Tachyarrhythmias in the emergency department

The tachyarrhythmias are managed in the emergency department by a single decision, made at the bedside before any drug: is the patient unstable? An unstable tachyarrhythmia is cardioverted whatever the rhythm; a stable one is then sorted by the QRS width and the regularity. The Fellowship candidate must know the algorithm cold, the drugs and their doses, and the two lethal traps — treating a regular broad-complex rhythm as SVT and giving verapamil, and giving an atrioventricular-node blocker to pre-excited atrial fibrillation.[1][2]

Definition and classification

A tachyarrhythmia is any rhythm with a ventricular rate over 100 per minute, and the emergency classification turns on two features. The first is the QRS width: a narrow-complex rhythm (under 120 ms) arises above the ventricles — from the atria or the atrioventricular node — and a broad-complex rhythm (120 ms or more) is either ventricular in origin or a supraventricular rhythm conducted with aberrancy. The second is the regularity. Together, the QRS width and the regularity sort the stable tachyarrhythmia into a narrow-regular (the supraventricular tachycardias), a narrow-irregular (atrial fibrillation or flutter), a broad-regular (ventricular tachycardia, presumed), or a broad-irregular rhythm (pre-excited atrial fibrillation, or torsades de pointes). [1]

Pathophysiology — why the regular broad-complex rhythm is presumed VT

Most tachyarrhythmias are re-entrant — a self-sustaining electrical circuit — and the remainder arise from enhanced automaticity or triggered activity. The reason a regular broad-complex tachycardia in an adult is treated as ventricular tachycardia until proven otherwise is statistical and clinical: the great majority of regular broad-complex tachycardias in adults are ventricular, and treating one as a supraventricular rhythm with aberrancy — particularly by giving verapamil — can collapse an already failing ventricle, because verapamil is a negative inotrope and blocks the atrioventricular node. The diagnosis is supported by independent P waves (atrioventricular dissociation), capture and fusion beats, and concordance of the precordial QRS, but the default treatment in the emergency department is to presume VT. [1]

Clinical presentation

The patient presents with palpitations, dyspnoea, chest pain, presyncope or syncope. The instability that mandates immediate cardioversion is the presence of any one of hypotension or shock, syncope, ischaemic chest pain, acute heart failure, or an altered conscious level. A tachyarrhythmia may also present as cardiac arrest — pulseless ventricular tachycardia or fibrillation — which is defibrillated as part of the advanced-life-support algorithm. [1]

Differential diagnosis

The differential is the rhythm itself, and the ECG resolves it. [1]

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Bedside assessment

The first assessment is the stability, because it decides between cardioversion and a drug. Look for the unstable features — hypotension, shock, syncope, ischaemic chest pain, acute heart failure, an altered conscious level — and if any is present, prepare for synchronized cardioversion at once. Then assess the QRS width and the regularity on the monitor and the 12-lead ECG, and seek the precipitant (ischaemia, electrolyte disturbance, hypoxia, sepsis, a drug, thyroid disease, structural heart disease). [1]

Investigations and the targets

The 12-lead ECG (and a rhythm strip) is the central investigation: the QRS width (the 120-ms threshold), the regularity, the P waves and their relation to the QRS (atrioventricular dissociation in VT), the axis, capture and fusion beats in VT, a delta wave and a short PR in Wolff-Parkinson-White, and the QT interval (a long QT raises torsades). The electrolytes — potassium, magnesium and calcium — are checked and corrected, the troponin identifies an ischaemic cause, the magnesium is checked in suspected torsades, and a thyroid function test and a digoxin level are sent where relevant. [1]

Immediate management — stability first, then the algorithm

Stabilise the airway and the breathing with oxygen, and decide the stability. [1]

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Adenosine terminates the common re-entrant supraventricular tachycardia by transiently blocking the atrioventricular node, and the 6-then-12-then-12 mg sequence is the standard escalation; the patient must be warned of the brief flush, dyspnoea and chest tightness, and the rhythm monitored throughout, because adenosine can produce a transient asystole.[2] It is contraindicated in asthma and in high-grade atrioventricular block. Torsades de pointes — a polymorphic broad-complex tachycardia with a twisting axis on a long QT — is treated with intravenous magnesium sulphate 2 g, withdrawal of the offending drug, and potassium correction, with overdrive pacing for recurrent episodes.

Subtypes and special scenarios

The AV-nodal-re-entrant tachycardia (AVNRT) is the commonest regular narrow-complex SVT and responds to vagal manoeuvres and adenosine; the atrioventricular-re-entrant tachycardia (AVRT) uses an accessory pathway (Wolff-Parkinson-White) and is flagged for catheter ablation. Atrial fibrillation is managed by a rate-control or a rhythm-control strategy: rate control with a beta-blocker or a rate-limiting calcium-channel blocker (digoxin in heart failure) is first-line for most; rhythm control by pharmacological or electrical cardioversion is considered when the onset is under 48 hours and the stroke risk is low, and anticoagulation is stratified on the CHA₂DS₂-VASc score (congestive heart failure, hypertension, age 65 or over, diabetes, stroke or transient ischaemic attack, vascular disease, and sex category). A cardioversion performed on a fibrillation of uncertain or prolonged duration is preceded by anticoagulation or a trans-oesophageal echocardiogram to exclude a left-atrial thrombus. Monomorphic ventricular tachycardia in structural heart disease is presumed and treated as above. Digoxin toxicity produces an atrial tachycardia with atrioventricular block and is treated with the digoxin-specific antibody fragment. The channelopathies — the long-QT syndrome (and the drug-induced QT prolongation that leads to torsades), the Brugada syndrome, and the catecholaminergic polymorphic ventricular tachycardia — produce characteristic arrhythmias and need cardiology input, an implantable defibrillator in selected cases, and the strict avoidance of the offending drug. [1]

Complications and pitfalls

The complications are the arrhythmia itself (haemodynamic collapse, cardiac arrest), thromboembolism after the cardioversion of unrecognised atrial fibrillation, amiodarone-induced hypotension, and the bronchospasm, heart block or asystole of adenosine. The pitfalls are the dangerous inverse of the algorithm: treating a regular broad-complex rhythm as SVT and giving verapamil; giving an atrioventricular-node blocker to pre-excited atrial fibrillation; giving adenosine in asthma; missing an electrolyte or drug cause; not recognising torsades; and delaying cardioversion in the unstable patient. [1]

Prognosis and disposition

The prognosis depends on the rhythm and the cause: ventricular tachycardia and fibrillation carry a high risk; the benign re-entrant supraventricular tachycardias do well. The unstable patient, the patient with ventricular tachycardia, and the patient with new atrial fibrillation needing rate or rhythm control are admitted to cardiology or a monitored bed; the precipitant is treated; and the anticoagulation decision is made by the CHA₂DS₂-VASc score and the rhythm's duration. Patients with a structurally normal heart and a clearly provoked, terminated arrhythmia may suit a short-stay pathway after cardiology review, whereas those with syncope, structural disease, a channelopathy, or a family history of sudden death are admitted for a full workup and the consideration of an implantable cardioverter-defibrillator. [1]

Each antiarrhythmic drug is itself pro-arrhythmic — amiodarone, flecainide and sotalol can each worsen a rhythm — so the response to any drug therapy is monitored on a continuous trace before the patient leaves the monitored area. [1]

Narrow-complex tachycardias in depth

A narrow-complex tachycardia (the QRS under 120 ms) is, by definition, supraventricular — the impulse uses the His–Purkinje system and the ventricles depolarise normally, so the complex is narrow. The emergency task is to separate the regular rhythms (the AV-nodal-re-entrant tachycardia, the AV-re-entrant tachycardia, the atrial tachycardia, the atrial flutter with a fixed block) from the irregular one (atrial fibrillation, and the atrial flutter with a variable block), because the regular one is terminated with adenosine while the irregular one is rate-controlled and anticoagulated. [1]

Vagal manoeuvres — the first step in the stable SVT

The modified Valsalva manoeuvre is the first-line termination for a haemodynamically stable regular narrow-complex tachycardia, recommended by both the ESC and the ACC/AHA/HRS guidelines before any drug.[1][8] The patient is positioned supine, blows into a 10 mL syringe to move the plunger for 15 seconds (a sustained intrathoracic pressure of about 40 mmHg), and is then laid flat with the legs passively elevated to 45 degrees for 15 seconds — the augmented venous return and the reflex vagal surge increase the success rate to around 43 per cent versus 17 per cent for the standard seated strain. Carotid sinus massage is the alternative, applied for 5 to 10 seconds to one carotid at a time after auscultation for a bruit (a bruit contraindicates it in the atherosclerotic patient) — never both carotids together, and never in the elderly without first excluding significant carotid disease.

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Adenosine — the escalation and the warnings

If the vagal manoeuvre fails, adenosine terminates the AV-node-dependent tachycardia (the AVNRT and the orthodromic AVRT) by transiently blocking the node. The dose is escalated through the 6 mg, then 12 mg, then 12 mg sequence, each as a rapid intravenous bolus through a large proximal cannula, immediately followed by a 20 mL saline flush, with the patient on a continuous cardiac monitor and a defibrillator at the bedside. The half-life is under 10 seconds, so a slow push fails — the drug is metabolised before it reaches the heart. The 6 mg dose terminates roughly 60 per cent; the first 12 mg dose raises this to over 90 per cent.[2]

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Atrial fibrillation and atrial flutter in the emergency department

Atrial fibrillation is the commonest sustained arrhythmia and the most frequent reason for an arrhythmia-related emergency presentation. The emergency-department decision is governed by two questions: how unstable is the patient, and when did the fibrillation start — because the answer to the first decides between the cardioversion and the rate control, and the answer to the second decides the stroke risk of a cardioversion. [1]

The rate-control versus the rhythm-control decision

The AFFIRM trial established that, for the older patient with the risk factors for stroke, a rate-control strategy is non-inferior to a rhythm-control strategy for survival — and is simpler and safer.[3] The rate control is therefore the first-line strategy for most stable patients, and the rhythm control (the pharmacological or the electrical cardioversion) is reserved for the patient with the new-onset fibrillation (the onset under 48 hours, when the stroke risk of the cardioversion is low) and the significant ongoing symptoms despite the adequate rate control, or the patient in whom a tachycardia-induced cardiomyopathy is developing. The RACE II trial further showed that a lenient rate target (a resting ventricular rate under 110 per minute) is non-inferior to a strict target (under 80 at rest, under 110 with the moderate exercise) for the cardiovascular outcome in the stable ambulatory patient.[4]

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A score of 0 in a man, or 1 in a woman with no other risk factor, is a low stroke risk and the anticoagulation is withheld; a score of 2 or more in a man, or 3 or more in a woman warrants the oral anticoagulation (a direct oral anticoagulant preferred, or the warfarin with the mechanical-valve or the moderate-to-severe mitral stenosis). The 2023 ACC/AHA/ACCP/HRS guideline reaffirmed this threshold and the preference for the direct oral anticoagulants in the non-valvular fibrillation.[10]

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Atrial flutter — the sawtooth and the 2:1 trap

Atrial flutter produces the characteristic sawtooth flutter waves (the negative deflections in the inferior leads, the typical "sawtooth" of the counterclockwise cavotricuspid-isthmus-dependent flutter) at an atrial rate around 300 per minute. The commonest conduction is 2:1, giving a regular ventricular rate of 150 per minute — a regular narrow-complex tachycardia at exactly 150 should prompt the search for the flutter waves, because the atrial tachycardia masquerades as an SVT. The adenosine is diagnostic here: it transiently increases the AV block to 4:1 or 8:1, slowing the ventricular rate and unmasking the flutter waves without terminating the flutter itself. The rate control, the rhythm control and the anticoagulation follow the same principles as the atrial fibrillation; the definitive treatment is the cavotricuspid-isthmus ablation (the success rate above 90 per cent). [1]

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Broad-complex tachycardia — the ventricular tachycardia

The stable regular broad-complex tachycardia in an adult is ventricular tachycardia until proven otherwise. The statistical justification is overwhelming — over 80 per cent of the regular broad-complex tachycardias in adults with the structural heart disease are ventricular — and the consequence of the misdiagnosis (the verapamil-induced collapse of the failing ventricle) is catastrophic. The Brugada algorithm (the four-step criteria for the QRS morphology) and the Vereckei aVR lead analysis help distinguish the VT from the SVT-with-aberrancy, but the emergency default is to treat as VT.[12]

The ECG features that support the VT diagnosis

The diagnosis of the ventricular tachycardia is supported by the independent P waves (the atrioventricular dissociation — the atria and the ventricles fire independently), the capture beats (a normal narrow QRS among the broad ones, where a sinus impulse captures the ventricles), the fusion beats (a hybrid of the sinus and the ventricular complexes), and the concordance of the precordial QRS (all positive or all negative in V1 to V6). Other supportive features are the extreme axis deviation (the northwest axis), the AV dissociation, the delay to the nadir of the S wave of over 100 ms, and the notching of the downstroke. None of these is universally present — their absence does not exclude the VT. [1]

The stable VT — amiodarone, or the lidocaine

The haemodynamically stable ventricular tachycardia (no hypotension, no shock, no chest pain, no heart failure, no altered consciousness) is treated with the intravenous amiodarone 300 mg over 20 to 60 minutes, followed by the infusion of 900 mg over 24 hours (the 900 mg in 500 mL of the 5 per cent dextrose, run over 24 hours).[7] The amiodarone terminates about 40 to 60 per cent of the stable monomorphic VT within the first hour. The alternative is the lidocaine (lignocaine) 1 to 1.5 mg/kg intravenously (a 100 mg dose in the average adult), repeated every 5 to 10 minutes to a maximum of 3 mg/kg, followed by the infusion of 1 to 4 mg/min — useful when the amiodarone is contraindicated or the VT is clearly ischaemia-mediated. The procainamide (a class Ia agent, 20 to 50 mg/min to a maximum of 17 mg/kg) is an alternative that some guidelines prefer for the stable monomorphic VT with the preserved ejection fraction, but it requires a monitored bed and carries the hypotension risk.

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Pulseless ventricular tachycardia and ventricular fibrillation — the ALS pathway

The pulseless ventricular tachycardia and the ventricular fibrillation are the shockable rhythms of the cardiac arrest, managed within the advanced-life-support algorithm as a continuous loop of the high-quality CPR and the defibrillation, with the adrenaline and the amiodarone added at the third shock.[9]

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Torsades de pointes and the long-QT syndromes

The torsades de pointes is a polymorphic ventricular tachycardia on a prolonged QT interval, characterised by the QRS complexes of the varying amplitude that appear to "twist" around the isoelectric baseline. The sustained torsades causes the syncope or the cardiac arrest; the self-terminating bursts cause the dizziness and the palpitations. The QT prolongation (a corrected QT over 500 ms, or an increase of over 60 ms on a new drug) is either congenital (the long-QT syndromes — the Romano-Ward, the Jervell and Lange-Nielsen) or, far more commonly in the emergency setting, acquired from a QT-prolonging drug (the macrolides, the fluoroquinolones, the antipsychotics — especially the haloperidol and the droperidol, the methadone, the ondansetron, the sotalol, the amiodarone), the electrolyte disturbance (the hypokalaemia, the hypomagnesaemia, the hypocalcaemia), the bradycardia, and the acute neurological injury. [1]

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The Vaughan-Williams classification and the antiarrhythmic drug profiles

The antiarrhythmics are classified by the Vaughan-Williams scheme — the class I agents block the sodium channel, the class II block the beta-receptors, the class III block the potassium channel, and the class IV block the calcium channel. The digoxin is sometimes the class V. The classification is imperfect — many drugs span the classes (the amiodarone has the class I, II, III and IV activity) — but it remains the framework for the Fellowship viva. [1]

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The synchronised cardioversion and the defibrillation — the technique

The synchronised DC cardioversion delivers the shock on the R wave of the QRS (the "sync" mode) to avoid the delivery of the shock on the T wave, which would precipitate the ventricular fibrillation. It is used for the unstable tachyarrhythmia with a QRS — the unstable SVT, the unstable atrial fibrillation and flutter, the unstable monomorphic VT — where the R wave is identifiable. The defibrillation is the unsynchronized shock, used when the R wave is not identifiable — the ventricular fibrillation, the polymorphic VT, and the pulseless VT — and is delivered at the higher energy from the first shock. [1]

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The precipitants — find and reverse the cause

A tachyarrhythmia is rarely an isolated event — the precipitant drives the recurrence, and the search for it is part of the emergency management. The common precipitants are the myocardial ischaemia and infarction (the troponin, the ECG), the electrolyte disturbance (the potassium, the magnesium, the calcium — the hypokalaemia is the classic precipitant of the atrial and the ventricular arrhythmias), the hypoxia and the respiratory failure, the sepsis, the thyrotoxicosis (the thyroid function test in the new atrial fibrillation), the alcohol excess (the "holiday heart" — the binge-drinking-induced atrial fibrillation), the sympathomimetic drugs (the cocaine, the amphetamines, the excessive caffeine), the pulmonary embolism (the cause of both the sinus tachycardia and the atrial fibrillation), the recreational and the prescribed drug withdrawal, and the structural heart disease (the cardiomyopathies, the valvular disease, the channelopathies). [1]

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The disposition and the safety net

The unstable patient, the patient with the ventricular tachycardia, the patient with the pre-excited atrial fibrillation, and the patient with the new atrial fibrillation needing the rate or the rhythm control are admitted to the monitored bed (the coronary care or the high-dependency unit). The patient with the clearly provoked and terminated benign SVT (the young, the structurally-normal heart, the clear precipitant removed) may suit the short-stay or the discharged-after-the-cardiology-review pathway, with the referral for the catheter ablation (the curative treatment for the AVNRT, the AVRT and the atrial flutter). The patient with the syncope, the structural heart disease, the channelopathy, or the family history of the sudden death is admitted for the full workup and the consideration of the implantable cardioverter-defibrillator. Every patient discharged after a tachyarrhythmia receives a written safety net — the return-if symptoms and the cardiology follow-up — because the recurrence and the first presentation of the channelopathy can be the cardiac arrest. [1]

Special populations

In pregnancy, adenosine is safe for the mother and the fetus, and amiodarone is avoided where possible because of its fetal thyroid effects; a synchronized cardioversion is also safe in pregnancy when the rhythm is unstable. The elderly and those with structural heart disease more often have ventricular tachycardia, decompensate at lower rates, and tolerate the rate-control and the anticoagulation less well, with a higher bleeding risk. The patient with a known accessory pathway (Wolff-Parkinson-White) is flagged for catheter ablation, and the electrolyte-depleted or the septic patient has the precipitant corrected alongside the rhythm itself. [1]

Evidence and regional guidelines

The contemporary framework is the advanced-life-support tachyarrhythmia algorithm (Resuscitation Council) and the 2019 ESC supraventricular-tachycardia guideline[1] with the ESC ventricular-arrhythmia guidance. The adenosine dosing is supported by emergency-department studies.[2] The algorithm and the drug doses are global; the cardioversion energies and the anticoagulation pathway are local.

SAQs — exam practice

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Exam pearls

• Unstable → synchronized cardioversion (any tachyarrhythmia).
• Regular broad complex = VT until proven otherwise → amiodarone 300 mg if stable; verapamil is dangerous.
• Irregular broad complex (pre-excited AF, WPW) → NO AV-node blockers → cardiovert.
• Stable narrow regular (SVT) → vagal then adenosine 6→12→12 mg.
• Adenosine: warn of the flush; contraindicated in asthma; can cause brief asystole.
• Torsades de pointes → magnesium 2 g, stop the offending drug, correct the potassium. [1]

Red flags

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References

1. [1]Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC) Eur Heart J, 2020.PMID 31504425
2. [2]Sert ET, Yilmaz MS, Ay MO, et al. Initial 12 mg Versus 6 mg Adenosine for Supraventricular Tachycardia in the Emergency Department Acad Emerg Med, 2026.PMID 42057249
3. [3]Wyse DG, Waldo AL, DiMarco JP, et al. (AFFIRM Investigators) A comparison of rate control and rhythm control in patients with atrial fibrillation N Engl J Med, 2002.PMID 12466506
4. [4]Van Gelder IC, Groenveld HF, Crijns HJGM, et al. (RACE II Investigators) Lenient versus strict rate control in patients with atrial fibrillation N Engl J Med, 2010.PMID 20231232
5. [5]Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A (ALIVE Investigators) Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation N Engl J Med, 2002.PMID 11907287
6. [6]Kudenchuk PJ, Brown SP, Daya M, et al. (ROC Investigators) Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest N Engl J Med, 2016.PMID 27043165
7. [7]Levine JH, Massumi A, Scheinman MM, et al. (intravenous amiodarone multicenter investigators) Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias. Intravenous Amiodarone Multicenter Trial Group J Am Coll Cardiol, 1996.PMID 8522712
8. [8]Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society J Am Coll Cardiol, 2016.PMID 26409258
9. [9]Soar J, Donnino MW, Maconochie I, et al. European Resuscitation Council Guidelines for Resuscitation: 2018 Update - Antiarrhythmic drugs for cardiac arrest Resuscitation, 2019.PMID 30496838
10. [10]Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines Circulation, 2024.PMID 38033089
11. [11]Tzivoni D, Banai S, Schuger C, et al. Terminology of torsades de pointes Cardiovasc Drugs Ther, 1991.PMID 1854659
12. [12]Antunes E, Brugada J, Steurer G, Andries E, Brugada P The differential diagnosis of a regular tachycardia with a wide QRS complex on the 12-lead ECG: ventricular tachycardia, supraventricular tachycardia with aberrant intraventricular conduction, and supraventricular tachycardia with anterograde conduction over an accessory pathway Pacing Clin Electrophysiol, 1994.PMID 7991423