Bradycardia: Difference between revisions

The right bundle branch is composed of one fascicle. Right bundle branch block is a unifascicular block of the right bundle and can be found in healthy people and is represented by a broad QRS complex (>120ms). However a new RBBB in a patient with a history of normal ventricular conduction warrens further cardiological investigation. The last activity is to the right and results in a RSR’ pattern in V1 where R’ > R. This results from the delayed activation of the right ventricle. In V6 a slurred S wave can be seen at the end of the QRS complex.

The left bundle branch is composed of two fascicles. One of the fascicle has an anterior location and activates the interventricular septum and the anterior of the ventricle. Clinically this is represented by a left axis deviation and an absent or very small S and normal q in lead I and a S>R in lead II and III. QRS duration should be <120ms.

The second fascicle of the left bundle branch is the posterior fascicle. This fascicle has a posterior location and activates the posterior and lateral part of the ventricle. This fascicular block results in a right axis deviation and is represented by a deep S in I and small q in III with a QRS duration of <120ms.

If the two fascicles of the left bundle branch show conduction block there is a left bundle branch block, this bifascicular block is uncommon in healthy patients and further cardiologic investigations need to be performed to screen for underlying disease. Left bundle branch block causes the left ventricle to activate later then the right ventricle. This results in typical ECG characteristics, most importantly a broad QRS of >120ms. In V1 a broad monomorphic S wave can be seen (sometimes with a small r wave) representing slow left ventricular activation. In the lead V6 a broad monomorphic R wave is seen with no Q waves.

In certain conditions a conduction disorder can arise on the ECG. This functional conduction disorder is called aberrant conduction and can mimic any form of interventricular conduction disorder. In most cases a right bundle branch block pattern can be seen on the surface ECG because the right bundle has a longer refractory period. There are a few mechanisms which can cause aberrant conduction.

Phase 3 aberration is a situation that occurs when the bundle branches receive a new impulse, before they are repolarized. The bundles are still in their refractory period. This is also called Ashman phenomenon. As a result of the refractionary state of the bundle, conduction can not proceed along the refractory bundle and a conduction block is visible on the surface ECG. Thus for instance short coupled atrial activity can procedure phase 3 abberant conduction.

During a prolonged interval the Purkinje fibers can depolarize spontaneously. This depolarisation results in the conduction slowing and can even produce a conduction block. This is usually a pathological response, resulting from an increased activity in the Purkinje fibers, but can be normal at very low heart rates. Phase 4 aberration thus only occurs after prolonged pause.

This kind of aberrant conduction resembles phase 3 aberrant conduction; however appearance of the conduction disorders is the result of a small increase in rhythm. The conduction disorder is a result of an abnormal response of tissue that has diminished excitability.

 

In the diagnosis of bradyarrhythmias the identification of reversible causes is important to prevent unnecessary treatment. After a detailed history and physical examination there are additional investigations which can give information about the location of the nature of the bradyarrhythmia. While not all investigations are necessary, a thorough work-up has to be performed to prevent serious clinical events or pacemaker implantation. Espaccially the differentiation between bradyarrhtyhmias and vasovagal syncope can be difficult, but is very important for the management of symptoms.

===Symptoms===

A patient with a bradyarrhythmia can be complete asymptomatic. However patients with bradycardia may present with a diversity of signs and symptoms. A complete cardiac standstill can result in syncope (pause >6 sec) or near syncope. More often symptoms are nonspecific and chronic and are a result of the chronotopic incompetence and reduced cardiac output. Symptoms like for example, dizziness, light-headedness or confusional states, episodes of fatigue or muscular weakness, exercise intolerance, heart failure or palpitations can be described by the patient.

* <b>X-ECG:</b> An exercise test can give information about the chronotropic competence of the cardiac conduction system.

* <b>Long-term ECG recording:</b> Holter recording can identify causes of paroxysmal or intermittent bradyarrhythmias. Importantly a correlation with symptoms can be made and pathological causes of bradyarrhythmias or long pause (>3sec) during the night can be identified. If 24h or 48h Holter recordings cannot identify the cause of symptoms longer duration of monitoring may be required.  Transient event recorders can record up to 30seconds of ECG when a patient activates the device. This device can be especially useful when non-invasive monitoring is required due to the low occurrence of the bradyarrhythmia. For longer monitoring an implantable loop recorder can be used. This small device can be implanted and observe rhythm over an extensive period.  

* <b>Electrophysiological testing:</b> If non-invasive testing does not discover the bradyarrhythmia underlying the symptoms and electrophysiologic study may be undertaken to assess sinus nodal function and atrioventricular conduction. The measurement of conduction intervals and reaction to standard electrophysiological pacing protocols can elucidate the cause of bradyarrhtyhmia.

Fortunately the human heart has a couple of backup mechanisms that can sustain a heart rate in case of severe bradycardia. These escape mechanisms can occur in every part of the heart (i.e. atrium, AV, node, ventricle). In general, the rate of the escape mechanism is faster when the escape rhythm is located higher in the conduction system. If no reversible cause for the bradyarrhythmia can be found and the bradyarrhythmia persist, further therapy is required if the patients remains symptomatic.

There are no options for chronic drug therapy in bradyarrhthmias. In the acute setting atropine or isoprenaline may be used to increase heart rate or AV-nodal conduction. Patients with severe bradyarrhythmias (Type 2 AV nodal Mobitz II block, Type 3 AV nodal block, sinus arrest >3 seconds) should be considered for permanent or temporary pacing therapy.

Temporary pacing can be used to bridge the time to pacemaker implantation or until the bradyarrhythmia is resolved. Transvenous pacing is the most accepted method and can be used to pace the right atrium or the right ventricle after insertion of a temporary pacemaker wire through venous access. Pacing through the oesophagus can only capture the atrium, due to the anatomical position of the heart in relation with the oesophagus. Transcutanous pacing is a painful and emergency option in which muscle and heart are stimulated with large electrodes. Finally epicardal pacing is usually performed after cardiac surgery and requires surgical implantation of the electrodes.

* <b>Sinus node disease:</b> Pacemaker implantation should be considered in patients with sinus node disease which manifests as symptomatic bradycardia in which the symptom-rhythm correlation must have been 1) spontaneously occurring or 2) drug-induced where alternative drug therapy is lacking. Furthermore other eligible candidates for permanent pacing are patients with syncope with sinus node disease, either spontaneously occurring or induced at electrophysiological study and sinus node disease manifests as symptomatic chronotropic incompetence which is 1) spontaneously occurring or 2) drug-induced where alternative drug therapy. Patients with sinus node disease without symptoms including use of bradycardia-provoking drugs, ECG findings of sinus node dysfunction with symptoms not due directly or indirectly to bradycardia or symptomatic sinus node dysfunction where symptoms can reliably be attributed to non-essential medication do not have an indication for permanent pacemaker therapy.

* <b>Atrioventricular Block:</b> The following patients with AV conduction block have an indication for pacemaker therapy; 1) chronic symptomatic third or second degree (Mobitz I or II) atrioventricular block 2) neuromuscular diseases (e.g. myotonic muscular dystrophy etc.) with third-degree or second-degree atrioventricular Block or 3) third or second degree (Mobitz I or II) atrioventricular block after catheter ablation of the atrioventricular junction or after valve surgery when the block is not expected to resolve. Patients with asymptomatic first degree atrioventricular block, asymptomatic second degree Mobitz I with supra-Hisian conduction block or atrioventricular block expected to resolve do not require a pacemaker implantation.

* <b>Intraventricular conduction Block:</b> Patient which show a intermittent third-degree atrioventricular block, second-degree Mobitz II atrioventricular block. alternating bundle branch block or findings on electrophysiological study of markedly prolonged His-Ventrical interval (≥100ms) or pacing-induced infra-His block in patients with symptoms have an indication for pacemaker therapy. Patients with a bundle branch block without atrioventricular block or symptoms and bundle branch block with first-degree atrioventricular block without symptoms should not have a pacemaker implanted.