Medicine chapters
SVT, VT, VF, torsades and cardiac arrest management
Narrow-complex SVT (AVNRT, AVRT and WPW), ventricular tachycardia, ventricular fibrillation and torsades de pointes, how to tell VT from SVT, and the adult cardiac arrest algorithm with shockable and non-shockable rhythms.
- SVT (usually AVNRT or AVRT) is a regular narrow-complex tachycardia; stable patients get vagal manoeuvres, then adenosine 6 mg then 12 mg IV; unstable patients get synchronised DC shock.
- Broad-complex tachycardia is VT until proved otherwise; clues are AV dissociation, capture and fusion beats, very wide QRS, concordance; torsades (long QT) is treated with IV magnesium.
- In cardiac arrest, VF and pulseless VT are shockable (shock, then 2 minutes CPR); asystole and PEA are non-shockable (CPR plus adrenaline 1 mg at once); always seek the 4 Hs and 4 Ts.
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Overview
Fast rhythms (rate over 100/min) are split by where they start:
- Supraventricular tachycardias (SVT) start in the atria or AV junction. They use the normal His-Purkinje system, so the QRS is usually narrow.
- Ventricular tachyarrhythmias start in the ventricles, giving a broad QRS (VT) or chaos (VF). These cause most sudden cardiac deaths.
For every tachycardia the first question is the same: is the patient stable? Shock, syncope, chest pain or heart failure mean electrical treatment now. Cardiac arrest management splits by rhythm into shockable and non-shockable pathways.
Mechanisms in one line each
- Re-entry: an impulse circles round two pathways with different speeds and refractory periods (AVNRT, AVRT, flutter, scar-related VT). The commonest mechanism of regular paroxysmal tachycardia.
- Increased automaticity: a focus fires too fast (sinus tachycardia, some atrial tachycardias).
- Triggered activity: after-depolarisations reach threshold (digoxin toxicity, long QT with torsades).
Supraventricular tachycardia (SVT)
Types
| Type | Circuit | ECG clue |
|---|---|---|
| AVNRT (commonest paroxysmal SVT) | Slow and fast pathways within the AV node | Regular, narrow, rate about 140–240; P waves hidden in or just after the QRS |
| AVRT | AV node plus an accessory pathway (WPW) | P wave seen after the QRS, in the ST segment |
| Atrial tachycardia | Focus in the atrium | Abnormal P waves before each QRS |
| Atrial flutter | Right atrial macro re-entry | Sawtooth waves; rate 150 with 2:1 block |
| Multifocal atrial tachycardia | Several foci | Three or more P wave shapes; seen in severe lung disease |
Clinical features
- Sudden-onset, sudden-offset regular palpitations, often in young people with normal hearts; AVNRT is commoner in women.
- Dizziness, breathlessness, chest discomfort, polyuria after the attack (atrial natriuretic peptide).
- Neck pounding ("frog sign") from atria contracting against closed valves.
- Attacks may stop with Valsalva.
Acute management of SVT
- Unstable (shock, syncope, ischaemia, heart failure): synchronised DC cardioversion under sedation.
- Stable: vagal manoeuvres: Valsalva (blowing into a syringe), carotid sinus massage (one side only, not if bruit or recent stroke), cold water to the face.
- Adenosine IV: 6 mg rapid push, then 12 mg if needed, via a large vein with a saline flush. It blocks the AV node for seconds (half-life under 10 seconds), breaking any circuit that uses the node.
- If adenosine is contraindicated or fails: verapamil IV (5–10 mg) or a beta-blocker.
Adenosine side effects are brief: flushing, chest tightness, a sense of doom, short asystole. Avoid in asthma (bronchospasm); use verapamil instead.
Never give verapamil to a broad-complex tachycardia or soon after IV beta-blockers. If the rhythm is actually VT, verapamil can cause collapse.
Long-term
Beta-blockers, verapamil or diltiazem; flecainide in normal hearts. Catheter ablation (slow pathway in AVNRT, accessory pathway in AVRT) cures over 95%.
Wolff-Parkinson-White (WPW) syndrome
An accessory pathway (bundle of Kent) bypasses the AV node.
- Resting ECG (pre-excitation): short PR interval, delta wave (slurred upstroke of the QRS), wide QRS.
- WPW syndrome = this ECG plus symptoms (palpitations).
- Orthodromic AVRT (down the node, up the pathway): narrow QRS; treat like any SVT.
- AF with WPW: fast, irregular, broad QRS; risk of VF. Avoid AV nodal blockers (digoxin, verapamil, adenosine, beta-blockers). Use DC cardioversion, or flecainide or procainamide if stable.
- Definitive: ablation of the pathway (first-line in symptomatic patients).
Ventricular tachycardia (VT)
Definition: a run of consecutive beats arising in the ventricles at a rate over 100/min. Sustained VT lasts over 30 seconds or needs termination; non-sustained VT stops by itself within 30 seconds.
- Monomorphic VT: identical QRS shapes; usually from scar after MI or cardiomyopathy.
- Polymorphic VT: changing shapes; includes torsades de pointes.
- Causes: ischaemic heart disease and old MI scar (commonest), cardiomyopathies, myocarditis, hypokalaemia, hypomagnesaemia, drugs (digoxin toxicity, QT-prolonging drugs), channelopathies.
Clinical features
Rate usually 120–220/min. Patients may be well, or have dizziness, syncope, hypotension, heart failure or arrest. Signs of AV dissociation: intermittent cannon a waves and variable first heart sound.
VT or SVT with aberrant conduction?
About 80% of broad-complex tachycardias are VT, and even more in patients with previous MI or heart disease.
Features favouring VT:
- Very broad QRS (over 0.14 s).
- AV dissociation: P waves marching independently.
- Capture beats (an occasional normal narrow beat) and fusion beats (hybrid of sinus and VT beat).
- Concordance: all chest lead QRS complexes pointing the same way.
- Extreme axis deviation ("north-west" axis).
- History of MI or structural heart disease.
A broad-complex tachycardia is VT until proved otherwise, especially after an MI. Treating VT as SVT can kill; treating SVT as VT is safe.
Being haemodynamically stable does not exclude VT. Many patients with VT have a normal blood pressure.
Management of VT (with a pulse)
- Unstable (shock, syncope, chest pain, heart failure): synchronised DC cardioversion.
- Stable: IV amiodarone (alternatives: lidocaine, procainamide; beta-blocker in ischaemia). Cardiovert if drugs fail.
- Correct potassium (keep around 4.5 mmol/L after MI) and magnesium.
- Pulseless VT: treat as cardiac arrest (shockable).
- Long-term: ICD for survivors of VT or VF without a reversible cause (secondary prevention); ablation for recurrent VT; beta-blockers. Idiopathic VT in a normal heart (outflow tract) has a good outlook and is often cured by ablation.
Ventricular fibrillation (VF)
Chaotic, disorganised ventricular activity with no cardiac output. The patient is pulseless and unconscious within seconds: this is cardiac arrest.
- ECG: irregular, shapeless waves with no recognisable QRS (coarse or fine).
- Often triggered by an R-on-T ectopic, especially in acute MI.
- Only effective treatment: immediate defibrillation (unsynchronised shock) with CPR.
- VF in the first day or two of acute MI does not usually need long-term prevention; VF without a reversible cause carries a high risk of recurrence, so an ICD is advised.
VF is treated by defibrillation (unsynchronised), not "cardioversion" (synchronised). A synchronised shock may not fire at all in VF because there is no QRS to sync to.
Torsades de pointes and long QT
Torsades de pointes is a polymorphic VT in which the QRS axis twists around the baseline, with changing amplitude. It occurs on a background of long QT and is often started by a pause or bradycardia. It may stop by itself (syncope) or turn into VF (sudden death).
Corrected QT
QT varies with heart rate, so it is corrected, usually with Bazett's formula: QTc = QT ÷ √(RR interval in seconds). In torsades the QTc is usually over 0.50 s.
QT = 480 ms; heart rate about 94/min, so RR = 0.64 s
√0.64 = 0.8
QTc = 480 ÷ 0.8 = 600 ms → markedly prolonged; high risk of torsades
Causes of long QT
| Congenital | Acquired: electrolytes | Acquired: drugs and others |
|---|---|---|
| Romano-Ward (autosomal dominant, normal hearing) | Hypokalaemia | Class Ia (quinidine, disopyramide), class III (sotalol, amiodarone) |
| Jervell and Lange-Nielsen (autosomal recessive, congenital deafness) | Hypomagnesaemia | Macrolides (erythromycin), quinolones |
| Hypocalcaemia | Antipsychotics (haloperidol), tricyclics, methadone, antimalarials (quinine, halofantrine) | |
| Bradycardia, hypothyroidism, organophosphate poisoning |
Congenital subtypes: LQT1 attacks with exercise, especially swimming; LQT2 with emotion or sudden noise; LQT3 during sleep or rest.
Management of torsades
- IV magnesium sulphate (for example 8 mmol over 10–15 minutes): first-line, even if the serum magnesium is normal.
- Stop QT-prolonging drugs; correct potassium and calcium.
- Raise the heart rate to shorten the QT: temporary overdrive pacing, or isoprenaline in acquired cases (not in congenital long QT).
- If pulseless: defibrillate (cardiac arrest algorithm).
- Congenital long QT long-term: beta-blockers, avoid QT drugs, ICD for high-risk patients.
Amiodarone is not the answer for torsades; it prolongs QT further. Give magnesium.
Brugada syndrome
Inherited sodium channel defect (often SCN5A), commoner in young men and in South-East Asia; sudden death in sleep. ECG: RBBB pattern with coved ST elevation in V1–V3, which can be unmasked by flecainide or ajmaline. Treatment: ICD.
Cardiac arrest
Most adult cardiac arrests are due to VF or pulseless VT from coronary artery disease. Survival depends on the chain of survival: early recognition and call for help, early CPR, early defibrillation, and good post-resuscitation care.
Basic life support (adult)
- Make sure the scene is safe.
- Check response; if unresponsive and not breathing normally, call for help and an AED.
- Chest compressions: centre of the chest, depth 5–6 cm, rate 100–120/min, full recoil.
- 30 compressions : 2 breaths (one or two rescuers). Children: 15:2 for healthcare rescuers.
- Attach the AED as soon as it arrives and follow its prompts.
Advanced life support: rhythm check
| Pathway | Rhythms | What to do |
|---|---|---|
| Shockable | VF and pulseless VT | One unsynchronised shock (biphasic 150–200 J, monophasic 360 J), then immediately 2 minutes CPR before the next rhythm check |
| Non-shockable | Asystole and pulseless electrical activity (PEA) | CPR 2 minutes at a time; adrenaline 1 mg IV as soon as access is obtained |
Drugs in arrest
- Adrenaline 1 mg IV or intraosseous: in non-shockable rhythms, give as soon as possible; in shockable rhythms, give after the third shock; then every 3–5 minutes (alternate cycles).
- Amiodarone IV after the third shock in refractory VF or pulseless VT (a further dose after the fifth shock). Lidocaine is an alternative.
- Atropine is no longer used routinely in asystole or PEA.
During CPR
- Minimise interruptions to compressions.
- Airway: bag-valve-mask, then supraglottic airway or intubation; once an advanced airway is in, give continuous compressions with ventilation at about 10 breaths/min.
- Waveform capnography to confirm tube position and spot return of circulation.
- IV or intraosseous access.
Reversible causes: 4 Hs and 4 Ts
| 4 Hs | 4 Ts |
|---|---|
| Hypoxia | Thrombosis (coronary or pulmonary): consider thrombolysis for PE |
| Hypovolaemia (commonest cause of PEA from haemorrhage) | Tension pneumothorax: needle decompression |
| Hypo- or hyperkalaemia and other metabolic causes (calcium for hyperkalaemia) | Tamponade (cardiac): pericardiocentesis |
| Hypothermia | Toxins: specific antidotes |
Shockable = "Vs": VF and pulseless VT. Non-shockable = "As and Ps": Asystole and PEA.
PEA means organised electrical activity without a pulse. It is non-shockable; look hard for the 4 Hs and 4 Ts, especially hypovolaemia, tamponade, tension pneumothorax and PE.
Asystole is never shocked. Check that a "flat line" is not fine VF by checking leads and gain; shocking true asystole does no good and wastes CPR time.
After return of spontaneous circulation (ROSC)
- ABCDE approach; give enough oxygen to avoid hypoxia but avoid excess, and aim for a normal CO2.
- 12-lead ECG; urgent coronary angiography and PCI if STEMI or likely coronary cause.
- Targeted temperature management: prevent fever; cooling to 32–36°C has been used, with no clear benefit for one target over another.
- Treat the cause; glucose control; organ support; judge the neurological outlook only after several days, not in the first hours.
- Survivors of VF or VT without a reversible cause: ICD.
Expect: vagal manoeuvres then adenosine 6 mg and 12 mg for stable SVT, verapamil if asthmatic, DC shock if unstable; WPW ECG (short PR, delta wave) and drugs to avoid; criteria favouring VT and the rule that broad-complex tachycardia is VT until proved otherwise; amiodarone for stable VT and synchronised shock for unstable VT; defibrillation for VF; torsades with long QT, its causes (hypokalaemia, hypomagnesaemia, macrolides, antipsychotics) and IV magnesium; shockable vs non-shockable rhythms; CPR 30:2 at 100–120/min; adrenaline 1 mg and amiodarone timing; and the 4 Hs and 4 Ts.
Quick revision
- SVT: regular narrow complex; vagal manoeuvres, adenosine 6 then 12 mg; verapamil if asthma; DC shock if unstable.
- WPW: short PR, delta wave; avoid digoxin and verapamil in AF with WPW; ablate.
- Broad-complex tachycardia = VT until proved otherwise (AV dissociation, capture and fusion beats, QRS over 0.14 s, concordance).
- Stable VT: amiodarone; unstable VT: synchronised DC cardioversion; pulseless VT: arrest algorithm.
- VF: immediate unsynchronised defibrillation and CPR.
- Torsades: long QT; IV magnesium, stop drugs, correct K+, pacing or isoprenaline.
- Arrest: VF/pVT shock (150–200 J biphasic) then 2 min CPR; asystole/PEA CPR plus adrenaline 1 mg at once.
- Adrenaline every 3–5 min; amiodarone after third shock; seek 4 Hs and 4 Ts.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
What is the first drug for a stable regular narrow-complex tachycardia?
Adenosine IV, given as a rapid bolus of 6 mg followed by 12 mg if needed, after vagal manoeuvres have failed.
Why is a broad-complex tachycardia treated as VT when unsure?
Most broad-complex tachycardias are VT, and drugs given for SVT, such as verapamil, can cause collapse in VT. Treating SVT as VT is far safer than the reverse.
What is the treatment of torsades de pointes?
Intravenous magnesium sulphate, stopping QT-prolonging drugs, correcting potassium, and speeding up the heart with pacing or isoprenaline in acquired cases. Defibrillate if pulseless.
Which cardiac arrest rhythms are shockable?
Ventricular fibrillation and pulseless ventricular tachycardia. Asystole and pulseless electrical activity are not shocked.
When is adrenaline given during cardiac arrest?
At once in asystole and PEA, and after the third shock in VF or pulseless VT, then every 3 to 5 minutes.