01Purpose and principlesWhat the treatment does and how it fits into care.
An emergency ECG is interpreted alongside the patient, not as an isolated pattern-recognition exercise. The same rapid rhythm can coexist with preserved perfusion or life-threatening collapse, and a normal-looking monitor trace may represent pulseless electrical activity. The first branching questions are whether a circulation exists and whether the rhythm is responsible for dangerous physiological compromise.
Once immediate threats are addressed, classify rate, regularity, QRS width, atrial activity and repolarisation changes. Record a twelve-lead tracing when it will not delay urgent treatment. Seek causes such as ischaemia, electrolyte disturbance, hypoxia and drug exposure; correcting these can prevent recurrence after a successful shock or temporary rate improvement.
Key points
- Check for a pulse and clinical instability before selecting a rhythm-specific treatment.
- Treat sinus tachycardia by correcting its cause; do not cardiovert a compensatory sinus response.
- Use synchronised cardioversion for an unstable tachyarrhythmia with a pulse, with appropriate sedation when feasible.
- An undifferentiated regular broad-complex tachycardia should usually be approached as ventricular tachycardia pending expert assessment.
- Avoid atropine in high-degree AV block with wide QRS complexes and in transplanted hearts; arrange expert alternatives.
- Hyperkalaemic ECG toxicity needs cardiac protection and potassium-lowering treatment, because calcium alone does not lower potassium.
02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.
Hypoperfusion, ischaemic chest pain, severe pulmonary oedema or syncope with severe ongoing hypotension makes prompt electrical treatment important. A numerical heart rate alone does not define instability.
Ventricular tachycardia is particularly likely with structural heart disease. Incorrect treatment as a benign supraventricular rhythm can worsen circulation, so uncertainty should prompt a cautious VT-based approach.
A slow ventricular escape, high-grade block, recurrent pauses or broad QRS complexes can precede asystole. Do not allow temporary improvement to defer pacing assessment when dangerous conduction disease persists.
Hyperkalaemia can produce peaked T waves, conduction slowing and QRS widening. QT prolongation with polymorphic VT suggests torsades, where amiodarone may worsen the underlying repolarisation problem.
03Assessment before treatmentTests and checks that guide safe selection.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Twelve-lead ECG and rhythm stripFirst step - Why
- Define the arrhythmia and retain a record for specialist review.
- Interpretation and limitations
- Compare previous tracings and inspect QRS duration, regularity and atrial activity. Obtain rhythm documentation during therapy when feasible, but do not postpone indicated cardioversion.
- 02
Electrolytes, glucose and renal function - Why
- Identify modifiable causes and safe treatment constraints.
- Interpretation and limitations
- Urgently check potassium and magnesium when arrhythmia or conduction slowing is unexplained. A haemolysed sample may need repeating, but severe clinical and ECG toxicity needs immediate action.
- 03
Haemodynamic and oxygenation assessment - Why
- Determine whether the rhythm is causing life-threatening compromise.
- Interpretation and limitations
- Assess pressure, conscious level, peripheral perfusion and pulmonary congestion. A palpable pulse separates peri-arrest arrhythmia treatment from the cardiac-arrest algorithm.
- 04
Drug history and targeted cardiac tests - Why
- Identify proarrhythmic exposure or an underlying cardiac event.
- Interpretation and limitations
- Ask about rate-limiting drugs, QT-prolonging agents and overdose. Troponin or echocardiography may clarify the cause, but tachycardia itself can increase troponin without plaque rupture.
04Treatment approachPreparation, options, escalation and aftercare.
01Electrical priorityUnstable tachyarrhythmia with a pulseFirst stepAn abnormal fast rhythm is accompanied by shock, ischaemia or severe cardiac failure.+
- 1Call senior resuscitation support, secure monitoring and access, and confirm that the rhythm is an arrhythmia rather than compensatory sinus tachycardia.
- 2Prepare synchronised shocks with sedation or anaesthesia for a conscious patient when feasible, checking that synchronisation markers align with R waves before delivery.
- 3If repeated cardioversion fails and instability persists, seek specialist antiarrhythmic treatment and repeat electrical therapy; if no pulse remains, immediately use the arrest pathway.
02Bradycardia branchSymptomatic slowing and pacing decisionsA slow rhythm accompanies poor perfusion, syncope or other adverse clinical signs.+
- 1Identify high-degree block with a wide QRS or a transplanted heart, where atropine should not be given; arrange prompt specialist support and pacing or appropriate pharmacological alternatives.
- 2For suitable symptomatic bradycardia, give atropine 500 micrograms IV, repeating every three to five minutes if needed to a total of 3 mg.
- 3If ineffective or conduction disease is high risk, prepare transcutaneous pacing as a bridge and obtain early transvenous pacing assessment, verifying mechanical as well as electrical capture.
03Hyperkalaemic toxicityCardiac protection while potassium is loweredA patient with marked hyperkalaemia develops ECG conduction abnormalities or arrhythmia.+
- 1Give IV calcium with ECG monitoring: UKKA recommends calcium chloride in cardiac arrest or peri-arrest, and calcium gluconate for other patients with hyperkalaemic ECG toxicity. Check the salt and concentration because their volumes are not equivalent.
- 2Start indicated potassium-shifting treatment and organise potassium removal, assessing renal function and urgent dialysis need; calcium protection is temporary.
- 3Recheck ECG, potassium and glucose, looking for recurrent toxicity and insulin-associated hypoglycaemia rather than assuming an improved tracing means potassium has normalised.
05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.
Atropine for appropriate symptomatic bradycardia
Give 500 micrograms IV initially, repeating every 3–5 minutes when necessary to a total dose of 3 mg, while reassessing perfusion and preparing escalation.Do not administer in high-degree AV block with a wide QRS or in a transplanted heart. Ineffectiveness must not postpone pacing or expert alternative treatment.
Calcium gluconate for hyperkalaemic ECG toxicity
For hyperkalaemic ECG toxicity outside cardiac arrest or peri-arrest, give 30 mL of 10% calcium gluconate IV over 10 minutes with ECG monitoring; reassess for further calcium if abnormalities persist or recur.Thirty millilitres of 10% gluconate provides calcium comparable to 10 mL of 10% chloride. Neither salt lowers potassium; monitor the cannula and avoid extravasation.
Magnesium for torsades de pointes with QT prolongation
Give 8 mmol magnesium IV over 10 minutes with ECG and blood-pressure monitoring in a patient with a circulation; obtain expert advice on repeat treatment or pacing if arrhythmia persists.Do not delay a required shock in unstable sustained polymorphic VT or cardiac arrest. Check renal function and cumulative magnesium, and avoid amiodarone when QT prolongation drives torsades.
06Complications, monitoring and follow-upAdverse effects, response and longer-term review.
- Continue ECG and repeated pressure monitoring after rhythm treatment because recurrence or drug-related hypotension can appear after apparent initial success.
- Document the rhythm, energy, synchronisation, sedation and response associated with every electrical intervention.
- For pacing, confirm a palpable pulse or arterial waveform corresponding to paced complexes; monitor artefact alone is not mechanical capture.
- After potassium treatment, arrange serial potassium and glucose measurement and specify who responds to rebound hyperkalaemia or delayed hypoglycaemia.
07Special situationsVariants, exceptions and circumstances that change the usual approach.
Regular narrow-complex rhythm
In an appropriate stable regular narrow-complex tachycardia without pre-excitation, vagal manoeuvres and the RCUK adenosine pathway may terminate AV-node-dependent re-entry.
Pre-excited atrial fibrillation
An irregular broad-complex rhythm can represent pre-excited AF; AV-nodal blocking drugs can be dangerous, so obtain expert help and consider appropriate electrical treatment.
Torsades treatment direction
For torsades with a circulation, give IV magnesium as well as correcting potassium and stopping QT-prolonging drugs; magnesium treatment does not depend on a low measured serum value. Unstable sustained polymorphic VT requires prompt electrical treatment.
The 2026 tachyarrhythmia pathway
Current RCUK guidance includes specific distinctions for structural heart disease, sedation risk and pre-excitation; an old shorthand algorithm can omit these clinically important branches.
08Common pitfallsFrequent interpretation and management errors.
- 01
Do not interpret monitor electrical activity as proof of a circulation without assessing the patient.
- 02
Do not give an AV-nodal blocking drug reflexively to every irregular broad-complex tachycardia.
- 03
Do not confuse synchronised cardioversion with unsynchronised defibrillation when choosing treatment for a rhythm with a pulse.
- 04
Do not describe calcium as potassium removal or omit the subsequent treatment and monitoring plan.