Resuscitation Council UK Adult Advanced Life Support Guidelines. Published: Oct 2025.
Article Last Updated: 20 September 2025
Content is updated to reflect the latest Resuscitation Council UK Advanced Life Support (ALS) 2025 Guidline.
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Peri-Arrest Tachycardia (Resus Council UK 2025)
Peri-arrest tachycardia refers to a tachyarrhythmia in a patient who still has a pulse but may be clinically unstable. Management depends first on whether life-threatening features are present, then on ECG pattern (narrow vs broad QRS, regular vs irregular rhythm).
Updated UKMLA guide to peri-arrest tachycardia based on the latest Resuscitation Council UK 2025 Advanced Life Support (ALS) guidelines.
Overview of New 2025 Guideline vs Old 2021 Guideline
Scenarios
Old 2021 guideline
New 2025 guideline (key changes)
Unstable
After 3x synchronised DC shocks → IV amiodarone
After 3x synchronised DC shocks → IV amiodarone or procainamide
Stable
Narrow QRS + regular
No changes
Narrow QRS + irregular
Rate control with a beta blocker
Consider digoxin or amiodarone if there is evidence of heart failure
Rate control with a beta blocker OR verapamil OR diltiazem OR digoxin
If ejection fraction <40%: avoid verapamil and diltiazem
Board QRS + regular
1st line: IV amiodarone
If ineffective: synchronised DC shock
Patients with structural heart disease → synchronised DC shock is recommended
If there is high sedation / anaesthesia risk → antiarrhythmics
1st line: IV procainamide
2nd line (if procainamide is unavailable or contraindicated): IV amiodarone
Board QRS + irregular
AF with BBB → treat as irregular narrow complex
Polymorphic VT (e.g. torsades de pointes) → give magnesium 2g over 10 min
AF with pre-excitation → procainamide or cardioversion
Polymorphic VT with QT prolongation (i.e. torsades de pointes) →
Magnesium 8 mmol (equivalent to 2g) over 10 min
Avoid amiodarone
Consider isoprenaline or temporary pacing to increase the heart rate
In addition,“immediately post-ROSC” has been introduced as a new life-threatening feature in peri-arrest management.
NB The latest guidelines on stable tachyarrhythmias have become increasingly complex, particularly for broad-complex, regular rhythms. It is therefore unlikely that examinations will test detailed nuances of this algorithm.
For example, in a question on the management of a stable, broad-complex, regular tachyarrhythmia, it is unlikely that both DC cardioversion and procainamide would be presented as options. More likely, the correct answer would be one of these, alongside clearly inappropriate distractors (e.g. magnesium, atropine, bisoprolol).
In contrast, it is more important to be familiar with the management of unstable tachyarrhythmias, as these pathways are more straightforward, high-yield, and clinically relevant. Consistent with clinical practice, the guidelines emphasise expert input when managing stable tachyarrhythmias.
Background Information
Cardiac Arrest vs Peri-Arrest
This article covers the algorithm for peri-arrest tachycardia, meaning in the presence of a pulse.
If there is no pulse, that is cardiac arrest, the ALSAdvanced life support algorithm should be used.
Approach to Tachycardia (Classification and Causes)
Any tachycardia could be approached with the following method. This is not an exhaustive list, but it includes the most important ones.
Polymorphic ventricular tachycardia (e.g. torsades de pointes)
Atrial fibrillation with aberrancy (e.g. bundle branch block)
Management
The first step is to check for ANY of the life-threatening features:
Shock – hypotension (SBP < 90 mmHg) and/or features of sympathetic compensation⦁ Tachycardia ⦁ cold pale skin ⦁ ↓ CRT ⦁ symptoms of ↓ cerebral blood flow (confusion, ↓ GCS)
Syncope
Only syncope is considered an unstable feature in the context of periarrest tachycardia guidelines; presyncope (near-syncope) does not qualify as an unstable feature. Syncope is defined as a transient, complete loss of consciousness with inability to maintain postural tone and rapid recovery, whereas presyncope refers to symptoms such as extreme lightheadedness or altered consciousness without complete loss of consciousness.
The unstable, high-risk period right after a pulse is regained (following a cardiac arrest), before the patient is physiologically stabilised.
The timingof adverse features must be current (i.e. present at the time of evaluation) to prompt consideration of immediate synchronised cardioversion. Past episodes of instability do not, by themselves, justify urgent cardioversion unless instability recurs or persists during clinical assessment.
Important: the adult tachyarrhythmia algorithm is for peri-arrest tachyarrhythmia of abnormal origin. It is NOT for sinus tachycardia.
Sinus tachycardia is defined as a heart rate >100 bpm originating from the sinus node, typically in response to physiological stressors (e.g., fever, hypovolemia, pain, anaemia, hypoxia). Sinus tachycardia is generally a sympathetic compensatory mechanism, rather than a primary arrhythmia. To manage sinus tachycardia, treat underlying cause, do NOT use antiarrhythmics and cardioversion to normalise the heart rate.
Typical ECG features of sinus tachycardia: 1) heart rate 100-150 bpm 2) identifiable and upright P wave in leads I, II and aVF.
Immediate management: synchronised DC shockShock must be synchronised to occur with the R wave of the ECG to avoid R on T phenomena which can induce ventricular arrhythmias up to 3 attempts, under sedation or anaesthesia (regardless of the rhythm)
For atrial fibrillation: initial shock at maximum defibrillator output is reasonable
For other rhythms: use a stepwise approach (use a lower initial energy level and increase in a stepwise manner)
If DC shock is unsuccessful in restoring sinus rhythm, and the patient remains unstable:
First, attempt pharmacological cardioversion
Amiodarone
Amiodarone is a class III antiarrhythmic drug
300mg IV over 10-20 min, or
Procainamide
Procainamide is a class Ia antiarrhythmic drug
10-15 mg/kg over 20 min
If pharmacological cardioversion failed → re-attempt synchronised DC shock
No Life-Threatening Features (Stable Tachycardia)
The management algorithm depends on the likely tachyarrhythmia, based on 1) QRS duration and 2) rhythm.
Narrow QRS (<120 ms)
Regular Rhythm
In the context of regular narrow complex tachycardia, SVTSupraventricular tachycardia or atrial flutter is most likely
Step up accordingly if there is an inadequate response:
Step 1: vagal manoeuvresManoeuvres that increases vagal tone to reduce the heart rate. Examples include Valsalva manoeuvre and carotid massage.
Asthma & chronic obstructive lung disease (can cause bronchospasm) → can safely use all other interventions besides beta-blockers/adenosine
Decompensated heart failure
Long QT syndrome
2nd / 3rd degree AV block and sick sinus syndrome (unless a pacemaker is fitted)
Severe hypotension
Irregular Rhythm
In the context of irregular narrow complex tachycardia, AF is most likely.
Offer rate control with:
Beta blocker
Most commonly used: bisoprolol, carvedilol, metoprolol
, or
Digoxin, or
Rate-limiting CCB (verapamil or diltiazem) (avoid in heart failure or ↓ LVEF)
Anticoagulation is necessary if the duration of the arrhythmia has lasted >24 hours
For detailed management of atrial fibrillation (non-acute), see the Atrial Fibrillation (AF) article.
Rate-limiting CCBs (verapamil and diltiazem) should be avoided if there is heart failure or an ejection fraction <40%. Beta blocker or digoxin should be used instead.
This is because rate-limiting CCBs (specifically non-DHP CCBsNon-dihydropyridine calcium-channel blocker) have a strong -ve inotropic and -ve chronotropic effects, which can depress myocardial contractility, worsening heart failure, and potentially triggering cardiac arrest.
Broad QRS (>120ms)
Regular Rhythm
Regular broad complex tachycardia is VT until proven otherwise, but it could also be SVT with aberrancy.
VT is likely if ANY of the following are present:
Known case of VT
Vagal manoeuvres and adenosine failed
Known / suspected heart disease
Uncertain mechanism of arrhythmia
Management approach:
Patients with structural heart disease (or unclear whether there is underlying heart muscle damage) → synchronised DC shock (under sedation / anaesthesia) is recommended
If there is high sedation / anaesthesia risk OR certainly no structural heart disease → antiarrhythmics
1st line: IVprocainamide
Procainamide is a class Ia antiarrhythmic drug
10-15 mg/kg over 20 min
2nd line (if procainamide is unavailable or contraindicated): IV amiodarone 300 mg over 10-60 min, then 900 mg over 24 hours
If antiarrhythmics are ineffective → synchronised DC shockShock must be synchronised to occur with the R wave of the ECG to avoid R on T phenomena which can induce ventricular arrhythmias up to 3 attempts
Procainamide contraindications:
Severe heart failure
Acute myocardial infarction
End-stage renal disease
Irregular Rhythm
In the context of irregular broad complex tachycardia, polymorphic VT or AF with aberrancy is most likely
Torsades de pointes (i.e. polymorphic VT) →
IV magnesium 8 mmol (equivalent to 2g) over 10 min
Avoid amiodarone
Consider isoprenaline or temporary pacing to increase the heart rate
This is because bradycardia worsens QT prolongation
Although torsades is a tachyarrhythmia, it is worsened by bradycardia (see below for full explanation)
Therefore, increasing the heart rate will shorten the QT interval and help terminate the arrhythmia
However, isoprenaline / temporary pacing is usually only used if magnesium alone is insufficient, and under specialist care.
For those who are interested, this is how torsades occur:
QTc prolongation (slow HR also lengthens QT further)
Early after depolarisation occurs (slow HR increases these)
Early after depolarisation triggers premature ventricular complex
If the premature ventricular complex lands on the T wave → R-on-T phenomenon → torsades de pointes
AF with pre-excitation (e.g. WPWWolff-Parkinson-White) →procainamide / cardioversion
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