I. The document discusses how to interpret timing on electrocardiograms (ECGs) and determine heart rates. Each large square on an ECG represents 0.2 seconds and is divided into 5 smaller squares of 0.04 seconds each.
II. It also provides methods for assessing regularity of heart rhythms using ECG tracings and distinguishing between bradycardias and tachycardias, as well as narrow and broad complex rhythms.
III. Specific arrhythmias discussed include ventricular tachycardia, polymorphic ventricular tachycardia, torsades de pointes, and broad complex rhythms that can originate from the atria like atrial fibrillation.
2. I. Each large square (5 mm long) on the ECG trace represents 0.2
s (200 ms) of time (ie five squares per second).
II. The large squares are subdivided into five smaller squares (1
mm long), each of which represents 0.04 s (40 ms) of time (ie 25
squares per second).
III. When interpreting the timing of events on an ECG, one should
count the number of squares over which the event in question
occurs in order to obtain an accurate reading of how long it has
taken.
3. Conti......
I. This allows you to compare it to the normal range for the event and decide whether or
not it is abnormal.
II. See the first reference in 'Further reading & references' below for an easy-to-read-and-
understand guide to basic interpretation of ECG timing, with sample traces.
III. 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.
IV. The same method can be used to determine the rate of atrial activity or any other
regular ECG event.
5. I. One useful method for determining this is to use a piece of paper and mark off
several examples of the event - eg, ventricular QRS complex - with a small mark.
II. By moving 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.
III. This can be very helpful when trying to determine the nature of an arrhythmia,
particularly in the case of tachycardias.
IV. Such an approach can help to distinguish between events such as fast atrial
fibrillation (irregular) and other atrial arrhythmias such as supraventricular
tachycardia (SVT) (regular).
7. • The normal ventricular rate is 60-100 beats per minute
(bpm). Bradycardias (<60 bpm) are usually caused by
diseases affecting the sinoatrial or atrioventricular (AV)
nodes or the conducting tissues of the heart (although
these may also cause some tachyarrhythmias). See also
separate ECG Identification of Conduction Disorders
article.
8. • If the ventricular rate is >100 bpm then there is a tachycardia and the next
question to consider is whether this is a broad complex or narrow complex
tachycardia, ie whether the ventricular complexes are 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
the 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
AV node, in the ventricles.
10. I. This is defined as >3 ventricular extrasystoles in a row at >120 bpm (at 100-120 bpm it is termed accelerated
idioventricular rhythm).
II. A change in frontal plane cardiac axis of >40° in either direction is indicative of VT.
III. Irregular QRS complexes are highly suggestive of an atrial origin for the tachycardia, with aberrant conduction.
IV. 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.
V. A diagnosis of VT is made more reliable by finding evidence of atrial activity independent of ventricular
contractions, such as:
VI. P waves dissociated from the QRS complex and usually present at a slower rate.
VII. Capture beats - occasionally ventricular depolarisation occurs along the normal conduction system with a
resulting early, narrow QRS complex.
VIII. Fusion beats - occur when a normal AV node beat fuses with a beat arising in the ventricles, causing a QRS
complex halfway between normal and abnormal beat.
12. I. Monomorphic VT - all QRS complexes are the same general, but peculiar, shape and 90% are >0.12 s
in duration (the longer the QRS, the greater the 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.
II. Fascicular VT - as monomorphic VT, but QRS is usually 0.11-0.14 s in duration. (NB: in fascicular VT
the QRS complexes are shorter where as in monomorphic VT they are broad.)
III. Right ventricular outflow tract origin VT - right axis deviation with left bundle branch block (LBBB)
pattern; may be brief or sustained.
IV. Polymorphic VT - 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.
V. 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.
14. I. As previously discussed, an atrial tachycardia with
aberrant conduction can produce a highly irregular
broad complex tachycardia.
II. 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.