A heart can be in trouble without any artery being blocked, and the rhythm disorders are where most of the decisions a person actually faces sit: whether to take an anticoagulant for the rest of your life, whether to have a wire burned inside your heart, whether to have a box implanted under your collarbone. This chapter takes each rhythm problem in turn — what it is, how it is found, what the treatment decisions are and what the numbers behind them say — with the UK and US positions. Cardiac arrest itself is the resuscitation chapter; what is looked for afterwards is here and in the every-test chapter.
1. Atrial fibrillation: the common one
The heart's upper chambers stop beating and quiver, driven by chaotic electrical activity; the lower chambers pick up an irregular, often fast, rhythm from it. About one adult in fifty has it, rising to one in ten over 80. It presents as palpitations, breathlessness, tiredness, faintness, reduced exercise capacity — or as nothing at all until the stroke. It is classified by how it behaves: paroxysmal (comes and goes within a week), persistent (lasts longer, or needs treatment to stop), permanent (accepted as the rhythm). The 2023 American guideline added stages before that: "at risk" and "pre-AF", to make the point that it is a progressive disease driven by blood pressure, weight, alcohol, sleep apnoea and diabetes, and that treating those is treatment for AF.
Why it matters: the stroke
Blood in a quivering atrium pools in a pouch called the appendage and clots; the clot travels to the brain. AF causes about a fifth of ischaemic strokes, and they are larger and more disabling than the average stroke. The decision that matters most is therefore not the rhythm but the anticoagulant, and it is made with a score:
| Item | Points |
|---|---|
| Congestive heart failure | 1 |
| Hypertension | 1 |
| Age 75 or over | 2 |
| Diabetes | 1 |
| Previous stroke, TIA or embolism | 2 |
| Vascular disease (a previous heart attack, peripheral artery disease, aortic plaque) | 1 |
| Age 65–74 | 1 |
| Female sex | 1 in CHA2DS2-VASc (UK); dropped in the European 2024 CHA2DS2-VA, because sex modifies risk with age rather than adding to it |
UK (NICE NG196): offer anticoagulation at a CHA2DS2-VASc of 2 or more, and consider it at 1 in men, taking bleeding risk into account with the ORBIT score. Europe 2024: anticoagulate at CHA2DS2-VA of 2 or more, consider at 1, same cut-off for both sexes. US 2023: anticoagulate when annual stroke risk is 2% or more, which lands in the same place. In every version the anticoagulant is a DOAC (apixaban, rivaroxaban, edoxaban or dabigatran) rather than warfarin, except with a mechanical valve or significant mitral stenosis, and aspirin is not a substitute: it barely reduces AF stroke and bleeds as much. The anticoagulant continues whether or not the rhythm is later restored, because the risk lives in the atrium, not in the current rhythm. A bleeding score is used to fix the things that raise bleeding risk — blood pressure, alcohol, anti-inflammatory drugs, unstable warfarin control — not as a reason to withhold the anticoagulant. For the minority who cannot take one at all, the appendage can be closed with a device.
Brief AF found by a monitor or a watch. Devices now find short runs of AF in people who never felt them. Two trials of anticoagulating device-detected AF (NOAH-AFNET 6 and ARTESIA) found a small reduction in stroke and a larger increase in bleeding, and the guidelines say the decision depends on how much AF there is and the person's stroke risk. A smartwatch alert is a reason for a proper ECG and a conversation, not a prescription.
Rate or rhythm
Two strategies. Rate control accepts the AF and slows the ventricles with a beta-blocker or a rate-limiting calcium-channel blocker (digoxin for the sedentary); it is the UK first line for most people because it is safe and simple. Rhythm control tries to restore normal rhythm: by cardioversion (a synchronised shock under sedation, or a drug), by antiarrhythmic drugs (flecainide, sotalol, dronedarone, amiodarone), or by catheter ablation, in which the areas that trigger AF, mainly around the pulmonary veins, are burned or frozen through a catheter from the groin. The evidence has moved towards rhythm control:
- Early rhythm control in the first year after diagnosis reduced the combined risk of cardiovascular death, stroke and hospitalisation by about a fifth in the EAST-AFNET 4 trial (2020).
- Ablation as first treatment for paroxysmal AF beat drugs at keeping people in rhythm in three trials, and is now a first-line option in the 2024 European guideline and "reasonable" in the American one. NICE still places it after a failed drug.
- Ablation in heart failure with AF reduced death and heart-failure admission (CASTLE-AF), and both guidelines recommend it there.
- Cardioversion for a new episode: the European guideline shortened the window for cardioverting without a prior period of anticoagulation from 48 to 24 hours, and endorses waiting a day to see if it stops on its own, which it usually does.
What ablation involves: a day-case or overnight procedure, success (freedom from AF at a year) of around 70–80% for paroxysmal AF and lower for persistent, often a second procedure, and a serious complication rate of around 2–4% (bleeding at the groin, stroke, perforation, damage to the oesophagus in the older heat-based technique). Pulsed-field ablation, a newer non-thermal method, has fewer of the tissue complications and is spreading through UK centres. Anticoagulation continues uninterrupted through the procedure and, for anyone with a stroke-risk score that warrants it, indefinitely afterwards regardless of the rhythm result.
What moves the risk more than any drug
The 2024 European guideline reorganised itself around comorbidity control, because the evidence is now hard to argue with. Alcohol abstinence halved AF recurrence in a randomised trial of regular drinkers (2020). Weight loss of 10% in obese patients reduced AF burden several-fold and made ablation more likely to work (the LEGACY and ARREST-AF cohorts). Treating sleep apnoea, blood pressure and diabetes each reduce recurrence. Endurance exercise at extreme volumes raises AF risk; moderate exercise lowers it. A person with new AF should be asked about alcohol, weight, snoring and blood pressure before being asked about ablation.
2. Supraventricular tachycardia: frightening, and curable
A short circuit above the ventricles, usually a congenital extra pathway, that starts suddenly and drives the heart at 150–220 beats a minute, then stops as suddenly. It presents from the teens onward, more in women, as pounding palpitations with breathlessness and faintness, often mistaken for panic. It is rarely dangerous. An episode can often be stopped with a vagal manoeuvre — the modified Valsalva, straining against a closed airway then lying flat with the legs lifted, which stopped 43% of episodes against 17% for the standard version in the REVERT trial — and in the emergency department with adenosine, a drug that stops the heart for a few seconds and lets it restart normally. For recurrent episodes, catheter ablation cures it in over 95% of cases with a complication rate under 1%, and is preferred to lifelong drugs in both countries' guidance. A wearable ECG recording during an episode is what gets the diagnosis (the consumer ECG chapter).
3. Ventricular tachycardia and fibrillation: the rhythms of collapse
Ventricular tachycardia (VT) arises in the ventricles, usually from scar left by a previous heart attack or from a cardiomyopathy, and can cause palpitations, faintness, collapse, or degenerate into ventricular fibrillation (VF), which is cardiac arrest. VF in the first 48 hours of a heart attack is a consequence of the acute injury and does not by itself mean a device is needed; VF or sustained VT after that, or without an acute cause, does.
The implantable cardioverter-defibrillator (ICD) is a box under the collarbone with a lead in the heart that detects VF or fast VT and shocks it, or paces it out. Two reasons to have one:
- Secondary prevention: after a cardiac arrest from VF or VT, or a sustained VT with collapse, not caused by a reversible event. The trials (AVID, CIDS, CASH) showed roughly a quarter to a third fewer deaths over a few years than drugs.
- Primary prevention: a weakened pump — an ejection fraction of 35% or less — measured at least 40 days after a heart attack or 90 days after a stent or bypass, on full medical treatment, with a reasonable life expectancy (NICE TA314; MADIT-II and SCD-HeFT). The waiting period exists because the pump often recovers, and because a device placed in the first weeks did not save lives (DINAMIT, IRIS). A wearable defibrillator vest can bridge the wait for those at highest risk.
An ICD does not treat the underlying disease and does not make anyone feel better; it prevents one way of dying. Inappropriate shocks (for a fast but harmless rhythm) happen to a minority and are distressing; modern programming has reduced them. The subcutaneous ICD, with no lead inside the heart, is an option for younger people without a pacing need. Driving stops for a period after implantation and after any shock (see the after-hospital chapter). Anti-arrhythmic drugs (beta-blockers, amiodarone) and VT ablation reduce the number of shocks in people who get many.
4. Heart block and the slow rhythms
The signal from the atria reaches the ventricles through one narrow electrical junction (the AV node and the bundle below it). When that junction fails, the ventricles either follow late, intermittently, or not at all:
| Degree | What the ECG shows | What it means | Treatment |
|---|---|---|---|
| First degree | Every beat conducted, but slowly | Common, usually harmless; sometimes a drug effect | None, unless very marked |
| Second degree, Mobitz I (Wenckebach) | Conduction slows progressively until a beat is dropped, then the cycle repeats | Often benign, especially at night or in athletes; the block is high in the junction | None if asymptomatic; a pacemaker if it causes symptoms |
| Second degree, Mobitz II | Beats dropped without warning | The block is low, in the bundle; it progresses to complete block unpredictably | A pacemaker, whether or not there are symptoms |
| Third degree (complete) | No relationship between atria and ventricles; the ventricles beat at their own slow escape rate, 20–40 | Faints, breathlessness, heart failure, sudden death | A pacemaker, urgently; temporary pacing or drugs (atropine, isoprenaline) while it is arranged |
| Sick sinus syndrome | The natural pacemaker pauses or slows; often alternating with AF | Faints, fatigue | A pacemaker if symptomatic; the AF still needs its anticoagulation decision |
Causes to look for before the pacemaker goes in, because some are reversible: a heart attack of the inferior wall (block often recovers within days) or of the anterior wall (it often does not); drugs that slow conduction (beta-blockers, diltiazem, verapamil, digoxin, amiodarone, some antidepressants, some drugs for dementia); an underactive thyroid; high potassium; Lyme disease in anyone with a tick exposure and a recent rash (heart block is its classic cardiac presentation and resolves with antibiotics); sarcoidosis and cardiac amyloidosis in the unexplained middle-aged or older patient, found on cardiac MRI or PET; a congenital block; and age-related fibrosis of the conduction system, which is the commonest cause and has no treatment but a pacemaker. Endocarditis and a recent valve operation cause it too.
The pacemaker is a small generator under the collarbone with one or two leads into the heart, placed under local anaesthetic in about an hour, with a battery lasting ten to fifteen years. Leadless pacemakers, the size of a large capsule and placed inside the ventricle through a leg vein, avoid the lead and the pocket and suit people at risk of infection. Where the pump is also weak and the ventricles beat out of step, a resynchronisation device with a third lead (CRT) improves symptoms and survival; conduction-system pacing, which threads the lead into the heart's own wiring, is the newer alternative. Driving stops for a week after a pacemaker; contact sport is avoided; phones and induction hobs are fine at a hand's width; MRI is possible with modern systems if the hospital knows the model.
5. The inherited rhythm conditions
A minority of arrests, faints and sudden deaths in people under 40 come from conditions present from birth, usually silent until they are not: long QT syndrome (a prolonged QT interval on the ECG; faints or arrests triggered by exertion, emotion, swimming or a startle; treated with beta-blockers and by avoiding a long list of QT-prolonging drugs), Brugada syndrome (a characteristic ECG pattern, sometimes only unmasked by a drug challenge; arrests in sleep or with fever; an ICD for those who have had events), catecholaminergic polymorphic VT (exercise-triggered; beta-blockers and flecainide), arrhythmogenic cardiomyopathy (a structural condition of the right ventricle in which exercise accelerates the disease), and hypertrophic cardiomyopathy (thickened muscle; the commonest cause of sudden death in young athletes; ICD by risk score). Each has genes that can be tested, and each is a reason to screen first-degree relatives with an ECG and an echocardiogram, and with the gene when one is found. The UK's inherited cardiac conditions clinics take referrals after any unexplained arrest, any unexplained faint with exercise, and any sudden death in a relative under 40; the every-test chapter lists what they do.
6. Palpitations, and what should happen
Most palpitations are extra beats (ectopics), harmless and made worse by caffeine, alcohol, lack of sleep and anxiety, or a fast regular rhythm from exertion or fear. The ones that need a proper look: an irregular pulse that persists (AF until proved otherwise); palpitations with faintness, collapse, chest pain or breathlessness; palpitations that start and stop abruptly like a switch (SVT); palpitations during exercise (the inherited conditions); and any palpitations in someone with a previous heart attack or a weak pump (VT until proved otherwise). What should happen: a 12-lead ECG, bloods including thyroid function and electrolytes, and a recording during the symptom — a 24-hour or 7-day monitor, a patch, or a personal ECG device with the trace kept — because a normal ECG between episodes tells nobody anything. An echocardiogram if there is any structural concern.
7. Where UK and US guidance differ
- The stroke score. UK: CHA2DS2-VASc with sex counted; Europe 2024: CHA2DS2-VA without it; US 2023: a risk-percentage threshold. Same decisions in nearly everyone.
- Ablation. Europe 2024 and the US 2023 allow it first-line for paroxysmal AF; NICE still requires a failed drug first. The evidence favours the newer position.
- Early rhythm control. Endorsed in Europe and the US after EAST-AFNET 4; NICE's rate-first default predates it.
- Cardioversion window. Europe 24 hours; UK and US 48 hours.
- Device-detected AF. All three now say "it depends"; none says anticoagulate every alert.
- ICD and pacing criteria are the same, from the same trials; the UK's NICE TA314 adds a cost-effectiveness frame.
- Comorbidity control is the organising principle of the 2024 European guideline and is stated more strongly there than anywhere.