Conductive disturbances. Treatment of conductive disturbances

Conductive disturbances. Treatment of conductive disturbances

When the heart's wiring slows or fails, from a sinus node that pauses to an atrioventricular block that leaves the ventricles to a slow escape rhythm; how to read the blocks on the ECG, which are harmless and which cause sudden blackouts, and when a pacemaker is needed.

At a glance

  1. The impulse starts in the sinus node and passes through the atria, the atrioventricular node, the His bundle and the bundle branches. A block anywhere slows the heart or changes the shape of the QRS.
  2. Sinus node dysfunction causes slow rates, pauses and often alternating fast atrial arrhythmias. Atrioventricular block is graded first, second (Mobitz I and II) and third degree.
  3. Where the block lies matters most: block in the node has a reliable narrow escape rhythm, while block below the node has a slow, unreliable broad escape rhythm that causes sudden blackouts and death.
  4. Reversible causes come first: drugs that slow the node, hyperkalaemia, ischaemia, hypothyroidism, Lyme disease and high vagal tone.
  5. Bradycardia with shock, syncope, ischaemia or heart failure is treated at once, with atropine when the block is in the node, and a drug infusion or pacing.
  6. A permanent pacemaker is needed for symptomatic sinus node dysfunction and for Mobitz II, high-degree or complete atrioventricular block without a reversible cause, with or without symptoms.

Definition and overview

The conduction system generates and spreads each heartbeat. The sinus node, high in the right atrium, fires spontaneously. The impulse spreads across the atria to the atrioventricular node, which delays it so the ventricles fill, then passes through the His bundle into the right and left bundle branches (the left dividing into anterior and posterior fascicles) and the Purkinje fibres.

Conduction disturbances are slowing or block anywhere along this path:

LevelDisturbance
Sinus nodesinus node dysfunction (sick sinus syndrome): sinus bradycardia, sinus pauses or arrest, sinoatrial exit block, chronotropic incompetence, tachy-brady syndrome
Atrioventricular node and His bundleatrioventricular block, first, second and third degree
Bundle branches and fasciclesright and left bundle branch block, fascicular blocks (hemiblocks), bifascicular block

Sinus node dysfunction and atrioventricular block slow the heart (bradyarrhythmias). Bundle branch and fascicular blocks widen or shift the QRS, and they matter mainly as markers of heart disease and of the risk of complete block.

Etiology and pathophysiology

Causes

GroupExamples
Degenerativefibrosis and calcification of the conduction system with age, the commonest cause in older people
Ischaemicacute infarction (the right coronary artery supplies the sinus node in about 60 per cent of people and the atrioventricular node in about 90 per cent), ischaemic cardiomyopathy
Drugsbeta-blockers, verapamil and diltiazem, digoxin, amiodarone and other antiarrhythmics, ivabradine
Metabolic and other extrinsichyperkalaemia, hypothyroidism, hypothermia, raised intracranial pressure, obstructive sleep apnoea
Vagalathletes, sleep, vasovagal and carotid sinus reflexes
Structural and infiltrativecalcific aortic stenosis, cardiomyopathies, amyloidosis, sarcoidosis, tumours
Inflammatory and infectivemyocarditis, Lyme disease, Chagas disease, an aortic root abscess in endocarditis, rheumatic fever, autoimmune diseases
Iatrogenicaortic valve replacement, especially transcatheter, valve and septal surgery, catheter ablation
Congenital and geneticcongenital complete block from maternal anti-Ro antibodies, congenital heart disease, myotonic dystrophy, variants in SCN5A or lamin A/C

Why the level of block matters

  1. 1

    Block in the node

    Block in the atrioventricular node is usually caused by vagal tone, drugs, ischaemia of an inferior infarction or inflammation, and it often recovers. The His bundle takes over with a narrow-complex escape rhythm of 40 to 60 a minute, which is fairly reliable and responds to atropine.
  2. 2

    Block below the node

    Block in the His bundle or the bundle branches is usually caused by fibrosis or a large anterior infarction and seldom recovers. The escape rhythm comes from the ventricles: broad, slow (20 to 40 a minute) and unreliable, and atropine does not help.
  3. 3

    The consequence

    When an infranodal escape rhythm pauses, the patient loses consciousness without warning, a Stokes–Adams attack, and may die. This is why Mobitz II, high-degree and complete block are paced even without symptoms; the danger is greatest when the escape is broad.

Prolonged right ventricular pacing activates the ventricles in the same abnormal sequence as left bundle branch block. In some patients this weakens the left ventricle, a pacing-induced cardiomyopathy.

Clinical features

  • Many conduction disturbances cause no symptoms and are found on an ECG.
  • Slow rates and pauses cause fatigue, dizziness, presyncope, syncope, breathlessness, reduced exercise tolerance, confusion in older people, and heart failure.
  • Stokes–Adams attacks: sudden collapse without warning, pallor, sometimes brief jerking, then a flush as the circulation returns, with rapid recovery.
  • Chronotropic incompetence, a heart that does not speed up with effort, causes breathlessness and fatigue on exertion only.
  • Tachy-brady syndrome: episodes of atrial fibrillation or flutter that end in a long pause, causing palpitations then dizziness or syncope.

In complete heart block the pulse is slow and regular and does not rise with effort, the jugular venous pressure shows intermittent cannon waves when the atria contract against closed valves, and the loudness of the first heart sound varies. Right bundle branch block widens the splitting of the second sound, and left bundle branch block reverses it.

Diagnosis and management

The ECG

DisturbanceECG
First-degree atrioventricular blockPR interval over 200 ms, every P wave conducted
Second-degree, Mobitz I (Wenckebach)the PR lengthens progressively until a P wave is not conducted; usually in the node
Second-degree, Mobitz IIa P wave fails to conduct without prior lengthening of the PR; usually below the node, often with a broad QRS
2:1 blockevery second P wave conducted; the level is decided by the QRS width and the response to exercise or atropine
High-degree (advanced) blocktwo or more consecutive P waves not conducted
Third-degree (complete) blockP waves and QRS complexes independent, the atrial rate faster than the ventricular
Right bundle branch blockQRS 120 ms or more, rsR′ in V1, broad S waves in I and V6
Left bundle branch blockQRS 120 ms or more, broad notched R waves in I, aVL, V5 and V6 without a septal q wave, deep S in V1
Left anterior fascicular blockleft axis deviation (beyond −45°), qR in aVL
Left posterior fascicular blockright axis deviation, once right ventricular hypertrophy is excluded; rare
Bifascicular blockright bundle branch block with a fascicular block, or left bundle branch block

Left bundle branch block makes the ECG hard to read for ischaemia, so left bundle branch block with symptoms of ongoing ischaemia is managed as a possible STEMI. Alternating right and left bundle branch block signals severe disease of the whole conduction system.

Other tests

  • Blood tests: potassium, thyroid function, digoxin levels, Lyme serology where exposure is possible, and troponin when ischaemia or myocarditis is suspected.
  • Ambulatory ECG monitoring, chosen by how often the symptoms occur: a 24-hour to 7-day recording, an external event recorder, or an implantable loop recorder for rare unexplained syncope.
  • An exercise test for chronotropic incompetence and for block that appears on exertion, which points below the node.
  • Echocardiography for structural heart disease, and cardiac MRI in a patient under about 60 with unexplained atrioventricular block, looking for sarcoidosis, myocarditis or a cardiomyopathy.
  • An electrophysiology study in selected patients with syncope and bundle branch block: an HV interval of 70 ms or more indicates pacing.

Acute management of bradycardia

Bradycardia is dangerous when it causes shock, syncope, myocardial ischaemia or heart failure, or when there is a high risk of asystole: a recent pause of more than 3 seconds, Mobitz II, or complete block with a broad QRS.

  • Reversible causes are treated at the same time: stopping the slowing drugs, treating hyperkalaemia, glucagon for a beta-blocker overdose, digoxin-specific antibody fragments for digoxin toxicity, reperfusion of an infarction.
  • Atropine intravenously, 0.5 to 1 mg depending on the guidance followed, repeated to a total of 3 mg. It works on vagal and nodal causes. It is not given in high-degree block with a broad QRS, where it does not work and may worsen the block, nor after heart transplantation, where it can cause complete block or sinus arrest; aminophylline is used there instead.
  • If it fails or is not suitable: an infusion of isoprenaline or adrenaline, and transcutaneous pacing, which is uncomfortable and needs sedation.
  • A temporary transvenous pacing wire, placed early in an unstable patient through a central vein into the right ventricle, until the cause resolves or a permanent pacemaker is fitted.

After an inferior myocardial infarction, atrioventricular block usually resolves within days, so a permanent pacemaker is considered only if it persists for at least about 5 days. Block after cardiac surgery is also watched for several days, and after transcatheter aortic valve implantation for 24 to 48 hours. In Lyme carditis the block usually resolves with intravenous ceftriaxone, and a temporary wire bridges the gap.

Permanent pacing

ConditionPacing
Sinus node dysfunctionwhen the symptoms are clearly caused by the bradycardia, including tachy-brady syndrome in which drugs for the fast rhythm would worsen the slow one; not without symptoms
Mobitz II, high-degree or complete atrioventricular blockrecommended with or without symptoms, once reversible causes are excluded
Mobitz Iwhen it causes symptoms or the block lies below the node
First-degree blockonly when a very long PR clearly causes symptoms
Atrial fibrillation with slow conductionwhen symptoms are caused by the slow rate or pauses; with high-degree or complete block, with or without symptoms
Bundle branch blockalternating bundle branch block; syncope with an HV interval of 70 ms or more, or with documented block; not for bundle branch or bifascicular block without symptoms, other than alternating block
Reflex syncopein selected patients over 40 with recurrent, unpredictable syncope and documented pauses

Pacemakers are implanted under local anaesthetic, with the generator under the skin below the clavicle and leads passed through the cephalic or axillary vein. They are described by a code:

ModeWhat it doesUsual use
VVI(R)paces and senses the ventriclepermanent atrial fibrillation with slow conduction
AAI(R)paces and senses the atriumsinus node dysfunction with normal conduction, now rarely used alone
DDD(R)paces and senses both chambers, keeping their sequenceatrioventricular block in sinus rhythm, and most sinus node dysfunction

The R means rate-responsive: a sensor raises the rate with activity. Leadless pacemakers, implanted in the right ventricle through the femoral vein, avoid leads and a pocket. Pacing the conduction system itself, at the His bundle or the left bundle branch area, keeps a near-normal activation and is increasingly used when much ventricular pacing is expected, to prevent pacing-induced cardiomyopathy. Patients with a reduced ejection fraction who need ventricular pacing receive cardiac resynchronisation instead. A patient who needs pacing and has cardiac sarcoidosis or a lamin A/C variant receives an implantable defibrillator, because of the high risk of ventricular arrhythmia.

Complications include pneumothorax, a pocket haematoma, lead displacement in the first weeks, tricuspid regurgitation, and infection, which needs removal of the whole system. A single-chamber ventricular pacemaker in sinus rhythm can cause pacemaker syndrome: dizziness, fatigue and pulsation in the neck as the atria contract against closed valves. Patients are followed in a device clinic, often remotely; batteries last about 7 to 12 years; most modern systems are safe in MRI under set conditions.

Epidemiology

First-degree block is found in about 1 to 2 per cent of young adults and becomes commoner with age. Right bundle branch block affects about 1 per cent of adults, left bundle branch block fewer, and both rise with age. Mobitz I is common in athletes and during sleep. Complete heart block is rare, mostly in older people, and congenital complete block occurs in about 1 in 15,000 to 20,000 births. European countries implant a median of about 740 pacemakers per million people a year, from under 50 to over 1,000 between countries, and more than 80 per cent go to people over 65; atrioventricular block and sinus node dysfunction are the commonest reasons.

Prognosis

Sinus node dysfunction is not life-threatening in itself: pacing relieves the symptoms but does not prolong life, and atrial fibrillation and stroke are the main later risks. First-degree block and Mobitz I in a healthy heart are usually benign. Complete heart block with blackouts was often fatal before pacemakers, about half of such patients dying within a year; with pacing, survival approaches that of people of the same age, and the outlook depends on the underlying heart disease. Isolated right bundle branch block in a normal heart has a good prognosis, while left bundle branch block marks a higher cardiovascular risk. Bifascicular block progresses to complete block in only about 1 to 2 per cent a year without symptoms, more often with syncope or a prolonged HV interval.

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

1An ECG shows a PR interval that lengthens with each beat until a P wave is not followed by a QRS complex, after which the cycle repeats. What is it?

2Which patient needs a permanent pacemaker even without symptoms?

3A 70-year-old with complete heart block and a broad-complex escape rhythm of 32 a minute has a blood pressure of 75/40 mmHg and is confused. What is the right first step?

4Before a permanent pacemaker is implanted for new complete heart block, which causes should be looked for and reversed?

5A 65-year-old with breathlessness on exertion is found to have left bundle branch block. What does it most often mean?

Linked topicsThe concepts this topic shares, and the topics they tie it to.

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Cardiac conduction

Sinoatrial and AV blocks slow or drop beats; a single bundle branch block widens the QRS instead.

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  • 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.
  • Rhythm abnormalities: supraventricular arrhythmiasCardiovascular diseasesFast rhythms that start above the ventricles, such as atrial fibrillation.
  • Rhythm abnormalities: ventricular arrhythmiasCardiovascular diseasesFast rhythms from the ventricles, which can turn into ventricular fibrillation.
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