Supraventricular (narrow complex) tachycardias
- DOI:
- 10.1093/med/9780198759935.003.0012
The term supraventricular tachycardia (SVT) includes an umbrella term used to describe tachycardias (atrial and/or ventricular rates in excess of 100bpm at rest), the mechanism of which involves tissues from the His bundle or above that explains the narrow QRS complex, except for the presence of bundle branch block or antidromic tachycardia in the presence of an accessory pathway. These narrow complex tachycardias (NCTs) can be due to two modalities. The first one, where only atrial tissue is involved, is called atrial tachycardia (AT), including inappropriate sinus tachycardia, focal and multifocal and macro-re-entrant AT (including typical atrial flutter). The second one is AVN-dependent tachycardia, the so-called junctional tachycardia, where the AVN is part of the circuit and blocking it with vagal manoeuvres or adenosine can stop the tachycardia, including AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia (in the presence of an accessory pathway) (AVRT).
The epidemiology is not completely known because of incomplete data and failure to discriminate AF, atrial flutter, and other supraventricular arrhythmias. The best available evidence indicates that the prevalence of SVTs in the general population is 2.29 per 1000 persons. SVTs can appear at any age but are especially prevalent in young age and are commoner among females. AF and atrial flutter are treated in 
Chapter 4.1. Here we will focus on NCTs.
AT can originate from the sinoatrial node, the peri-sinoatrial tissue, or any site in the right or the left atria. It may not be easy to determine the nature of a regular NCT on presentation, and often acute treatment is necessary in the absence of an established diagnosis. Nevertheless, some clinical clues can help in the diagnosis, as shown in Table 4.2.1, and some ECG criteria are helpful for the differential diagnosis (see Fig. 4.2.1). In AVNRT, palpitations are generally referred to the neck, and it is difficult to clearly localize the P-wave on the ECG, because it occurs simultaneously with the R-wave. Sometimes, as shown in Fig. 4.2.2, it is possible to see a P-wave mimicking an S-wave in inferior leads or a pseudo-RBBB (RSr′) in lead V1. In the case of AVRT via an accessory pathway, the P-wave can be found at 120–140ms after the beginning of the R-wave, as shown in Fig. 4.2.3.
Table 4.2.1 Clinical clues to the differential diagnosis of supraventricular tachycardia
Type of tachyarrhythmia |
Typical age at onset of symptoms |
Underlying condition |
Usual presentation |
Findings on baseline ECG |
|---|---|---|---|---|
Paroxysmal SVT |
All ages |
None (normal heart) |
Abrupt onset and termination of regular palpitations, diaphoresis |
Pre-excitation common in AVRT |
AF, atrial flutter, multifocal atrial tachycardia |
≥60 years |
Heart disease common (hypertension, ischaemic or valvular heart disease) |
Abrupt onset of paroxysmal, irregular palpitations; symptoms sometimes persistent and occasionally mild or absent |
Signs of LVH; non-specific repolarization abnormalities common |
Sinus tachycardia |
10–30 years |
None (normal heart) |
Progressive onset and termination of palpitations |
Normal |
Ventricular tachycardia |
≥50years |
Ischaemic heart disease |
Abrupt onset and termination of regular palpitations, syncope, or sudden death from cardiac causes |
Pathological Q-waves common |
AVRT, atrioventricular re-entrant tachycardia through an accessory pathway; AF, atrial fibrillation; LVH, left ventricular hypertrophy; SVT, supraventricular tachycardia.
Fig. 4.2.1 Guide to electrocardiographic differential diagnosis of supraventricular tachycardia/regular narrow complex tachycardia. AVNRT, atrioventricular node re-entrant tachycardia; AVRT, atrioventricular re-entrant tachycardia through an accessory pathway; MAT, multifocal atrial tachycardia; PJRT, permanent junctional re-entrant tachycardia.
Fig. 4.2.3 AVRT by an accessory pathway. The P-waves can be seen clearly at 140ms after the beginning of the R-wave (as shown by arrows). In this case, the patient was successfully ablated in the mitral annulus using a retro-aortic approach.
Vagal manoeuvres (Valsalva manoeuvre, carotid sinus massage, or facial immersion in cold water, rather than eye compression) can be performed, with a reported efficacy of 19–54%. Carotid sinus compression should be performed with caution in older patients, ruling out murmurs by carotid auscultation. Compression should be for 15 and 20s and can be repeated twice. If this fails, adenosine/ATP injection can help to distinguish atrial tachycardia from tachycardia involving the AVN. In addition, the efficacy and safety of etripamil (a short-acting CCB) as nasal spray have recently been reported to terminate paroxysmal SVT induced in the electrophysiological laboratory. It is possible that, in the future, self-administration of such drug would prove useful in patients with tachycardias involving the AVN. Fig. 4.2.4 shows an algorithm indicating the use of IV adenosine for the diagnosis of an underlying rhythm in patients with NCT and how to manage this type of arrhythmia.
Fig. 4.2.4 Usefulness of vagal manoeuvres or adenosine in the diagnosis of NCT. AVNRT, atrioventricular nodal reciprocating tachycardia; AVRT, atrioventricular reciprocating tachycardia.
Notes:
* Continuous ECG recording should commence on administration.
Adenosine should be given as a push IV injection through the antecubital fossa vein (adenosine is more likely to induce atrial fibrillation if given via a central venous line).
Adenosine is contraindicated in the severely asthmatic, owing to bronchiolar constriction.
Adenosine effects are potentiated by dipyridamole.
Higher rates of atrioventricular block are seen if concomitantly administered with carbamazepine.
Verapamil IV can be used as an alternative atrioventricular-blocking agent for diagnosis/arrhythmia/termination, but it is only recommended to be used by experienced cardiologists.
AT originating in, or very close to, the sinoatrial node is mainly treated with pharmacological agents, and ablation is only restricted to some cases of perisinus reciprocating tachycardia not responding to pharmacological therapy.
Ectopic AT originating from any site in the right or left atrium and AVN-dependent tachycardias are usually treated by catheter ablation, which, in recent years, has become the cornerstone treatment for these arrhythmias, reserving pharmacological management for the emergency room scenario. Multifocal AT is difficult to treat pharmacologically. Its presence usually reflects severe chronic lung disease.
Pharmacotherapy
The pharmacological management of supraventricular arrhythmias is summarized in Tables 4.2.2–4.2.4.
Table 4.2.2 Pharmacological options for NCT originating in the sinoatrial node
Type of NCT |
Acute treatment |
Long-term treatment |
|---|---|---|
Physiological sinus tachycardia |
Vagal manoeuvres |
β-blockers Non-dihydropyridine CCBs |
Inappropriate sinus tachycardia |
As above |
β-blockers Non-dihydropyridine CCBs Ivabradine (anecdotal evidence, no approved indication) Ablation |
Paroxysmal orthostatic tachycardia syndrome (POTS) |
As above |
β-blockers Fludrocortisone ± bisoprolol SSRIs Other agents; midodrine, clonidine, octreotide, erythropoietin |
Sinus node re-entry tachycardia |
As above, plus IV amiodarone, non-dihydropyridine CCBs, β-blockers, or digoxin |
Little scope for pharmacotherapy—ablation is the mainstay if poorly tolerated or symptoms present |
CCB, calcium channel blocker; SSRI, selective serotonin reuptake inhibitor.
Table 4.2.3 Pharmacotherapy for atrial (non-sinus node)-origin NCT
Type of NCT |
Acute treatment |
Long-term treatment |
|---|---|---|
Focal AT |
Reverse digitoxicity/hypokalaemia Vagal manoeuvres IV adenosine, β-blockers, non-dihydropyridine CCBs, procainamide, flecainide, propafenone, amiodarone, sotalol |
β-blockers, non-dihydropyridine CCBs Disopyramide, flecainide, propafenone (in absence of structural/ischaemic heart disease) Sotalol, amiodarone (NB. Class I agents should not be used without AV nodal-blocking agent) |
Multifocal AT (irregular rhythm often mistaken for AF) |
Correct pulmonary disease or electrolyte disturbances |
Non-dihydropyridine CCBs β-blockers often contraindicated due to pulmonary disease No role for antiarrhythmics |
AF, atrial fibrillation; AT, atrial tachycardia; AV, atrioventricular; CCB, calcium channel blocker.
Table 4.2.4 Pharmacotherapy for junctional/AV nodal rhythms (NB. Ablative therapies have become the mainstay treatment of these rhythms)
Type of NCT |
Acute management |
Chronic management |
|---|---|---|
AV nodal reciprocating tachycardia (AVNRT) |
Vagal manoeuvres IV adenosine IV amiodarone |
Non-dihydropyridine CCBs, β-blockers, digoxin Flecainide or propafenone if no ischaemic or structural heart disease ‘Pill-in-the-pocket’ treatment for infrequent and well-tolerated episodes (further evidence required). Diltiazem 120mg + propranolol 80mg more effective than flecainide |
AV reciprocating tachycardia (AVRT)—including WPW syndrome |
Vagal manoeuvres IV adenosine (contraindicated in pre-excited AF owing to risk of rapid ventricular response deteriorating into VF) |
Non-dihydropyridine CCBs, β-blockers, digoxin (should not be used as monotherapy in those with accessory pathway that may be capable of rapid conduction during AF) Propafenone, flecainide, sotalol, amiodarone. ‘Pill-in-the-pocket’—as above |
Focal junctional tachycardia |
As above IV flecainide |
Variable responsiveness to β-blockers, flecainide |
Non-paroxysmal junctional tachycardia May be precipitated by: myocardial ischaemia/myocarditis, cardiac surgery, COPD, hypokalaemia, digitoxicity |
Correct underlying abnormality, i.e. correct digitoxicity or hypokalaemia |
Usually not required, but persisting tachycardia can be suppressed by β-blockers or non-dihydropyridine CCBs |
AF, atrial fibrillation; AV, atrioventricular; CCB, calcium channel blocker; COPD, chronic obstructive pulmonary disease; VF, ventricular fibrillation; WPW, Wolff–Parkinson–White.
Further reading
Blomström-Lundquist C, Sheinman MM, Aliot EM, et al. ACC/AHA/ESC Practice Guidelines for the management of patients with supraventricular arrhythmias. Eur Heart J 2003;24:1857–97.Find this resource:
Dan GA, Martínez-Rubio A, Agewall S, et al. Antiarrhythmic drugs—clinical use and clinical decision making: a consensus document from the European Heart Rhythm Association (EHRA) and European Society of Cardiology (ESC) Working Group on Cardiovascular Pharmacology, endorsed by the Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS) and International Society of Cardiovascular Pharmacotherapy (ISCP). Europace 2018;20:731–2an.Find this resource:
Delacretaz E. Supraventricular tachycardia. N Engl J Med 2006;354:1039–51.Find this resource:
Link MS. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med 2012;367:1438–48.Find this resource:
Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adults patients with supraventricular tachycardia. J Am Coll Cardiol 2016;67:e27–115.Find this resource:
Wellens HJJ. The value of ECG in the diagnosis of supraventricular tachycardias. Eur Heart J 1996;17(Suppl C):10–20.Find this resource:
