An AV block can have several degrees of severity.

A first degree AV block (1° AVB) causes slow conduction through the AV node. Each impulse does eventually reach the ventricles, but the PR interval will be longer than normal (> 200 msec or 1 large grid square).

A second degree AV block (2° AVB) does not always conduct the impulse through to the ventricles, so there can be some P waves without a QRS following them (i.e. an abnormal P:QRS ratio). This block can occur in regular repeating patterns, or more unpredictably. There are several different subtypes of second degree block that can be explored later.

A third degree AV block (3° AVB) is also known as complete heart block, because all of the atrial impulses are completely blocked from entering the ventricles. There may still be regular P waves, but the QRS complexes will be marching out on their own in an escape rhythm (junctional or ventricular) that is completely unrelated to the P waves. The PR intervals and P:QRS ratio can be all over the place because of this dissociation, and the ventricular rate will usually be a bradycardia.

Second degree AV blocks also vary in their severity.

A Wenckebach (aka Mobitz type I) AVB features progressively lengthening PR intervals, until the delay is so long that there is a dropped beat (a P wave without a following QRS), then the cycle starts again.

A Mobitz 2 has intermittently dropped beats, sometimes in a fixed ratio e.g. 3 P waves for every 1 QRS (3:1 block).

If the P:QRS ratio is 2:1, there isn't an opportunity to see if the PR interval is lengthening, which makes it hard to work out if it is a Mobitz 1 or 2 type of block. Instead it can be simply named a 2:1 AV block.

If the P:QRS is 3:1 or higher, it can also be named a high grade block.

Sometimes the SA node fails to produce an impulse. This can be called a sinus pause if it is brief, or a sinus arrest if it is prolonged (i.e. > 2-3 seconds). There are various definitions, and sometimes the terms are used interchangeably.

Some pauses are caused by a failure of the SA node to generate an impulse (e.g. sinus arrest), whereas some are caused by an exit block as the impulse tries to leave the SA node. Classically, if the R-R intervals continue to march out through the pause, it is more likely an SA block, whereas if there is a compensatory pause it is more likely a sinus arrest.

SA exit blocks have similar degrees of severity as AV blocks, but only 2nd degree SA blocks can be seen on a normal ECG.

A first degree SA block causes a delay between SA activation and the P wave appearing on the ECG, but because SA node depolarisation is not visible on the ECG no change is seen.

A second degree SA block causes intermittently dropped P waves, either in a pattern of Wenckebach (Mobitz 1) with progressively lengthening intervals between SA activation and exit to atria, or Mobitz 2 with intermittent dropped P waves. Type 1 will have a progressively shortening P-P interval (beats will get closer together) then a pause due to a dropped beat. Type 2 will have pauses that are exact multiples of the P-P interval.

A third degree SA block causes complete block and no P waves will be visible. This appears on the ECG the same as a sinus arrest.

A Left Bundle Branch Block features a wide QRS (>120 msec), negative QRS in V1 and a broad R in V6 without a Q wave.

A Right Bundle Branch Block features a wide QRS, an RSR’ in V1 and deep slurred S waves in the lateral leads.

An Intraventricular conduction delay (IVCD) can be any form of widened QRS (>100 msec) when the rhythm is supraventricular in origin. This includes conduction blocks to the bundle branches or fascicles, pre-excitation, hypertrophy / cardiomyopathy, or toxins/ electrolytes causing slowed conduction.

If no cause can be identified, a widened QRS can be name a non-specific IVCD.

A wide QRS is not an IVCD if the rhythm is ventricular in origin, as ventricular rhythms are expected to have a wide QRS.

A Left Anterior Fascicular Block (LAFB) features a left axis deviation (< -45 deg), long R wave peak time in aVL (> 45 msec) and a slightly wide QRS (80-110 msec).

A Left Posterior Fascicular Block (LPFB) features a right axis deviation and long R wave peak time in aVF. It is a diagnosis of exclusion for right axis deviation, e.g. there should be no other identifiable cause such as right ventricular hypertrophy.

Incomplete Bundle Branch Blocks have similar features but are not yet wide enough (QRS <120 msec) to be complete.

Intermittent Bundle Branch Blocks are not always present.

Rate related Bundle Branch Blocks may only be present with tachycardia.

A bifascicular block affects the RBBB and either the LAFB or LPFB. It features a RBBB with axis deviation to the left (LAFB) or right (LPFB) in the absence of other causes.

A true trifascicular block affects the RBBB + LAFB + LPFB. It can be seen as a 3°AVB + RBBB + (LAFB or LPFB). The term trifascicular block is often misused to represent a 1° or 2° AVB + bifascicular block, but this is no longer recommended as on its own does not increase the risk of progression to complete block above the risk of its individual components.

Artificial pacemakers have several different types. Their mode of operation can be represented by a code up to 5 characters representing the chamber(s) paced, sensed, response to sensing, rate modulation and multisite pacing.

A paced ECG can show sharp vertical pacing spikes. They will appear before P waves if atrial pacing, before QRS complexes if ventricular pacing, or before both if dual chamber A-V-sequential pacing is present. There may be two spikes before the QRS complex if there is biventricular pacing (aimed at re-synchronising ventricular contraction).

Normal ventricular paced beats will be wide complex. They will normally have a LBBB-like shape because the electrode is inserted in the right ventricle. The exception is biventricular pacing, when the left ventricle is paced slightly before the right, as this produces a RBBB shape.

Native or non-paced beats may have a very different QRS shape unless there is a pre-existing wide complex rhythm.

Pacemaker problems can be divided into sensing problems and pacing problems.

Sensing problems include undersensing, where extra pacing spikes may be seen because the native beats are not sensed. Conversely, oversensing means that pacing spikes/beats may be missing. Some sensing problems can temporarily be managed by placing a magnet over the pacemaker. This removes the sensing function.

Pacing problems include failure to capture or output failure, e.g. from wire damage, lead displacement, oversensing, infarction or electrolyte problems.

Pacemakers can also cause dysrhythmias. Pacemaker mediated tachycardia, sensor induced tachycardia, a runaway pacemaker or lead displacement dysrhythmias can lead to presyncope or syncope. As above, if the problem is related to abnormal sensing, a magnet may be of use to terminate the dysrhythmia.

Transcutaneous pacing can produce a broad artifact that is easily confused for a QRS complex, but it does not have a T wave following it.