Rhythm abnormalities: ventricular arrhythmias

Rhythm abnormalities: ventricular arrhythmias

Rhythms that start in the ventricles, from harmless extra beats to ventricular tachycardia and fibrillation, the main causes of sudden cardiac death; how to recognise them on the ECG, the inherited syndromes behind them in young people, the emergency treatment, and who needs an implantable defibrillator.

Contents6 sections

At a glance

  1. Ventricular arrhythmias range from ectopic beats, which are common and usually harmless, to ventricular tachycardia and fibrillation, which cause most sudden cardiac deaths.
  2. Most arise in a diseased heart, above all in the scar of a myocardial infarction and in cardiomyopathies. In young people inherited channelopathies and cardiomyopathies matter most.
  3. A broad-complex tachycardia is ventricular tachycardia until proven otherwise, especially after a myocardial infarction.
  4. Ventricular fibrillation and pulseless ventricular tachycardia are cardiac arrest, treated with CPR and defibrillation at once. Ventricular tachycardia with a pulse but with shock, syncope, ischaemia or heart failure needs synchronised cardioversion.
  5. Torsades de pointes comes with a long QT interval and is treated with magnesium, potassium, removal of the drugs that prolong the QT, and a faster heart rate.
  6. An implantable defibrillator prevents sudden death in survivors of ventricular fibrillation or unstable ventricular tachycardia without a reversible cause, and in patients at high risk.

Definition and overview

Ventricular arrhythmias start below the His bundle, in the ventricular muscle or the Purkinje fibres. The ventricles are activated cell to cell rather than through the conduction system, so the QRS is usually broad, typically 120 ms or more; fascicular tachycardia, which uses the Purkinje network, can be only slightly broad.

ArrhythmiaDefinition
Ventricular premature beats (ectopics)single early broad QRS complexes, usually followed by a pause
Non-sustained ventricular tachycardia3 or more ventricular beats in a row at over 100 a minute, ending within 30 seconds
Sustained ventricular tachycardialasting 30 seconds or more, or needing termination earlier because of collapse
Monomorphic ventricular tachycardiaevery QRS the same shape, usually from a re-entry circuit around a scar
Polymorphic ventricular tachycardiathe QRS shape changes from beat to beat, typically in acute ischaemia or a channelopathy; with a long QT interval it is torsades de pointes
Ventricular fibrillationchaotic activation with no QRS complexes and no cardiac output
Accelerated idioventricular rhythma slow ventricular rhythm, under about 120 a minute, common after reperfusion of an infarct and usually harmless
Electrical storm3 or more separate episodes of sustained ventricular tachycardia or fibrillation within 24 hours, at least 5 minutes apart, each needing a shock, pacing or cardioversion to end it

Sudden cardiac death is an unexpected natural death from a cardiac cause, within an hour of the first symptoms, or, if no one saw it, in a person who was well in the previous 24 hours. Most are caused by ventricular tachycardia degenerating into ventricular fibrillation; a few by bradycardia or asystole.

Etiology and pathophysiology

Causes

GroupExamples
Ischaemic heart disease, the commonest causeacute ischaemia, which causes polymorphic ventricular tachycardia and fibrillation; the healed scar of an old infarction, which causes monomorphic ventricular tachycardia years later
Cardiomyopathies and inflammationdilated, hypertrophic and arrhythmogenic cardiomyopathy, sarcoidosis, myocarditis, Chagas disease
Inherited channelopathies, in a structurally normal heartlong QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome
Electrolytes, drugs and toxinslow potassium and magnesium, high potassium, drugs that prolong the QT interval, digoxin toxicity, cocaine, hypoxia and acidosis
Other heart diseaseaortic stenosis, heart failure of any cause, repaired congenital heart disease such as tetralogy of Fallot
Idiopathicventricular tachycardia and ectopics from the right ventricular outflow tract or the left fascicles, in a normal heart

Drugs that prolong the QT interval include antiarrhythmics (sotalol, amiodarone, quinidine, disopyramide), macrolide and quinolone antibiotics, antipsychotics such as haloperidol, tricyclic antidepressants, methadone, ondansetron and azole antifungals. The risk rises with low potassium or magnesium, bradycardia, female sex, heart disease and several such drugs together.

Mechanisms

  • Re-entry: an infarct scar leaves channels of surviving muscle that conduct slowly, so an impulse can circle round the scar again and again. This is the usual mechanism of monomorphic ventricular tachycardia in heart disease.
  • Triggered activity: afterdepolarisations, small depolarisations during or after repolarisation, can fire a new beat. Early afterdepolarisations in a long QT interval trigger torsades de pointes; delayed afterdepolarisations, from calcium overload, cause the arrhythmias of digoxin toxicity and of catecholaminergic polymorphic ventricular tachycardia.
  • Enhanced automaticity: ischaemic or stretched cells depolarise spontaneously, as in accelerated idioventricular rhythm.
  1. 1

    A substrate

    Scar, fibrosis, hypertrophy or an abnormal ion channel creates regions that conduct or recover unevenly.
  2. 2

    A trigger

    An ectopic beat, ischaemia, a surge of catecholamines, low potassium or a drug arrives at a vulnerable moment.
  3. 3

    Ventricular tachycardia

    A re-entry circuit or triggered firing sustains a fast ventricular rhythm. The ventricles fill poorly and contract out of step, so the output and pressure fall, more so in a weak heart.
  4. 4

    Ventricular fibrillation

    Fast ventricular tachycardia, or polymorphic tachycardia in ischaemia or a long QT, breaks up into chaotic activation. There is no output, and without defibrillation death follows within minutes.

Clinical features

  • Ectopic beats: a missed or thumping beat, or no symptoms. When they are very frequent, fatigue, and rarely a weak ventricle (ectopic-induced cardiomyopathy).
  • Ventricular tachycardia: palpitations, dizziness, syncope, chest pain, breathlessness, shock or cardiac arrest. Some patients, especially with a slow tachycardia and a good ventricle, tolerate it well, which does not make it supraventricular.
  • Signs of atrioventricular dissociation in ventricular tachycardia: intermittent cannon a waves in the neck and a first heart sound of varying loudness.
  • Ventricular fibrillation: sudden collapse, no pulse, and absent or gasping (agonal) breathing, which must not be mistaken for normal breathing.

Some features point to an inherited cause and need specialist assessment: syncope during exercise, swimming, a sudden noise or emotion; syncope while lying down or asleep; and a family history of sudden unexplained death, drowning or a single-car accident at a young age.

Diagnosis and management

The ECG

A 12-lead ECG during the tachycardia is the most valuable test. About 80 per cent of broad-complex tachycardias are ventricular, and more in patients with an old infarction. Features that favour ventricular tachycardia over a supraventricular rhythm with bundle branch block:

  • atrioventricular dissociation, with P waves marching through at their own rate;
  • capture beats (a normal narrow beat conducted from the atria) and fusion beats (a hybrid of a normal and a ventricular beat), which prove ventricular tachycardia;
  • a very broad QRS, over 140 ms;
  • concordance, all chest-lead QRS complexes pointing the same way;
  • an extreme axis, and a QRS shape that does not look like typical bundle branch block.

A broad-complex tachycardia is treated as ventricular tachycardia unless it is certain to be supraventricular. Verapamil given to ventricular tachycardia can cause collapse.

In sinus rhythm the ECG looks for the cause: Q waves of an old infarction, a long or short QT interval (corrected for heart rate), a Brugada pattern, T-wave inversion in V1 to V3 with epsilon waves in arrhythmogenic cardiomyopathy, left ventricular hypertrophy, and pre-excitation.

Other tests

  • Blood tests: potassium, magnesium, calcium, troponin, drug levels such as digoxin, and thyroid function.
  • Echocardiography for ventricular function and structural disease, and cardiac MRI for scar, cardiomyopathy, myocarditis and sarcoidosis.
  • Coronary angiography after ventricular fibrillation or polymorphic tachycardia when ischaemia is possible, and urgently after a cardiac arrest with ST elevation.
  • Ambulatory ECG monitoring, an exercise test (which provokes catecholaminergic tachycardia and unmasks long QT), a sodium channel blocker challenge (ajmaline or flecainide) for Brugada syndrome, and an electrophysiology study in selected patients.
  • Genetic testing for suspected inherited disease, and screening of first-degree relatives of patients with inherited arrhythmias or of young people who died suddenly. After a sudden unexplained death in a young person, an autopsy with genetic testing of stored tissue can find the cause.

Cardiac arrest

  1. 1

    Recognise and call

    Unresponsive with absent or abnormal breathing is cardiac arrest. Help and a defibrillator are called for at once.
  2. 2

    CPR and early defibrillation

    High-quality chest compressions with minimal pauses, and a shock as soon as a defibrillator shows ventricular fibrillation or pulseless ventricular tachycardia, followed straight away by 2 minutes of CPR before the rhythm is checked again.
  3. 3

    Drugs

    After the third shock, adrenaline 1 mg intravenously, repeated every 3 to 5 minutes, and amiodarone 300 mg, with 150 mg more after the fifth shock. Lidocaine, 100 mg and then 50 mg after the fifth shock, is an alternative to amiodarone.
  4. 4

    Reversible causes

    Hypoxia, hypovolaemia, hypo- or hyperkalaemia and other metabolic causes, and hypo- or hyperthermia; coronary or pulmonary thrombosis, tension pneumothorax, tamponade and toxins.
  5. 5

    After return of circulation

    Oxygen and blood pressure targets, an ECG, urgent coronary angiography if there is ST elevation, temperature control and assessment of the brain.

Ventricular tachycardia with a pulse

  • With shock, syncope, myocardial ischaemia or severe heart failure: synchronised electrical cardioversion at once, under sedation, starting at about 120 to 150 J and increasing. If it fails, amiodarone 300 mg intravenously over 10 to 20 minutes (not as a bolus, unlike in cardiac arrest), or procainamide, and further shocks. Verapamil is never given for a broad-complex tachycardia of uncertain origin.
  • Stable: electrical cardioversion under sedation is often the first choice. Procainamide or amiodarone are alternatives when there is structural heart disease. Idiopathic ventricular tachycardia in a normal heart responds to a beta-blocker, and the fascicular type to verapamil.
  • Potassium and magnesium are corrected, and ischaemia is treated.
  • Polymorphic ventricular tachycardia with a normal QT usually means acute ischaemia and needs urgent coronary angiography, with a beta-blocker and amiodarone.

Torsades de pointes

Electrical storm

Electrical storm is treated with sedation, an intravenous beta-blocker, amiodarone, correction of triggers such as ischaemia, electrolytes and heart failure, and reprogramming of a defibrillator. Catheter ablation is often needed, and some patients need general anaesthesia or mechanical circulatory support.

Preventing recurrence and sudden death

  • Treat the cause: revascularisation of ischaemia, heart failure drugs (beta-blockers and the other foundational drugs reduce sudden death), and correction of electrolytes and drugs.
  • Implantable cardioverter-defibrillator (ICD). It senses ventricular tachycardia or fibrillation and ends it, with painless rapid pacing or a shock. It is recommended after ventricular fibrillation or unstable ventricular tachycardia without a reversible cause, unless the arrhythmia occurred in the first 48 hours of an acute infarction. For primary prevention, it is recommended for patients whose ejection fraction stays at 35 per cent or less despite at least 3 months of full treatment, in NYHA class II or III, at least 40 days after an infarction, and considered when the cause is not ischaemic; the patient should be expected to live more than a year in good health, as described in treatment of chronic heart failure, and to high-risk patients with inherited diseases. A subcutaneous device, with no lead in the heart, suits patients who need no pacing. A wearable defibrillator vest can bridge a period of uncertain risk.
  • Catheter ablation of the circuit is preferred to escalating drugs for recurrent ventricular tachycardia after an infarction, and is first-line for idiopathic tachycardia and ectopics from the right ventricular outflow tract or the left fascicles, succeeding in about 75 to 90 per cent or more. From other sites, a beta-blocker, verapamil or diltiazem comes first.
  • Antiarrhythmic drugs. Beta-blockers come first. Amiodarone and sotalol reduce recurrences and shocks but do not prolong life. Class Ic drugs such as flecainide are avoided after a myocardial infarction and in structural heart disease, because in a large trial they suppressed ectopics but increased deaths.
  • Ectopic beats and non-sustained ventricular tachycardia in a normal heart need only reassurance, or a beta-blocker or a rate-limiting calcium channel blocker for symptoms. An ectopic burden of 10 per cent or more with an otherwise unexplained low ejection fraction suggests ectopic-induced cardiomyopathy, which ablation can reverse.

Inherited arrhythmia syndromes

SyndromeDiagnosisTypical triggersTreatment
Long QT syndromeQTc of 480 ms or more on repeated ECGs, a high diagnostic score, or a disease-causing variant whatever the QT; 460 to 479 ms with arrhythmic syncope once other causes of a long QT are excluded; genetic subtypes of potassium and sodium channelstype 1, exercise, especially swimming; type 2, a sudden noise or emotion; type 3, rest and sleepa non-selective beta-blocker (nadolol or propranolol), avoidance of QT-prolonging drugs, normal potassium; an ICD after cardiac arrest or for high risk
Brugada syndromecoved ST elevation of 2 mm or more in V1 or V2 (type 1), spontaneous; a pattern brought out by a sodium channel blocker or fever counts only with cardiac arrest, arrhythmic syncope or a suggestive family history; reduced sodium currentrest, sleep, fever, some drugs, alcohol, large meals; men, and more common in Southeast Asiaprompt treatment of fever, a list of drugs to avoid; an ICD after cardiac arrest or sustained ventricular tachycardia, considered after arrhythmic syncope; quinidine or ablation in selected patients
Catecholaminergic polymorphic ventricular tachycardianormal resting ECG; bidirectional or polymorphic tachycardia on exercise testing; calcium release channel variantsexercise and emotion, in children and young adultsa beta-blocker, flecainide, avoidance of strenuous exercise, sympathetic denervation, an ICD
Arrhythmogenic cardiomyopathyfibrofatty replacement, mainly of the right ventricle; T-wave inversion in V1 to V3, ventricular tachycardia with a left bundle branch block shapeexercise, especially in young athletesno competitive or endurance sport, a beta-blocker, ablation, an ICD

Epidemiology

Sudden cardiac death causes about half of all cardiovascular deaths, and for many it is the first sign of heart disease. In Europe emergency services attempt resuscitation for an out-of-hospital cardiac arrest in about 55 people per 100,000 each year. Coronary disease causes about 80 per cent of sudden cardiac deaths in Western countries, and cardiomyopathies most of the rest in older people. Under the age of 35 sudden death is rare, and its causes are inherited cardiomyopathies and channelopathies, myocarditis and coronary anomalies; in a substantial share the heart is normal at autopsy. Ventricular ectopic beats are common in healthy people and become more frequent with age. Long QT syndrome affects about 1 in 2,000 people.

Prognosis

Fewer than 1 in 10 people who have an out-of-hospital cardiac arrest survive to leave hospital (about 7 to 8 per cent across Europe, from 3 to 35 per cent between countries), and bystander CPR and early defibrillation, including public defibrillators, can double or triple the chance. Survivors of ventricular fibrillation or unstable ventricular tachycardia without a reversible cause have a high risk of recurrence, and a defibrillator improves their survival. In patients with a low ejection fraction after an infarction or from heart failure, defibrillators reduced deaths by about a quarter to a third, although many later die of progressive heart failure. Ventricular fibrillation in the first 48 hours of an infarction raises the risk of dying in hospital but not the long-term risk of sudden death.

Ectopic beats and idiopathic ventricular tachycardia in a normal heart have an excellent outlook. With diagnosis, treatment and family screening, most people with inherited arrhythmia syndromes live normal lives, while undiagnosed relatives remain at risk.

Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.

1A 68-year-old who had a myocardial infarction 5 years ago has a regular broad-complex tachycardia at 170 a minute. He is alert, with a blood pressure of 110/70 mmHg. What is the right approach?

2Which patient should receive an implantable cardioverter-defibrillator?

3A patient in cardiac arrest remains in ventricular fibrillation after three shocks with good CPR between them. Which drugs are given now?

4A 74-year-old woman taking erythromycin and haloperidol has runs of polymorphic ventricular tachycardia whose QRS axis twists around the baseline. Between them her QTc is 580 ms. What is the first drug treatment?

5A 32-year-old man faints during a febrile illness. His ECG shows coved ST elevation of 3 mm in V1 and V2 followed by negative T waves, and it returns to near normal when the fever settles. What is the most likely diagnosis?

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Cardiac conduction

Fast rhythms from the ventricles, which can turn into ventricular fibrillation.

  • The resting membrane potentialPhysiologyNot written yetThe ion gradients and channels behind every cardiac action potential.
  • Antiarrhythmic drugsPharmacologyNot written yetGrouped by what they block: sodium channels (I), β-receptors (II), potassium channels (III), calcium channels (IV).
  • Calcium channel blockersPharmacologyNot written yetVerapamil and diltiazem slow conduction through the AV node; the dihydropyridines hardly do.
  • Drugs for the treatment of heart failurePharmacologyNot written yetDigoxin slows conduction through the AV node.
  • Local anaestheticsPharmacologyNot written yetLidocaine, a local anaesthetic, is also a class Ib antiarrhythmic: both effects come from blocking sodium channels.
  • Conductive disturbances. Treatment of conductive disturbancesCardiovascular diseasesSinoatrial and AV blocks slow or drop beats; a single bundle branch block widens the QRS instead.
  • Rhythm abnormalities: supraventricular arrhythmiasCardiovascular diseasesFast rhythms that start above the ventricles, such as atrial fibrillation.
  • Antiarrhythmic drugsCardiovascular diseasesThe same drug classes seen from the bedside: which to choose for which rhythm.