My Stepwise Approach to ECG Interpretation

 I have been questioned a few times recently as to my own personal approach to 12-Lead ECG Interpretation. I am aware that there are a variety of methods out there, yet this is the method that works for me. By employing a stepwise approach to each and every ECG trace that you interpret throughout your career, not only will you have a much more thorough analysis available at your fingertips, those initially ‘daunting’ traces on first inspection can be broken down into bitesize chunks, which make them much more digestible to interpret. It is also good practice to question the ‘Initial ECG Checklist’ prior to the ‘Stepwise Approach’, to ensure that you always obtain a consistent, standardised, reliable trace of much more clinical significance. This is very important further down the line, where a patient may need repeat electrocardiograms and therefore already have a reliable baseline trace to make a comparison with.

My personal opinion is that there are three main categories that must be considered for every 12-Lead ECG, which are all as important as each other (and therefore do not need to be considered in any particular order, depending on the clinical scenario/urgency).

  1. Initial ECG Checklist

  2. My Stepwise Approach to 12-Lead ECG Interpretation

  3. Clinical Correlation

So let’s take a look at the suggested Initial ECG Checklist, followed by my own Stepwise Approach to 12-Lead ECG Interpretation. At each stage where there is an anomaly or specific finding, either an action should be immediately taken depending on the clinical correlation, or differentials are considered as to the cause/presentation. For example, the deteriorating patient in a regular Wide-Complex Tachycardia (WCT) should be treated as Ventricular Tachycardia until proven otherwise, and the patient should receive urgent Synchronised DC Cardioversion; this is not the type of ECG trace and/or situation that requires detailed scrutinisation of findings! This is similar to situations such as Advanced Life Support (ALS) arrhythmias in Cardiac Arrest. However, Patients that present to EMS following the insult of Transient Loss of Consciousness (TLOC), syncope following exertion, unexplained weakness/dizziness, palpitations, shortness of breath, pulse irregularities, new onsets of pain, familial cardiac history and so forth.. the 12-Lead ECG deserves, as a minimum, a thoroughly detailed interpretation by the attending clinician, and a variety of differentials can be explored that correlate with specific findings.

No matter where you are on your journey to learning 12-Lead ECG Interpretation, the most important ability is differentiating the ‘Normal Resting 12-Lead ECG’ and the ‘Abnormal ECG’ that requires immediate/urgent attention.

This may be the first electrocardiogram the patient has ever received, or it may be one of several taken over a period of time for ongoing complaints and symptoms. Your interpretation could make a real difference to that person’s life.

This stepwise approach will not teach you how to interpret each individual finding, but it should provide you with a better framework to make your 12-Lead Analysis.



  • Is the vertical scale set to a standardised 10.0 mm/mV (1 small square = 0.1mV, 1 large square = 0.5mV)? Have a quick look at the calibration mark at the beginning of the ECG trace.
  • Is the horizontal scale (paper speed) set to a standardised 25.0 mm/s (1 small square = 0.04s or 40ms, 1 large square 0.2s or 200ms)?
  • Is the frequency set as 0.05 – 150 Hz? A compromise of 0.05 to 40 Hz can be made if muscle artefact is severe, every effort has been made to reduce artefact and that the provider understands that there may be amplitude distortions as a result. Note: A low cutoff frequency may hide pacing spikes!
  • Does the ECG contain (as a minimum) the Patient’s Name, DOB, ID Number & Date/Time of Recording?
  • Is the Patient in a Semi-Recumbent position? i.e not sat completely upright or fully laid down.
  • Has the skin been adequately prepped, and are the electrodes in the correct anatomical positions?
  • Are the leads appropriately attached to their respective electrodes? Does the ECG trace suggest inadvertent transposal of the limb leads? Could this ECG show Dextrocardia?
  • Is there any artefact present on the 12-Lead ECG that needs your attention? Can it be reduced? Does the presented artefact have any clinical significance? How is the Patient presenting? (Excessive ‘noise’, Loose leads, Somatic muscle potentials (tremors/tension), Large movements of the baseline, AC electrical interference (electromagnetic interference EMI), Sloping/wandering baselines, CPR compression artefact, Neuromodulation artefact, Echo Distortion, Arterial pulse tapping, Temporary loss of electrical contact, Complete absence of electrical activity).


My Stepwise Approach to 12-Lead ECG Interpretation

1 – Rate

  1. Regular – Calculated from the R-R Intervals (300 / Large Squares, or 1500 / Small Squares).
  2. Irregular – Calculated from the Number of QRS complexes over a period of time.
  3. Is the Rate 60-100bpm? Note: Consider Intrinsic Pacemakers!

2 – Rhythm

  1. Is the Rhythm Regular?
  2. Is the Rhythm Regularly Irregular? (Patterns of irregularity).
  3. Is the Rhythm Irregularly Irregular (No patterns or regularity whatsoever).
  4. Are there Regular P waves?
  5. Is every P wave followed by a QRS?
  6. Is every QRS preceded by a P wave?
  7. Does the PR Interval remain constant and between 0.12 and 0.20 seconds (3-5 small squares)?
  8. Are the P waves upright in I and II?
  9. Are there any Premature Atrial, Junctional or Ventricular Complexes?
  10. Does the ECG show Pacing Spikes in any of the leads? Note: Bipolar pacing spikes may be extremely small.Visible either prior to P waves, prior to QRS complexes, or both. Added Note: Just because a Patient has a pacemaker, does not mean that it is always ‘firing’ !

3 – Axis (QRS)

  1. Is the Cardiac Axis Normal (Dominant R wave in Lead I & II)? (-30° to +90°)
  2. Is the Cardiac Axis Leftward? (-30° to -90°)
  3. Is the Cardiac Axis Rightward? (+90° to +/-180°)
  4. Is there an Extreme Cardiac Axis? (+/-180° to -90°)
  5. Is there an Indeterminate Axis? (?°)

4 – Intervals

  1. Is the PR Interval 0.12 – 0.20 seconds (120 – 200 ms)?
  2. Is the QRS Duration 0.11 seconds (110 ms) or less? Note: If the QRS is Wide, this is the point where you must stop and determine WHY it is wide. QRS width will give explanation to many other findings later in your Interpretation!
  3. Is the corrected QT (QTc) 0.35 to 0.45 seconds (350-450 ms)? Note: If the heart rate and QT values stated on the ECG strip are accurate, then the QTc value will be accurately calculated (however, the calculation is less accurate at faster heart rates).

5 – Hypertrophy / Conduction Abnormalities

  1. Does the ECG show any Fascicular Blocks, Bundle Branch Blocks or NSIVCD? Note: LAFB, LPFB, RBBB, Bifasicular Block, LBBB, Trifasicular Block, NSIVCD.
  2. Does the ECG demonstrate Preexcitation? Note: Shortened PR with slurred ‘Delta Waves’ going into the QRS complex.
  3. Are P waves neither tall and peaked nor broad and notched? Note: Consider Right Atrial and/or Left Atrial Conduction Abnormalities.
  4. Is there at least one QRS amplitude > 0.5mV in the Limb Leads?
  5. Is there at least one QRS amplitude > 1.0mV in the Chest Leads?
  6. Does the ECG suggest both the Voltage & Non-Voltage criteria for LVH? Notes: S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm, accompanied with ST-Depression/T-Wave Inversion in left-sided leads.
  7. Does the ECG suggest both Voltage & Non-Voltage criteria for RVH? Notes: Right Axis Deviation >110°, Dominant R wave in V1 (> 7mm, R/S > 1), Dominant S Wave in V5/V6 (>7mm Deep, R/S < 1), QRS Duration  ≤ 110ms, supported with Right Atrial Enlargement, RV-Strain (ST-Depression / T Wave Inversion in Right Sided leads i.e V1-V4 + Inferior II, III aVF), Deep S waves in the lateral leads (I, aVL, V5-V6).
  8. Does this ECG show Electrical Alternans? Note: Variation in QRS amplitude.
  9. Is there a Prolonged Intrinsicoid Deflection in any of the Leads? (Prolonged R-Wave Peak Time RWPT).

6 – Ischaemia / Infarction

  1. Are there any ST/T changes? Note: Consider STEMI territories i.e Inferior, Lateral, Anterior etc.
  2. Are there any Reciprocal changes? Note: If present, scrutinise the ECG for changes!
  3. Are there any ‘HyperAcute’ T Waves? How do the T waves appear in proportion to their respective QRS complexes?
  4. Are there any Q waves >25% amplitude of following R wave or > 0.04 seconds (40 ms) in width?
  5. Does the R:S ratio increase from V1 to V6, with an initial small r-wave in V1, an equiphasic QRS in V3/V4, with a dominant R wave in V6? Is there a Poor R-Wave Progression? (PRWP)

7 – STEMI Equivalents

  1. If the ECG was found to be a LBBB or a Ventricular Paced Rhythm, does the trace meet the modified Sgarbossa criteria for Acute MI?
  2. Does the ECG show De Winter’s T waves?
  3. Does the ECG show the reciprocal changes of an Isolated Posterior STEMI?
  4. Consideration to Wellens Syndrome
  5. Could this be a Left Main Coronary Occlusion? 3VD? Critical Stenosis?

8 – STEMI Mimics

  1. Does the ECG show Early Repolarisation ‘High Take-Off’?
  2. Does the ECG show the Brugada Sign in V1/V2 +/- V3?
  3. Could this ECG be a result of Raised Intracranial Pressure?
  4. Does this ECG suggest Pericarditis? Note: Pericarditis is a prehospital diagnosis of exclusion. Clinical Correlation is key.

9 – Sudden Cardiac Death Syndromes, Cardiomyopathy & Electrolyte Imbalance

Consideration to the changes associated with Arrhythmogenic Right Ventricular Dysplasia (ARVD), Dilated Cardiomyopathy (DCM), Hypertrophic Cardiomyopathy (HCM), Restrictive Cardiomyopathy (RCM), Long QT Syndromes, Short QT Syndrome, TakoTsubo Cardiomyopathy, Hyperkalaemia, Hypokalaemia, Hypercalcaemia, and Hypocalcaemia.


Clinical Correlation

Clinical Correlation is very important when it comes to making an interpretation of a resting 12-Lead ECG. For example, in a young fit athlete with no complaints of pain, but an ECG showing widespread concave ST-Elevation with notching or slurring at the J-Point – the likely diagnosis would be Early Repolarisation, and therefore further scrutinisation of the trace and relative investigations could be made if warranted. On the other hand, ST-Depression and T-Wave Inversion in aVL, along with T waves much bigger in proportion to the QRS complexes in the Inferior Leads (II/III/aVF – Hyperacute!) would likely suggest the early signs of an acute coronary occlusion; also linked clinically with central crushing chest pain in a mid-50’s male who has been a heavy smoker for 30 years!

It is vitally important to link your clinical findings with the 12-Lead ECG. This gives your interpretation much more value and significance, especially in terms of supporting your Patient Assessment, Differential Diagnosis and Treatment Plan.

Here are a list of a few considerations in terms of correlating clinical findings with the descriptive analysis of a 12-Lead ECG:

  • Hyperkalaemia or Hypokalaemia?
  • Hypercalcaemia or Hypocalcaemia?
  • Could this be Beta-Blocker Toxicity?
  • Could this be Calcium-Channel Blocker Toxicity?
  • Does this ECG show the Digoxin Effect?
  • Could this be Digoxin Toxicity?
  • Could this ECG be the result of a Pulmonary Embolism? Note: Sinus Tachycardia, Rightward Axis, RBBB/iRBBB, T-Wave Inversions in the Right-Sided Leads, S1Q3T3
  • Could this ECG be the result of Chronic Pulmonary Disease?
  • Could this ECG be the result of Hyperthyroidism / Hypothyroidism?
  • Could this ECG be the result of Increased Intracranial Pressure?
  • Could this ECG be Left Ventricular Aneurysm as opposed to Acute STEMI?
  • Does this ECG suggest Pericardial Effusion / Tamponade?
  • Could this ECG be the result of a Sodium-Channel Blocker Overdose?
  • Does this ECG suggest a Tricyclic Antidepressant Overdose?
  • Does this ECG contain findings that correlate with the use of Cocaine?
  • Could the changes on this ECG be the result of Aortic Dissection?
  • Does the clinical scenario match that to suggest Wellens Syndrome?

…..and so forth!

Using the Initial ECG Checklist, My Stepwise Approach and Clinical Correlation, there is enough information to write the following example for a standardised normal resting 12-Lead ECG.

‘’Initial ECG Checklist: 10 mm/mV, 25 mm/s, 0.05 – 150 Hz, Patient’s Name, DOB, ID Number, Date/Time of Recording, Patient Semi-Recumbent, Artefact Minimised’’
‘’A resting 12-Lead ECG of a 25 year old male with a recent history of general fatigue. 12-Lead ECG shows a Normal Sinus Rhythm of 68bpm, Normal Cardiac Axis (+60°), Normal PR (160ms), Normal QRS (100ms), QTc of 420ms, QRS voltages normal, No suggestion of any Atrial or Ventricular Conduction Abnormalities, Nil ST/T changes, Septal Q Waves I/aVL/V5/V6, Good RWP. Nil Acute’’

Although the above interpretation may seem a little ‘overkill’ for a Normal 12-Lead ECG, it is just an example to evidence how effective the Stepwise Approach can be to ensure a thoroughly detailed interpretation is made; and that all anomalies, if any, are identified.

I hope that this blog post will assist in giving your 12-Lead ECG Interpretation greater structure, and that it makes those initially ‘daunting’ traces much easier to break down into smaller chunks. The only other advice I can give, is to learn your differentials for specific findings/anomalies. For example, if you came across a short PR interval, what could that be the result of? Scrutinise your differentials when you come across them! And the best advice anyone can give for ECG Interpretation…. Practice, Practice, Practice.


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