A very short guide to ECG interpretation

This is a very short guide to ECG interpretation. This article will focus on to quickly enable you to read ECG strips, and not an in-depth understanding of the ECG. It's targeted for the people who are new to ECG and are willing to make a jump-start at reading ECG before studying it further in more detail.

You can get the most out of this article if you have some idea about the anatomy and the physiology of the heart.

The article will start with a few basic things about ECG, and then proceed to a step by step guide to read and interpret an ECG strip.

The Basics

There are 4 basic things you need to know about to understand ECG—

The Leads

The leads collect electrical information from the skin of the subject. Usually ECG is done with 12 leads, of them 3 are limb leads, 3 are augmented limb leads and 6 are chest leads.

Einthoven's triangle
Figure: Direction of limb leads

Limb Leads

Lead nameLead position
Lead IRight Arm
Lead IILeft Arm
Lead IIILeft Foot

A neutral lead is also positioned at the right foot.

Augmented Limb Leads

  • Lead aVR
  • Lead aVL
  • Lead aVF

Chest Leads

Lead nameLead position
Lead V14th intercostal space, right side of sternum
Lead V22nd intercostal space, left side of sternum
Lead V3Midway between lead V2 and lead V4
Lead V45th intercostal space, mid-clavicular line
Lead V55th intercostal space, anterior-axillary line
Lead V65th intercostal space, mid-axillary line

Views of the Heart

There are four different views of heart that helps to identify the location of an abnormal reading.

Every view is best appreciated by a specific set of leads. They are also called lead groups

AnteriorV2, V3, V4
Left lateralI, aVL, V5, V6
InferiorII, III, aVF
Right ventricularaVR, V1
Lead angles
Figure: ECG lead angles

ECG strip

ECG strip is composed of 1 cm × 1 cm cells. Every line at the gap of such 5 cells (5 cm) is drawn in thick line.

ECG has a paper speed of 25 cm/second, so a small cell of ECG measures 0.04 second horizontally (so every large cell equals 0.2 second).

ECG strip plots voltage vertically. Each small cell represents 0.1 mV vertically (so every large cell equals 0.5 mV).

There are usually 12 plottings representing 12 leads and one long lead II for better inspection of the rate and rhythm.

Waves and intervals

Normally the heart is depolarized from SA node at the right atrium (depolarizing both atria) and after passing through AV node the depolarization continues to the ventricles (through Bundle of His and Purkinje fibers). The repolarization occurs in the same direction.

When a wave comes towards a lead, it registers a positive deflection (upward curve on paper) and when a wave goes away from it, it registers a negative deflection (downward curve on paper). When a wave travels parallel to a lead, it registers a biphasic curve.

An interval is the time between the start of the previous wave and the start of the following wave, whereas a segment is the time between the end of the previous wave and the start of the following wave.

The important waves and intervals and their relations to cardiac physiology is mentioned below.

ECG featurePhysiologyNormal duration
P waveAtrial depolarization< 0.08 second (2 small cells)
PR intervalAV nodal delay0.12 - 0.2 second (3 - 5 small cells)
QRS complexVentricular depolarization0.08 - 0.12 second (2 - 3 small cells)
ST segmentTime between ventricular depolarization and ventricular repolarization
T waveVentricular repolarization
ECG waves
Figure: ECG waves and intervals

The atrial depolarization coincides with ventricular repolarization, so it's hidden within the QRS complex and can't be detected.

Reading ECG

You can easily read ECG strip by following the 10 steps described below—

Heart Rate

The heart rate is best determined by looking at the long lead II. It can be calculated by the following procedure:

Find the R-R interval: First find two consecutive QRS complex. Now count the number of cells (small cell for precision or large cell for ease of calculation) between the tip of the two consecutive R waves.

`"Heart Rate" = 300 / "R-R interval in large cells"`


`"Heart Rate" = 1500 / "R-R interval in small cells"`

If you find bradycardia or tachycardia, the next thing to look for would be arrhythmias.


R-R interval
Figure: R-R interval

In this figure the R-R interval is 20 small cells or 4 large cells

So the heart rate is—
`1500 / 20 = 75 // "min"` or `300 / 4 = 75 // "min"`

Atrial Rate

Atrial rate is measured by the same method, except R-R interval is replaced by P-P interval.

`"Atrial Rate" = 300 / "P-P interval in large cells"`


`"Atrial Rate" = "1500" / "P-P interval in small cells"`

Cardiac Axis

Cardiac axis is the direction in which the depolarization wave travels within the cardiac electrophysiological circuit. Normally the axis is downwards and leftwards. We already know that if a wave is moving towards a lead it will show an upward curve (+), if away from it it will show a downward curve (-).

The most important leads to determine the cardiac axis is Lead I and Lead aVF. The following table illustrates it—

Lead ILead aVFAxis
(+)(-)Left axis deviation
(-)(+)Right axis deviation
(-)(-)Extreme right axis deviation

In case of axis deviation look for cardiac hypertrophy, conduction blocks.


Right axis deviation
Figure: Right axis deviation

In the above picture the lead I shows negative deflection and the lead aVF shows positive deflection. So it is a case of right axis deviation.

For more precise estimation of cardiac axis: Find the limb lead with the closest biphasic curve i.e. almost equal negative and positive deflection in QRS complex. The cardiac axis lies almost perpendicularly to this lead. For example in the above figure the most biphasic limb lead is aVR (-150°), so the cardiac axis lies close to either -60° or +120°. But since we already know that it is a right axis deviation from lead I (-ve) and aVF (+ve), we can conclude that the cardiac axis is close to +120°. (Note that normal cardiac axis may range from -30° to +90°)

Atrial axis: Cardiac axis and the ventricular axis is the same. Similarly an Atrial axis can be determined. It is done by the same method using P wave in lead I and aVF.


Most important intervals are PR interval, QT interval and the width of QRS complex. The normal values have already been discussed. Any shortening or lengthening of these values may be clinically significant.

  • Long PR interval: look for heart blocks.
  • Short PR interval: look for pre-excitation syndromes.
  • Long QT interval: investigate any predisposing factor as described later.
  • Wide QRS complex: look for ventricular arrhythmia, conduction blocks, WPW syndrome etc.


Atrial enlargement is identified by examining the P wave, whereas Ventricular hypertrophy is determined by the QRS complex.

Right Atrial Enlargement

Tall P wave with normal duration, best seen in the lead II. It is also known as P pulmonale.

P wave height is > 2.5 small cells in the inferior leads. Right axis deviation of the P wave may be present (-ve P wave in lead I, +ve P wave in lead aVF).

Right Atrial Enlargement
Figure: Right Atrial Enlargement, tall P wave in lead II.

Left Atrial Enlargement

Bifid or M shaped P wave in the lead II with prolonged duration, called P mitrale

Last part of P wave is > 1 small cell in duration. In V1 (biphasic P wave) the last part of P wave is > 1 small cell below iso-electric line.

P mitrale
Figure: P Mitrale in Left Atrial Enlargement, bifid P wave seen in lead II.

Right Ventricular Hypertrophy

  1. Right axis deviation.
  2. In V1: R wave > S wave and In V6: R wave < S wave.
Right Ventricular Hypertrophy
Figure: Right Ventricular Hypertrophy

Normally R wave gradually increases from V1 to V6, this is known as R wave progression. This pattern is disrupted in case of Right Ventricular Hypertrophy.

Left Ventricular Hypertrophy

  1. Left axis deviation.
  2. (R wave in V5 or V6) + (S wave in V1 or V2) > 35 small cells
Left Ventricular Hypertrophy
Figure: Left Ventricular Hypertrophy

Ventricular Strain Pattern is often seen in case of ventricular hypertrophies. They are characterized by—

  • Down sloping ST segment depression.
  • T wave inversion.

They appear in V1, V2 in Right ventricular hypertrophy and in I, aVL, V5, V6 in Left ventricular hypertrophy.


Cardiac rhythm is best ascertained by looking at the long lead II.

Arrhythmia can be classified under three broad groups. Exclude them one by one.

  1. Ventricular arrhythmia
  2. Supra-ventricular arrhythmia
  3. Conduction blocks

They are explained below along with their sub-types.

Ventricular Arrhythmia

Ventricular arrhythmia is identified by wide and bizarre shaped QRS complex.

They are of 4 types—

Premature Ventricular Contractions (PVC)

Appearance of wide and bizarre shaped QRS complex followed by a compensatory pause followed by normal resumption of beat. Usually they occur randomly but sometimes they may appear with alternate sinus beats regularly.

Figure: Premature Ventricular Contraction.

Accelerated Idioventricular Rhythm

Wide QRS complex without P wave. Heart rate is 50/min to 100/min (difference from VT, in which the rate is usually >120/min).

If the rate is below 50/min it is simply called Idioventricular Rhythm.

Ventricular Tachycardia (VT)

Consecutive appearance of wide and bizarre shaped QRS complex with a heart rate usually between 120/min 200/min. (By definition appearance of 3 or more PVC is called VT).

Ventricular Tachycardia
Figure: Ventricular Tachycardia, Lead II.

Torsades de pointes is a special type of ventricular tachycardia where the height of QRS complex varies periodically, so that it appears to rotate around an axis.

Ventricular Fibrillation (VF)

No identifiable QRS complex. The ECG tracing shows random deflections.

Ventricular Fibrillation
Figure: Ventricular Fibrillation, Lead II.

Supra-ventricular Arrhythmia

Supra-ventricular arrhythmia is differentiated from ventricular arrhythmia by presence of narrow QRS complex with normal morphology.

Sinus Tachycardia / Bradycardia
  • Normal sinus rhythm.
  • Tachycardia: Heart rate > 100.
  • Bradycardia: Heart rate < 60.
Paroxysmal Supra-Ventricular Tachycardia (PSVT)
  • No visible P wave. (Retrograde P wave is present, but they are usually buried within QRS complex, hence not visible.)
  • Rhythm regular.
  • Heart rate: 150/min - 250/min.
Figure: Paroxysmal Supra-ventricular Tachycardia.

Atrial Flutter
  • Saw-tooth shaped P waves.
  • Rhythm regular.
  • Atrial rate: 250/min - 350/min.
  • Heart rate is lower due to AV block. Atrial rate:Heart rate is 2:1, 3:1, 4:1 etc.
Atrial Flutter
Figure: Atrial Flutter.

Atrial Fibrillation
  • P waves appear as an undulating baseline.
  • Rhythm irregular.
  • Atrial rate: 350/min - 500/min.
  • Heart rate is variable.
Atrial Fibrillation
Figure: Atrial Fibrillation.

Multi-focal Atrial Tachycardia (MAT)
  • At least 3 different morphology of P wave present.
  • Rhythm irregular
  • Heart rate: 100/min - 200/min
Paroxysmal Atrial Tachycardia (PAT)
  • Similar to PSVT.
  • Differentiated by carotid massage. Carotid massage terminates PSVT but PAT remains unaffected.
  • On ECG PAT may show warm-up period (when the heart rate gradually increases) or cool-down period (when heart rate gradually decreases). No such feature present in PSVT.

Conduction blocks

They are of three main types, AV block, Bundle branch block and hemiblock.

AV block (Heart Block)
First degree AV block

Identification: Only PR interval is increased. No change in P wave or QRS complex.

Cause: Increased conduction delay in AV node.

Second degree AV block

Identification: Ratio of P:QRS is more than 1. E.g. 4:3, 3:2 etc.

Cause: In 2° AV block some of the P waves fail to pass through the AV node. The failed P waves doesn't give rise to any QRS complex causing this altered ratio.

Types: In addition to the above feature the PR interval may show some changes.

Most commonly PR interval gradually increases in each cycle, followed by a drop of QRS complex, then the PR interval resets to initial short length and again prolongs with each cycle. This type of AV block is known as Mobitz type I.

Less commonly the PR interval remains fixed and only drop of QRS complex is observed. This is known as Mobitz type II.

2° AV block
Figure: Second degree AV block with 4:3 block.

Third degree AV block

Identification: Complete dissociation of P and QRS, there is no correlation between them. P wave and QRS complex occurs at different rates.

Cause: No impulse can pass through the AV node. P wave appears at sinus rhythm and QRS complex at junctional rhythm.

Bundle branch block

It has two types, Right and Left. Both causes widening of the QRS complex. There is also a RSR' pattern (upstroke, down-stroke and upstroke again. Looks like a rabbit's ear) in the QRS complex. In RBBB RSR' appears in the right sided leads i.e. V1, V2 whereas in LBBB RSR' is present in left sided leads i.e. V5, V6, I, aVL.

Right Bundle Branch Block (RBBB)
  1. Wide QRS complex
  2. RSR' pattern in V1, V2
  3. Reciprocal changes in V5, V6, I, aVL
Left Bundle Branch Block (LBBB)
  1. Wide QRS complex
  2. RSR' pattern in V5, V6, I, aVL
  3. Reciprocal changes in V1, V2
Right bundle branch block
Figure: Right Bundle Branch Block. (RSR' pattern in both V1 & V2 and also in V3)


Hemiblock is of two types, Left Anterior and Left Posterior. In both cases QRS complex is NOT widened (difference with Bundle branch block). But both types are associated with axis deviation.

Left Anterior Hemiblock

Left axis deviation without any other cause.

Left Posterior Hemiblock

Right axis deviation without any other cause.

Mnemonic: RIP (Right is Posterior)

Bifascicular block

Right bundle branch block and hemiblock can occur at the same time, it is known as bifascicular block.

It is characterized by presence of features of both RBBB and hemiblock at the same time. Such as:

RBBB with Left Anterior hemiblock = (Wide QRS + RSR' in V1, V2) + (Left Axis Deviation)

RBBB with Left Posterior hemiblock = (Wide QRS + RSR' in V1, V2) + (Right Axis Deviation)

Figure: Right Bundle Branch Block with Left Anterior Hemiblock. Note the notched R wave in V2 and the left axis deviation.

Summary of Arrhythmia

  • First check QRS complex.
  • If QRS complex is wide then look for ventricular arrhythmia.
  • If QRS complex is narrow then look for supra-ventricular arrhythmia
  • At last check if there is any conduction block present.

Pre-excitation Syndrome

Pre-excitation syndrome occurs when the impulse from SA node bypasses the AV nodal delay through an abnormal pathway and reaches the ventricles too early. They are identified by short PR interval. There are two common types—

Wolff-Parkinson-White Syndrome (WPW)

  1. Short PR interval.
  2. Wide QRS complex (difference from LGL syndrome).
  3. Sometimes delta waves may be seen, characterized by a slurred upstroke of the QRS complex.
Delta wave in WPW syndrome
Figure: WPW syndrome showing short PR interval, wide QRS complex and Delta wave.

Lown-Ganong-Levine Syndrome (LGL)

  1. Short PR interval.
  2. Normal QRS complex.
  3. No delta wave.

Pre-excitation syndrome often causes arrhythmias, most commonly PSVT and Atrial fibrillation.

Coronary Artery Disease

Myocardial Infarction

Myocardial infarction has different ECG pattern for three different stages of evolution.

Hyper-acute Myocardial Infarction
  • ST segment elevation.
  • Tall T wave.
Fully evolved Myocardial Infarction
  • Appearance of Q waves.
  • Elevated ST segment.
  • T wave inversion.
Old Myocardial Infarction

All other features disappear except for the persistent Q wave.

Reciprocal Changes

These changes appear in the leads at the opposite side of the leads showing features of MI, i.e if lead I shows MI changes, lead aVR may show the reciprocal changes. Reciprocal changes include—

  1. ST segment depression. (reciprocal to ST elevation)
  2. Tall R wave. (reciprocal to deep Q wave)
Localizing the lesion

The ECG changes appear in the leads overlying the position of the lesion, whereas leads in opposite side shows reciprocal changes.

Depending on the leads showing the changes, the site of lesion can be determined as follows—

MI changes in lead Reciprocal changes in lead Site of lesion Vessel commonly involved
I, aVL, V5, V6 (Left lateral leads) aVR, V1 (Right ventricular leads) Left lateral wall of the heart Left circumflex coronary artery
aVR, V1 (Right ventricular leads) I, aVL, V5, V6 (Left lateral leads) Right ventricle of the heart Right coronary artery
II, III, aVF (Inferior leads) - Inferior wall of the heart Right coronary artery
V2, V3, V4 (Anterior leads) - Anterior wall of the heart Left Anterior Descending Artery
- V2, V3, V4 (Anterior leads) Posterior wall of the heart Right coronary artery
Myocardial Infarction
Figure: Inferior wall and right ventricular myocardial infarction.

Not all myocardial infarction causes ST segment elevation. Depending on which they are divided into two types—

  1. ST segment elevated Myocardial Infarction (STEMI)
  2. Non ST segment elevated Myocardial Infarction (NSTEMI)


  1. ST segment elevation over affected area.
  2. Reciprocal changes in opposite leads i.e. ST segment depression.
  3. T wave inversion

Other common conditions causing ECG changes


Hyperkalemia produces different changes with increasing levels of serum potassium.

  1. Initially Tall peaked T wave.
    (Difference with MI: in Myocardial Infarction T wave changes occur only in the leads overlying the lesion, but in hyperkalemia the changes are diffuse)
  2. With further increase, P-R interval prolongs.
    T waves flattens and then disappears.
  3. Ultimately, QRS complex widens and merge with T wave to form sine wave pattern.
    Ventricular fibrillation may develop.


  1. ST segment depression.
  2. T wave flattening.
  3. Appearance of U wave


Short QT interval


Prolonged QT interval


  1. Sinus bradycardia.
  2. ST segment elevation with an abrupt up-slope followed by an abrupt down-slope. It is known as Osborn wave.
  3. Various arrhythmias.
  4. Muscle tremor artifact. (Not to be confused with atrial flutter)


  1. Digitalis

    Therapeutic level of Digitalis may produce ST elevation and T inversion.

    Digitalis Toxicity may cause sinus node suppression, conduction blocks and/or tachy-arrhythmias.

  2. Drugs causing QT prolongation

    Anti-arrhythmic drugs like quinidine, procainamide, amiodarone etc.

    Other drugs include tricyclic anti-depressants, erythromycin, quinolone etc.

    Prolong QT predisposes to arrhythmias. For more precise measurement QTc or corrected QT is used.


ST elevation and T inversion. Changes appear diffusely in many leads (difference from MI).

In large effusion heart rotates freely causing variable voltage of QRS complex.

Hypertrophic Obstructive Cardiomyopathy

Left ventricular hypertrophy may be present. Q wave may be seen in lateral and inferior leads.


Conduction blocks may be present.

Chronic Obstructive Pulmonary Disease

  1. Low voltage ECG.
  2. Right axis deviation.
  3. Right atrial enlargement (P pulmonale) and right ventricular hypertrophy may be present.

Pulmonary Embolism

  1. Right ventricular hypertrophy.
  2. S1Q3 pattern: Large S wave in lead I and deep Q wave in lead III.
  3. Arrhythmias may be present.

Cerebrovascular accident

  1. T wave inversion.
  2. Prominent U wave.


We have discussed the ECG interpretation in short. While it's a good way to get started with ECG, it's still a good idea to go through a standard book to understand ECG in a more detailed level.



Copyright © 2012-2024 Dr. Agnibho Mondal
E-mail: mondal@agnibho.com