ECG Identification of Conduction Disorders

See also: ECG a Methodical Approach; ECG Abnormal.

• Each large square (5mm long) on the ECG trace represents 0.2 s (200 ms) of time (i.e. 5 squares per second).
• The large squares are subdivided into 5 smaller squares (1mm long), each of which represents 0.04 s (40 ms) of time (i.e. 25 squares per second).
• When interpreting the timing of events on an ECG, one should count the number of squares over which the event in question occurs to get an accurate reading of how long it has taken. This allows you to compare it to the normal range for the event and decide whether or not it is abnormal.

See the first reference in the further reading section below for an easy-to-read-and-understand guide to basic interpretation of ECG-timing, with sample traces. The table below shows an easy way to calculate the heart rate by counting the number of squares between successive ventricular electrical complexes, measured from the gap between R-waves – the first upward deflection of the ventricular QRS complex. This is known as the R–R interval. The same method can be used to determine the rate of atrial activity or any other regular ECG event.

• Each normal cardiac electrical cycle starts with the generation of a regular depolarisation in a specialised area of cardiac tissue in the right atrial wall, known as the sino-atrial (SA) node.
• The electrical impulse spreads from here as a wave of depolarisation that causes atrial contraction. This corresponds with the P-wave of the ECG.
• The process of spread of the electrical impulse from the SA node to the myocardium corresponds with the P–R interval of the ECG. The spread of conduction is as follows:
  • The depolarising wave reaches the atrioventricular (AV) node at the atrioventricular junction, where the electrical impulse is conducted more slowly by another specialised area of cardiac tissue.
  • From here, the wave of depolarisation is then rapidly conducted down a specialised bundle of tissue in the interventricular septum, known as the Bundle of His.
  • This bundle divides in its course in the septum into the right and left bundle branches that conduct the electrical impulse to the right and left ventricular myocardium respectively.
• A nebulous network of smaller conducting fibres known as Purkinje fibres spread the electrical impulse, from the bundles, throughout the myocardial tissues, causing ventricular systole.
• The spread of the wave of depolarisation through the myocardium and consequent ventricular activation corresponds with the QRS complex of the ECG.
• The T-wave that follows the QRS complex represents the repolarisation of the ventricular myocardium, ready for the next heartbeat.

First-degree heart block

• This is delayed conduction of the electrical impulse between the SA node, AV node and His-Purkinje system. Despite the delay in conduction there is a normal correspondence between atrial and ventricular activation. In an ECG, this process is represented by the P–R interval. The P–R interval is measured from the beginning of the P-wave to the first impulse of the R-wave.
• In 1st-degree heart block the P–R interval is prolonged but each atrial activation leads to a ventricular activation with a 1:1 correspondence. There is a delay in electrical conduction through the AV node or the His-Purkinje system, or in a combination of the two. It is commoner for the conduction delay to be in the AV-node. If the QRS complex is of normal width then the delay is almost certainly arising in the AV-node. If the QRS complex is widened the His-Purkinje system is the likely site of the problem.
• It is a relatively common condition with a prevalence of 0.65–1.6% in young adults, becoming increasingly common with advancing age. It is found much more commonly in highly-trained athletes with supranormal cardiovagal tone. It is usually asymptomatic and often an incidental ECG finding. Possible pathological causes are listed below:¹
  • Following myocardial infarction
  • Intrinsic congenital or acquired AV-nodal disease
  • Myocarditis
  • Electrolyte derangement
  • Medication-induced (particularly disopyramide, flecainide, encainide, propafenone, beta-blockers, calcium-channel blockers, digoxin and magnesium).
• The condition does not usually require investigation or treatment if it is asymptomatic, particularly in young, healthy people. If there is reason to suspect metabolic disturbance (e.g. in someone taking potassium-losing diuretics or with other symptoms or signs of illness) then it might be worth checking U&Es. If the patient has experienced cardiac symptoms or there is reason to suspect occult ischaemic heart disease then cardiological referral may be appropriate. Follow-up ECGs on an annual basis can be used to monitor for progression of the heart block if a pathological cause is suspected, or the patient is on AV-node blocking medication.
• 1st-degree heart block is a relative contraindication to the use of drugs that may delay AV nodal conduction, such as those listed above, and they must be used with caution in this scenario and preferably under specialist supervision.

Second-degree heart block

This is prolongation of the P–R interval with intermittent failure of conduction of atrial impulses to the ventricles, causing 'dropped' beats. There are 2 types:

• Mobitz Type I AV block (a.k.a. Wenkebach block/phenomenon):
  • There is progressive prolongation of the P–R interval following each atrial impulse, until an atrial impulse fails to be conducted to the ventricles.
  • A ventricular impulse is 'dropped', and following this AV conduction recovers to its baseline optimal level and the cycle repeats itself.
  • The increments in AV-nodal conduction are usually greatest at the start of the Wenkebach sequence, leading to the somewhat paradoxical finding that, as the sequence progresses towards the 'dropped' beat, the QRS complexes actually move closer together.²
  • Sometimes the non-conducted P-wave can be seen superimposed on the preceding beat's T-wave, making it appear larger or biphasic.
  • Remember that the trace will not necessarily start with the shortest P–R interval (as it does in most textbook illustrations of the phenomenon), so a long trace and careful interpretation may be needed to see the characteristic pattern.²
  • Usually due to impaired AV-nodal conduction, so the QRS complexes tend to be of normal width.²
• Mobitz Type II AV block
  • There is intermittent failure of conduction of atrial impulses to the ventricles without progressive lengthening of the P–R interval, thus the P–R interval of conducted beats is constant.
  • There may be a regular pattern to the number of atrial impulses that do actually lead to ventricular activation (e.g. every second or third atrial impulse may 'get through', termed 2:1 and 3:1 block respectively).
  • Not all cases of Mobitz II AV block have this regular relationship and the ratio between conducted and non-conducted impulses can vary.²
  • The non-conducted P-waves may be difficult to see if they are superimposed on the preceding T-wave.²
  • Usually due to impaired conduction in Bundle of His or bundle branches, so the QRS complexes tend to be wider than normal.

If Type I block is due to AV nodal disease then it is usually relatively benign and non-progressive, with a good long-term prognosis. Type I block caused by His-Purkinje abnormalities (an unusual subgroup) is likely to progress to complete heart block. Type II block often progresses to complete heart block and so has a poorer prognosis. Type II block may cause symptoms in the form of Stokes-Adams attacks, where episodes of syncope are caused by significant slowing of the ventricular rate.

2nd-degree AV block is usually associated with cardiac pathology. Around 3% of patients with underlying structural heart disease develop some form of 2nd-degree block.³ Possible causes include:

• Medication – Digoxin, beta-blockers, calcium-channel blockers and other anti-arrhythmics.
• Structural abnormalities of the heart such as congenital abnormalities (and their surgical correction) and valvular heart disease (especially aortic stenosis and following aortic valve replacement).
• Idiopathic age-related fibrosis of the cardiac matrix.
• Ischaemic heart disease and MI.
• Inflammatory cardiac disease such as SLE, ankylosing spondylitis, Reiter's syndrome, dermatomyositis, rheumatoid arthritis, scleroderma, endocarditis, myocarditis, Lyme disease and rheumatic fever.
• Cardiac infiltration caused by tumour, leukaemia, amyloidosis, haemochromatosis and sarcoidosis.
• Endocrine and metabolic disorders such as hyperkalaemia, hypermagnesaemia and Addison's disease.
• Disorders of the myocardium caused by cardiomyopathies and muscular dystrophies.
• Familial cases are usually inherited in an autosomal dominant fashion (SCN5A-gene mutations have been identified).
• There are cases of 2nd degree block in highly-trained athletes with supranormal cardiovagal tone. This type of block improves with exercise; if it causes symptoms it tends to do so during sleep when parasympathetic tone predominates.³

Acutely symptomatic patients with low ventricular rates can be treated with atropine and/or temporary pacemaker insertion. Patients with 2nd-degree AV block should be referred for cardiological assessment (after adjusting the dose of or discontinuing any culprit medications). More detailed investigations such as 24-hour ECG monitoring, electrophysiological studies, cardiac imaging and cardiac catheterisation may be carried out. Treatment by insertion of a permanent cardiac pacemaker may be required, particularly for Mobitz Type II AV block.

Third-degree or complete heart block

This occurs when there is complete failure of transmission of atrial impulses to the ventricles. P waves will occur regularly, usually at a rate of around 75 bpm. They are completely unconnected to the rhythm of the QRS complexes.

3rd-degree AV block can occur at the AV node (~40% of cases) or infra-nodally in the His-Purkinje system.

• In nodal block the new, subsidiary distal pacemaker will arise above, or in, The Bundle of His.
  • Unless there is accompanying bundle branch block, the QRS complexes in such cases will be narrow.
  • These pacemakers normally fire reliably and at a reasonably rapid rate (~45–60 bpm). They increase their rate in response to exercise and atropine.
  • Patients with this type of complete heart block may remain asymptomatic for appreciable periods of time and are usually haemodynamically stable. They may experience mild or non-specific symptoms such as fatigue, dizziness, reduced exercise tolerance, chest discomfort and palpitations.
• AV-blocks occurring in or below the His-bundle usually have a subsidiary pacemaker in the right or left bundle branches.
  • These pacemakers produce wide QRS complexes and are usually slow (<45 bpm).
  • Patients with this type of complete heart block are usually haemodynamically compromised and overtly symptomatic. Common symptoms include syncope, confusion, dyspnoea, severe chest pain or decompensation of pre-existing cardiac failure. Sudden death may occur.

Complete AV block can co-exist with cases of atrial fibrillation or flutter where there are no P waves, but the characteristic baseline irregularity (in AF) or saw-tooth waves at a rate of ~300 bpm in atrial flutter. The term AV dissociation should be reserved for cases where the ventricular escape rate is faster than the atrial rate. It should be distinguished from the more common types of 3rd-degree AV block. Sometimes, in this scenario, the occasional atrial impulse will fire at just the right moment to 'capture' the ventricles via the AV node before the next escape pacemaker discharge, causing premature ventricular activation. This is termed AV dissociation with capture beats. It may occur during acute MI or thrombolysis and does not usually require pacemaker insertion in a haemodynamically stable patient (which is the norm for this situation).²

Complete heart block may occur as a progression from 2nd-degree heart block, or acutely, particularly after MI, thus its causative conditions are as listed above for 2nd-degree heart block. It is treated acutely with atropine and temporary pacemaker insertion if the patient is haemodynamically compromised. Permanent pacemaker insertion is usually required in the long-term.

Abnormally fast AV conduction

This occurs as part of the Wolff-Parkinson-White syndrome (WPW syndrome), one of the ventricular pre-excitation syndromes. Follow link for full information. The characteristic ECG abnormalities are a shortened P–R interval and a 'slurred' upstroke to the QRS complex, so that it is widened. This feature of the QRS complex is known as the delta wave. It occurs due to conduction of atrial impulses down a congenital accessory pathway, rather than via the AV node. The atrial impulse is conducted more quickly than normal, hence the short P–R interval. This pathway is known as The Bundle of Kent. Patients with WPW may be in sinus rhythm, but are prone to fast atrial fibrillation and paroxysmal supraventricular tachycardias.

The Bundle of His divides into left and right bundle branches. The left bundle branch subdivides further into the anterior and posterior hemi-fascicles. Abnormal conduction through the bundles or hemi-fascicles causes characteristic lengthening of the QRS complex and may cause abnormalities in the axes of the QRS complexes in the chest leads (V1–V6), or the limb leads (I, II, aVF, III, aVR and aVL). Interpretation of the cardiac axis requires an understanding of the hexaxial reference system where activity in the various limb leads reflects the direction of the electrical impulse in the frontal plane (i.e. looking at the body from the front). See the diagram below for further information on understanding the axis of cardiac conduction.

Left bundle branch block (see diagram below)

The interventricular septum is normally activated by the left bundle branch. When its conduction is slowed the septum is activated 'in reverse' by impulses from the right bundle branch. This has the following electrical consequences:

• A prolonged QRS complex
• Replacement of the usual small Q-wave in the left-ventricular leads (V5, V6, I and aVL) by a large, prolonged positive R-wave
• Secondary R-waves in the left-ventricular leads, causing an M-shaped pattern in leads I and V4, V5 or V6
• Left-axis deviation may be seen.

Right bundle branch block (see diagram below)

The activation of the right ventricle is delayed and slowed conduction from the left to right ventricles results in:

• A prolonged QRS complex
• A secondary R-wave in leads oriented to the right ventricle (V1 and V2) – giving an M-shaped ventricular complex in these leads
• T-wave inversion may be seen in leads V1 and V2
• A deep, slurred S-wave is seen in leads I and V6.

Left anterior fascicular block (a.k.a. left anterior hemi-block) – see diagram below

• Left axis deviation (mean frontal plane axis counterclockwise to –30°)
• Small initial R-wave in leads II and aVF
• No other cause for left-axis deviation is identified.

Left posterior fascicular block (a.k.a. left posterior hemi-block)

• Right axis deviation (mean frontal plane axis clockwise to 90°)
• No other cause of right axis deviation such as right ventricular hypertrophy/strain or young, thin-built patient is identified.

Bi-fascicular block – see diagram below

• Combined right bundle branch block and, usually, associated left anterior hemiblock.
• Results in characteristic pattern of RBBB in the relevant leads and deviation of axis in frontal plane to counterclockwise to –30°.