Bradyarrhythmias and Heart Block

Introduction

A bradyarrhythmia is a heart rate below 60 beats per minute arising from failure of impulse generation at the sinus node, or failure of impulse conduction through the AV node and His-Purkinje system.

The most important principle is that a slow heart rate is not automatically abnormal. A resting rate of 45/min in a trained athlete, or 50/min during sleep, is physiological. What matters is whether the rate is adequate for the patient's needs, whether it causes symptoms, and whether the conducting system is showing signs that it may fail altogether.

This last point - the risk of progression - is what separates the benign bradyarrhythmias from the dangerous ones, and it turns almost entirely on where in the conducting system the problem lies. Disease at the level of the AV node is usually reversible, responsive to atropine, and backed up by a reliable junctional escape. Disease below the AV node, in the His-Purkinje system, is not reversible, does not respond to atropine, and is backed up only by an unreliable ventricular escape that may stop without warning.

Aetiology

Physiological

• Athletic training - high vagal tone with sinus bradycardia, and first degree or Mobitz I block during sleep
• Sleep - rates in the 40s are common and normal
• Vasovagal responses - during vomiting, straining, pain, or a needle procedure

Intrinsic conducting system disease

• Idiopathic fibrosis of the conducting system - the commonest cause of complete heart block in older people, sometimes named Lev disease (fibrosis of the cardiac skeleton) or Lenegre disease (fibrosis of the conducting tissue itself)
• Ischaemic heart disease - both acute and chronic. Inferior myocardial infarction commonly causes AV block, because the right coronary artery supplies the AV node in about 90% of people. This block is usually transient, atropine-responsive and does not require permanent pacing. Anterior infarction causing AV block indicates extensive septal necrosis affecting the bundle branches themselves - a much more ominous finding requiring pacing and carrying a poor prognosis.
• Infiltrative disease - amyloidosis, sarcoidosis and haemochromatosis. Cardiac sarcoidosis is an important and treatable cause of heart block in a younger patient.
• Infection - Lyme disease (a classic and reversible cause of AV block in a young patient with a rash or arthritis), infective endocarditis with an aortic root abscess, myocarditis, rheumatic fever, and Chagas disease
• Connective tissue disease - systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis, and maternal anti-Ro or anti-La antibodies causing congenital complete heart block
• Congenital complete heart block
• Cardiac surgery and interventions - aortic and mitral valve surgery, and TAVI, all risk damage to the conducting system, which lies close to the aortic valve
• Neuromuscular disease - myotonic dystrophy and Kearns-Sayre syndrome

Extrinsic and reversible causes

• Drugs - beta-blockers (including eye drops for glaucoma, which are systemically absorbed), rate-limiting calcium channel blockers, digoxin, amiodarone, ivabradine, adenosine, lithium, and cholinesterase inhibitors such as donepezil
• Hyperkalaemia - and other electrolyte disturbance
• Hypothyroidism
• Hypothermia - with J waves on the ECG
• Raised intracranial pressure - the Cushing reflex of bradycardia with hypertension
• Obstructive sleep apnoea - nocturnal bradycardia and pauses
• Hypoxia
• Cholestatic jaundice and anorexia nervosa

Sinus node disease

Sick sinus syndrome describes a spectrum of sinoatrial node dysfunction, most often from age-related fibrosis. It encompasses several ECG patterns, and one patient may show all of them at different times.

Atrioventricular block

First degree AV block

A PR interval above 200 ms that is constant, with every P wave followed by a QRS. No beats are dropped - the term "block" is really a misnomer, since this is delay rather than block.

It is usually benign and asymptomatic, requiring no treatment. Consider reviewing rate-limiting drugs, and note that a markedly prolonged PR (over 300 ms) can occasionally cause symptoms resembling pacemaker syndrome, because atrial contraction occurs too early relative to ventricular filling.

Second degree AV block

Some P waves are not conducted. Distinguishing the two types is one of the highest-yield discriminations in cardiology, because the implications are entirely different.

2:1 AV block - where every alternate P wave is conducted - cannot be classified as Mobitz I or II from the ECG alone, because there are never two consecutive conducted beats to compare PR intervals. Clues favouring a Mobitz II mechanism are a broad QRS and worsening with exercise or atropine. If in doubt, treat it as the more dangerous possibility and seek specialist assessment.

High-grade AV block describes two or more consecutive non-conducted P waves with some conduction preserved. It is managed as Mobitz II.

Third degree (complete) heart block

No atrial impulses reach the ventricles at all. The atria and ventricles beat entirely independently, each at its own intrinsic rate, and ventricular activity depends on an escape rhythm arising below the level of block.

• Regular P waves at the sinus rate, marching through the trace at a constant P-P interval
• Regular QRS complexes at a slower rate, with a constant R-R interval
• Complete dissociation - no fixed relationship between P waves and QRS complexes, and a variable PR interval. P waves may be buried in QRS complexes and T waves.
• The QRS width indicates the origin and reliability of the escape rhythm

Clinical features

Symptoms

• Fatigue, lethargy and reduced exercise tolerance - often insidious, attributed to ageing, and only recognised in retrospect after pacing
• Dizziness and presyncope
• Syncope, classically as a Stokes-Adams attack
• Breathlessness - from reduced cardiac output, or frank heart failure
• Confusion - a common presentation of bradycardia in older patients
• Falls - bradycardia is an important and frequently missed cause of unexplained falls in older people
• Chest pain - if there is coexisting coronary disease
• Asymptomatic - many are found incidentally

Examination

• Slow, regular pulse - typically 30-40/min in complete heart block, and characteristically it does not increase with exertion
• Wide pulse pressure - a large stroke volume compensates for the slow rate
• Cannon a waves in the JVP - intermittent, irregular, large waves occurring when the atrium contracts against a closed tricuspid valve. A cardinal sign of AV dissociation.
• Variable intensity of the first heart sound - varying PR interval means varying valve position at the onset of systole
• Signs of heart failure if the rate is inadequate
• Signs of a cause - hypothyroidism, an erythema migrans rash, a new aortic regurgitation murmur suggesting an aortic root abscess, or a sternotomy scar

Investigations

• 12-lead ECG - the essential investigation. Measure the PR interval, look for dropped beats and their pattern, assess QRS width, and look for evidence of infarction and bifascicular block.
• Continuous cardiac monitoring - if there are symptoms, adverse features or any risk of asystole
• U&Es - particularly potassium; hyperkalaemia is a rapidly reversible cause
• Thyroid function tests
• Troponin - if ischaemia is suspected
• Digoxin level where relevant, and a full review of every rate-limiting drug
• Lyme serology - in a young patient, or with a suggestive exposure history or rash
• Blood cultures - if endocarditis with an aortic root abscess is a possibility
• Echocardiogram - to assess ventricular function, valve disease and structural causes
• Ambulatory monitoring or an implantable loop recorder - for intermittent symptoms, particularly unexplained syncope
• Cardiac MRI - where infiltrative disease such as sarcoidosis or amyloidosis is suspected
• Electrophysiological study - occasionally, to localise the level of block where it is uncertain

Acute management

Follow the Resuscitation Council UK bradycardia algorithm. Begin with an ABCDE assessment, give oxygen if hypoxic, obtain intravenous access and monitor the rhythm.¹

Drug treatment

1. Atropine 500 micrograms IV, repeated every 3-5 minutes to a maximum total of 3 mg
2. If the response is inadequate, move to second-line measures without delay

Second-line measures

• Transcutaneous pacing - the fastest route to a guaranteed rate. It is painful, so give analgesia and sedation, and confirm mechanical capture by feeling a pulse, not just by seeing pacing spikes on the monitor.
• Isoprenaline infusion (5 micrograms/min, titrated) or adrenaline infusion (2-10 micrograms/min)
• Alternative drugs - aminophylline, dopamine, glucagon in beta-blocker or calcium channel blocker overdose, and digoxin-specific antibody fragments in digoxin toxicity
• Percussion pacing - a fist struck rhythmically over the lower left sternal edge, as a holding measure while awaiting equipment
• Transvenous pacing - the definitive temporary measure, arranged urgently through cardiology or critical care

Treat the cause

Stop rate-limiting drugs, correct hyperkalaemia, treat hypothyroidism, rewarm the hypothermic patient, treat Lyme disease with intravenous ceftriaxone, and reperfuse an acute infarct. Complete heart block complicating inferior myocardial infarction is often transient and resolves with reperfusion, which is why permanent pacing decisions are generally deferred for several days in that setting.

Permanent pacing

A permanent pacemaker is indicated where bradycardia is symptomatic and irreversible, or where there is a high risk of progression to asystole regardless of symptoms.²

Device choice depends on the underlying rhythm: a single-chamber ventricular (VVI) device for permanent atrial fibrillation with slow ventricular response, a dual-chamber (DDD) device for AV block in sinus rhythm to preserve atrioventricular synchrony, and cardiac resynchronisation therapy where there is heart failure with a broad QRS. Pacemakers are covered in more detail in the article on pacemakers and implantable defibrillators.

Complications

• Asystole and sudden cardiac death - the outcome that pacing exists to prevent
• Syncope and consequent injury - fractures, head injury, and road traffic collisions
• Heart failure - cardiac output is the product of rate and stroke volume, and a persistently inadequate rate causes decompensation
• Bradycardia-related ventricular arrhythmia - a slow rate prolongs the QT and permits pause-dependent torsades de pointes
• Cognitive impairment and falls in older people from chronic cerebral hypoperfusion
• Complications of pacing - lead displacement, pneumothorax, infection, tamponade, and pacemaker syndrome from loss of AV synchrony in single-chamber ventricular pacing

Red flags

Prognosis

Prognosis depends on the level of block and whether the cause is reversible.

First degree block and Mobitz I in an asymptomatic patient carry an excellent prognosis and generally require nothing more than periodic review and attention to rate-limiting drugs.

Untreated complete heart block has a poor outlook, with a substantial annual mortality from asystole and heart failure, and syncope carries a high risk of injury in the interim. With permanent pacing, life expectancy approaches that of the general population, and the improvement in symptoms is often dramatic - patients frequently describe a return of energy they had attributed to ageing. Pacing for complete heart block is one of the clearest examples in medicine of a treatment that reliably restores both length and quality of life.

Reversible causes carry the prognosis of the underlying condition. AV block from drugs, hyperkalaemia, hypothyroidism or Lyme disease usually resolves completely with treatment, and identifying these avoids an unnecessary lifelong device. Conversely, complete heart block complicating anterior myocardial infarction carries a poor prognosis, not because of the block itself but because it indicates a large septal infarct with extensive myocardial loss.