Understanding ECGs: tachycardias

In the third article in our series Dominic Cox and Hamish Dougall discuss the main types of tachycardia

Tachycardias are the most exciting part of learning about ECGs. It is of course important to understand the mechanism causing tachycardias, but it is equally important to remember to look at the patient first. "Benign" arrhythmias can compromise a person, and "serious" arrhythmias can be asymptomatic. Look at the patient and act with commonsense, rather than treating the ECG.

We are not going to try to explain the emergency treatment of arrhythmias, but this should be something on all doctors' minds (and hearts). All the emergency treatment protocols are available from the European Resuscitation Council (website www.erc.edu/).

Tachyarrhythmias can be divided into two broad categories: supraventricular tachycardias (SVT) and ventricular tachycardias (VT). It is useful to think of these as narrow complex (QRS complex <120ms) tachycardias (SVT) and broad complex (QRS >120 ms) tachycardias (VT).

Why is the QRS complex narrow?

As described in the previous articles,^{1, 2} normally the atrium passes the sinoatrial (SA) node's signal to the atrioventricular (AV) node. This then passes on through the ventricular specialised conducting tissue, which gives rapid, synchronous activation of the whole of the ventricle. Thus to get a narrow complex you must have an electrical signal that passes forward through the AV node, and you must have specialised conducting tissue, that works. A broad QRS complex means that either your conducting system is not working (bundle branch block) or the electrical circuit is not involving the AV node correctly.

So what causes arrhythmias?

Only two things cause abnormal heart rhythms. The most common mechanism involves an abnormal electrical circuit which allows the heart beat to cycle around it. This is called re-entry. The other is where a focal area of the heart starts to "spark off" and send out a shower of extra heart beats (increased automaticity or triggered activity; see figure 1).

Narrow complex tachycardias

Atrial fibrillation (AF)

• The most common sustained arrhythmia of all
• Affects 2% of 65-75 year-olds, 5% over 75 years
• Associated with any disease affecting the heart
• Other narrow complex tachycardias can degenerate to AF--for example, atrial flutter
• Re-entrant mechanism.

Arrhythmia anatomy: Multiple wavelets of re-entry swashing around the atria. The AV node is inundated with cascades of chaotic activity (see figure 2).

ECG: Irregular ventricular rate with no true P waves, baseline irregularities representing atrial activation (ECG 1).

Useful drugs: anticoagulation to prevent thromboembolism; ß blockers, sotalol, propafenone, flecainide, and amiodarone to prevent paroxysmal AF; digoxin ß blocker, diltiazem, and verapamil (often in selected combinations) to control heart rate.

Atrial flutter

• Mistakenly thought of as a variant of atrial fibrillation
• Occurs at any age
• Can be difficult to control with drug therapy
• Re-entrant mechanism.

Arrhythmia anatomy: Typically involves a large circuit created by the structures in the right atrium (figure 3).

ECG: Saw tooth baseline with atrial rate of 300 and ventricular response of 150. Always be suspicious of flutter if you see a narrow QRS tachycardia at a heart rate of 150(ECG 2). Flutter waves are seen before each QRS and after each QRS in the middle of each T wave.

Useful drugs: Digoxin and verapamil (or diltiazem) can be used to slow the response of the AV node. You still get an atrial rate of 300 but hopefully a slower ventricular rate. Type 1c agents (propafenone or flecainide) can be used to stop the atrial circuit and terminate the tachycardia.

Atrioventricular nodal re-entry tachycardia (AVNRT)

• Also known as AV nodal tachycardia (AVNT), or AV junctional tachycardia (AVJRT)
• Commonest type of narrow QRS
• Typically starts in the later teens and 20s
• Re-entrant mechanism.

Arrhythmia anatomy: The basis of this arrhythmia is that the AV node can have two pathways as part of it (see figure 3). These paths allow a circuit to be set up at the AV node itself, giving rise to the arrhythmia.

ECG: Narrow QRS tachycardia of about 180 bpm with P waves often absent: they are hidden in the QRS, as atrial and ventricular depolarisation occur at the same time. You may see changes in the QRS complex in lead V1 as compared with the resting ECG: these are due to simultaneous P wave activation. This is a small positive deflection before the onset of the T wave and is shown in ECG 3 and 4. Look at the subtle difference in the QRS during tachycardia and during normal rhythm.

Useful drugs: Drugs which affect the AV node--that is, digoxin, diltiazem, and verapamil; adenosine can acutely stop the tachycardia as it transiently blocks the AV node (as can vagotonic manoeuvres); ß blockers; type 1c agents (propafenone or flecainide).

Atrial tachycardias

• Second most common SVT
• Can occur at any age, but increased likelihood if the atria are diseased (hypertension, pulmonary disease, previous cardiac surgery, etc)
• Either focal automatic activity (mainly) or due to re-entrant mechanism. Can have multiple foci of automatic activity.

Arrhythmia anatomy: Varied anatomical basis (see figure 4): they can be due to a focal area in the atria with increased automaticity, or re-entry around an abnormal area of atrial tissue.

ECG: Abnormal looking P waves; may have different types of P waves on same ECG. Heart rate very variable from 140 to 240 bpm.

Useful drugs: ß blockers; verapamil or diltiazem; type 1c agents (propafenone or flecainide); amiodarone.

Atrioventricular re-entrant tachycardia (AVRT) and Wolff-Parkinson-White syndrome

• Can occur from infancy onwards
• In infants it may be associated with congenital heart defects
• Re-entrant mechanism
• One to three people in every 1000 have an obvious extra pathway on the resting ECG--that is, Wolff Parkinson White syndrome. It may even be you!

Arrhythmia anatomy: Figure 5 shows that the re-entry mechanism is due to a congenital addition of a small piece of atrial tissue which crosses the isolating fibrous ring separating the atria and ventricles. This gives a large circuit with the heart beat passing down through the AV node, around the ventricle, back up the pathway, and across the atrium back to the AV node. This illustrates why SVT is not such a good name for these arrhythmias: most of this tachycardia's circuit lies in the ventricle.

ECG: The resting ECG can be normal but it can show evidence of the pathway's existence if the path allows some of the atrial depolarisation to pass quickly to the ventricle before it gets though the AV node (Wolff-Parkinson-White (WPW) syndrome; ECG 5). The early depolarisation of part of the ventricle leads to a shortened PR interval and a slurred start to the QRS (delta wave). The QRS is narrow; the message via the AV node eventually predominates because it uses the rapid conducting system to depolarise most of the ventricle.

The tachycardia ECG may be unremarkable, with P waves absent (hidden in the QRS). If the circuit is long or slow enough the P wave may occur at the end of the QRS and can be visible as a distortion in the T wave (this is best seen in lead V1).

Useful drugs: ß blockers; adenosine can acutely stop the tachcardia as it transiently blocks the AV node (as can vagotonic manoeuvres); type 1c agents (oropafenone or flecainide); type 1a agents (procainamide or quinidine).

Atrial fibrillation has an atrial rate of 300-600 bpm. Fortunately, the AV node protects the ventricle from experiencing such a heart rate. In patients with accessory paths there is a mechanism for this very fast heart rate to bypass the AV node and cause AF with a dangerously fast ventricular response (ECG 1). Treating this with drugs such as digoxin, verapamil, or diltiazem would further block the AV node but not prevent the AF from passing down the accessory path. The situation would be made a lot worse in this case. This is why the drugs are stated as being contraindicated in atrial fibrillation in the presence of an accessory pathway.

Broad complex tachycardias

To have a narrow complex you need functioning specialised conducting tissue, and the cardiac impulse must pass through the AV node normally. All of the SVTs can give a broad complex tachycardia if bundle branch block is present. Much time is spent by cardiologists considering ECGs and asking whether they show VT or SVT with bundle branch block. To the majority of doctors it does not matter. Think of it as VT and you will do little harm in the acute situation. Always treat the patient and not the ECG. So if you see a broad complex tachycardia look at the patient.

Ventricular tachycardia

• Broad complex tachycardia means ventricular tachycardia until proved otherwise
• Likely in patients with established heart disease
• Mainly, but not exclusively, re-entrant mechanism (see figure 6).

ECG: Broad complex >120 ms; bizarre QRS morphology; no P waves preceding each QRS; abnormal axis; concordant QRS (all point in the same direction); capture or fusion beats may be present (see ECG 7).

Useful treatments: Check the patient; if the patient is pulseless get help and treat as per resuscitation guidelines.

Ventricular fibrillation (VF)

• VF is the rapid, totally uncoordinated contraction of ventricular myocardial fibres
• Causes circulatory arrest; unconciousness develops within 10 to 20 seconds.

ECG: Irregular, chaotic electrical activity (ECG 8).

Useful treatment: Defibrillation.

The main message about tachycardias is at all times to assess the patient, not treat the ECG. Obviously, ventricular arrhythmias cause most concern as they are most likely to upset the heart's ability to pump blood effectively. But remember that relatively benign rhythms can be devastating if they are fast enough or in a patient with little physiological reserve. If the patient is well there will be enough time to assess even the most serious rhythm disturbance. If the patient is threatened by their heart rhythm then following life support protocols is essential. These give everyone dealing with the situation a proper structure so that they can think and act together.

Dominic Cox, specialist registrar in cardiology, Newcastle upon Tyne

Hamish Dougall, general practitioner and research fellow in general practice, University of Dundee


studentBMJ 2001;09:399-442 November ISSN 0966-6494

1. Cox D, Dougall H. What's so difficult about ECGs--a bundle of what? studentBMJ 2001;9:315-7. (September.)
2. Cox D, Dougall H. Understanding ECGS: minding your Ps and Qs. studentBMJ 2001; 9: 374-6. (October.)