تحديد اضطرابات النظم بواسطة تخطيط القلب

See also the separate articles ECG A Methodical Approach, ECG Identification of Conduction Disorders, Supraventricular Tachycardia in Adults, Paediatric Supraventricular Tachycardia, Ventricular Tachycardias, Narrow Complex Tachycardias و Broad Complex Tachycardias.

Notes on arrhythmia ECG and timing

• Each large square (5 mm long) on the ECG trace represents 0.2 s (200 ms) of time (ie five squares per second).

• 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).

• 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.

• 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 'Further reading and references' 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.

Quick method to calculate the ventricular heart rate from the number of large squares in the R-R interval

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 - eg, ventricular QRS complex - with a small mark.

• 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.

• This can be very helpful when trying to determine the nature of an arrhythmia, particularly in the case of tachycardias.

• 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).

Bradycardia or tachycardia? Narrow or broad ventricular complexes?

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 the separate ECG Identification of Conduction Disorders مقالة.

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.

Characteristics of atrial tachyarrhythmias¹

A brief guide to help determine the nature of atrial arrhythmias (narrow complex tachycardia, unless there is associated bundle branch block)

تسرعات القلب ذات المركب العريض^{2 3}

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 halfway 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 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.

• 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.)

• Right ventricular outflow tract origin VT - right axis deviation with left bundle branch block (LBBB) pattern; may be brief or sustained.

• 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.

• 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.