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............................................................................................................................................................................. 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 (618 mg i.v. bolus) is the first drug of choice.9294 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 atrialHis (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 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 2030 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 6498% of patients, but is associated with a risk of hypotension.92,9498,128 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 (2.515 mg given i.v. in ©ESC 2019 Narrow QRS tachycardia Vagal manoeuvres (I B) i.v. adenosine (I B) i.v. verapamil or diltiazem (IIa B) i.v. beta-blocker (IIa C) Synchronized cardioversion (I B) Yes No If ineffective If ineffective If ineffective Haemodynamic instability Figure 4 Acute therapy of narrow QRS tachycardia in the absence of an established diagnosis. i.v. = intravenous. Downloaded from academic.oup.com/eurheartj/article/41/5/655/5556821 by guest on 07 October 2026