Electrocardiography – Basic Principles and Interpretations


Dr Felix James

Electrocardiography is concerned with the recording and analysis of the electrical activity of the heart. The instrument used for recording the electrical activity is a sophisticated galvanometer called as electrocardiograph. The graphic record is called as the electrocardiogram (ECG)

The first ECG was obtained by Wallen in 1887 with the help of a capillary electrometer. Einthoven in 1903 introduced the string galvanometer for recording ECG, which was largely supplanted by vacuum tube amplifier driven oscillograph n 1930s. Cathode ray oscilloscopes are presently being used in ECG monitors for continuous visual display of ECG.

Elementary Electrophysiology:
In a healthy resting muscle cell, certain molecules dissociate into positive and negative ions. The positively charged ions are on the outer surface and the negatively charged ions on the inner surface of the cell membrane. The positive charges are exactly equal in number to the negative charges. When this occurs the cell is in a state of electrical balance and is said to be POLARIZED.

When two electrical charges of equal and opposite directio are juxtaposed on either side of a membrane they constitute a dipole. When two charged ions of equal and opposite direction are situated next to each other on the surface of an excitable tissue, they constitue a doublet.

When the cell is stimulated or injured, the negative ions migrate to the outer surface of the cell and the positive charges pass into the cell i.e. the polarity is reversed. This process is termed as DEPOLARISATION. With recovery, positive charges migrate into the cell. This process is termed REPOLARISATION, i.e. the polarity or the electrical balance of the cell is reestablished.

The chief extra cellular cation (+) is sodium and the chief intracellular cation is potassium. Potassium and Calcium ions and to a less extend the sodium ions have influence in the contractility and excitability of the heart muscles. Depolarization wave in myocardial cells and cells of Purkinge system is brought about by fast inward movement of sodium where as in the SA node and proximal region of AV node it is brought about by slow inward movement of Calcium.
Injured cells emit a continous negative charge to and electrode oriented to its surface.

Measurement of the electrical activity:
The instrument:
Electrocardiograph is a sophisticated galvanometer, a sensitive electromagnet, which can detect and record changes in electromagnetic potential. It has a positive pole and a negative pole. The wire extensions from these poles have electrodes at each end; a positive electrode at the end of the extension from the positive pole, and a negative electrode at the end of the extension from the negative pole. The paired electrodes together constitute a electrocardiographic lead.

The record:
The record is called as Electrocardiogram. It is a paper that is divided into smaller and larger squares, which are formed by fainter and darker lines respectively. The squares form a grid which facilitates the measurement of
1. Time parameter (horizontal measurement)

2. Deflexion amplitudes (vertical measurement)
The distance between the fainter lines is 1mm and the distance between two darker lines is 5mm. Conventionally ECG is recorded at the speed of 25mm per second.

The method:
electrical field of the heart

The heart is situated at the centre of the electrical field which it generates. The electrical intensity recorded by an electrode diminishes rapidly when the electrode is moved a short distance from the heart, and less and less as the electrode is moved still further away from the heart. With distances greater than 15 cm from the heart the decrement is hardly noticeable, so all the leads placed at a distance greater than 15 cm are considered to be equidistant from the heart.

Electocardiographic leads (conventional)
There are 12 conventional lead which may be physiologically divided into 2 groups:
1. The frontal plane leads: These are oriented to the frontal or coronal plane of the body. The standard leads I,II,III and leads AVR, AVL AND AVF belongs to this category

2. The horizontal plane leads: these are oriented in the transverse or horizontal plane of the body and are formed by the precordial leads- leads V1 to V6.

1. Frontal plane leads:
Einthoven deliberately placed the electrodes of the three standard limbs as far as away from the heart as possible i.e. on the right arm, left arm and left leg. These three electrodes thus electrically equidistant from the heart.

The leads derived from these three electrodes are:
1. Standard lead I: negative electrode on the right arm and positive electrode on left arm
2. Standard lead II: negative electrode on the right arm and the positive electrode on the left foot
3. Standard lead III: negative electrode on the left arm and the positive electrode on the left foot.
The three lead axis forms an equilateral triangle called as the Einthoven’s triangle.

Unipolar limb leads
The electrode of a unipolar lead constitutes the exploring electrode which is the positive electrode of the lead. The negative electrode is so constructed that it is considered to be at zero potential. All unipolar leads are termed V leads. Extremity leads are of low electrical potential and are therefore instrumentally augmented. These augmented extremity leads are thus prefixed by the letter “A”.

1. Lead AVR is the augmented unipolar right arm lead
2. Lead AVL is the augmented unipolar left arm lead
3. Lead AVF is the augmented unipolar left leg lead

The horizontal plane leads:
They are designated by the alphabet ‘V’. There are 6 chest leads (V1 to V6)

1. Lead V1 is placed over the fourth intercostal space immediately to the right of the sternum.
2. Lead V2 is placed over the fourth intercostal space immediately to the left of the sternum.
Please note that the next electrode to be placed is V4
3. Lead V4 is placed over the fifth intercostal space in the mid clavicular line
4. Lead V3 is placed on the chest exactly midway between the lead V2 and V4 electrode positions
5. Lead V5 is placed at the same horizontal level as lead V4 on the anterior axillary line
6. Lead V6 is placed at the same horizontal level as leads V4 and B5 on the mid axillary line

The basic electrocardiographic deflexions
Electrocardiology is based on one essential and fundamental principle, which can be succinctly reflected by two statements

1. When an electromagnetic force (current, vector, activation front, depolarization front) flows, or is directed, towards the positive electrode of a lead, the electrocardiograph will record an upward or positive deflexion.
2. When an electromagnetic force flows, or is directed, away, from the positive electrode of a lead and thus towards the negative electrode of the lead, the electrocardiograph will record a downward or negative deflexion.
Galvanometer writing on paper in zero position; paper moving from left to right.
Representation of vector principle

It is the deflection produced by atrial depolarization. It is the sum of the right and the left atrial activation, the right preceding the left because SA node is located in the right atrium.

1. It is upright in most of the leads except lead AVR. It is best seen in leads L2 and V1. In lead V1 , the P wave is generally biphasic with a small terminal negative deflection produced by atrial activation.
2. The P wave normally does not exceed 0.11 sec in duration or width. The P wave notch is not easily visible.
3. The P wave amplitude or height does not exceed 2.5mm normally
4. The normal P wave axis is in the range of +40 degrees to +60 degrees.

The major positive deflection, from the beginning of the Q wave (or the R wave if no Q wave is visible) to the termination of the S wave is known as the QRS complex. It represents the sequence, time and synchronization of total ventricular muscle depolarization. It is upright in most leads except aVR.

1. The normal duration on the horizontal axis is .04 to .08sec.
2. The amplitude in the limb leads except aVR should be at least 5mm
S wave is prominent in the right-sided chest leads and R is prominent in the left-sided chest leads. The amplitude of R wave should exceed in the left sided chest leads.
3. The ventricular activation time (V.A.T) should not exceed 0.035 sec in leads V1, V2 and should not exceed 0.055 sec in leads V5 and V6

The Q wave is the initial negative deflection of the QRS complex, which precedes the first positive deflection, the R wave.

1. They represent septal activation from left to right. It may be observed in the following leads – L1, aVL, V5-V6 with a horizontal heart position. In L2, L3 and aVF with a vertical heart position.

T Wave
The T wave is a deflection following the QRS complex. It is produced by ventricular depolarization. The normal T wave is upright in most leads except aVR, and taller in lead V6 than V1

U Wave
The U wave is a small positive deflection after the T wave produced by slow and late repolarization of the ventricular Purkinje fibers. It is best appreciated in the precordial transition zone V2 to V4, during a slow rhythm and when the Q-T interval is short in which case it is clearly separable from the T wave.

P – R Segment
It is the portion tracing form the end of the P wave to the onset of the QRS complex. The P-R segment is at the same level as the S-T segment, which is the isoelectric line.

S – T Segment
It is the portion tracing from the J point (termination of S wave) to the onset of the T wave. Normally it is in the isoelectric line at the same level as P-R segment.

P – R Interval
The interval between beginning of P wave and the onset of the QRS complex, irrespective of whether it begins with a Q wave or R wave. The normal P-R interval is in the range 0.12 –0.20 sec.

Q – T Interval
It is the interval between the onset of Q wave and the end of the T wave duration represents ventricular repolarization time. It measures the total duration of electrical activity of the ventricles.

The electrocardiograph is conventionally standardized so that one millivolt will result in 10mm vertical deflexion.

The Electrical Axis
The interpretation of the ECG deflexions in terms of axis direction and deviation constitute a most important diagnostic aid to the accurate and deductive evaluation of electrocardiogram. ECG interpretation is then removed from the realm of pure empiricism and becomes elevated to a logical and deductive discipline.

Using leads I and aVF the axis can be calculated to within one of the four quadrants at a glance.
If the axis is in the “left” quadrant take your second glance at lead II.

  • both I and aVF +ve = normal axis
  • both I and aVF -ve = axis in the Northwest Territory
  • lead I -ve and aVF +ve = right axis deviation
  • lead I +ve and aVF -ve
  • lead II +ve = normal axis
  • lead II -ve = left axis deviation

Causes of a Northwest axis (no man’s land)
a. Emphysema
b. Hyperkalemia
c. Lead transposition
d. Artificial cardiac pacing
e. Ventricular tachycardia

Causes of right axis deviation
a. Normal finding in children and tall thin adults
b. Right ventricular hypertrophy
c. Chronic lung disease even without pulmonary hypertension
d. Anterolateral myocardial infarction
e. Left posterior hemiblock
f. Pulmonary embolus
g. Wolff-Parkinson-White syndrome – left sided accessory pathway
h. Atrial septal defect
i. Ventricular septal defect

Causes of left axis deviation
a. Left anterior hemiblock
b. Q waves of inferior myocardial infarction
c. Artificial cardiac pacing
d. Emphysema
e. Hyperkalaemia
f. Wolff-Parkinson-White syndrome – right sided accessory pathway
g. Tricuspid atresia
h. Ostium primum ASD
i. Injection of contrast into left coronary artery

Causes of abnormal waves
1. Tall P wave: The P wave exceeding 2.5mm in height are seen in
a. Right atrial hypertrophy
b. Hypokalemia
2. Wide P wave: P waves exceeding 0.11 seconds in width are observed in
a. Left atrial hypertrophy
b. Hyperkalemia
3. Inverted P wave:
a. Occurs in nodal rhythm (impulses of AV nodal origin),
b. Impulses of ventricular origin,
c. Impulses bypass to SA node after activating AV node (WPW syndrome)
4. Absent P Wave
a. Atrial fibrillation
b. AV nodal rhythm
c. Ventricular tachycardia
d. Hyperkalemia
e. SA block
5. Abnormal P wave axis
a. With right atrial hypertrophy, the axis is +60 degrees to +90 degrees
b. With left atrial hypertrophy, the axis is –30 degrees to +40 degrees
6. Change in P wave morphology
a. P-pulmonale is common in pulmonary hypertension
b. P-mitrale seen in left atrial hypertrophy

QRS complex abnormalities
1. Wide QRS complex: The normal QRS width is 0.04 to 0.08sec
a. Interventricular conduction defect or hemi block
b. Left ventricular hypertrophy
c. Myocardial infarction
d. Incomplete bundle branch block
e. WPW syndrome

2. Abnormal QRS Amplitude
a. Tall R wave in lead V1
i. Right ventricular hypertrophy
ii. Right bundle branch block
iii. WPW syndrome type A
iv. Persistent juvenile pattern of right ventricular dominance
v. Mirror image dextocardia
vi. Duchenne’s muscular dystrophy with cardiomyopathy
vii. Hypertrophic obstructive cardiomyopathy
viii. Left ventricular extra systole
ix. Posterior wall myocardial infarction

b. Tall R wave in lead V6
i. Left ventricular systolic overload
ii. Left ventricular diastolic overload
iii. Left bundle branch block
c. Deep S wave in lead V1 (rS pattern): The normal S wave in V1 does not exceed 2.5 mV. Deep S waves in V1 with tall R waves in lead V6 is a feature of left ventricular hypertrophy.
d. Deep S wave (rS pattern) in lead V6:

The normal S wave voltage in V6 does not exceed 0.7mV and the R wave is generally taller than the S wave. A deep S wave in V6 may be due to
i. Right ventricular dominance
ii. Mirror image dextrocardia
iii. Right bundle branch block with left anterior hemi block
iv. Ventricular ectopy
v. Marked clock wise rotation
e. Non-progression of R wave from V1 to V4:
i. Anterior wall myocardial infarction
ii. Diffuse myocardial disease
iii. Pulmonary emphysema
iv. Left ventricular hypertrophy
v. Left bundle branch block
vi. WPW syndrome Type B
vii. Anomalous pulmonary origin of left coronary artery

f. Low QRS voltage: The voltage of QRS complex should be atleast 5mm in the standard leads and atleast 10mm in the precordial leads. Voltage below these values are considered as low.
i. With normal T wave
1. Thick chest wall
2. Marked obesity
3. Pulmonary emphysema
ii. With inverted T wave
1. Pericardial effusion or constrictive pericarditis
2. Hypothyroidism
3. Hypopitutarism
4. Diffuse myocardial disease
g. Electrical Alterans: A condition in which the voltage of the P wave, T wave, and the QRS complex re all variable in the same lead. Reasons
i. Paroxysmal atrial tachyarrhythmia with fast heart rate like atrial tachycardia, flutter or fibrillation
ii. Serious organic heart disease e.g. ischaemic or hypertensive heart disease, cardiomyopathy or myocarditis.
iii. Pericardial effusion e.g. malignant or tubercular.

3. Prolonged Ventricular Activation time:
a. Ventricular hypertrophy
b. Bundle branch block or hemi block
c. Hyperacute phase of myocardial infarction
4. Abnormal QRS morphology:
a. Abnormal R wave Peak:
i. RSR’ Pattern or ‘M’ pattern in the presence of bundle branch block. The RSR’ pattern is observed in lead V1 in right bundle branch block and in lead V6 in left bundle branch block.
b. Delta wave on Ascending limb:
i. Occurs in WPW syndrome due to Bundle of Kent
c. Osborne wave on Descending limb:
i. A hump like deflection on the descending limb of R wave due to prolonged intra ventricular conduction observed in hypothermia.
5. Wide QRS complex:
a. Occurs from various myocardial diseases and conduction defects.

Q Wave Abnormalities:
1. Q waves in Myocardial infarction:
a. Necrosed myocardial tissue is electrically inert and cannot be depolarized. If the full myocardial thickness is necrosed (transmural infarction), there is an electrical hole in the muscle wall. If an electrode is placed over this hole (area of transmural necrosis) it reflects activation of the opposite ventricular wall. Since the activation is in a direction away from the electrode, it is reflected as a Q wave, which is negative, and not followed by R wave, the so called QS complex. The location of Q waves on the ECG can help to localize the area of myocardial infarction.
i. V1-2: septal;
ii. V3-4: anterior;
iii. V5-6, L1, aVL: Lateral;
iv. V1-4: Antero septal;
v. V3-6, L1, aVL: Antero lateral;
vi. V1-6, L1, aVL: Extensive anterior;
vii. L1, aVL: High lateral;
viii. L2, L3, aVF: Inferior

Causes of T Wave Inversion:
1. Non specific causes:
a. Anxiety
b. Hyperventilation
c. Heavy metals
d. Smoking
e. Tachycardia
f. Cerebro vascular Haemorrhage
g. Pancreatitis, cholecystitis
h. Pulmonary embolism
i. Myxoedema
j. Shock
2. Specific Causes
a. Primary
i. Digitalis and Quinidine poisoning
ii. Hypokalemia
iii. Cardiomyopathy
iv. Myocarditis
v. Pericarditis
vi. Pericardial effusion
vii. Acute coronary insufficiency
viii. Acute myocardial infarction
b. Secondary
i. Ventricular hypertrophy
ii. Bundle branch block
iii. WPW syndrome
c. Giant T wave inversion
i. Myocardial ischaemia or infarction
ii. Cerebrovascular accident
iii. Apical myocardiopathy
iv. After resuscitation from ventricular fibrillation

Causes of Tall T Wave
1. Tall T wave:
a. Hyperkalemia
b. Myocardial ischaemia / injury
i. Hyperacute myocardial infarction
ii. Prinzmetal’s angina
iii. Coronary insufficiency
iv. Recovering inferior wall infarction
c. True posterior wall myocardial infarction (in V1 & V2)
d. Left ventricular diastolic overload (in V5 & V6)
e. Cerebrovascular accident
f. In psychotic individuals
g. As a normal variant in vagotonic persons.
2. Notched or Broad T waves
a. Pericarditis
b. CNS disorders
c. Prolonged Q-T interval
d. Alcoholic Cardiomyopathy
e. Quinidine effect
f. Myocarditis

U Wave Abnormalities:
1. Prominent U wave:
a. Hypokalemia
b. Sympathetic stimulation
c. Intra-cranial events
2. U wave inversion
a. Coronary artery disease and myocardial ischaemia
b. Aortic and / or mitral valve regurgitation
c. Hypertension with left ventricular hypertrophy
d. Right ventricular hypertrophy

P R Segment Depression:
1. Secondary causes
a. Sinus tachycardia in normal persons
b. Atrial enlargement or hypertrophy
2. Primary causes
a. Acute pericarditis
b. Atrial infarction
c. Mechanical injury

S-T Segment Depression:
1. Non specific causes:
a. Physiological
i. Anxiety
ii. Hyperventilation
iii. Heavy metals
iv. Smoking
v. Tachycardia
b. Extra cardiac causes
i. Subarachnoid haemorrhage
ii. Pancreatitis, cholecystitis
iii. Pulmonary embolism
iv. Myxoedema
v. Shock
2. Specific causes
a. Primary
i. Digitalis, Quinidine effect
ii. Hypokalemia
iii. Cardiomyopathy
iv. Myocarditis
v. Acute coronary insufficiency
vi. Non-Q myocardial infarction
b. Secondary
i. Ventricular hypertrophy or systolic overload
ii. Bundle branch block
iii. WPW syndrome

S-T Segment Elevation:
1. Myocardial infarction
2. Prinzmetal’s angina
3. Acute pericarditis
4. Early repolarization variant
5. Ventricular aneurysm
6. Post cardiotomy syndrome

Causes of P- R Interval Change
1. Prolonged P-R interval:
a. Prolonged P-R interval in all beats:
i. Acute rheumatic fever and diphtheria
ii. Drug acting on the A-V node – digitalis, verapamil, propranolol
iii. Coronary artery disease
iv. Congenital heart disease
v. Hyperkalaemia or hypokalemia
vi. Vagotonia
vii. Sympathetic blockade
viii. Rapid atrial placing
ix. Hypothyroidism and hypothermia
b. Prolonged P-R interval in isolated beats:
i. Atrial ectopic
ii. A-V dissociation
iii. Interpolated ventricular ectopic
c. Progressive prolongation of P-R
i. Second degree A-V block
2. Shortened P-R interval
a. Shortened P-R interval in all beats
i. A-V nodal rhythm
ii. Accessory by-pass tract
iii. Vagolytic drugs – atropine, quinidine
iv. Sympathetic stimulation
b. Shortened P-R interval in Isolated beats
i. Atrial ectopic
ii. A-V dissociation
iii. End-diastolic ventricular ectopic
c. Progressive shortening of P-R interval
i. Isorhythmic A-V dissociation
ii. Reverse Wenckebach phenomenon
3. Variable P-R interval
a. With Identical P waves
i. A-V dissociation
b. With changing P wave morphology:
i. Multiple supraventricular ectopics
ii. Wandering pacemaker rhythm
iii. Chaotic atrial rhythm or multifocal atrial tachy cardia.

Causes of Q-T Interval Change:
1. Shortened Q-T interval
a. Hyperkalaemia
b. Hypercalcaemia
c. Digitalis effect
d. Acidosis
e. Hyperthermia
f. Vagal stimulation
2. Prolonged Q-T interval:
a. Acquired causes:
i. Hypocalcaemia and hypomagnesaemia
ii. Acute myocardial infarction or coronary insufficiency
iii. Acute myocarditis and rheumatic fever
iv. Intra-cranial events – head injury, cerebral or subarachnoid haemorrhage.
v. Liquid protein diet
vi. Sympathetic stimulation
vii. Hypothermia
viii. Bradyarrhythmias e.g. third-degree A-V block, marked sinus bradycardia.


1. Essentials of applied electrocardiography – Athul Luthra
2. Introduction to electrocardiography – U.N. Panda and Laxmi chand
3. ECG pocket guide – Bradford C. Lipman and Bernard S. Lipman
4. A primer of Electro cardiography – Natoobhai.J.Shah and Sailesh.N.Shah
5. The ECG made easy – John R. Hamptom
6. Electrocardiography -Leo schamroth
7. Text book of medicine – K.V. Krishnadas
8. Clinical Medicine – K.V.Krishnadas
9. Hutchison’s Clinical Methods – Michael Swash
10. Davidson’s Principles and practice of Medicine

 Dr Felix James BHMS,MD(Hom)
Medical Officer, Dept. of Homoeopathy, Govt. of Kerala