Code Ready

Level 2 of 6Must-remember

Tachyarrhythmias

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Define it and classify it in three answers: a tachyarrhythmia is any abnormal rhythm with a ventricular rate above 100 beats/min, and the whole of the emergency treatment follows from stable or unstable, narrow or broad, regular or irregular.
  • Narrow QRS (< 0.12 sec, under three small squares at 25 mm/sec) means the ventricles were depolarised through the normal His–Purkinje system, so the rhythm arose at or above the AV junction — sinus tachycardia, AVNRT, AVRT, atrial fibrillation, atrial flutter, focal atrial tachycardia or multifocal atrial tachycardia.
  • Broad QRS (≥ 0.12 sec) means ventricular tachycardia, or a supraventricular rhythm with bundle branch block (aberrancy) or antegrade accessory-pathway conduction — approximately 80% of all broad-complex tachycardias are VT, a proportion that rises further with previous myocardial infarction or structural heart disease, and in all cases of doubt a broad-complex tachycardia is diagnosed and treated as VT.
  • The most important bedside judgement is not the name of the rhythm but whether the patient is stable or unstable. Any one adverse feature mandates electrical rather than pharmacological treatment: shock (systolic BP < 90 mmHg, pallor, sweating, cold peripheries, capillary refill > 3 sec, confusion, oliguria); syncope; myocardial ischaemia (new ischaemic chest pain, or new ST depression or elevation); heart failure (breathlessness, orthopnoea, raised JVP, crackles, frothy sputum); or an extreme rate > 150/min with evidence of poor perfusion.
  • Absence of a palpable central pulse converts the problem into cardiac arrest, treated with *unsynchronised* defibrillation.Not available at your setup — Defibrillator.
  • History of the palpitation: rate, regularity, and abruptness of onset and offset — sudden onset and termination that the patient can pinpoint favour a paroxysmal re-entrant tachycardia, a rate that climbs and falls gradually favours sinus tachycardia, and termination by a Valsalva manoeuvre is characteristic of AVNRT and AVRT.
  • Two symptoms deserve emphasis: polyuria, from atrial natriuretic peptide release, characteristic of AVNRT and atrial fibrillation; and prominent jugular venous pulsations from atrial contraction against closed AV valves in AVNRT. Syncope occurs in 10–15% of patients with SVT, usually at onset or during the pause after termination.
  • Hunt for the trigger, because sinus tachycardia is a sign and not a diagnosis: exercise, emotion, pain, fever and sepsis, hypovolaemia and haemorrhage, heart failure, pulmonary embolism, hypoxia, pregnancy, anaemia, thyrotoxicosis, phaeochromocytoma, and drugs — beta-agonists, caffeine, alcohol intoxication and withdrawal, cocaine, amphetamines, anticholinergics.
  • Examine the pulse: in atrial fibrillation it is irregularly irregular and, unlike the occasional irregularity of ectopic beats, the irregularity persists during exercise; in VT it is typically 120–220/min with signs of AV dissociation — intermittent cannon a waves and a first heart sound of varying intensity.
  • A normal blood pressure does not exclude VT — blood pressure may be well maintained in sustained VT.
  • Record three ECGs: a 12-lead during the tachycardia, a rhythm strip running through every intervention, and a 12-lead after conversion. Measure the QRS in the lead where the complex is widest, because isoelectric segments make a broad complex look deceptively narrow in one lead, and establish regularity with calipers or a marked card rather than by eye, since a fast irregular rhythm looks regular at 180/min.
  • A regular narrow tachycardia at almost exactly 150/min is atrial flutter with 2:1 block until proven otherwise — sawtooth F waves at about 300/min, negative in II, III and aVF, revealed by carotid sinus pressure or adenosine, which will not terminate it.
  • Features that make it VT: a history of previous myocardial infarction (the strongest single clinical predictor); AV dissociation with independent P waves marching through, and capture or fusion beats (both pathognomonic); a very broad QRS (> 0.14 sec, especially > 0.16 sec); extreme left or right axis deviation; concordance of QRS polarity across V1–V6; a bifid upright QRS in V1 with a taller first peak and a deep S in V6; and failure to respond to carotid massage or adenosine.
  • Three rhythms carry the highest immediate lethality: VT with haemodynamic compromise; torsades de pointes (complexes twisting about the baseline, QTc > 0.50 sec between runs); and pre-excited atrial fibrillation — an irregular, very broad, very fast tachycardia often > 200/min with beat-to-beat variation in QRS width, which can degenerate into ventricular fibrillation.
  • Bedside and urgent bloods: potassium (aim 4.0–4.5 mmol/L in ventricular arrhythmia), magnesium, calcium, glucose, troponin, full blood count, a digoxin concentration in anyone taking it, blood gases if shocked, hypoxic or acidotic, and thyroid function, which is mandatory in unexplained new atrial fibrillation.Not available at your setup — Serum electrolytes, Cardiac troponin, Arterial blood gas.
  • Children: a fast heart is far more often shock, fever, dehydration, pain, hypoxia or anaemia than a primary arrhythmia — sinus tachycardia is usually below 220/min in an infant and below 180/min in an older child, whereas true infant SVT runs above 220/min, is monotonously unvarying, and presents with poor feeding, pallor, irritability, sweating and tachypnoea, often for many hours and eventually in heart failure.

Management— do this, in order

  • Unstable, any rhythm — synchronised DC cardioversion. Sedate or anaesthetise the conscious patient, because cardioversion is intensely painful, and confirm the synchronisation markers before every shock, since most defibrillators revert to unsynchronised mode after each discharge.Doctor / NurseNot available at your setup — Defibrillator.
  • Cardioversion energies (biphasic): regular narrow-complex SVT 100 J (70–120 J) escalating; atrial flutter 100–200 J; atrial fibrillation 200 J escalating to 360 J or the machine maximum; pre-excited AF treated as AF with high energy from the outset; VT with a pulse 100–200 J escalating with each shock; paediatric 1 J/kg for the first shock, then 2 J/kg.Doctor / NurseNot available at your setup — Defibrillator.
  • Up to three synchronised shocks are given. If three fail, give amiodarone 300 mg intravenously over 10–20 minutes and repeat the shock, followed by amiodarone 900 mg over 24 hours; failure is most often uncorrected potassium or magnesium, or high thoracic impedance, and an anteroposterior pad position may succeed where anterolateral failed.Doctor / NurseNot available at your setup — Defibrillator.
  • Stable, narrow, regular — vagal manoeuvres first, which terminate 20–50% of episodes. Modified Valsalva: semi-recumbent at 45 degrees, blow into a 10 mL syringe hard enough just to move the plunger (about 40 mmHg of intrathoracic pressure) for at least 15 seconds, then lie flat with both legs passively raised to 45 degrees for a further 15 seconds; conversion typically occurs during the leg raise. In infants use the diving reflex — an iced flannel over forehead, eyes and bridge of the nose for up to 15 seconds.
  • Carotid sinus massage: firm but gentle pressure over the right carotid sinus for 10–20 seconds with the ECG running, then the left if unsuccessful — never both sides simultaneously, never if a bruit is present, never after stroke or transient ischaemic attack or with known carotid disease, and not in children.Doctor / Nurse
  • Adenosine is the first-line drug and terminates AVNRT and AVRT in approximately 90% of cases. Adult: 6 mg by rapid intravenous push over 1–2 seconds, immediately followed by a 20 mL sodium chloride 0.9% flush and arm elevation; if no effect after 1–2 minutes, 12 mg; if still none, a further 12 mg (Davidson's expresses this as 3–12 mg in rapid incremental doses). Start at 3 mg if the line is central, or the patient takes dipyridamole or has a transplanted heart.Doctor / Nurse
  • Adenosine, paediatric: 0.1 mg/kg (maximum first dose 6 mg), then 0.2 mg/kg (maximum 12 mg), then 0.3 mg/kg (maximum 12 mg), each with a rapid 5–10 mL flush.Doctor / Nurse
  • Give adenosine properly or not at all: use the largest, most proximal vein — adenosine given into a small hand or foot vein is metabolised before reaching the heart — push drug and flush as one continuous movement, and warn the patient of about ten seconds of chest heaviness, flushing, breathlessness and a sense of dread, which passes and is harmless.Doctor / Nurse
  • If adenosine fails or is contraindicated, choose one AV nodal blocking class and stay within it: verapamil 5–10 mg IV over 5–10 min, or 2.5 mg boluses every 1–3 min to a total of 20 mg over 20 min; diltiazem 0.25 mg/kg IV over 2 min, a second bolus of 0.35 mg/kg after 15 min if inadequate, then a 5–15 mg/hour infusion; metoprolol 5 mg IV every 5 min up to 3 doses (15 mg total), orally 25–200 mg daily; esmolol 500 micrograms/kg IV over 1–2 min then 50–300 micrograms/kg/min; propranolol 1–3 mg IV every 5 min to a total of 5 mg.Doctor / Nurse
  • Stable, broad, regular — treat as VT with amiodarone 300 mg intravenously over 20–60 minutes, then 900 mg over 24 hours (Kumar and Clark: 900–1200 mg per 24 hours; CMDT and Harrison's: 150 mg over 10 minutes, then 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours). In the peri-arrest patient give the 300 mg over 10–20 minutes; dilute in 5% dextrose and give through the largest available vein or a central line. Paediatric dose 5 mg/kg over 20–60 minutes.Doctor / NurseNot available at your setup — Infusion pump.
  • Lidocaine as an alternative that may be given peripherally: 1 mg/kg intravenously as a bolus (Kumar and Clark: 50–100 mg), then 1–4 mg/min by infusion; an intravenous beta-blocker (metoprolol 5 mg, or esmolol 50–300 micrograms/kg/min) is useful in ischaemic VT and electrical storm.Doctor / NurseNot available at your setup — Infusion pump.
  • Torsades de pointes: magnesium sulphate 2 g (8 mmol of magnesium) intravenously over 10–15 minutes in every case, irrespective of the serum magnesium, followed by 72 mmol over 24 hours; paediatric 25–50 mg/kg, maximum 2 g, over 10–15 minutes. Stop every QT-prolonging drug and correct potassium to 4.0–4.5 mmol/L along with magnesium and calcium.Doctor / Nurse
  • Torsades — raise the heart rate, because it is bradycardia- and pause-dependent: overdrive pacing at 90–120/min shortens the QT rate-dependently and is definitive, and isoprenaline 2–20 micrograms/min is the alternative where pacing is unavailable. If the pulse is lost, defibrillate immediately with an unsynchronised shock.Doctor / NurseNot available at your setup — Defibrillator. Where pacing is unavailable, isoprenaline 2–20 micrograms/min is the alternative to raise the rate.
  • Pre-excited atrial fibrillation is an emergency and synchronised DC cardioversion is the treatment of choice. If the patient is genuinely stable and a drug is required, use procainamide (loading 10–17 mg/kg at 20–50 mg/min, stopping if the QRS widens by more than 50% or the blood pressure falls) or ibutilide 1 mg over 10 minutes, repeated once.Doctor / NurseNot available at your setup — Defibrillator.
  • Atrial fibrillation, stable — rate control first, with metoprolol where there is ischaemia or infarction and diltiazem where blood pressure is low, never the two classes combined intravenously. Digoxin may be added: loading 0.5 mg intravenously over 20 minutes, then increments of 0.25 mg or 0.125 mg to a total of 1–1.5 mg over 24 hours (or the same total orally over 24–36 hours in divided doses); maintenance 0.125–0.5 mg daily, or 0.0625–0.25 mg daily in heart failure and the elderly. Rate targets: below 110/min suffices without symptoms or left ventricular dysfunction, below 80/min where symptoms persist.Doctor / Nurse
  • The timing rule for cardioversion in stable AF: acceptable without prior anticoagulation if AF has been present less than 48 hours (Davidson's uses a more cautious 24-hour threshold, and the safer figure should be preferred); beyond 48 hours or where onset is unknown, either perform transoesophageal echocardiography to exclude left atrial thrombus or anticoagulate therapeutically for at least 3 weeks first, and continue anticoagulation for at least 4 weeks afterwards.Not available at your setup — Ultrasound. Where transoesophageal echocardiography is unavailable, anticoagulate therapeutically for at least 3 weeks before cardioversion and continue for at least 4 weeks afterwards.
  • Pharmacological cardioversion: flecainide 2 mg/kg intravenously over 30 minutes, maximum 150 mg restores sinus rhythm in about 75% within 8 hours — but only in structurally normal hearts; use amiodarone where structural or ischaemic heart disease is present. In the unstable patient in whom 200 J then 360 J both fail, cardioversion may succeed after loading with ibutilide 1 mg intravenously over 10 minutes, repeated once.Doctor / Nurse
  • Correct the substrate in parallel and treat the precipitant: potassium to 4.0–4.5 mmol/L, magnesium, calcium, hypoxia, acidosis and ischaemia — no antiarrhythmic drug and no shock works reliably in a hypokalaemic, hypomagnesaemic, hypoxic or acidotic patient. Wide-complex tachycardia in tricyclic antidepressant, diphenhydramine or class Ia overdose is treated with sodium bicarbonate 8.4%, 50 mmol (50 mL) intravenously, repeated as necessary, even without acidosis.Doctor / NurseNot available at your setup — Serum electrolytes.

Caution— what harms

  • Broad means ventricular until proven otherwise: giving verapamil to VT in the belief that it is SVT with aberrancy causes cardiovascular collapse.
  • Never give verapamil when the QRS is broad; never give verapamil to a patient who has received a beta-blocker, or the reverse, since the combination causes profound bradycardia, AV block and hypotension; and never give verapamil, diltiazem or digoxin in AF with pre-excitation.
  • In pre-excited AF, verapamil, diltiazem, digoxin, beta-blockers and adenosine are absolutely contraindicated — all block the AV node, which is the protective route, diverting atrial impulses down the fast unprotected pathway and precipitating ventricular fibrillation. Cardiovert instead.
  • Verapamil is contraindicated in infants under 1 year, in whom it causes refractory hypotension, bradycardia and cardiac arrest.
  • One antiarrhythmic at a time — stacking a second agent on a failed first is proarrhythmia; when a drug fails the next step is usually electricity. If the drug fails or the patient deteriorates, sedate and cardiovert rather than adding a second antiarrhythmic.
  • Never give amiodarone, sotalol or any other QT-prolonging antiarrhythmic in torsades — this is the commonest error in this rhythm.
  • Polymorphic VT with a normal QT is myocardial ischaemia until proven otherwise, and the treatment is treatment of the ischaemia, not magnesium.
  • Accelerated idioventricular rhythm at 60–100/min, common during reperfusion, is benign and self-limiting; it should be neither cardioverted nor loaded with amiodarone.
  • Adenosine cautions: use with great caution or not at all in asthma; the effect is potentiated by dipyridamole and antagonised by theophylline and caffeine; it provokes atrial fibrillation in up to 12% of patients, so a defibrillator must be to hand.Not available at your setup — Defibrillator.
  • Class Ic agents such as flecainide are contraindicated in coronary artery disease and left ventricular dysfunction, where the CAST trial showed increased mortality, and contraindicated in atrial flutter, where slowing the flutter rate may permit 1:1 conduction and a catastrophic ventricular rate.
  • Carotid sinus massage: never both sides simultaneously, never with a bruit, never after stroke or transient ischaemic attack or with known carotid disease, and never in children.
  • Confirm synchronisation before every shock: an unsynchronised shock landing on the T-wave vulnerable period ('R on T') can induce ventricular fibrillation, and most defibrillators revert to unsynchronised mode after each discharge.Not available at your setup — Defibrillator.
  • Digoxin is not a rescue agent: it peaks at 6 hours and is easily overwhelmed by catecholamines, so it will not control a rapid rate in an acutely unwell patient; verapamil's long half-life means hypotension may persist well after sinus rhythm is restored.
  • Anticoagulation errors kill: aspirin should not be used for stroke prevention in AF; direct oral anticoagulants must not be used in mechanical prosthetic valves or moderate-to-severe mitral stenosis, where warfarin with a target INR of 2.0–3.0 remains first-line; and a post-conversion pause or bradycardia may follow termination of a tachycardia, particularly dangerously in sinoatrial disease.

Refer / escalate

Escalate or transfer urgently any tachyarrhythmia with an adverse feature (shock, syncope, myocardial ischaemia, heart failure or a rate above 150/min with poor perfusion), any broad-complex tachycardia, torsades de pointes, pre-excited atrial fibrillation, any patient who needs cardioversion, an amiodarone infusion, pacing or a defibrillator, and any newly diagnosed atrial fibrillation needing echocardiography, thyroid assessment and an anticoagulation decision.

Read the full lesson free

Create a free account to unlock every page, the level exams, and progress tracking.

Sign up freeLog in