The Complete Basics of ECG Interpretation

Author: Mr Vik Veer MBBS(Lond) MRCS(Eng) DoHNS(Eng) — December 2007. Updated 2025.

This document is for doctors, nurses, or medical students who have forgotten — or never fully understood — ECGs. This is not an exhaustive textbook account; it is a guide to help you work out whether the patient in front of you is having a major cardiac event. It is particularly aimed at FY1 doctors who are suddenly faced with an ECG on the ward, and new A&E SHOs who are routinely asked to interpret ECGs. Some basic knowledge of medicine and cardiac physiology is assumed throughout.

Understanding the ECG Layout

Most departments use a standard 12-lead ECG layout. Familiarise yourself with this format — understanding the geography of the ECG is the first step to interpreting it reliably.

Each lead shows the electrical activity of the heart as seen from a different anatomical direction. No single lead tells the whole story — you need to interpret all 12 leads together to understand what is happening. Different groups of leads correspond to different regions of the heart:

• Inferior: leads II, III, aVF — supplied by the right coronary artery (RCA)
• Anterior/septal: leads V1–V4 — supplied by the left anterior descending artery (LAD)
• Lateral: leads I, aVL, V5, V6 — supplied by the circumflex artery (Cx)

Knowing these territories is important because ST changes confined to a particular group point towards a specific vessel as the culprit.

The ECG Complex — P, QRS, T

Before interpreting an ECG, remind yourself of what each part of the complex represents.

Normal values to know

• PR interval: 120–200 ms (3–5 small squares). Longer = heart block; shorter = pre-excitation (WPW)
• QRS duration: <120 ms (<3 small squares). Wider = bundle branch block or ventricular rhythm
• QT interval: Corrected QTc should be <440 ms in men and <460 ms in women. Prolonged QT predisposes to torsades de pointes
• Heart rate calculation: Count the number of large squares between two R waves and divide 300 by that number. Alternatively, count the R waves in a 10-second rhythm strip and multiply by 6

Assessing the Rhythm

At the bottom of the ECG printout there is a long rhythm strip — usually lead II — showing the heart rate across the full width of the page. This is the primary strip used for rhythm assessment. Look at the QRS complexes and compare the distances between them. In sinus rhythm the spaces should be approximately equal (there may be a slight variation with respiration — this is called sinus arrhythmia and is normal, particularly in young people).

Atrial Fibrillation (AF)

Now compare this with the ECG below, where the peaks of the QRS complexes are highlighted. There are obvious differences in the spaces between them — this is an irregular rhythm.

AF occurs when the atria lose their organised, co-ordinated contraction and instead fire randomly and rapidly — often described as a "bag of worms" appearance rather than a controlled pumping action. This disordered atrial activity results in a completely irregular ventricular response.

To diagnose AF on an ECG, look for two features:

1. Irregularly irregular rhythm — no two RR intervals are the same
2. Absent P waves — no discrete P waves are visible; the baseline may appear to flutter (fibrillatory baseline)

Other common rhythms to recognise

• Atrial flutter: Regular "sawtooth" flutter waves at approximately 300 bpm, with a ventricular rate typically 150 bpm (2:1 block). Flutter waves are best seen in leads II, III, and aVF.
• SVT (supraventricular tachycardia): Regular narrow complex tachycardia, typically 150–250 bpm, often with no visible P waves or with retrograde P waves just after the QRS. Causes palpitations and often resolves with vagal manoeuvres or adenosine.
• Ventricular tachycardia (VT): Regular broad complex tachycardia (QRS >120 ms), rate 100–250 bpm. The patient may be haemodynamically stable or in extremis. Always treat as VT until proven otherwise.
• Ventricular fibrillation (VF): Chaotic, disorganised broad complexes with no recognisable pattern. The patient will be pulseless and in cardiac arrest. Requires immediate defibrillation.

Ventricular tachycardia and ventricular fibrillation are nearly always associated with a patient who looks seriously unwell. If the patient is pulseless and unresponsive — call the crash team and begin CPR immediately. Attend a resuscitation course to be prepared for these situations.

Looking for Ischaemia (Angina) on an ECG

A good history and clinical examination are vital — an ECG can be completely normal in someone with genuine, severe angina. Bear this in mind before reading on.

Wherever possible, obtain a previous ECG taken when the patient was not in pain, so you can identify any new changes. A dynamic, changing ECG is far more significant than a single abnormal tracing.

The main area to examine is the ST segment — the flat region between the end of the QRS complex and the beginning of the T wave. In ischaemia, the ST segment sinks below the baseline. This is called ST depression.

Also note in the ECG above that the T wave is inverted (upside down). T wave inversion or flattening is another marker of ischaemia, though it is less specific and can also indicate a previous infarction or other pathology.

Important points before diagnosing ischaemia

• ECGs are not infallible. If you are convinced the patient has angina from the history but the ECG is normal — still contact your senior. The ECG can be entirely normal during genuine ischaemia.
• Ectopic beats (single abnormal complexes that look completely different from the surrounding beats) should not be interpreted in isolation if the rest of the ECG is normal.
• ST depression in 2 or more consecutive leads in the same anatomical territory is needed before you can confidently attribute the finding to ischaemia.
• Dynamic changes matter most. Repeat the ECG every 15–30 minutes in chest pain. A worsening ECG is more significant than a single abnormal tracing.
• GTN trial: If you are confident the patient has angina, give GTN spray or tablet sublingually and repeat the ECG. Improvement (normalisation of the ST segment) supports the diagnosis. Do not do this unless you are fairly sure of the diagnosis — GTN causes headaches and drops in blood pressure.
• T wave inversion requires 2 or more consecutive leads (not including aVR) to be significant. A single lead with T wave inversion is non-specific.
• Broad QRS complex: If the QRS is wide (>120 ms, more than 3 small squares), you cannot reliably interpret the ST segment. Bundle branch block — particularly left bundle branch block — completely invalidates standard ST segment interpretation. Fall back on the history and discuss urgently with a senior.

Bundle Branch Block

Left Bundle Branch Block (LBBB)

LBBB is identified by a wide QRS (>120 ms) with a broad, notched (W-shaped) QRS in V1 and a broad, notched (M-shaped) R wave in V6 — remembered by the mnemonic WiLLiaM (W in V1, M in V6 = LBBB). In the context of new chest pain, new LBBB should be treated as a STEMI equivalent — it indicates complete failure of the left bundle branch, which can occur because the LAD territory supplying the bundle is occluded. Activate the primary PCI pathway immediately.

Right Bundle Branch Block (RBBB)

RBBB shows a wide QRS with an RSR' pattern (rabbit ears) in V1 and a wide S wave in V6 — remembered by MaRRoW (M in V1, W in V6 = RBBB). RBBB may be a normal variant, may be seen in right heart strain (pulmonary embolism, pulmonary hypertension), or can follow a right-sided myocardial infarction.

Myocardial Infarction — Looking for ST Elevation

In acute myocardial infarction (AMI) — specifically a STEMI (ST-elevation myocardial infarction) — the ST segment rises above the baseline. This is called ST elevation and represents transmural (full-thickness) ischaemia of the myocardium in the territory supplied by the occluded coronary artery.

Important points before diagnosing STEMI

• ST elevation can occur anywhere in the heart and therefore in any leads of the ECG. Common locations: anteroseptal infarction (LAD territory) = ST elevation in V1–V4; inferior infarction (RCA territory) = ST elevation in II, III, aVF; lateral infarction (Cx territory) = ST elevation in I, aVL, V5, V6.
• Reciprocal changes: ST depression in the leads opposite to the territory of elevation is a very supportive finding — e.g., inferior STEMI (ST elevation II, III, aVF) with reciprocal ST depression in I and aVL.
• Significance thresholds: ST elevation is considered significant if it is ≥1 mm in limb leads or ≥2 mm in precordial leads (V1–V6) in 2 or more contiguous leads.
• Do not wait for the ECG to become "fully significant" before calling your senior. If you can see a trend of worsening changes with a compelling clinical picture — call urgently for advice.
• Ectopic beats: As with ischaemia, do not interpret lone ectopic complexes when the surrounding beats are normal.
• Broad QRS: Wide QRS makes ST elevation unreliable — new LBBB is treated as a STEMI equivalent regardless.

Evolution of STEMI changes

ECG changes in STEMI evolve over time in a characteristic sequence:

1. Hyperacute T waves — tall, broad, peaked T waves (very early, often missed)
2. ST elevation — the classic finding of acute occlusion
3. Development of Q waves — pathological Q waves (wider than 1 small square, deeper than 2 mm) represent established full-thickness infarction; they are usually permanent
4. T wave inversion — as the ST segment settles, T waves invert
5. Persistent Q waves with normalised ST and T waves — the appearance of an old MI

Pericarditis

Pericarditis (inflammation of the pericardial sac) can mimic STEMI on the ECG. Key differentiating features:

• ST elevation is saddle-shaped (concave upward, like a smile) rather than the convex (tombstone) elevation of STEMI
• ST elevation is present in all leads simultaneously (diffuse / global), not confined to a single coronary territory
• PR segment depression is a classic and relatively specific sign of pericarditis
• No reciprocal ST depression (unlike STEMI)

Common Patterns — Additional Recognition Points

Hyperkalaemia

Elevated serum potassium (hyperkalaemia) produces a characteristic sequence of ECG changes: tall, peaked, tented T waves (early); prolonged PR interval; widening of the QRS; eventually a sine wave pattern, and finally ventricular fibrillation. Any patient with suspected hyperkalaemia should have an urgent ECG and an immediate electrolyte result.

Hypokalaemia

Low serum potassium (hypokalaemia) causes: flattening and inversion of T waves, prominence of U waves (a positive deflection after the T wave, best seen in V2–V3), prolongation of the QU interval (which can be misread as QT prolongation). Hypokalaemia predisposes to ventricular arrhythmias.

Wolff-Parkinson-White (WPW) Syndrome

WPW is a pre-excitation syndrome caused by an accessory conduction pathway (Bundle of Kent) that bypasses the AV node. ECG shows: shortened PR interval (<120 ms); delta wave (a slurred upstroke to the QRS); wide QRS. Patients are at risk of rapid accessory pathway-mediated tachyarrhythmias and, rarely, sudden cardiac death via pre-excited AF.

Long QT Syndrome

A prolonged QT interval (corrected QTc >440 ms in men, >460 ms in women) predisposes to torsades de pointes — a polymorphic ventricular tachycardia that can degenerate into VF. Causes include congenital channelopathies, many drugs (antipsychotics, antiemetics, macrolide antibiotics, quinolones), electrolyte disturbances, and myocardial disease.