Bradycardia and heart block

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Bradyarrhythmia may reflect sinus-node dysfunction, AV nodal block, infranodal His-Purkinje disease, drugs, ischaemia or systemic illness. The acute task is to support perfusion while correcting a reversible cause and anticipating asystole.

RCUK 2025 is the acute authority. NICE TA88/TA324 address device mode for symptomatic bradycardia; ESC pacing guidance adds detailed diagnostic and indication context where NICE is narrower.

Atropine, catecholamines and pacing are parallel conditional tools. Repeated atropine is not an acceptable delay to pacing in distal high-grade block.

Key points

Bradycardia is a rate, not a diagnosis; athletes and sleep can be physiological, while symptoms and conduction level determine urgency.
First-degree AV block: every P conducts with a constant PR over 200 ms.
Mobitz I: progressive PR lengthening before a dropped QRS; Mobitz II: fixed PR intervals with sudden non-conducted P waves.
A 2:1 AV block cannot be reliably called Mobitz I or II from the ratio alone; QRS width and specialist assessment help localise it.
Complete AV block shows independent atrial and ventricular activity; a slow broad escape implies distal disease and higher asystole risk.
RCUK life-threatening features are shock, syncope, myocardial ischaemia, severe heart failure and immediately post-ROSC.
With adverse features give atropine 500 micrograms IV, repeating every 3-5 minutes to a total of 3 mg—except cardiac transplant or high-grade broad-QRS AV block.
If response is inadequate, use transcutaneous pacing and/or isoprenaline 5 micrograms/min starting infusion or adrenaline 2-10 micrograms/min while arranging expert transvenous pacing.
Even after a satisfactory response, recent asystole, Mobitz II, complete block with broad QRS or a ventricular pause over 3 seconds signals risk of asystole.
Permanent pacing is driven by symptoms, block type, reversibility and rhythm; NICE recommends dual-chamber pacing for symptomatic SSS/AV block with specific exceptions.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Physiological sinus slowing

Sleep, athletic conditioning and increased vagal tone can slow sinus discharge without disease. Preserved perfusion, absence of symptoms and an appropriate rate rise with activity support a physiological explanation.

Conduction-system disease

Sinus-node dysfunction may cause pauses or tachy-brady episodes, while degeneration within the atrioventricular node or His–Purkinje system can produce intermittent or higher-grade block and unreliable escape rhythms.

Ischaemic or structural heart disease

Myocardial ischaemia, infarction, valve disease and ventricular dysfunction can impair impulse generation or conduction. New block with chest pain or heart failure therefore requires urgent assessment of the underlying cardiac process.

Medicines, toxins and systemic disturbance

Beta-blockers, rate-limiting calcium-channel blockers, digoxin, antiarrhythmics, lithium and overdose can slow conduction. Hyperkalaemia, other electrolyte disorders and thyroid disease provide potentially reversible systemic causes.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Reduced sinus-node discharge
Slower impulse generation produces sinus bradycardia; intermittent failure can create sinus pauses or sinoatrial block. Symptoms arise when the remaining rate cannot maintain output during rest or exertion.
2
Atrioventricular nodal delay
Conduction through the atrioventricular node may progressively slow until an atrial impulse is dropped, creating the Mobitz I pattern. After the blocked beat, nodal conduction often recovers and the next atrial impulse conducts.
3
Infranodal conduction failure
Disease below the atrioventricular node can abruptly block impulses despite fixed conducted intervals, producing Mobitz II or complete block. A slow broad ventricular escape is less reliable and signals greater asystole risk.
4
Loss of atrioventricular coordination
In complete heart block, atria and ventricles beat independently. The escape rhythm determines ventricular rate, while lost atrial contribution and bradycardia together reduce filling efficiency and forward flow.
5
Low-output physiology
A markedly slow ventricular rate can reduce cardiac output and organ perfusion. Cerebral hypoperfusion may cause syncope, coronary flow may become inadequate, and raised filling pressures can produce acute heart failure.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Sinus bradycardia or sinus-node dysfunction

Sinus P before each QRS at a rate below 60/min; sinus-node disease may also cause pauses, sinoatrial block, chronotropic incompetence or tachy-brady episodes. Correlate symptoms rather than pacing an incidental number.

Second-degree AV blockRed flag

Mobitz I has progressive PR prolongation then a dropped QRS; Mobitz II has constant conducted PR intervals with unexpected dropped QRS. Mobitz II indicates RCUK asystole risk even after symptoms improve.

Complete AV blockRed flag

P waves and QRS complexes are independent. A narrow junctional escape may be temporarily more reliable; a slow broad ventricular escape suggests infranodal disease and high risk.

Life-threatening featuresRed flag

Shock, syncope, myocardial ischaemia, severe heart failure or immediately post-ROSC. Extreme bradycardia may progress to effective cardiac arrest even before a pulse disappears.

Risk of asystole despite initial improvementRed flag

Recent asystole, Mobitz II AV block, complete heart block with broad QRS, or ventricular pause over 3 seconds.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
ABCDE, repeated pulse/BP/perfusion assessment and continuous ECG/SpO2First step
Why
Identify symptomatic low output and deterioration while treatment is prepared.
Interpretation and limitations
Treat life-threatening features, not an arbitrary rate threshold; attach pads early in high-risk block.
02
12-lead ECG plus a long rhythm strip
Why
Define P waves, PR behaviour, dropped beats, QRS width, escape rhythm, ischaemia and QT.
Interpretation and limitations
Check apparent asystole carefully for P waves: ventricular standstill may respond to pacing whereas true asystole generally will not.
03
Medication/toxin review
Why
Identify beta-blockers, verapamil/diltiazem, digoxin, antiarrhythmics, lithium and overdose.
Interpretation and limitations
Stop/withhold contributors where safe; beta-blocker/CCB overdose requires toxicology/NPIS-guided antidotal and metabolic treatment, not atropine alone.
04
U&E/creatinine, potassium, magnesium, calcium, glucose; TFT, troponin and drug levels when indicated
Why
Find electrolyte, endocrine, ischaemic and toxic causes and guide drug clearance.
Interpretation and limitations
Hyperkalaemia can cause broad-QRS bradycardia/heart block and needs its own emergency protocol.
05
Echocardiography
Why
Assess LV/valve/structural disease when new conduction disease, heart failure or pacing is being considered.
Interpretation and limitations
Structural findings affect pacing strategy and urgency but should not delay temporary support in an unstable patient.
06
Ambulatory ECG/implantable monitor or exercise testing
Why
Correlate intermittent symptoms/pauses and assess chronotropic response when the resting ECG is nondiagnostic.
Interpretation and limitations
Symptom-rhythm correlation is central in sinus-node dysfunction; documented Mobitz II or complete block does not require recurrent syncope to be taken seriously.
07
Specialist pacing/electrophysiology assessment
Why
Determine temporary/permanent pacing indication and device mode.
Interpretation and limitations
Continuous AF with AV block generally requires ventricular rather than atrial tracking; frailty/comorbidity and LV function influence device choice.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Physiological sinus bradycardia

Each sinus P wave conducts normally, perfusion is preserved and symptoms are absent, often during sleep or in a trained athlete. A rate alone does not establish pathological bradyarrhythmia.

Sinus-node dysfunction

Sinus pauses, sinoatrial block, chronotropic incompetence or alternating atrial tachyarrhythmia and bradycardia suggest sinus-node disease. Correlation between symptoms and the recorded rhythm is particularly important.

Mobitz I atrioventricular block

Progressive lengthening of the PR interval before a dropped ventricular complex defines Mobitz I. This distinguishes it from Mobitz II, where the conducted PR intervals remain constant.

Mobitz II or complete block

Unexpected dropped complexes with fixed conducted PR intervals suggest Mobitz II; persistent atrioventricular dissociation supports complete block, although a long rhythm strip helps distinguish other causes of dissociation. A broad QRS or slow escape favours distal, high-risk disease.

Drug or metabolic bradycardia

A recent dose change, overdose, renal decline or compatible electrolyte abnormality favours a reversible toxic or metabolic cause. Broad-QRS bradycardia with hyperkalaemia needs its dedicated emergency pathway.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01No adverse featuresObserve, treat cause and assess asystole riskFirst stepBradycardia without shock, syncope, ischaemia, severe heart failure or immediate post-ROSC state.

1Perform ABCDE, monitor, obtain 12-lead and identify reversible causes.
2If none of recent asystole, Mobitz II, complete block with broad QRS or pause over 3 seconds is present, observe and treat the cause.
3If an asystole-risk feature is present, seek urgent expert help, monitor in an appropriate area and consider transvenous pacing even if the current response appears satisfactory.
4Do not treat physiological asymptomatic sinus bradycardia purely to normalise the number.

02Adverse featuresAtropine-responsive branchLife-threatening features with a rhythm likely to respond and no transplant or high-grade broad-QRS block.

1Give atropine 500 micrograms IV and reassess immediately.
2If the response is unsatisfactory, repeat atropine 500 micrograms every 3-5 minutes to a maximum total of 3 mg while preparing pacing/chronotropic support.
3Do not allow repeated dosing to delay transcutaneous pacing in a deteriorating patient.
4Once stabilised, treat the cause and obtain expert assessment for transvenous/permanent pacing when indicated.

03Atropine unsuitable or ineffectivePacing and chronotropic bridgeUnsatisfactory atropine response, cardiac transplant, or high-grade AV block with broad QRS.

1Start transcutaneous pacing as a bridge; provide analgesia/sedation if conscious while preserving haemodynamics.
2Use isoprenaline IV infusion at a starting rate of 5 micrograms/min OR adrenaline 2-10 micrograms/min, titrated to perfusion/rate under continuous monitoring.
3Seek expert help early and establish transvenous pacing in unstable symptomatic bradycardia; do not give atropine after cardiac transplant or in high-grade broad-QRS AV block per RCUK.
4DefinitiveIf pacing equipment is not immediately available and atropine is ineffective, RCUK permits fist pacing while equipment is brought; this is a short bridge, not definitive care.
5For transplant/spinal cord injury consider aminophylline 100-200 mg by slow IV injection. For suspected beta-blocker/CCB overdose, RCUK names glucagon but gives no dose—contact NPIS/TOXBASE and follow the local toxicology regimen rather than inventing one.

04Permanent therapyPacing after reversible causes are addressedSymptomatic sinus-node dysfunction/AV block or prognostically important conduction disease.

1NICE recommends dual-chamber pacing for symptomatic bradycardia due to sick-sinus syndrome, AV block or both.
2Use single-chamber ventricular pacing for AV block with continuous AF; patient-specific frailty/comorbidity may also favour single-chamber ventricular pacing.
3NICE TA324 supports dual-chamber pacing for symptomatic sick-sinus syndrome without AV block, with rare individual exceptions.
4Do not implant before considering reversibility (drug, electrolyte, acute ischaemia/infection) unless the need for pacing is emergent or the block is expected to persist.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

First acute drug for symptomatic bradycardia with adverse features when the block is likely to be nodal/vagally mediated.

Atropine IV

500 micrograms IV; repeat every 3-5 minutes if needed to a maximum total of 3 mg.

Do not give after cardiac transplant or in high-grade AV block with broad QRS per RCUK. It may be ineffective in distal block and should not delay pacing; monitor for tachyarrhythmia/ischaemia and anticholinergic effects.

Interim chronotropic support when atropine is ineffective/unsuitable and pacing is being arranged.

Isoprenaline IV infusion

RCUK starting rate 5 micrograms/min IV; titrate under continuous expert monitoring to perfusion and heart rate while pacing is arranged.

Can provoke tachyarrhythmia and myocardial ischaemia and increase oxygen demand; continuous ECG/BP, correct hypovolaemia and avoid uncontrolled titration.

Interim support for unstable bradycardia, particularly with hypotension, while pacing/cause treatment proceeds.

Adrenaline IV infusion

2-10 micrograms/min IV, titrated to clinical response.

This is a monitored infusion, not the 1 mg cardiac-arrest bolus. Watch for ischaemia, ventricular arrhythmia, severe hypertension and extravasation.

RCUK alternative in bradycardia after cardiac transplant or spinal cord injury.

Aminophylline

100-200 mg by slow IV injection.

Narrow therapeutic index and proarrhythmia/seizure risk; check interacting xanthines/drugs and obtain expert input.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Syncope and traumatic injury

Transient cerebral hypoperfusion causes dizziness or abrupt loss of consciousness. Recurrent unpredictable episodes create substantial risk of falls, injury and unsafe driving even if the resting examination later appears normal.

Hypotension and shock

When stroke volume cannot compensate for a slow ventricular rate, cardiac output and arterial pressure fall. Confusion, cool peripheries and oliguria indicate clinically important systemic hypoperfusion.

Myocardial ischaemia

Low arterial pressure and cardiac output may compromise coronary perfusion, particularly in existing coronary disease. Ongoing chest pain attributable to myocardial ischaemia is therefore a life-threatening feature requiring immediate bradyarrhythmia treatment.

Acute heart failure

Low output and loss of atrioventricular coordination raise cardiac filling pressures. Severe breathlessness, pulmonary oedema or worsening ventricular function indicate haemodynamic intolerance rather than an incidental slow rhythm.

Progression to asystole

Mobitz II, broad-QRS complete block, recent asystole or significant ventricular pauses can precede escape-rhythm failure. Early pacing or chronotropic support may prevent deterioration from a perfusing rhythm to cardiac arrest.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuous ECG, BP, SpO2 and perfusion/mental-state reassessment during acute treatment; pads attached for high-risk block.
Confirm electrical capture and then mechanical capture during transcutaneous pacing; monitor skin, pain and haemodynamics, not monitor spikes alone.
Isoprenaline/adrenaline: titrate by perfusion and rate with continuous ECG/BP and ischaemia surveillance.
Repeat electrolytes/renal function after correction and review all rate-limiting drugs before restart.
After permanent pacing: wound/infection, lead/device checks and remote/in-person follow-up per device service; reassess LV function when pacing burden may be high.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

A satisfactory atropine response does not erase asystole risk

Mobitz II, broad-QRS complete block, recent asystole and pauses over 3 seconds remain RCUK escalation features after the rate improves.

2:1 block is deliberately noncommittal

With every other P blocked there is not enough PR sequence to prove Mobitz I versus II. Treat high-risk clinical/QRS features and seek expert localisation.

Transcutaneous pacing needs a pulse check

Electrical spikes followed by QRS complexes show electrical capture; a palpable pulse/arterial waveform confirms mechanical capture. Muscle twitch alone is not enough.

Transplant hearts are different

The denervated transplanted heart may not respond normally to atropine; RCUK warns atropine can cause high-grade AV block or sinus arrest and recommends aminophylline instead.

Device mode follows atrial usefulness

Continuous AF makes atrial tracking ineffective, so NICE favours single-chamber ventricular pacing for AV block in that setting.

11Common pitfallsFrequent interpretation and management errors.

01
Treating every rate below 60/min without establishing symptoms or physiology.
02
Calling 2:1 AV block Mobitz II solely from the conduction ratio.
03
Repeating atropine in high-grade broad-QRS block while delaying pacing.
04
Giving atropine to a cardiac-transplant recipient despite the current RCUK warning.
05
Mistaking pacing spikes or muscle twitch for mechanical capture.
06
Using the 1 mg arrest adrenaline bolus for a perfusing bradycardic patient instead of a titrated infusion.