See also:

ECG identification of conduction disorders
ECG a methodical approach

Some basic notes on the ECG and timing

• 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.

Determining regularity of events on an ECG

• One useful method for determining this is to use a piece of paper and mark off several examples of the event – e.g. ventricular QRS complex – with a small mark.
• By removing the piece of paper from the ECG trace and finding the distance between marks (either accurately by measurement, or approximately by eye), one can make a judgement on whether or not the event in question is regular.
• This can be very helpful when trying to determine the nature of an arrythmia, particularly in the case of tachycardias.
• Such an approach can help to distinguish between events such as fast atrial fibrillation (irregular) and other atrial arrythmias such as supraventricular tachycardia (regular).

Bradycardia or tachycardia? Narrow or broad ventricular complexes?

The normal ventricular rate is 60–100 bpm. Bradycardias (<60 bpm) are usually caused by diseases affecting the sinoatrial or atrioventricular nodes or the conducting tissues of the heart (although these may also cause some tachyarrhythmias). See article on ECG and conduction disorders for more detail.

If the ventricular rate is >100 bpm then there is a tachycardia, and the next question to ask yourself is whether this is a broad complex or narrow complex tachycardia, i.e. are the ventricular complexes of normal width? The normal QRS duration should be <0.08–0.12 s (2–3 small squares). A narrow complex tachycardia is usually due to an arrhythmia arising in the atria or junctional region. The exception to this rule of thumb is if there is a co-existing bundle branch block which will cause the ventricular complexes to be wider. Broad complex tachycardias usually arise from a focus below the atrioventricular node, in the ventricles.

Characteristics of atrial tachyarryhthmias¹

Broad complex tachycardias²

Ventricular tachycardia (VT)

• This is defined as >3 ventricular extrasystoles in a row at >120 bpm (at 100–120 bpm it is termed accelerated idioventricular rhythm).
• A change in frontal plane cardiac axis of >40° in either direction is indicative of VT.
• Irregular QRS complexes are highly suggestive of an atrial origin for the tachycardia, with aberrant conduction.
• QRS concordance throughout the chest leads – all QRS complexes in chest leads either mainly positive or negative; positive suggests origin in posterior ventricular wall and negative suggests origin in anterior ventricular wall.
• A diagnosis of VT is made more reliable by finding evidence of atrial activity independent of ventricular contractions, such as:
  • P waves dissociated from the QRS complex and usually present at a slower rate.
  • Capture beats – occasionally ventricular depolarisation occurs along the normal conduction system with a resulting early, narrow QRS complex.
  • Fusion beats – occur when a normal AV node beat fuses with a beat arising in the ventricles causing a QRS complex half way between normal and abnormal beat.

Types of VT

• Monomorphic VT – all QRS complexes are the same general, but peculiar, shape and 90% are >0.12 sec duration (longer QRS greater is chance of it being VT instead of SVT); rate is 120–300 bpm and rhythm is regular except where there are fusion or capture beats.
• Fascicular VT – as monomorphic VT, but QRS is usually 0.11–0.14 s duration.
• Right ventricular outflow tract origin VT – right axis deviation with LBBB pattern; may be brief or sustained.
  • Polymorphic ventricular tachycardia – there are the same ECG characteristics as monomorphic VT but there are repeated progressive changes in the QRS axis, so that the complexes appear to twist about the ECG baseline.
  • Torsades de pointes tachycardia – this is a subgroup of polymorphic VT associated with prolongation of the QT interval; the cardiac axis rotates over 5–20 beats first in one direction and then the other; it has a variety of causes and the arrhythmia is often not sustained; anti-arrhythmic drugs can aggravate this rhythm.

Broad complex tachycardias originating in the atria

• As previously discussed an atrial tachycardia with aberrant conduction can produce a highly irregular broad complex tachycardia.
• In Wolff-Parkinson-White syndrome there may be broad, bizarre complex tachycardias that occur from either antidromic AV re-entrant tachycardia, or atrial fibrillation with conduction from the atria to the ventricles via an accessory pathway.