmic drugs are administered.67

9.2.1.3 QRS axis

As VT circuits (especially post-MI or in cardiomyopathies) frequently lie outside the normal His Purkinje network, significant axis shifts are likely to occur, enabling diagnosis. Therefore, in patients with SVT and aberrancy, the QRS axis is confined between -60 and þ120 . In particular, extreme axis deviation (axis from -90 to ±180 ) is strongly indicative of VT, both in the presence of RBBB and LBBB.65

9.2.1.4 Chest lead concordance

The presence of negative chest lead concordance (all QRS complexes negative V1 V6) (Figure 3) is almost diagnostic of VT, with a specificity >90%, but is only present in 20% of VTs. Positive concordance can be indicative of VT or an antidromic tachycardia utilizing a left posterior or left lateral AP.68

9.2.1.5 Right bundle branch block morphology

Lead V1: Typical RBBB aberrancy has a small initial r’, because in RBBB the high septum is activated primarily from the left septal bundle. Therefore, the following patterns are evident: rSR0, rSr0, or rR0 in lead V1. However, in VT, the activation wavefront progresses from the left ventricle (LV) to the right precordial lead V1, in a way that a prominent R wave (monophasic R, Rsr0, biphasic qR complex, or broad R >40 ms) will be more commonly seen in lead V1. Additionally, a double-peaked R wave (M pattern) in lead V1 favours VT if the left peak is taller than the right peak (the so-called ‘rabbit ear’ sign). A taller right rabbit ear characterizes the RBBB aberrancy but does not exclude VT.

Lead V6: A small amount of normal right ventricular voltage is directed away from lead V6. As this is a small vector in RBBB aberrancy, the R:S ratio is >1. In VT, all of the right ventricular voltage, and some of the left, is directed away from V6, leading to an R:S ratio <1 (rS and QS patterns). An RBBB morphology with an R:S ratio in V6 of <1 is seen rarely in SVT with aberrancy, mainly when the patient has a left axis deviation during sinus rhythm.

Differentiating fascicular VT from SVT with bifascicular block (RBBB and left anterior hemiblock) is very challenging. Features that indicate SVT in this context include QRS >140 ms, r’ in V1, overall negative QRS in aVR, and an R/S ratio >1 in V6.44

9.2.1.6 Left bundle branch block morphology

Lead V1: As stated above for RBBB, for the same reasons, the presence of a broad R wave, slurred or notched-down stroke of

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the S wave, and delayed nadir of the S wave are strong predictors of VT.

Lead V6: In true LBBB, no Q wave is present in the lateral precordial leads. Therefore, the presence of any Q or QS wave in lead V6 favours VT, indicating that the activation wavefront is moving away from the LV apical site.

These morphology criteria are not fulfilled in any lead in 4% of SVTs and 6% of VTs, and in one-third of cases when one lead (V1 or V6) favours one diagnosis, the other favours the opposite diagnosis (VT in one lead and SVT in the other, and vice versa).69,70

A number of algorithms have been developed to differentiate VT from SVT.69,71,72 Detailed presentation and comments are beyond the scope of these Guidelines, and can be found in the 2018 European Heart Rhythm Association/Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Sociedad Latinoamericana de Estimulacion Cardıaca y Electrofisiologıa consensus document.3

All of these criteria have limitations. Conditions such as bundle branch re-entrant tachycardia, fascicular VT, VT with exit site close to the His Purkinje system, and wide QRS tachycardia occurring during antiarrhythmic drug treatment are difficult to diagnose using the mentioned morphological criteria. Differentiating VT from antidromic AVRT is extremely difficult for the very fact that the QRS morphology in antidromic AVRT is similar to that of a VT, with its origin at the insertion of the AP in the ventricular myocardium. An algorithm has been derived for differential diagnosis, based on the analysis of 267 wide QRS tachycardias, consisting of VT and antidromic

AVRT. The derived criteria were found to offer sensitivity of 75% and specificity of 100%,73 and the algorithm was also validated in another study,74 but experience is still limited.

In fact, several independent studies have found that various ECGbased methods have specificities of 40 80% and accuracies of75%.44,68,75 80 Indeed, a similar diagnostic accuracy of 75% would be achieved effortlessly by considering every wide QRS tachycardia to be a VT, because only 25 30% are SVTs. Therefore, emerging approaches to integrate these algorithms and provide more accurate scoring systems are being evaluated.81 Furthermore, conventional ECG criteria have reduced the sensitivity to distinguish VT from SVT with aberrancy in patients with idiopathic VT. This is most pronounced in VTs originating from septal sites, particularly Purkinje sites and the septal outflow tract regions.82

9.2.2 Electrophysiology study

On certain occasions, an EPS is necessary for diagnosis.

9.3 Irregular tachycardias

An irregular ventricular rhythm most commonly indicates AF, multifocal AT, or focal AT/atrial flutter with variable AV conduction, and may occur in the context of both narrow and broad QRS complexes. When AF is associated with rapid ventricular rates, the irregularity of this ventricular response is less easily detected and can be misdiagnosed as a regular SVT.83 If the atrial rate exceeds the ventricular rate, then atrial flutter or AT (focal or multifocal) is usually present. Polymorphic VT and, rarely, monomorphic VT may also be irregular. Occasionally, a junctional, non-re-entrant tachycardia may have a variable rate.

Specifically, the differential diagnosis of an irregular wide QRS tachycardia is either pre-excited AF or polymorphic VT, or AT with variable block in the context of aberrancy. Pre-excited AF manifests itself by irregularity, a varying QRS morphology, and a rapid ventricular rate (owing to the short RP of the AP). The changing QRS morphology results from varying degrees of fusion due to activation over both the AP and the AVN, which also result in variation in the width of the delta wave. A further cause of varying QRS morphology in this context will be if more than one antegrade AP is present with intermittent conduction over each. The ventricular rate tends to be higher than in those with non-pre- excited AF.84

10 Acute management in the absence of an established diagnosis

10.1 Regular tachycardias

10.1.1 Narrow QRS ( 120 ms) tachycardias

Patients with SVT are common and potentially recurrent attenders in emergency departments, with an estimated 50 000 visits each year in the USA.85 The initial approach to acute management tends to be non-drug-based, with escalation to intravenous (i.v.) drugs or electrical cardioversion in the absence of early correction (Figure 4).

Recommendations for the acute management of narrow QRS tachycardia in the absence of an established diagnosis

	Recommendation		Classa	Levelb
	Haemodynamically unstable patients
	Synchronized DC cardioversion is recom-
	mended for haemodynamically unstable		I	B
	patients.86 88
	Haemodynamically stable patients
	A 12 lead ECG during tachycardia is		I	C
	recommended.
	Vagal manoeuvres, preferably in the supine
	position with leg elevation, are		I	B
	recommended.41,89 91
	Adenosine (6 18 mg i.v. bolus) is recom-		I	B
	mended if vagal manoeuvres fail.92 94
	Verapamil or diltiazem (i.v.) should be consid-
	ered, if vagal manoeuvres and adenosine		IIa	B
	fail.92,94 98
	Beta-blockers (i.v. esmolol or metoprolol)
	should be considered if vagal manoeuvres and		IIa	C
	adenosine fail.97,99,100
	Synchronized direct-current cardioversion is
	recommended when drug therapy fails to con-		I	B
	vert or control the tachycardia.87,88

i.v. beta-blockers are contraindicated in the presence of decompensated HF.

i.v. verapamil and diltiazem are contraindicated in the presence of hypotension or HFrEF.

DC = direct current; ECG = electrocardiogram; HF = heart failure; HFrEF = heart failure with reduced ejection fraction; i.v. = intravenous.

aClass of recommendation. bLevel of evidence.

.	10.1.1.1 Haemodynamically unstable patients
.
.
.	Immediate direct-current (DC) cardioversion is the first choice in
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.
.	haemodynamically compromised					patients with narrow QRS
.
.			86 88,101
.	tachycardia.
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.
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.	10.1.1.2 Haemodynamically stable patients
.
.
.	Vagal manoeuvres can be used to terminate an episode of narrow
.
.
.		41		The effectiveness of conventional vagal manoeuvres in
.	QRS SVT.
.
.	terminating SVT, when correctly performed, has been reported as
.
.
.	between 19 and 54%.				41,89 91,102,103	Vagal manoeuvres include differ-
.
.
.	ent techniques used to stimulate the receptors in the internal carotid
.
.
.	arteries. This stimulation causes a					reflex stimulation of the vagus
.
.
.
.	nerve, which results in the release of acetylcholine, which may in turn
.
.
.	slow the electrical impulse through the AVN and slow the heart rate.
.
.
.	Many of these manoeuvres can be performed with minimal risk at the
.
.
.	bedside or in an office setting, and can be both diagnostic and thera-
.
.
.
. peutic. The Valsalva manoeuvre is a safe and internationally recom-
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.
. mended first-line emergency treatment for SVT, although a recent
.
.	Cochrane review found insufficient evidence to support or refute its
.
.	89
.
.	utility.	The Valsalva manoeuvre has generally been shown to be
.
.	most effective in adults, and in AVRT rather than AVNRT. A modified
.

				Narrow QRS
				tachycardia
				Haemodynamic
				instability
			No				Yes
		Vagal manoeuvres					Synchronized
			(I B)				cardioversion
If ineffective							(I B)
		i.v. adenosine
			(I B)
If ineffective
i.v. verapamil or				i.v. beta-blocker
diltiazem
				(IIa C)
(IIa		B)
									2019
									©ESC
		If ineffective

Figure 4 Acute therapy of narrow QRS tachycardia in the absence of an established diagnosis.

i.v. = intravenous.

approach to the Valsalva manoeuvre provides a considerable enhancement of conversion success rates (43 vs. 17% conversion rate).41 This enhanced method requires the Valsalva to be completed semi-recumbent, with supine repositioning and passive leg raise after the Valsalva strain. Blowing into a 10 mL syringe with sufficient force to move the plunger may standardize the approach.104 Carotid sinus massage is performed with the patient’s neck in an extended position, with the head turned away from the side to which pressure is applied. It should always be unilateral as there is a potential risk with bilateral pressure, and it should be limited to 5 s. The patient should be monitored. This technique should be avoided in patients with previous transient ischaemic attack or stroke, and in patients with carotid bruits.3

Other manoeuvres, such as facial immersion in cold water or forceful coughing, are rarely used now.

Adenosine, an endogenous purine nucleoside (6 18 mg i.v. bolus) is the first drug of choice.92 94 Pharmacologically relevant electrophysiological influences are mediated through cardiac adenosine A1 receptors.105,106 Clinical EPSs have documented progressive doserelated prolongation of AV conduction [due to effects on the atrial His (AH) interval, and none on the HV interval], culminating in transient AV block that is then responsible for tachycardia termination.107

The mean dose required for termination is 6 mg. To achieve efficient rhythm correction, injection should be as a rapid bolus with immediate saline flush. Large, centrally located (e.g. antecubital) veins are likely to deliver more effective drug concentrations to the heart

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than smaller distal veins.108 Dosing should then be incremental, starting at 6 mg in adults followed by 12 mg. An 18 mg dose should then be considered, also taking into account tolerability/side effects in the individual patient. Adenosine has a very short plasma half-life due to enzymatic deamination to inactive inosine being achieved in seconds, with end-organ clinical effects complete within 20 30 s.107 Thus, repeat administration is safe within 1 min of the last dose.2,3 The dose range between patients may be very wide,107 with >90% success generally expected.94,109 Some drugs (e.g. dipyridamole and theophylline) may on occasion affect dose requirements, but any influence of recent intake of caffeinated beverages is disputed.110,111

Transient dyspnoea is common with increased ventilation, and is more likely to result from the stimulation of pulmonary vagal C fibres.112 Facial flushing may occur, associated with vasodilatation and increased skin temperature.107 Chest pain, variable in terms of radiation over the thorax, may suggest ischaemic or oesophageal origins, and has been associated with increased coronary sinus blood flow so may well be of cardiac origin.107

Depression of sinoatrial node function is to be expected based on established pharmacology, but prolonged bradycardia is unusual.105,107 Nonetheless, adenosine administration should be approached cautiously in those with known sinus node disease.113 Perceived risks of bradycardia in recipients of denervated orthotropic heart transplants, in whom SVT is common, have prompted a relative contraindication.114,115 However, more recent substantive evidence supports adenosine use in this group with no particular cautions.116 AF may occur following adenosine administration as a result of either direct pulmonary vein (PV) triggering117 or increasing heterogeneity of repolarization,118 and appears more commonly associated with AVRT than AVNRT.93 Adenosine may also occasionally cause or accelerate pre-excited atrial arrhythmias.119,120

Clinically important bronchoconstriction has been rarely reported in those receiving i.v. adenosine for SVT,121 and this observation is further supported by the large experience obtained when adenosine infusions have been given for cardiac stress testing.105,122,123 Furthermore, despite inhaled adenosine producing bronchoconstriction in people with asthma,124 i.v. administration has had no impact on the airways in clinical experimental studies.125 There have been isolated reports of clinically well-documented bronchoconstriction occurring in patients with or without respiratory disease, thus suggesting that care is required in patients with asthma.121,126,127 However, adenosine can be used cautiously in those with asthma, although verapamil may be a more appropriate choice in patients with severe asthma.

Adenosine triphosphate may also be used but clinical experience is limited.

Calcium channel blockers (verapamil/diltiazem i.v.) and betablockers (e.g. esmolol and metoprolol i.v.) are of value, particularly in patients with frequent atrial or ventricular premature beats. Verapamil [0.075 - 0.15 mg/kg i.v. (average 5 - 10 mg) over 2 min] or i.v. diltiazem [0.25 mg/kg (average 20 mg) over 2 min] has been

shown to terminate SVT in 64 98% of patients, but is associated with a risk of hypotension.92,94 98,128 These drugs should be avoided

in patients with haemodynamic instability, HF with reduced LV ejection fraction (<40%), a suspicion of VT, or pre-excited AF. Betablockers (i.v.), such as short-acting esmolol (0.5 mg/kg i.v. bolus or 0.05 - 0.3 mg/kg/min infusion) or metoprolol (2.5 15 mg given i.v. in

2.5 mg boluses), are more effective in reducing the tachycardia rate than in terminating it.97,99,100,128 Although evidence for the effectiveness of beta-blockers in terminating SVT is limited, they have an excellent safety profile in haemodynamically stable patients. Betablockers are contraindicated in patients with decompensated HF. Caution is needed with concomitant use of i.v. calcium channel blockers and beta-blockers, because of possible potentiation of hypotensive and bradycardic effects. In the first clinical trial of etripamil, a short-acting L-type calcium channel blocker with a rapid onset of action after intranasal administration, conversion rates from SVT to sinus rhythm ranged from 65 95%.129

10.1.2 Wide QRS (120 ms) tachycardias

The acute management of a patient with wide QRS tachycardia depends on the haemodynamic stability of the patient

(Figure 5).106,130,131

Recommendations for the acute management of wide QRS tachycardia in the absence of an established diagnosis

	Recommendation	Classa	Levelb
	Haemodynamically unstable patients
	Synchronized DC cardioversion is recom-
	mended in haemodynamically unstable	I	B
	patients.86,130
	Haemodynamically stable patients
	A 12 lead ECG during tachycardia is	I	C
	recommended.
	Vagal manoeuvres are recommended.	I	C
	Adenosine should be considered if vagal
	manoeuvres fail and there is no pre-excitation	IIa	C
	on a resting ECG.
	Procainamide (i.v.) should be considered if	IIa	B
	vagal manoeuvres and adenosine fail.132
	Amiodarone (i.v.) may be considered if vagal	IIb	B
	manoeuvres and adenosine fail.132
	Synchronized DC cardioversion is recom-
	mended if drug therapy fails to convert or	I	B
	control the tachycardia.86,130
	Verapamil is not recommended in wide QRS-
	complex tachycardia of unknown	III	B
	aetiology.64,133,134

DC = direct current; ECG = electrocardiogram; i.v. = intravenous. aClass of recommendation.

bLevel of evidence.

10.1.2.1 Haemodynamically unstable patients

Haemodynamic instability may occur with any wide QRS tachycardia, regardless of the cause, but is more likely in patients with VT. Synchronized cardioversion is recommended for any persistent wide QRS tachycardia resulting in hypotension, acutely altered mental status, chest pain, acute HF symptoms, or signs of shock.86,87

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					Wide QRS
					tachycardia
					Haemodynamic
						instability
			No						Yes
		Vagal manoeuvres							Synchronized
			(I C)						cardioversion
If ineffective									(I B)
		i.v. adenosine
		(if no evidence of
		pre-excitation
		on resting ECG)
If ineffective			(IIa		C)
i.v. procainamide					i.v. amiodarone
(IIa		B)				(IIb		B)			2019
											©ESC
		If ineffective

Figure 5 Acute therapy of wide complex tachycardia in the absence of an established diagnosis.

AVRT = atrioventricular re-entrant tachycardia; i.v. = intravenous.

10.1.2.2 Haemodynamically stable patients

In a patient with wide QRS tachycardia who is haemodynamically stable, the response to vagal manoeuvres may provide insight into the mechanism responsible for the arrhythmia. SVT with aberrancy, if definitively identified, may be treated in the same manner as narrow complex SVT, with vagal manoeuvres or drugs (adenosine and other

AVN-blocking agents such as beta-blockers or calcium channel blockers).117 119,129

Some drugs used for the diagnosis or treatment of SVT (e.g. verapamil) can cause severe haemodynamic deterioration in patients with a previously stable VT.64,133,134 Thus, they should only be used for the treatment of patients in whom the diagnosis of SVT is fully established and secure. Adenosine may be helpful by means of allowing a diagnosis or interrupting an adenosine-sensitive VT, but it must be avoided if pre-excitation on resting ECG suggests a pre-excited tachycardia. There is a risk that in antidromic re-entry, adenosine may precipitate cardiac arrest if there is induction of AF by adenosine, as may occasionally occur.135

For pharmacological termination of a haemodynamically stable wide QRS-complex tachycardia of unknown aetiology, i.v. procainamide or amiodarone can be used in-hospital.132,136 138 In the PROCAMIO trial132 in patients with well-tolerated wide QRS

tachycardia, with or without reduced LV ejection fraction, procainamide was associated with fewer major cardiac adverse events and a higher proportion of tachycardia termination within 40 min compared with amiodarone.

In case the mechanism of the arrhythmia is not fully understood, the arrhythmia should be treated as VT.

10.2 Irregular tachycardias

A wide QRS irregular tachycardia is usually a manifestation of AF. Rarely, polymorphic VT and, very rarely, monomorphic VT may also present as irregular tachycardias. Electrical cardioversion is the acute treatment of choice in irregular pre-excited tachycardias associated with haemodynamic instability. Specific therapy of pre-excited AF is discussed in section 11.

If the rhythm is well tolerated with a narrow QRS-complex irregular tachycardia, this should be considered likely to be AF, and rate control with beta-blockers or calcium channel blockers, and elective chemical or electrical cardioversion once thromboprophylaxis is in place, may be appropriate.4

11 Specific types of supraventricular tachycardia

11.1 Atrial arrhythmias

11.1.1 Sinus tachycardia

Sinus tachycardia is defined as a sinus rate >100 b.p.m. On the ECG, the P wave is positive in leads I, II, and aVF, and biphasic/negative in lead V1.

11.1.1.1 Physiological sinus tachycardia

The determinants of physiological sinus tachycardia are, by definition, physiological (effort, stress, or pregnancy), and may also arise secondary to other medical conditions or drugs (Table 10). The 12 lead ECG shows P-wave morphology typical of normal sinus rhythm. Physiological sinus tachycardia is treated by identifying and eliminating the cause.

11.1.1.2 Inappropriate sinus tachycardia

IST is defined as a fast sinus rhythm (>100 b.p.m.) at rest or minimal activity that is out of proportion with the level of physical, emotional, pathological, or pharmacological stress.139 The tachycardia tends to be persistent, and most of the affected patients are young and female, but this disorder is not limited to that population.140 The underlying

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mechanism of IST remains poorly understood and is likely to be multifactorial (e.g. dysautonomia, neurohormonal dysregulation, and intrinsic sinus node hyperactivity). Recently, a gain-of-function mutation of the pacemaker hyperpolarization-activated cyclic nucleotidegated 4 (HCN4) channel has been reported in a familial form of IST.141 There is also evolving evidence that immunoglobulin G antibeta receptor antibodies are found in IST.142 The prognosis of IST is generally considered benign140 and the arrhythmia has not been associated with tachycardia-induced cardiomyopathy.

11.1.1.2.1Diagnosis. Patients with IST have a wide spectrum of clinical presentations ranging from usually asymptomatic or minimally symptomatic palpitations to dyspnoea, exercise intolerance, dizziness, and light-headedness. The diagnosis of IST is one of exclusion of POTS, sinus re-entrant tachycardia, or focal AT from the superior part of the crista terminalis or right superior PV. Characteristically, 24 h Holter monitoring demonstrates a mean heart rate >90 b.p.m. with an exaggerated heart rate response >100 b.p.m. during waking hours.140 Tolerance exercise testing might also be considered to document the exaggerated heart rate or blood pressure response to minimal exercise. An EPS is generally not required in making the diagnosis, and should not be routinely performed unless, rarely, sinus node re-entry is suspected.

11.1.1.2.2Therapy. Reassurance and lifestyle interventions such as exercise training, volume expansion, and avoidance of cardiac stimulants should be tried before drug treatment (Figure 6).139,143,144 As the prognosis of IST is benign, treatment is aimed at symptom reduction and may not be necessary. Beta-blockers have been used in patients with IST for several years, but may be needed at doses high enough to cause intolerable side effects such as chronic fatigue. Nondihydropyridine calcium channel blockers may also be used, but at

doses that may cause hypotension, and the evidence regarding these drugs is limited.139,145 Ivabradine, a selective blocker of the ‘pace-

maker current’ (If) in sinoatrial myocytes that directly slow the heart rate, has been found to be safe and effective in several small trials.146 150 However, blockade of the If may perturb the feedback loop underlying baroreceptor control of autonomic balance, thereby increasing sympathetic activity to the heart.151 If this effect occurred chronically at therapeutic dosages, it would be a matter of concern for its remodelling and pro-arrhythmic potential. Ivabradine should be preferably co-administered with a beta-blocker when possible; this combination may also be more beneficial than each drug alone for IST.152 Ivabradine should not be taken during pregnancy or

breastfeeding.153 As a substrate of cytochrome p450 (CYP) 3A4, ivabradine should be avoided or used with caution with concomitant administration of CYP44A inhibitors (ketoconazole, verapamil, diltiazem, clarithromycin, and grapefruit juice) or inducers (rifampin and carbamazepine).154 The limited and disappointing evidence, reported from small observational studies, suggests that catheter ablation should not be considered as part of the routine management of most patients with IST.155 161

Recommendations for the therapy of sinus tachycardias

	Recommendation		Classa	Levelb
	Inappropriate sinus tachycardia
	Evaluation and treatment of reversible causes		I	C
	is recommended.139,144,162
	Ivabradine alone or in combination with a
	beta-blocker should be considered in sympto-		IIa	B
	matic patients.146 149,151,152
	Beta-blockers should be considered in symp-		IIa	C
	tomatic patients.139,147
	Sinus nodal re-entrant tachycardia
	Non-dihydropyridine calcium channel block-
	ers (verapamil or diltiazem) in the absence of		IIb	C
	HFrEF, may be considered in symptomatic
	patients.163
	Catheter ablation should be considered in
	symptomatic patients who do not respond to		IIa	C
	drug therapy.164 166
	Postural orthostatic tachycardia syndrome
	A regular and progressive exercise pro-		IIa	B
	gramme should be considered.167 169
	The consumption of <2 3 L of water and
	10 12 g of sodium chloride daily may be		IIb	C
	considered.170,171
	Midodrine, low-dose non-selective beta-
	blocker, or pyridostigmine may be		IIb	B
	considered.167,170,172 174
	Ivabradine may be considered.175		IIb	C

HFrEF = heart failure with reduced ejection fraction. aClass of recommendation.

bLevel of evidence.

11.1.1.3 Sinus node re-entrant tachycardia

Sinus node re-entrant tachycardia arises from a re-entry circuit involving the sinus node and, in contrast to IST, is characterized by paroxysmal episodes of tachycardia.176 This uncommon arrhythmia may be associated with paroxysmal symptoms of palpitation, dizziness, and light-headedness. On the ECG, the polarity and configuration of the P waves are similar to the configuration of sinus P waves.163

11.1.1.3.1 Diagnosis. The diagnosis of sinus node re-entrant tachycardia is suspected on ECG and Holter ECG. It can be confirmed with an EPS.

				Sinus tachycardia
				Treatment of reversible causes
				If ineffective		(I		C)
		Ivabradine						Beta-blocker
			(IIa B)					(IIa C)
	If ineffective							If ineffective
					Symptomatic
				and recurrent sinus
				node re-entry
				Yes				No
			Drug therapy					Ivabradine with a
								beta-blocker
			desirable					(IIa B)
	Yes					No
	Verapamil or							Catheter		2019
	diltiazem							ablation
	(IIb C)		If ineffective					(IIa C)		©ESC
Figure 6 Therapy of sinus tachycardias.

.	11.1.1.3.2 Therapy. Medical treatment is empirical, and no drugs have
.
.
.	been studied in controlled trials. Verapamil and amiodarone have
.
.
.	demonstrated variable success, whereas beta-blockers are often inef-
.
.	163
.		Sinus node re-entrant tachycardia may be effectively and
.	fective.
.
.	safely treated with catheter ablation targeting the site of earliest atrial
.
.
.	activation with respect to the P wave. This approach has been shown
.
.				164	166
.
.	to be feasible with a good long-term outcome.
.
.
.
.
.	11.1.1.4 Postural orthostatic tachycardia syndrome
.
.
.	POTS is defined as a clinical syndrome usually characterized by an
.
.
.	increase in heart rate of >30 b.p.m. when standing for >30 s (or >40
.
.
.	b.p.m. in individuals aged 12 - 19 years) and an absence of orthostatic
.
.
.								177,178
.	hypotension (>20 mmHg drop in systolic blood pressure).
.
.	The prevalence of POTS is 0.2% and it represents the most com-
.
.
.						178
.								with most
.	mon cause of orthostatic intolerance in the young,
.
.	patients aged between 15 and 25 years, and >75% being female.
.
.
.	Although	the long-term prognosis		of POTS	has		been poorly
.
.
.	explored, 50% of patients spontaneously recover within 1 - 3 years.
..
.	A number of mechanisms have been described					in patients			with
.
.
.	POTS,	including	autonomic nervous system				dysfunction,
.
.
.
. peripheral autonomic denervation, hypovolaemia, hyperadrenergic
.
.	stimulation, diabetic neuropathy,			deconditioning,			anxiety,		and
.
.		178 181
.
.	hypervigilance.
.
.
.
.
.	11.1.1.4.1 Diagnosis. POTS is diagnosed during a 10 min active stand
.
.
.	test or	head-up	tilt test with	non-invasive		haemodynamic
.
.
.