Author: Gavin Lloyd, Beth Newstead / Editor: Steve Fordham / Reviewer: Reuben Cooper, Jessie Lynch / Codes: CC10, CC3, CP1, CP2, CP3, CP4, RP7, RP8, SLO1, SLO3Published: 20/01/2023

This session covers management of tachycardias in the Resuscitation Room. It builds on the Resuscitation Council UK [1] ALS Guidelines (2021) using selected evidence.

ALS certification is assumed.

Is My Patient Stable?

When you are given an ECG with a tachycardia to review, or, when you are summoned to a patient with a tachycardia on their monitor ask “Is my patient stable?”

Adverse clinical features that identify your patient is clinically unstable due to their tachycardia:

  • Systolic blood pressure less than 90
  • Breathlessness
  • Sweating
  • Confusion
  • Peripherally shut-down

Here are some useful questions to help you decide whether or not your patient is stable.

1. Does your patient have clinical evidence of a reduced cardiac output?

Are they peripherally shut down, sweaty, hypotensive or showing signs of confusion or drowsiness?

Have they had a syncopal event or transient loss of consciousness?

Patients with excessive tachycardias (>150 bpm) are more likely to be unstable.

2. Does your patient have chest pain?

This would suggest ischaemia due to inadequate perfusion.

Many patients with SVT have mild chest discomfort or tightness however and this does not always reflect instability.

3. Does your patient have signs of heart failure?

Are they breathless with pulmonary crepitations on auscultation?

Does they have peripheral or sacral oedema with evidence of liver engorgement and a raised JVP?

4. Simple measures you should apply to all unstable patients:

  • Move the patient to the resuscitation room
  • Give high-low oxygen
  • Attach an ECG monitor and get a 12-lead ECG if not already done
  • Establish intravenous access

A venous gas should give you a reliable and prompt K+.

Assume hypomagnasemia if hypokalaemia exists.

Order a calcium level.

5. Simple principles to remember:

  • Unstable patients need ‘electricity’.
  • Recognising the exact rhythm is not essential.
  • Treat the patient and not the ECG: if the patient is stable, take your time in making the ECG diagnosis and get advice if you’re unsure.

Learning bite

An unstable patient requires electrical cardioversion rather than drugs regardless of the underlying rhythm.

The ALS Tachycardia algorithm asks the following question: Are there any life-threatening features present?

Tachycardia Algorithm 2021. Resuscitation Council UK

If so, synchronised DC cardioversion is indicated.

Clearly stability/instability is a spectrum — if in doubt, give electricity. Sedation should be administered by a doctor experienced and competent in the technique used.

Deliver a synchronised DC shock. The current recommendations for different tachyarrhythmias are:

  • Initial synchronised shock at maximum defibrillator output rather than an escalating approach for atrial fibrillation (Resus Council UK advises that this is a reasonable strategy based on current data)
  • Initial shock of 70-120J, with stepwise increases in electricity for subsequent shocks, for atrial flutter or supraventricular tachycardia
  • Initial shock of 120-150J, with stepwise increases in electricity for subsequent shocks, for ventricular tachycardia

If the patient is unstable and you deliver three shocks to them without success, administer amiodarone 300mg IV over 10-20 minutes and repeat synchronised DC shock (ensure maximum recommended shock level is given).

Other things to consider include:

  • Seeking a cardiology opinion
  • Changing pad position to anterior/posterior
  • Correcting potential underlying causes e.g. hypovolaemia or electrolyte abnormalities
  • Overdrive pacing

If the patient is stable, you can ask:

  • Is the tachycardia narrow (QRS <120 ms or three small squares on the ECG) or broad complex (QRS >120 ms)?
  • Is the tachycardia regular or irregular?

These questions allow you to subdivide the rhythms into four categories (regular narrow complex/ irregular narrow complex/ regular broad complex/ irregular broad complex).

Tachycardia Algorithm 2021. Resuscitation Council UK

Three most common causes of a regular narrow complex tachycardia:

  • Sinus tachycardia
  • Atrial Flutter
  • Re-entrant SVT

Tips on Differentiating Between The Different Rhythms

Sinus tachycardia 1. Sinus tachycardia: Scrutinise the ECG carefully for P waves. These can be difficult to see at faster heart rates. Remember that very fast rates are unlikely in sinus rhythm; maximum heart rate = 220-age is a helpful formula. Direct treatment at the underlying cause (e.g. pain, anxiety, sepsis, shock….). Be wary of discharging a patient with an unresolved tachycardia.

Atrial Flutter

  • Look at the rate and suspect flutter if it is 140-160 and stays more or less constant. Look carefully for flutter waves in all leads but especially in leads V1 and II.  Treatment is broadly the same as for atrial fibrillation (see AF later). If symptoms have been present <48 hours than electrical cardioversion is probably the treatment of choice.  Pharmacological cardioversion is generally less effective than in atrial fibrillation. Flecainide can paradoxically lead to an increase in the ventricular rate by causing 1:1 conduction and is best avoided

Re-entrant SVT  If you cannot spot flutter or P waves that precede the QRS complex then you can safely assume a re-entrant SVT.

Vagal Manoeuvre

The Valsalva manoeuvre appears better than carotid sinus massage (54% vs 17%) in restoring sinus rhythm [3]  It is also safe, whereas carotid sinus massage rarely may be complicated by stroke – avoid in patients with carotid bruits (listen first).

A Valsalva manoeuvre (forced expiration against a closed glottis) can be easily achieved by asking your patient to try and blow the plunger back on a 20ml syringe.

Physiology of the Valsalva Manoeuvre

Here’s a refresher on the physiology of the Valsalva in order to maximise your chance of success.

Phase 1: (Initiation of manoeuvre): Raised intra-thoracic pressure leads to a transient increase in venous return leading to a rise in BP. Note that phase 1 does NOT start at time 0 in the figure.

Phase 2: (Straining): The sustained rise in intra-thoracic pressure leads to reduced venous return, reduced filling of the heart,  reduced cardiac output and a fall in BP. There is a compensatory increase in heart rate.

Phase 3: (Release): The sudden reduction in intra-thoracic pressure means that the venous reservoir is momentarily empty and there is a fall in BP.

Phase 4: There is rapid return of cardiac output and a corresponding rise in BP. This elicits a parasympathetically mediated reflex bradycardia. This is what hopefully terminates the SVT.

To increase the chances of a Valsalva being successful you therefore need to:

  • Explain carefully to the patient that they may feel faint and experience an initial increase in heart rate. Insufficient explanation may result in high anxiety (and high sympathetic activity) which will antagonise the desired parasympathetic bradycardia
  • Make sure the patient performs the manoeuvre for long enough (15-20 seconds if possible). Insufficient time spent in phases 1 and 2 may not elicit the necessary compensatory changes
  • Words of encouragement are allowed
  • The Valsalva manoeuvre should be augmented by putting the patient head down and raising his/her legs just prior to release of the ‘strain’ phase (by further increasing venous return) as per the REVERT study [4]. This simple modification improved the success of the valsalva manoeuvre from 17% to 43%.

Learning bite In a patient with re-entrant SVT, a Valsalva is the vagal manoeuvre of choice.


Second-line Treatments

Tachycardia Algorithm 2021. Resuscitation Council UK

If vagal manoeuvres fail to terminate the tachyarrhythmia, adenosine is recommended as second-line treatment. Adenosine works by slowing conduction thorough the AV node.

It is given as a rapid IV bolus (6 mg, 12 mg, 18mg) via a large vein and is followed by a rapid flush. Note the recent update in dosing regimen.

Side-effects include:

  • Nausea
  • Dizziness
  • Breathlessness
  • Flushing
  • Chest tightness

Ensure you alert your patient to adenosine’s very unpleasant side effects before administration. Be ready to reassure your patient shortly after administration of adenosine.

Adenosine has a success rate in excess of 90%.

Adenosine is contraindicated in heart block and sick sinus syndrome. Heart transplant patients should be given a small dose (3 mg) as the donor AV node may be exquisitely sensitive to adenosine. Asthma is discussed below.

Verapamil is an alternative option and is recommended if adenosine is ineffective. It has a longer onset of action and more potential side effects than adenosine.[5] It can be given IV over 2 minutes at a dose of 5-10 mg in otherwise well patients.

Verapamil is contraindicated in patients with heart block or impaired left-ventricular function. It should also be avoided in patients who take beta-blockers as you risk asystole.

Beta-blockers may be considered if all of the above options are ineffective.

The three main causes are:

  • Atrial Fibrillation
  • Atrial flutter with variable block
  • Multifocal Atrial Tachycardia

Differentiating Between the Different Rhythms

Atrial flutter8 is identified by the presence of:

  • Loss of isoelectric line
  • Regular atrial activity ~300 beats/minute
  • Saw-tooth pattern of inverted flutter waves (II, III, aVF)
  • Upright flutter waves in V1 (these may be mistaken for P waves)

In atrial flutter with a fixed AV conduction ratio, the ventricular rate is a fraction of the atrial rate, for example in a 3:1 block  the ventricular rate would be ~100bpm (1/3 of atrial rate ~300bpm).

Atrial flutter with a variable AV conduction ratio, there may be alternating 2:1, 3:1 and 4:1 ratios, creating an irregular ventricular response which mimics atrial fibrillation.

Multifocal atrial tachycardiais identified by the presence of:

  • HR >150 beats/minute (can be as high as 250bpm, usually ~100-150bpm)
  • Irregularly irregular rhythm
  • Varying PP/PR/RR intervals
  • 3 different P wave morphologies in same lead
  • No flutter waves

Atrial fibrillation10 is identified by the presence of:

  • Irregularly irregular rhythm
  • Loss of isoelectric line
  • No P waves
  • Narrow (<120ms) QRS complex (unless BBB/accessory pathway/rate-related aberrancy)
  • Fine or coarse fibrillatory waves.

NICE Recommendations

The management of patients presenting with AF is further complicated by the need to consider the important role of anticoagulation. This is beyond the scope of this session. See the NICE recommendation.

Please also refer to the dedicated RCEMlearning session on Atrial Fibrillation.

Learning bite

  • An unstable patient in atrial fibrillation should be electrically cardioverted
  • Attempt cardioversion in patients with atrial fibrillation/flutter of less than 48 hours.


Four main causes of a regular broad complex tachycardia:

  1. Ventricular tachycardia (VT)
  2. Supraventricular tachycardia (SVT) with bundle branch block (BBB) – this is sometimes called SVT with aberrancy/SVT with aberrant conduction
  3. Sinus tachycardia with BBB
  4. Atrial flutter with BBB

Differentiating VT from Other Rhythms

So, how can we differentiate VT from these other rhythms?

  • Any patient with a history of ischaemic or structural heart disease should be assumed to have VT
  • A prior history of MI = 98% chance the rhythm is VT
  • History of structural heart disease = 90% chance the rhythm is VT [7]

This may save attempts at detailed ECG analysis.

Learning bite

  • In differentiating between VT and SVT with aberrant conduction – if the patient is >50 and/or has a history of structural or ischaemic heart disease, assume the rhythm is VT
  • If there is any doubt whatsoever – treat a regular broad complex tachychardia as VT.

Following features are suggestive of VT:

  • Evidence of independent atrial activity – dissociated P waves
  • Fusion/Capture beats
  • A bizarre axis
  • QRS >140 msec
  • Concordance of the QRS complexes in the chest leads

Brugada Criteria

The following should be noted:

Is there an absence of RS complexes in all the chest leads


Is the R-S interval (interval between the tip of the R wave and the lowest part of the S wave) > 100mS in any V lead?


Are there capture beats, fusion beats, or evidence of AV dissociation?


Does the morphology of the QRS complex in leads V1/ V6 suggest VT?


Morphologic Criteria suggestive of VT

1. RBBB morphology

V1:     Monophasic R wave

QR wave

RS wave

V6:     Monophasic R wave

QR wave

R wave smaller than the S wave

2. LBBB morphology

V1:      R wave > 30 msec wide

RS wave > 60 msec wide

V6:     QR wave

QS wave

If the answer to any of these questions is YES then the diagnosis is VT.

If the answer to all of these questions is NO then the diagnosis is SVT with a bundle branch block.

Brugada et al. showed that application of these criteria to a sample of 554 patients had a sensitivity of 98.7% and a specificity of 96.5% in making the correct diagnosis [8].

The main pitfall with these criteria is that they are not easy to apply or remember.

Learning bite

Objective criteria for distinguishing between VT and SVT with aberrant conduction are irrelevant if the patient is unstable. Synchronised DC cardioversion is required.

Treatment of Stable VT


Tachycardia Algorithm 2021. Resuscitation Council UK

Assuming the underlying rhythm is VT and that the patient is stable, first-line treatment is conventionally amiodarone (Resus Council UK guidance).

However, amiodarone is poorly effective in the treatment of acute VT. In a small, retrospective study of 33 patients given 150 mg amiodarone it had only a 29% success rate after 20 minutes. Four patients deteriorated and 55% of the patient group ultimately required electrical treatment [9]. A more recent study of 41 patients substantiated these findings: only 15% of the patient group cardioverted with a bolus dose of 300 mg amiodarone after 20 minutes and 17% of patients deteriorated [10].

Sotalol appears more effective  One cross-over study showed a 69% success rate in the treatment of stable VT (compared with lignocaine, which was the ALS recommendation at that time) [11]. The AHA 2020 Adult Tachycardia algorithm suggests using a dose of 100mg (1.5mg/kg) over 5 minutes.

Procainamide has class 2a evidence supporting its usage in this situation but is slow to work. A recent RCT published in 2017 comparing procainamide to amiodarone in the haemodynamically stable patient with acute monomorphic VT – procainamide was more efficacious in terminating arrhythmia, and was associated with less major cardiac adverse events. The AHA 2020 Adult Tachycardia algorithm suggests using a dose of 20-50 mg/min until:

  • Resolution of arrhythmia
  • Maximum dose 17 mg/kg given
  • Adverse events:
  • Hypotension develops
  • QRS duration increases >50%

If the arrhythmia has been successfully treated, adverse events have not occurred & maximum dose not reached, a maintenance infusion of 1-4 mg/min can be commenced.

Both sotalol and procainamide have the potential to prolong the QT interval and are best avoided in patients who already have QT prolongation on ECG.

DC cardioversion is reasonable as first-line treatment of stable VT.

Learning bite

Amiodarone is poorly effective in the treatment of stable VT. Consider electrical cardioversion or soltalol instead.


The most common causes of an irregular broad complex tachycardia are:

  • Atrial fibrillation with a bundle branch block
  • Torsades de pointes
  • Pre-excited atrial fibrillation

Atrial fibrillation occurs in between 11-38% of patients with WPW and can degenerate into VF.

Many AV nodal blocking drugs that are used in the treatment of atrial fibrillation are contraindicated or not recommended in the treatment of pre-excited AF associated with WPW:

  • Verapamil
  • Adenosine
  • Beta blockers
  • Amiodarone
  • Digoxin

Recommended 1st line drug treatments are IV procainamide or IV ibutilide.17 IV flecainide is also effective in this setting.17,18

Consider pre-excited atrial fibrillation as a diagnosis where the rhythm is irregular and broad complex.

‘Torsades de pointes’ specifically refers to polymorphic VT due to a prolonged QT interval.

Prolongation of the QT can be congenital or acquired (most commonly due to drugs)19. Other causes of VT are ischaemia or myocarditis. Polymorphic VT is a form of VT in which there are rapid, irregular QRS complexes which seem to be twisting around the baseline.

Polymorphic VT

Do you have:

  • An unstable patient with polymorphic VT?

Treatment is by synchronised DC cardioversion. The defibrillator may have difficulty recognising the QRS complexes (as they are of varying morphology) and consequently fail to discharge. If this is the case, administer an unsynchronised shock.

  • Stable patient with polymorphic VT?

Rectify the QT prolongation by giving IV Magnesium, stopping any causative drugs and addressing any other causes of a prolonged QT such as hypokalaemia.

  1. Resuscitation Guidelines 2021. Resuscitation Council UK.
  2. National Institute for Health and Care Excellence. Atrial fibrillation: diagnosis and management. NICE [NG196], 2021.
  3. Mehta D. Wafa S. Ward DE. et al. 3. Mehta D. Wafa S. Ward DE. et al. Relative efficacy of various physical manoeuvres in the termination of junctional tachycardia. Lancet 1998; 1(8596):1181-5.
  4. Walker S. Cutting P. Impact of a modified Valsalva manoeuvre in the termination of supraventricular tachycardia. Emerg Med J 2010; 27:287-291.
  5. Holdgate A. Foo A. Adenosine versus intravenous calcium channel antagonists for the treatment of supraventricular tachycardia in adults. Cochrane Database of Systematic Reviews 2006; (4):CD005154.
  6. Terry P. Lumsden G. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Using intravenous adenosine in asthmatics. Emergency Medicine Journal 2001; 18(1):61.
  7. Royal College of Emergency Medicine (RCEM). Best Practice Guideline: Procedural Sedation in the Emergency Department. August 2022.
  8. Buttner R, Burns E. Atrial Flutter. Life In The Fast Lane (LITFL). February 2022.
  9. Burns E, Buttner R. Multifocal Atrial Tachycardia (MAT). Life In The Fast Lane (LITFL). June 2021.
  10. Burns E, Buttner R. Atrial Fibrillation. Life In The Fast Lane (LITFL). December 2021.
  11. Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J; PROCAMIO Study Investigators. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2017 May 1;38(17):1329-1335.
  12. Brugada P. Brugada J. Mont L. et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991; 83(5):1649-59.
  13. Marill KA. deSouza IS. Nishijima DK. et al. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med 2006; 47(3):217-24.
  14. Tomlinson DR. Cherian P. Betts TR. et al. Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emergency Medicine Journal 2008; 25(1):15-8.
  15. Ho DS. Zecchin RP. Richards DA. et al. Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia. Lancet 1994; 344(8914):18-23.
  16. Fengler BT. Brady WJ. Plautz CU. Atrial fibrillation in the Wolff-Parkinson-White syndrome: ECG recognition and treatment in the ED. Am J Emerg Med 2007; 25(5):576-83.
  17. Di Biase L, MD, Walsh EP. Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome. UpToDate. Updated July 2022.
  18. Crozier I. Flecainide in the Wolff-Parkinson-White syndrome. American Journal of Cardiology 1992; 70(5):26A-32A.
  19. Burns E. Drugs Causing QT Prolongation. Life In The Fast Lane (LITFL). February 2021