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Ten top tips – ECG interpretation

1. Don’t make an easy job hard 

If it’s important that an ECG is done, it’s important that it’s legible. Asking patients to hold their breath for a couple of seconds can help, or if fine tremor is a problem, try moving the limb leads up to a more proximal position on the arms.

2. Switch off (or cover up) the computer interpretation

Most GPs are aware that these computer-generated diagnostics can be over-sensitive, but perhaps more alarming is when cases of barn door atrial fibrillation, for example, are reported as ‘normal sinus rhythm’. Whatever you do, don’t trust it.1 Once you’ve made your own interpretation, it can be reassuring to compare with the machine, but if it is different, don’t be afraid to go with your hunch.

3. Know your four times tables

All you really need to know to spot a problem on the ECG is your four-times table and the normal waveform interval values. Assuming standard paper speed of 25mm/sec, then one small square = 0.04msec.

The P wave should be 2-3 small squares in duration (0.08-0.11 sec)

The P-R interval should be 3-5 squares in duration (0.12-0.20 sec)

The QRS complex should be 1.5-2.5 small squares in duration (0.06-0.11sec)

The QT interval should be 9-11 small squares (0.36-0.44 sec)

4. A quick rate estimation helps diagnose any ectopic activity

To calculate the rate of a regular ECG, simply divide 300 by  the number of large squares between two complexes.  For irregular rhythms, count the number of complexes between 30 large squares and multiply by 10 (30 large squares = 6 seconds, assuming standard paper speed of 25mm/sec).

In irregular rhythms, it’s important then to calculate both the ventricular and the atrial rate separately. This helps establish any mathematical relationship between them (use blank paper to map them out). This is a really quick way of spotting 2:1 or 3:1 blocks, dropped beats, or random ectopy. 

5. The key to heart block is the P wave

P waves aren’t just about AF. The relationship of the P waves to the QRS complex is the bread and butter of ‘heart block’ diagnostics.

If the rhythm looks irregular, check for P waves (usually best seen, if present, in leads V1 and V2). If you can’t make out P waves, and it’s irregularly-irregular, then think AF. But, if you can see P waves, it’s useful to work out both the atrial rate and the ventricular rate to determine any consistent relationship between them.

Damaged myocardium – commonly age related or old infarct trauma – gives rise to heart blocks. Heart blocks occur when there is any interruption of electrical impulse either between its initiation in the sinus node and subsequent atrial depolarization (sino-atrial block - see below), or during its journey between the atria and the ventricles (atrioventricular block). Both of these types of block can be further sub-divided into first, second and third degree. Click here for more information on heart blocks.

Heart blocks, unlike Bundle branch blocks, indicate a non-sinus rhythm. Bundle branch blocks can occur in normal sinus rhythm, and signify a block in electrical conduction through the right or left branch of the Bundle of His. Any widening of the QRS complex beyond 2.5 small squares should alert you to a total or partial bundle branch block. See more about LBBB and its causes.

6. Be very suspicious if you suspect sinus arrhythmia in the elderly

Sinus arrhythmia occurs with respiration in the young and healthy. The rise and fall of the heart rate is gradual, with respiration. 

In the elderly, sinus arrhythmia is rare. Study the R-R interval. If the distance is always a multiple of the basic rate, then a sino-atrial block is far more likely in this age group. In a sino-atrial block, the P-P interval remains regular but an entire P-QRS complex will occasionally be missing.

7. When considering left ventricular hypertrophy, don’t just look at the chest leads

Interestingly, there is no one universally agreed criteria for left ventricular hypertrophy (LVH) by ECG. Whilst LVH can only be truly diagnosed by ECHO measurement, there are various ECG ‘voltage criteria’ which can be suggestive of LVH.

Hypertension and aortic stenosis commonly cause a thickening of the left ventricular muscle, which gives rise to an LVH ‘strain’ pattern - a downwardly concave ST depression, with a flipped asymmetric T wave. Strain pattern is usually greatest in the lead with the tallest/deepest QRS.

The left ventricle is represented by chest leads v5 and v6, so in LVH we expect the ‘R’ waveforms to be enlarged/tall in these leads. Conversely, we expect the ‘S’ waves to be deep in the right ventricular leads (V1 and v2). Many are familiar with the voltage criteria for LVH in the chest leads – the combined height/depth of the S wave (in V1 or V2) plus the R wave (V5 or V6) is =35mm. However, this measurement is very sensitive to body habitus of the chest wall – a tall slim man, with little chest wall adipose tissue, may well have voltage criteria for LVH in the absence of any hypertrophy.

The limb leads are less affected by body habitus, so always take a glance at the amplitudes in Leads I and aVL. Even without voltage criteria being met in the chest leads, the criteria for LVH are met if lead I = 12mm, or lead aVL = 11 mm. 

However, voltage criteria are cumulative, so the more leads which qualify, the more likely the accuracy of a diagnosis.

8. If the digital analysis states ‘anteroseptol infarct, probably old’, ask if there really are and pathological Q waves

First thing to check is whether or not there is any positive upward deflection – no matter how small – which indicates an ‘R’ wave prior to the suspect Q waves. If so, the deep waves are ‘S’ waves, not Q waves.

Second, check the amplitude and width of the Q waves. As a general rule of thumb the Q wave should be at least 25% as deep as the corresponding R wave is tall, and in at least two contiguous leads.

9. Bizarre ectopic waveform or simple artefact?

Remember, that each ‘column’ of leads on a 12-lead ECG trace records the heart rate at the same moment in time, for all three leads in that column. So the first column simultaneously records the view from the limb leads (I, II and II). The recording will then switch to the second column, which in turn records simultaneous beats in the augmented limb leads (AvR, aVL, avF). The third column records V1, V2 and V3 simultaneously, and the fourth records V4, V5 and V6. 

While the heart rate and rhythm might well change between columns, within each of the columns it should always remain the same.

So, a genuine ectopic waveform or anomaly will always appear in all three leads of any one column. A bizarre complex seen in V6 for example, which isn’t present in V4 and V5, can only be an artifact - such as sudden movement of the electrode (see image 3).

10. Think of the ST segments in relation to the baseline

They should be described as isoelectric (or baseline), elevated, or depressed.

Elevated ST segments can be described as convex (for instance STEMI), coved (Brugada Type 1), saddle-shaped (as in pericarditis, Brugada Type 2), or upsloping (in benign high take-off).

Depressed ST segments can be described as upsloping (often normal on exercise, or very early ischaemia), horizontal or downsloping (correlating respectively, to more progressive ischaemia).


Dr Heather Wetherell is a GPSI in cardiology at James Cook University Hospital, Middlesbrough

If you’d like to polish your ECG skills further, or find more detailed explanations and examples of cases, see

This website can be used as stand-alone, but for Twitter users, it runs alongside a Twitter educational forum for GPs called #ECGclass.  Run by Dr Heather Wetherell, via @ECGclass, new ECG cases are uploaded to this free interactive discussion forum on a fortnightly basis. No registration is necessary and the emphasis is on fun.



  1. Salerno SM, Alguire PC, Waxman HS. Training and Competency Evaluation for Interpretation of 12-Lead Electrocardiograms: Recommendations from the American College of Physicians and Competency in interpretation of 12-lead electrocardiograms: a summary and appraisal of published evidence. Ann Intern Med 2003;138: 747-61



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