ECG Interpretation: A Reasoning-Based Revision Guide 🫀

Interpreting an ECG isn’t just about spotting abnormalities — it’s about understanding the heart’s electrical story in the context of the patient. This guide breaks down the process step by step. 

If you need a reminder of the electrophysiology of the heart you can find that here 

🎯 Step 1: Check the Rate

Heart rate reflects autonomic tone, metabolic demand, and cardiac output. Tachycardia may be compensatory (e.g., fever, hypovolemia) or pathological (e.g., SVT). Bradycardia may be physiological (e.g., athletes) or due to conduction disease or drug effects.

How to calculate:

• 300 Rule (regular rhythm): Count large squares between R waves → 300 ÷ squares = bpm
• 6-Second Rule (irregular rhythm): Count R waves in 6 seconds (30 large squares) → multiply by 10

Examples

Here's an example ECG - lets calculate the rate 

✅ 1. 300 Rule (for regular rhythms)

• Step 1: Choose two consecutive R waves in a lead with clear definition — Lead II works well here.
• Step 2: Count the number of large squares between them → In this ECG, there are between 2 and 2.5 large squares between R waves.
• Step 3: Apply the formula: →  300 ÷ 2.5 = 120 bpm or → 300 ÷ 2 = 150 bpm
• Therefore, rate is between 120–150 bpm

The rhythm is regular, so the 300 Rule gives a reliable estimate. Each large square represents 0.2 seconds, and 300 large squares fit into one minute — hence the shortcut.

✅ 2. 6-Second Rule (for irregular rhythms or confirmation)

• Step 1: Identify a 6-second strip — this is 30 large squares.
• Step 2: Count the number of R waves within that strip → In this ECG, there are 13 R waves in 6 seconds.
• Step 3: Multiply by 10: → 13 × 10 = 130 bpm

This method averages the rate over time and is especially useful when the rhythm is irregular — though in this case, it confirms the regular rhythm calculation.

Heart rate = ~130 bpm, consistent across both methods.

Lets try again?

✅ 300 Rule:

• In Lead II, the R–R interval spans ~6.5 large squares.
• So: → 300 ÷ 6.5 ≈ 46 bpm

✅  6-Second Rule:

• Count the number of R waves in 30 large squares.
• There are 4–5 R waves.
• So: → 4 × 10 = 40 bpm → 5 × 10 = 50 bpm

Final rate: ~46 bpm

🎯 Step 2: Assess the Rhythm

Rhythm reveals whether the pacemaker is functioning and conduction is coordinated.

Look for:

• Regular rhythm with P before every QRS: Sinus rhythm — SA node pacing.
• Irregular rhythm:
• Irregularly irregular: Atrial fibrillation — chaotic atrial activity.
• Regularly irregular: May suggest second-degree AV block or grouped ectopics.

Example

✅ Rhythm analysis

• The R–R intervals are consistent across the strip.
• This is a regular rhythm.
• There is a P before every QRS 
• This is normal sinus rhythm

Example

✅ Rhythm analysis

• The R–R intervals are inconsistent across the strip.
• This is an irregularly irregular rhythm.
• There are no distinct P waves
• “Quivering” baseline between QRS complexes — fibrillatory waves (‘f’ waves) — replace normal isoelectric intervals.
• This is atrial fibrillation

Example

✅ Rhythm analysis

• The R–R intervals are not equal, but they change in a repeating, predictable pattern.
• This is a regularly irregular rhythm.
• You can see a grouped beating pattern — several normal beats followed by a dropped QRS complex, then the cycle repeats.
• There is a P wave before every QRS until one P wave fails to conduct — i.e. a P wave not followed by a QRS complex. The PR interval progressively lengthens with each consecutive beat until a QRS is dropped. After the dropped beat, the PR interval resets (shortens again) and the cycle repeats.
• This is a second degree heart block - Mobitz I  which is usually due to AV nodal conduction delay (often benign).

🎯 Step 3: Analyze the P Wave

The P wave represents atrial depolarization — the SA node firing and atrial contraction.

Clues:

• Upright in II, III, aVF: Normal atrial vector.
• Absent P waves: AF, sinoatrial block, junctional rhythm.
• Peaked P waves: Right atrial enlargement (e.g., pulmonary hypertension).
• Bifid P waves (P mitrale): Left atrial enlargement (e.g., mitral stenosis)

Example

• Leads II, III, and aVF: Tall, peaked P waves, typically >2.5 mm in amplitude.
• Leads V1–V2: Prominent, upright P waves.
• Lead I: Usually normal or smaller amplitude (since the depolarisation vector is directed inferiorly and rightward).
• In right atrial enlargement, the right atrium contributes a larger depolarisation vector, which moves more vertically and rightward.
• This increases the amplitude of the initial part of the P wave — the “peaked” portion — without broadening it.
• The total P-wave duration remains normal (<120 ms) because atrial conduction time isn’t prolonged, only the right atrial mass and voltage are increased.

Example

• In lead I, the P waves are broad (>120 ms) and notched, forming a small “M”-shaped appearance — the so-called “P mitrale.”
• In lead V1, the P wave is biphasic — a small initial positive deflection followed by a deep and wide negative terminal component.
• A bifid (M-shaped) P wave indicates left atrial enlargement 
• The first hump = right atrial depolarisation.
• The second hump = delayed left atrial depolarisation.
• Because the left atrium is enlarged, depolarisation takes longer and creates that “double peak.”
• The P-wave shape depends on the direction of atrial depolarisation relative to each lead’s axis.

🎯 Step 4: Look at the PR Interval

Reflects AV nodal conduction time.

Interpretation:

• Normal: 0.12–0.20 sec
• Prolonged PR: First-degree AV block — delayed conduction.
• Short PR: Pre-excitation (e.g., WPW) — accessory pathway bypasses AV node.

Example

• The PR interval is the time from the start of the P wave to the start of the QRS complex.
• Normal PR = 120–200 ms (3–5 small squares).
• In this ECG, the PR interval is clearly prolonged — approximately 240 ms (6 small squares) in multiple leads (e.g. lead II and V1)→ This confirms a first-degree AV block.
• Caused by delayed conduction through the AV node.
• Common benign finding, but can also reflect:
• High vagal tone (e.g. in athletes)
• Drugs: beta-blockers, calcium channel blockers, digoxin
• Myocarditis or ischaemia affecting the AV node
• Degenerative conduction disease in older adults

🎯 Step 5: Examine the QRS Complex

Ventricular depolarization — impulse through His-Purkinje system.

Duration:

• Normal: <0.12 sec
• Wide QRS: Bundle branch block or ventricular origin.

Morphology clues:

• RSR’ in V1: Right bundle branch block.
• Broad R in V6, deep S in V1: Left bundle branch block.

Example

Left bundle branch block

In V1 (right precordial lead)

• You see a deep, broad, and entirely negative QS or rS complex — no initial R wave.
• This is the classic finding in LBBB, because depolarisation of the right ventricle occurs late, moving away from V1.

In V6 (left lateral lead)

• There is a broad, tall, notched (“M-shaped”) R wave.
• No Q wave is present.
• This reflects delayed left ventricular activation and is another hallmark of LBBB.

Example

Right bundle branch block

In V1–V3 (right precordial leads):

• You can clearly see an rSR′ pattern — a small initial R wave, a deep S wave, and then a tall, broad terminal R′ (the second upward deflection).
• This gives the classic “M-shaped” or rabbit ears appearance in V1–V2.
• The terminal R′ represents delayed right ventricular depolarisation.

In lateral leads (I, V5, V6):

• There is a broad, slurred S wave.
• The terminal portion of the QRS is directed rightward and inferiorly, producing that wide S wave

You can see discordant T-wave inversions and ST depression in the right precordial leads (V1–V3). These are secondary repolarisation changes associated with RBBB — not ischaemic in themselves.

🎯 Step 6: Check the ST Segment

Reflects the plateau phase of ventricular repolarization — should be isoelectric.

Changes:

• ST elevation: STEMI (transmural infarction), pericarditis (diffuse elevation + PR depression).
• ST depression: Subendocardial ischemia, reciprocal changes, digoxin effect

Example

Marked ST elevation is present in:

• V1–V4 (anterior leads)
• V6 and I, aVL (lateral leads)

The ST elevation is convex (“tombstone”) in shape, and merges with tall peaked T waves — classic for acute transmural injury.

Reciprocal ST depression can be seen in inferior leads (III, aVF).

Distribution: 

Anterior + lateral = anterolateral MI.

This suggests occlusion of the left anterior descending (LAD) artery — possibly extending to diagonal or circumflex branches if lateral involvement is prominent.

Evolutionary features

• Hyperacute T waves in V2–V4 — broad-based and tall.
• Loss of R-wave height in anterior precordial leads — early sign of necrosis.
• ST elevation continuous across anterior and lateral leads without interruption.

Example

ST elevation:

• Leads II, III, and aVF show marked ST elevation with convex (“tombstone”) morphology → consistent with inferior wall infarction.
• Lead III shows the greatest elevation, which is a useful clue.

Reciprocal ST depression:

• Leads I and aVL show reciprocal ST depression, confirming this is a true STEMI pattern (not early repolarisation or pericarditis).

Acute inferior STEMI due to RCA occlusion

❤️ ST Elevation in STEMI

When an area of myocardium becomes ischaemic:

• The affected cells cannot maintain their resting potential because of ATP depletion.
• Na⁺/K⁺-ATPase pumps fail → extracellular K⁺ increases and intracellular Na⁺ and H⁺ accumulate.
• The ischaemic cells therefore become partially depolarised compared to normal myocardium.

This difference in resting membrane potential creates a “current of injury” between normal and ischaemic zones.

The current of injury alters the baseline electrical potential:

• During diastole (rest phase): the injured region is less negative, so the ECG baseline (TP segment) shifts downward relative to the uninjured tissue.
• During systole (plateau phase): both normal and ischaemic regions are depolarised, but because of the baseline shift, the ST segment appears elevated relative to the ECG baseline.

In reality, the potential difference during diastole causes the apparent ST elevation — the actual action potential of the injured cells is lower and shorter.

• Transmural (full-thickness) ischaemia: ST elevation because the current of injury is directed outward (toward the chest electrodes).
• Subendocardial (partial-thickness) ischaemia: ST depression because the current of injury is directed inward (away from surface electrodes).

The leads facing the injured wall record ST elevation because the injury current is directed toward them.
The reciprocal leads (opposite wall) record ST depression, as the current vector points away.

• Inferior STEMI: elevation in II, III, aVF; reciprocal depression in I, aVL.
• Anterior STEMI: elevation in V1–V6; reciprocal depression in inferior leads.

🎯 Step 7: Evaluate the T Wave

Ventricular repolarization — a vulnerable phase for arrhythmias.

Clues:

• Inverted T waves: Ischemia, CNS events, ventricular strain.
• Hyperacute T waves: Early STEMI.
• Tall, peaked T waves: Hyperkalemia.

Example

The T waves are tall, narrow, and symmetrical, especially in the precordial leads V2–V5.

• They rise sharply and fall steeply — the classic “tented” shape.
• The base of the T wave is narrow, unlike the broad-based T waves seen in early ischaemia or hyperacute infarction.
• The QRS complexes are still narrow and the P waves are visible, suggesting this is early or moderate hyperkalaemia (before severe conduction effects develop).

Potassium plays a key role in setting the resting membrane potential of cardiac myocytes.

When extracellular potassium concentration rises:

1. The resting membrane potential becomes less negative (depolarised).
2. Phase 3 repolarisation (mediated by potassium efflux) occurs more rapidly.
3. This produces taller and narrower T waves because repolarisation happens faster and more synchronously across the ventricular myocardium.

As hyperkalaemia progresses, other ECG changes appear:

Severity	Typical ECG features
Mild (5.5–6.5 mmol/L)	Tall, peaked T waves; normal QRS
Moderate (6.5–7.5 mmol/L)	Widened QRS, prolonged PR, flattened P waves
Severe (>7.5 mmol/L)	Loss of P waves, sine-wave pattern, ventricular arrhythmia, asystole

🎯 Step 8: QT Interval

Why it matters: Reflects total ventricular activity — depolarization + repolarization.

Prolonged QT:

• Risk of Torsades de Pointes — polymorphic VT.
• Causes: drugs (antiarrhythmics, antipsychotics), electrolyte disturbances, congenital syndromes.

Example

The QT interval (beginning of QRS to end of T wave) is clearly prolonged — it spans nearly half or more of the R–R interval.

A quick rule of thumb:

• If the QT interval is more than half the R–R distance → it’s prolonged.

T wave morphology

• Broad, flattened T waves and possibly notched or late-peaking T waves can be seen, depending on the underlying cause.

• In some leads (especially V2–V5), there’s prolonged repolarisation with delayed return to baseline — typical of long QT states.

The QT interval represents the total time for ventricular depolarisation and repolarisation.

When this interval is prolonged, it reflects delayed ventricular repolarisation, which can create electrical instability and a substrate for torsades de pointes.

👉 Additional Tips for ECG Interpretation

🎯 Axis Matters

• Normal axis: -30° to +90°
• Left axis deviation: LVH, left anterior fascicular block, inferior MI.
• Right axis deviation: RVH, pulmonary embolism, lateral MI, congenital heart disease.

🎯 Look for Artifacts

• Artifacts can mimic pathology — always correlate with clinical context.
• Examples: Tremor, loose leads, electrical interference.

🎯 Don’t Miss the P Waves

• Absent P waves: AF, flutter (sawtooth), junctional rhythm.
• Inverted P waves: Retrograde atrial activation — AV or junctional origin.

🎯 ST Segment Changes

• ST elevation in ≥2 contiguous leads: STEMI — urgent reperfusion needed.
• ST depression: Ischemia, reciprocal changes, digoxin effect

🎯 Bundle Branch Blocks

• RBBB: RSR’ in V1 (“bunny ears”), wide S in lateral leads.
• LBBB: Broad R in I, V6; deep S in V1 — can mask ischemia.

🧠 Remember

When you interpret an ECG, don’t just tick boxes — ask yourself:

• What’s the underlying physiology?
• What’s the clinical context?
• Could this be a normal variant?
• What’s the risk if I miss this?