Bradyarrhythmias and atrioventricular block

• A bradyarrhythmia is a heart rhythm that is too slow for the body's needs. It arises either because the sinus node (the natural pacemaker) fires too slowly, or because impulses are delayed or blocked on the way from the atria to the ventricles (atrioventricular or AV block).
• Many slow rhythms are harmless: athletes, sleeping people and first-degree AV block need no treatment. The question is always whether the slow rate is causing symptoms or is likely to progress.
• AV block comes in grades. First degree is a long PR interval; second degree drops some beats (Mobitz I is usually benign, Mobitz II is dangerous); third degree is complete block, with atria and ventricles beating independently.
• Always look for a reversible cause first: drugs, ischaemia, electrolytes, hypothyroidism, hypothermia, infection (Lyme disease).
• Unstable patients get atropine, then pacing or an infusion. Long-term, a pacemaker is indicated for symptomatic sinus node disease and for Mobitz II, high-grade and complete AV block even without symptoms.

By the end of this page you should be able to:

1. Describe the cardiac conduction system and how the autonomic nervous system changes the rate and AV conduction.
2. Recognise and define sinus bradycardia, sinus pauses, sick sinus syndrome and tachy-brady syndrome, and say when a slow sinus rate needs treatment.
3. Identify first-degree, Mobitz I, Mobitz II, 2:1, high-grade and third-degree AV block on an ECG, and state where in the conduction system each is usually located.
4. Work through the reversible-causes checklist in any patient with a slow rhythm.
5. Manage symptomatic bradycardia in the emergency setting, including doses of atropine, infusions and pacing.
6. State the indications for permanent pacing, and decode pacemaker letter codes such as VVI and DDDR.

The heart is a pump that depends on an electrical wiring system. When the wiring fires too slowly or conducts too poorly, the ventricles beat too slowly to supply the brain and other organs. The patient feels faint, short of breath or tired, or collapses without warning.

This page covers the whole spectrum of slow rhythms, from the physiological to the life-threatening. Faster rhythms, including atrial fibrillation, are covered in atrial fibrillation and flutter; the ECG skills used throughout are in ECG interpretation.

The terms below recur throughout the page.^[1]

• Sinus pause: the sinus node fires more than 3 seconds after the last atrial beat.
• Sinus arrest: no sign of sinus node activity.
• Sinoatrial exit block: the sinus node fires but the impulse fails to leave it and depolarise the atria, so P waves drop out (often as "group beating").
• Sinus node dysfunction (SND): abnormal sinus node impulse formation or exit, producing bradycardia, pauses or arrest, alongside symptoms.
• Chronotropic incompetence: the heart cannot raise its rate in proportion to activity; in many studies this means failing to reach 80% of the expected heart rate reserve during exercise.
• Atrioventricular dissociation: the atria and ventricles beat independently, not necessarily because of block. In isorhythmic dissociation the two rates are almost equal, the atria being slightly slower, so the P waves drift in and out of the QRS complexes.

The impulse starts in the sinus node, a cluster of pacemaker cells high in the right atrium near the entry of the superior vena cava. It spreads across the atria (producing the P wave) and reaches the AV node, in the septum low in the right atrium near the coronary sinus. The AV node is the only normal electrical bridge between atria and ventricles, and it conducts deliberately slowly. That delay, shown by the PR interval, gives the atria time to empty into the ventricles before they contract.

Beyond the AV node the impulse enters the bundle of His, which runs down the septum and divides into the right and left bundle branches, and then into the Purkinje fibres that spread the impulse quickly through the ventricular muscle. Fast conduction here explains the narrow QRS complex. Block in a bundle branch widens the QRS (see bundle branch blocks).

Two features of this system explain much of the clinical picture:

• Backup pacemakers. Every part of the system can generate impulses at its own, slower rate. If the sinus node fails or conduction is blocked, a lower pacemaker takes over as an escape rhythm. The further down the system, the slower and less reliable the escape: a junctional escape (from the AV node region) fires at about 40 to 60 bpm and is usually narrow-complexed and relatively dependable, whereas a ventricular escape fires at about 20 to 40 bpm, is broad-complexed and is prone to failing.^[12]
• Blood supply and autonomic control. The sinus node artery comes from the right coronary artery in about 65% of people,^[9] and the AV node is also usually supplied by the right coronary artery. So right coronary or inferior infarction often disturbs the sinus and AV nodes. The vagus nerve (parasympathetic) slows the sinus node and slows AV conduction, while sympathetic activity speeds both. Heightened vagal tone therefore causes sinus bradycardia and AV nodal block, in sleep, in athletes, during vomiting or after pain or fright.^[1] The His-Purkinje tissue is much less influenced by the vagus nerve, which matters when judging whether atropine will help.

Conduction disease becomes more common with age, because degenerative fibrosis of the sinus node and the conduction system accumulates over the decades; most patients who need a pacemaker for sinus node disease or AV block are elderly.^[1][2] Sinus bradycardia and first-degree or Wenckebach block are common and benign in athletes and young people with high vagal tone. Acute bradycardia seen in the emergency department is most often due to drugs, then myocardial infarction (see the reversible-causes checklist for the figures).^[2]

Sinus bradycardia is a normal P wave before every QRS complex, with a rate below 50 bpm.^[1] The rhythm is regular and the PR interval is normal.

Sinus bradycardia is normal in well-conditioned athletes, in young people, and during sleep.^[2] Training raises vagal tone and stroke volume, so the heart needs fewer beats. No treatment is needed, and the guideline states that permanent pacing should not be performed in asymptomatic people whose slow rate or pauses come from physiologically raised parasympathetic tone, or whose pauses occur only in sleep.^[1]

A slow rate with symptoms needs a cause. The main groups, with the mechanism in each case, are in the table.

Reduced cardiac output causes light-headedness, fatigue, breathlessness, syncope (fainting), chest pain or hypotension. In sinus node disease, the guideline stresses that no particular minimum rate or pause length justifies pacing; what counts is a demonstrated link between the slow rhythm and the symptoms.^[1] A pause of several seconds in a sleeping patient or a trained athlete is not itself an indication.

Treatment principles:

1. If the patient is well and the rate is physiologically explained, do nothing.
2. If symptoms are present, find and correct reversible causes (below).
3. If severe or unstable, treat acutely (see the emergency section).
4. If symptomatic and the bradycardia persists without a reversible cause, consider permanent pacing.

Sick sinus syndrome (SSS), also called sinus node dysfunction, is a group of disorders in which the sinus node cannot keep the atrial rate matched to the body's needs.^[9] It can show as sinus bradycardia, pauses or arrest, sinoatrial exit block, or alternating slow and fast atrial rhythms.

The commonest cause is progressive, age-related fibrosis of the sinus node and the surrounding atrial muscle.^[1] Other intrinsic causes include infiltrative disease (amyloidosis, sarcoidosis, haemochromatosis), ion channel defects and remodelling of the node in heart failure and atrial fibrillation. Drugs and the metabolic causes in the table may unmask or mimic it.^[9]

In tachy-brady syndrome, bradycardia or sinus pauses alternate with episodes of atrial tachycardia, flutter or fibrillation.^[1] A scarred atrium is prone to re-entrant tachycardias. When such a tachycardia stops suddenly, the diseased sinus node, suppressed by the fast rate, may take several seconds to restart, giving a long pause and a faint or collapse. At least half of patients with SSS have supraventricular tachyarrhythmias, usually atrial fibrillation or flutter.^[9]

This creates a treatment dilemma. The drugs that slow the fast phase (beta-blockers, calcium channel blockers, digoxin, many antiarrhythmics) worsen the slow phase. A pacemaker protects against the pauses, and the rate-slowing drugs can then be used safely.

About half of patients with SSS have syncope or near-syncope at some point; others have fatigue, palpitations, confusion, angina, breathlessness, or stroke and transient ischaemic attack.^[9] Early on the 12-lead ECG is often normal, so diagnosis depends on catching the rhythm during symptoms. Monitoring is chosen by how often symptoms occur: a 24 to 48-hour Holter for daily symptoms, weeks of event monitoring for less frequent ones, and an implantable loop recorder for rare events.^[1][9] Exercise testing helps when symptoms occur with exertion, to look for chronotropic incompetence.^[1]

Sinus node dysfunction and AV block are the two commonest indications for a pacemaker. Which ranks first varies between registries and populations; sick sinus syndrome is often quoted as the commonest (historically about half of implants) and is the standard exam answer.^[9] Sinus node disease can coexist with AV conduction disease: AV block develops in about 0.5 to 1.5% of patients per year.^[9]

AV block is delayed or failed conduction between atria and ventricles. It is graded by what the ECG shows.^[1]

Every P wave is followed by a QRS (1:1 conduction), but the PR interval is longer than 200 ms (five small squares at standard paper speed). Strictly it is a delay rather than a block, since no beat is lost.^[1]

• Site: usually the AV node.
• Causes: raised vagal tone (athletes, sleep), beta-blockers, calcium channel blockers, digoxin, inferior ischaemia, myocarditis, Lyme disease, ageing.
• Symptoms: none. It is found on ECG.
• Treatment: none for an isolated finding; routine imaging is not needed if the patient is asymptomatic with no sign of structural heart disease.^[1] Review the drugs. Marked first-degree block (PR above 240 ms together with a bundle branch or fascicular block) is considered for pacing only when symptoms are attributed to it; neuromuscular disease and lamin A/C mutations lower the threshold (see pacing indications).^[1] The European Society of Cardiology (ESC) likewise does not recommend a pacemaker for first-degree block without a clear link to symptoms.^[2]

Some P waves conduct and some do not. There are two main types, separated by whether the PR interval changes before the dropped beat.^[1]

Mobitz type I (Wenckebach). The PR interval lengthens progressively over successive beats until one P wave fails to conduct. After the pause, the PR interval resets to its shortest and the cycle repeats. The R-R intervals shorten as the PR lengthens, giving the characteristic "grouped beating".

• Site: usually the AV node, particularly when the QRS is narrow. The cause is decremental conduction: each successive impulse is conducted more slowly through the node until one fails.^[1] The ESC regards supranodal Mobitz I as benign and infranodal Mobitz I as an indication for pacing.^[2]
• Causes: vagal tone, beta-blockers, calcium channel blockers, digoxin, and right coronary (inferior) ischaemia or infarction.^[1]
• Symptoms: usually none.
• Treatment: remove the cause. Observe if asymptomatic. Atropine may be used if symptomatic. Pacing is considered if symptoms are clearly caused by the block, or when there is evidence that the block is infranodal.^[1][2]

Mobitz type II. The PR interval is constant before and after the dropped P wave, which appears suddenly and without warning.^[1]

• Site: below the AV node (infranodal), in the His bundle or the bundle branches. The QRS is often wide, because bundle branch disease commonly coexists, although a narrow QRS does not exclude it.
• Causes: fibrosis of the conduction system (degenerative), and acute, subacute or old myocardial infarction, particularly anterior infarction, in which septal necrosis damages the bundle branches.
• Symptoms: may be silent, but syncope occurs, and the block can progress suddenly to complete block. That risk is the reason for its management.
• Treatment: permanent pacing is recommended whatever the symptoms, once reversible and physiological causes are excluded.^[1][2] Atropine is unreliable (the His-Purkinje tissue is poorly vagally controlled), so temporary pacing is the bridge in an unstable patient.

2:1 AV block (pitfalls). Every second P wave conducts. There is only one PR interval to look at (the conducted beat), so one cannot tell whether the PR interval was lengthening, and the block cannot be labelled Mobitz I or II from a short strip.^[1]

• A narrow QRS makes nodal block (benign) more likely; a wide QRS raises the chance of infranodal block.
• Look on a long rhythm strip for a stretch where 3:2 or 4:3 conduction reveals Wenckebach behaviour, or where the PR changes.
• As a teaching rule of thumb, atropine or exercise often improves nodal block (the node responds to sympathetic and vagal changes) and may worsen infranodal block, because a faster atrial rate delivers more impulses to a failing His-Purkinje system. This is a clue to the site, not a test to rely on without monitoring.
• When the site stays unclear, guidelines suggest exercise testing if asymptomatic, and an electrophysiology study if symptomatic.^[1]

Advanced (high-grade) AV block. Two or more consecutive P waves fail to conduct, but some conduction remains.^[1] The ESC defines it as a P:QRS ratio of 3:1 or higher.^[2] It is managed like Mobitz II.

No atrial impulse reaches the ventricles.^[1] The atria (usually sinus) and ventricles beat independently, a state called AV dissociation. P waves march regularly across the strip with no consistent relation to the QRS complexes, and the ventricles are driven by an escape rhythm.

• Junctional escape (block in the AV node): narrow QRS, a faster and more stable rate of about 40 to 60 bpm. Typical of congenital block and of high AV nodal block in inferior infarction.^[12]
• Ventricular escape (block below the node): wide QRS, slow (about 20 to 40 bpm) and unreliable. Typical of acquired infranodal block.^[12]
• Causes: congenital block (often linked to maternal systemic lupus erythematosus and anti-Ro antibodies, or to congenital heart defects); degenerative fibrosis (Lev and Lenègre diseases); acute myocardial infarction; drugs (beta-blockers, verapamil, diltiazem, digoxin, antiarrhythmics); infection (Lyme carditis, endocarditis with an abscess in the valve ring, rheumatic fever, Chagas disease); infiltration (amyloid, sarcoid); inflammatory disease (myocarditis, systemic lupus, rheumatoid arthritis, systemic sclerosis); neuromuscular disease (myotonic dystrophy); and iatrogenic causes (valve surgery, ablation, alcohol septal ablation, transcatheter aortic valve replacement).^[1]
• Symptoms: fatigue, dizziness, breathlessness and acute heart failure from a slow, fixed rate; hypotension; and syncope. A sudden faint caused by a pause before an escape rhythm takes over is called a Stokes-Adams attack: the patient goes pale, loses consciousness without warning, and usually recovers within seconds as the rhythm resumes.^[11]
• Signs: a regular slow pulse, a variable-intensity first heart sound, and cannon a waves in the jugular venous pulse. These large waves appear because the atria sometimes contract while the tricuspid valve is shut by ventricular contraction, driving blood back up the neck veins. Cannon waves are intermittent because atrial and ventricular timing drift in and out of phase.^[11]
• Treatment: pacemaker, after correcting any reversible cause.^[1]

Before any permanent device, ask whether the slow rhythm can be corrected. The 2018 guideline gives a Class I recommendation (the strongest) to assess for and treat reversible causes in acute bradycardia.^[1] In an emergency-department series cited by the ESC, adverse drug effects accounted for 21% of bradycardia, acute myocardial infarction for 14%, intoxication for 6% and electrolyte disturbance for 4%.^[2]

Work through the list in order:

1. Drugs: beta-blockers (including eye drops), non-dihydropyridine calcium channel blockers, digoxin, amiodarone and other antiarrhythmics, clonidine, lithium, donepezil and others. Check for overdose and for interactions, and consider kidney function, as renal failure raises digoxin and some beta-blocker levels.^[1][2]
2. Myocardial ischaemia: a 12-lead ECG for inferior ST elevation, and troponin.
3. Electrolytes: potassium (high and low), calcium and magnesium.
4. Hypoxia, hypercapnia and acidosis, including sleep apnoea. Screen for sleep apnoea when bradycardia or pauses occur during sleep; treating it reduces the arrhythmia.^[1]
5. Endocrine and temperature: hypothyroidism and hypothermia.
6. Raised intracranial pressure (slow pulse with hypertension and irregular breathing).
7. Infection: Lyme disease, and endocarditis (look for a new PR prolongation, which suggests an aortic root abscess).
8. Vagal triggers: vomiting, pain, procedures, defecation.
9. Recent cardiac procedure: valve surgery, ablation or transcatheter aortic valve replacement.

When a drug is the likely cause and it cannot be stopped because it is essential, the guideline allows permanent pacing, since the patient needs the drug.^[1]

• 12-lead ECG in every patient: rate, P-wave relation to QRS, PR interval, QRS width, signs of ischaemia, and possible Lyme or hyperkalaemia patterns.
• Prolonged ECG monitoring when the 12-lead trace is normal but symptoms suggest bradycardia (Holter, event monitor or implantable loop recorder, chosen by symptom frequency).^[1]
• Exercise ECG for exertional symptoms: helps decide whether a block is nodal (improves as the sinus rate rises) or infranodal (worsens), and detects chronotropic incompetence.^[1][2]
• Blood tests: electrolytes, urea and creatinine, thyroid function, troponin, digoxin level if on digoxin; Lyme serology if there has been tick exposure.
• Echocardiography: recommended in new left bundle branch block, Mobitz II, high-grade or complete AV block, to look for structural heart disease; not routinely needed for asymptomatic sinus bradycardia or isolated first-degree block.^[1]
• Advanced imaging (cardiac MRI, FDG-PET for sarcoidosis, CT) when infiltrative disease or other structural causes are suspected, particularly in younger patients with conduction disease.^[1][3]
• Sleep apnoea screening when events occur at night.^[1]
• Electrophysiology study is not done for sinus node dysfunction alone; it may help to localise an unclear AV block.^[1]

Not every slow pulse is a slow heart rhythm, and not every slow rhythm is the same disorder. Check the ECG for the following.

The principle is to treat the patient, not the number. Assess whether the slow rhythm is causing harm: hypotension, altered consciousness, signs of shock, ischaemic chest pain or acute heart failure (the "adverse features").^[4][5]

1. Airway, breathing, circulation, disability and exposure (ABCDE assessment). Give oxygen if hypoxaemic.
2. Attach a cardiac monitor with blood pressure and oximetry; obtain intravenous access and a 12-lead ECG, without delaying treatment.
3. Identify and treat reversible causes (drugs, ischaemia, electrolytes, hypoxia).^[4][5]

• Transcutaneous pacing (large adhesive pads on the chest and back connected to the defibrillator) is the rescue when atropine fails; it is a bridge, and the 2018 guideline gives it a Class IIb recommendation for a critically unwell patient with bradycardia.^[1] It is painful, so conscious patients need analgesia and sedation, and you must confirm mechanical capture, not only electrical capture on the monitor. Palpating a pulse can mislead, because skeletal muscle twitching from the pads can mimic one, so confirm capture with a second method such as the pulse oximetry trace, an arterial line or ultrasound.^[4]
• Transvenous temporary pacing (a wire passed through a vein to the right ventricle) follows when pacing will be needed for longer. If prolonged temporary pacing is needed, an externalised permanent lead is an option.^[1]
• Temporary pacing carries its own risk of infection: the ESC cites an odds ratio of 2.5 for later device infection after temporary pacing.^[3] Pacemaker implantation should be done as soon as it is safe.

• Inferior myocardial infarction with AV block. The block is usually in the node, often transient, and often responds to atropine; aminophylline is an option.^[1] Treat the infarction first.
• Anterior infarction with new block. This is more worrying because the block is below the node; early pacing is needed.
• Beta-blocker overdose. Give glucagon and high-dose insulin, and prepare to pace at the same time.^[1]
• Calcium channel blocker overdose. Give intravenous calcium and high-dose insulin, and prepare to pace at the same time.^[1]
• Digoxin toxicity. Give digoxin-specific antibody fragments.^[1]
• Lyme carditis (below).

Lyme disease is a tick-borne infection by Borrelia burgdorferi, and carditis is one of its manifestations. Up to 90% of cases of Lyme carditis show up as AV block, and complete block occurs in up to two-thirds.^[7] It affects men about three times as often as women and typically people aged 20 to 40, in the months after tick bites (carditis is commoner from June to December in the northern hemisphere), and only about 40% of patients recall a rash.^[7] In a Polish study of 130 patients being considered for pacemakers, Lyme carditis was thought to be the cause in 16 (about 12%), and fluctuating AV block was more common in them (75% against about 50%).^[8] Thus, a young patient with unexplained AV block, especially one that fluctuates, in an area where Lyme disease occurs, needs serology and a low threshold for antibiotics.

Treatment depends on severity:

• Mild (first-degree block with PR 300 ms or below): oral antibiotics for 14 to 21 days, for example doxycycline 100 mg twice daily, amoxicillin 500 mg three times daily or cefuroxime 500 mg twice daily.^[7]
• Severe (symptoms, PR above 300 ms, or second- or third-degree block): the 2020 Infectious Diseases Society of America, American Academy of Neurology and American College of Rheumatology guideline strongly recommends admission with continuous ECG monitoring for a PR above 300 ms, other arrhythmias or myopericarditis. Give intravenous ceftriaxone (2 g daily), then switch to oral doxycycline, amoxicillin, cefuroxime axetil or azithromycin when conduction recovers (PR below 300 ms), to complete 14 to 21 days.^[7][10]
• Pacing: for symptomatic bradycardia that cannot be managed medically, the guideline recommends temporary pacing rather than a permanent pacemaker,^[10] because block usually resolves, with more than 90% of high-degree block receding within a week of antibiotics.^[7] Permanent pacing is considered if 1:1 conduction is not restored after about two weeks.^[7]

A permanent pacemaker is a small battery-powered generator placed under the skin below the collarbone. Leads run through a vein into the right atrium and/or right ventricle, sensing the heart's own activity and pacing when needed. Leadless devices, placed directly inside the right ventricle, are used where venous access is poor or infection risk is high.^[3]

1. For sinus node disease, treat symptoms. Pacing is for symptomatic bradycardia that has been linked to the rhythm. Pacing asymptomatic sinus node dysfunction has not been shown to improve prognosis, and the 2018 guideline gives it a Class III (harm) recommendation.^[1][2]
2. For infranodal AV block, treat the risk. In acquired Mobitz II, high-grade or third-degree AV block not caused by a reversible or physiological cause, permanent pacing is recommended regardless of symptoms.^[1] For other types of AV block, pacing is generally considered only when symptoms correlate with the block.^[1]

When the QRS is wide or the ejection fraction is low, tailored choices apply. The 2018 guideline prefers physiological pacing over right ventricular pacing when the left ventricular ejection fraction is 36 to 50% and ventricular pacing will be needed more than 40% of the time, to prevent heart failure: cardiac resynchronisation is Class IIa and His-bundle pacing Class IIb.^[1] For AV block with an ejection fraction below 40% and a high expected ventricular pacing burden, the 2021 ESC guideline recommends cardiac resynchronisation rather than right ventricular pacing (Class I, level A).^[2] See heart failure for resynchronisation therapy. A pacing indication in a patient with a very short life expectancy or whose goals preclude it should be weighed carefully; the guidelines recommend shared decision-making and respecting a capable patient's right to decline or later withdraw pacing.^[1]

• Sinus node disease with normal AV conduction: a dual-chamber device (DDD), programmed to avoid unnecessary ventricular pacing, is the ESC's first choice; atrial-only pacing (AAI) is considered inferior (more atrial fibrillation and reoperations) in the ESC's analysis.^[2][1]
• AV block: dual-chamber pacing preferred in sinus rhythm, to maintain AV synchrony and avoid pacemaker syndrome; single-chamber ventricular pacing is used in permanent atrial fibrillation, and for frail patients or those who need pacing only infrequently.^[1][2]
• Long-term right ventricular pacing can cause left ventricular dysfunction, so the amount of ventricular pacing is kept as low as possible where conduction is intact.^[2]

Pacemaker modes are described by a code of up to five letters. The generic NASPE/BPEG (NBG) code uses these positions.^[6]

Examples:

• VVI: paces the ventricle, senses the ventricle, and is inhibited by a sensed beat. It fires only if the heart's own ventricular beat does not arrive in time. Suitable for permanent atrial fibrillation.
• AAI: the same logic in the atrium.
• DDD: paces and senses both chambers. If the atrium does not fire, the device paces it; if the ventricle does not follow the atrial beat in time, the device paces the ventricle. It keeps the natural AV sequence.
• DDDR / VVIR: the added "R" lets a built-in sensor (movement or breathing rate) raise the pacing rate during exercise, which helps chronotropic incompetence.
• VOO: asynchronous pacing at a fixed rate, with no sensing (used briefly, for example in surgery).^[6]

Untreated, severe bradycardia can cause syncope with injury (falls, road accidents), heart failure from a slow fixed rate, and sudden death, the last being the reason Mobitz II and complete block are paced even when the patient has no symptoms.^[1][2] The prognosis of benign forms (athletic bradycardia, first-degree block, supranodal Mobitz I) is good. Pacing does not improve the prognosis of asymptomatic sinus node dysfunction.^[2] Complications of the devices themselves are listed under follow-up.

• Review the drug list regularly, especially in older adults on beta-blockers, rate-limiting calcium channel blockers, digoxin or several slowing drugs together.^[1]
• Recognise and treat obstructive sleep apnoea, which causes nocturnal bradycardia and pauses.^[1]
• Prevent Lyme disease by avoiding tick bites, removing ticks promptly and treating early infection, before carditis develops.^[10]
• Keep potassium and thyroid function in range in patients at risk.

After implantation, patients need a wound check in the first weeks and regular device interrogation, in person or by remote monitoring, to test lead function, battery life, pacing percentage and recorded arrhythmias. The schedule differs between centres and countries, so follow local policy. Counsel patients on device identification cards, driving rules (which differ by country), magnets and MRI compatibility, and what to do if symptoms recur.

Complications include pocket haematoma, infection, lead displacement and pneumothorax. A clinically significant pocket haematoma increases later device infection risk almost eightfold; infection is more likely after device replacement or upgrade and after temporary pacing.^[3]

Patients who do not receive a pacemaker (for example Mobitz I observed, or reflex bradycardia) need advice to report syncope or presyncope, and review of drugs. Patients with SSS and atrial fibrillation need continuing stroke-prevention review.^[9] Patients with congenital block need lifelong specialist follow-up.

• Athletes: sinus bradycardia and first-degree or Wenckebach block can be normal at rest and resolve with exercise. Symptoms, a wide QRS, structural heart disease or a block that worsens with exercise need investigation.
• Older adults: degenerative fibrosis makes sinus node disease and AV block common; always review drugs, as polypharmacy is a common cause.
• Long QT and bradycardia: a slow rate prolongs the QT interval and can trigger torsades de pointes, and congenital complete block with a long QT is a pacing indication (see long QT syndrome).^[3]
• Children and pregnancy: congenital complete block is associated with maternal lupus antibodies; paediatric pacing is a specialist matter. A pregnant woman with complete block needs specialist obstetric-cardiology care.
• Transplant recipients: atropine is ineffective; aminophylline or theophylline can be used.^[1]

• A pulse check and a rhythm strip from any monitor or 12-lead ECG often settle the diagnosis. Learn to recognise Mobitz II and complete block, because they decide referral.
• Treat reversible causes first. Stop beta-blockers, calcium channel blockers and digoxin when appropriate, correct potassium, and treat Lyme disease or other infection.
• Where pacing is unavailable, atropine and adrenaline or dopamine infusions can bridge patients to referral, with careful monitoring. Dopamine and adrenaline need infusion pumps or very careful manual titration. Do not delay transfer to a centre that can pace.
• A transcutaneous pacing defibrillator may be present in a district hospital even if no pacemaker service is; know how to use it.
• Chagas disease (in Latin America), Lyme disease, rheumatic fever and endocarditis are important local causes of block in different regions.^[1]