ECG in Medical Practice ABM Abdullah
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Basic Concepts of ECGCHAPTER I

“Workout the best method for examination and practice it until it is a second nature to you”
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Standard Leads
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Chest Leads
There are 5 specialized tissues called conductive system of the heart. These are:
  • SA node.
  • AV node.
  • Bundle of His.
  • Right bundle branch (RBB) and left bundle branch (LBB).
  • Purkinje fibers.
These specialized conductive pathways allow the heart to be electrically activated in a predictable manner (see the sequence below).
The impulse arises in SA node (called primary pacemaker), spreads across the atria (by three internodal pathways and Bachmann's bundle), causing depolarization of both atria. From the atria, the impulse reaches the AV node, where there is some delay, which allow atria to contract and pump blood into the ventricles. The impulse then spreads along the bundle of His, then along the left and right bundle branch, finally into the ventricular muscles through Purkinje fibers, causing ventricular depolarization.
First the ventricular septum is activated, followed by the endocardium and finally the epicardium.
Sequence of impulse formation and conduction.
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This is the normal sequence of stimulation of the specialized tissue. If any disturbance of this sequence occurs, there is rhythm disturbance, called arrhythmia or abnormality of conduction, called heart block.
SA node is the dominant pacemaker. Other pacemaker sites in the heart are atria, AV node and ventricles. All these are dormant, but can initiate impulse at a slow rate when SA node fails.
  1. SA node: Located in the superior and right side of right atrium, near the root of superior vena cava. Normally, the impulse arises in SA node called sinus rhythm. From SA node, impulse spreads along 3 internodal pathways (anterior, middle and posterior) into both right and left atrium. Finally, these 3 internodal pathways enter into the AV node. An additional internodal pathway called Bachmann's Bundle is present, which transmits impulse to the left atrium.
    Normal rate in SA node is 60 to 100/minute.
  2. AV node: AV node smaller than SA node. It is located in the subendocardial surface of right side of right atrium, at the posterior part of interatrial septum, close to the opening of coronary sinus, just above the tricuspid valve.
    If SA node is blocked or fails, AV node can initiate cardiac impulse and perform as a pacemaker. Normal rate of AV node is 40 to 60/ minute. According to the electrical response, AV node is divided into 3 parts:
    • High nodal (AN region).
    • Mid nodal (N region).
    • Low nodal (NH region).
    In ECG, these 3 regions can be detected by looking at the configuration of P wave.
  3. Bundle of His: It is an extension of the tail of AV node, that extends downward and to the left to enter the interventricular septum, near the junction of muscles and fibrous part of ventricular septum. Then, it is divided into 2 right and left bundle branch.
    When there is AV block, bundle of His can initiate cardiac impulse and perform as a pacemaker. Normal rate of bundle of His is 20 to 40 /minute.
  4. Right bundle branch: Extends on the right side of interventricular septum and spreads into the right ventricle through Purkinje fibers.
  5. Left bundle branch: It divides into anterior and posterior fascicles. Anterior fascicle spreads into anterosuperior part of left ventricle. Posterior fascicle spreads into posteroinferior part of left ventricle, through Purkinje fibers.
  6. Purkinje fibers: These are the terminal network of fibers diffusely spread in the ventricular muscles in subendocardial and subepicardial myocardium.
    Normal intrinsic rate of Purkinje fibers is 15 to 40/minute.
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NB: Most specialized cardiac fibers contain large number of automatic cells, whereas atrial and ventricular muscle fibers, under normal condition, have no automatic activity.
There are 2 major coronary arteries: (1) Right and (2) Left.
1. Right Coronary Artery
It arises from right coronary sinus of Valsalva, runs along the right atrioventricular groove, gives marginal branch that supplies right atrium and right ventricle. It continues as posterior descending artery, which runs in posterior interventricular groove and supply posterior part of interventricular septum and posterior left ventricular wall.
Right coronary artery supplies the following parts:
  • SA node—60% cases.
  • AV node—90% cases.
  • Right atrium and right ventricle.
  • Inferoposterior aspect of left ventricle.
So, the occlusion of right coronary artery results in sinus bradycardia, AV block, infarction of inferior part of left ventricle and occasionally of right ventricle.
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2. Left Coronary Artery
It arises from left coronary sinus of Valsalva. Within 2.5 cm of its origin, left main coronary artery divides into 2 branches: (1) Left anterior descending artery and (2) Circumflex artery.
  • Left anterior descending artery: It runs in anterior interventricular groove and gives branches to supply the anterior part of interventricular septum, anterior wall and apex of left ventricle.
  • Circumflex artery: It runs posteriorly in left atrioventricular groove and supply by marginal branch to left atrium and lateral and posteroinferior part of left ventricle.
Left coronary artery also supply:
  • SA node in 40% cases.
  • AV node in 10% cases.
  • Bundle of His.
  • Right and left bundle branch.
Occlusion of left anterior descending artery and circumflex artery causes infarction of the corresponding territories of left ventricle.
Occlusion of left main coronary artery causes extensive damage and is usually fatal.
Venous system mainly follows coronory arteries, but drains to the coronory sinus in the atrioventricular groove, then to the right atrium.
Coronary vessels receive sympathetic and parasympathetic innervations. Stimulation of α-receptor causes vasoconstriction and β2 causes vasodilatation. Sympathetic stimulation in coronary artery causes dilatation, parasympathetic stimulation also causes mild dilatation of normal coronary artery. Healthy coronary endothelium releases nitric oxide, which promotes vasodilatation. Systemic hormones, neuropeptides and endothelin also influence arterial tone and coronary flow.
Cardiac muscles have some special properties:
  • Automaticity: Without external stimulus, heart muscle can initiate normal cardiac impulse by SA node.
  • Autorhythmicity: Cardiac muscle can contract after a regular interval, called autorhythmicity.
  • Excitability: Cardiac muscle can be excited by adequate external stimulus.
  • Conductivity: Cardiac muscle has the ability to conduct impulse from one muscle cell to another cell.
  • Contractility: Ability to contract after depolarization.
  • Refractory period: It is a period during which activated muscle fibers do not respond to further stimulus. It is of 2 types: (1) Absolute refractory period and (2) Relative refractory period.
    • Absolute refractory period—during this period, muscle fibers do not respond to any stimulus.
    • Relative refractory period—with very strong stimulus, muscle fibers may respond.
  • All or none law: If external stimulus is too little, no cardiac impulse is initiated. But with adequate stimulus, all muscle fibers contract with its best ability.
  • Functional syncitium: Cardiac muscle fibers are electrically connected with one another by a gap junction. When one muscle fiber is excited, the action potential spreads to whole cardiac muscle fibers, because of presence of intercalated disk. It is called syncytium.
NB: Remember the following points:
The heart is supplied by both sympathetic and parasympathetic (in cardiac plexus).
  • Sympathetic (adrenergic) supply both atria and ventricular muscle, also conductive specialized tissue.
  • Parasympathetic preganglionic fibers and sensory fibers reach the heart through vagus nerves. Cholinergic nerves supply SA node and AV nodes via muscarinic (M2) receptors.
Nerve supply is mainly through β1 and β2 receptors.
  • β1 receptor is predominant in heart, having both inotrophic and chronotrophic effect.
  • β2 receptor is predominant in vascular muscles and causes vasodilatation.
Under basal condition, predominant effect is parasympathetic through vagus nerve over sympathetic, resulting in slow heart rate. So during sleep, heart rate is slow. Also in athlete, there is predominant vagal effect (so heart rate may show bradycardia).
It is the graphical representation of electrical potentials produced when the electric current passes through the heart. Electrical activity is the basic characteristic of heart and is the stimulus for cardiac contraction. Disturbance of electrical function is common in heart disease.
Electrocardiogram (ECG) records the electrical impulse on ECG paper by electrodes placed on body surface called waves or deflections.
One beat is recorded as a grouping of waves called P-QRS-T.
• P
Represents atrial depolarization.
• PR interval
Represents the time taken for the cardiac impulse to spread over the atrium and through AV node and His-Purkinje system.
Represents ventricular depolarization.
• T wave
Represents ventricular repolarization.
In a normal ECG recording, there are 12 leads:
  • 3 bipolar standard leads.
  • 3 unipolar limb leads.
  • 6 chest leads.
    (Leads are different view parts of heart's electrical activity).
  1. Bipolar standard leads (also called limb leads) designated as LI, LII and LIII.
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  2. Unipolar limb leads (also called augmented limb leads) designated as aVR, aVL and aVF. Three unipolar leads have very low voltage, which cannot be recorded satisfactorily. For this reason, recordings of these leads are increased in amplitude. So, they are called augmented unipolar leads, which are represented as aVR, aVL and aVF.
  3. Chest leads (Unipolar) Designated by ‘V’.
    Electrodes are placed in the following places on the chest wall.
  • V1—4th intercostal space at right sternal border.
  • V2—4th intercostal space at left sternal border.
  • V3—midway between V2 and V4 lead on left side.
  • V4—5th intercostal space in left midclavicular line.
  • V5—5th intercostal space in left anterior axillary line.
  • V6—5th intercostal space in left midaxillary line.
By looking the following leads, the site and surface of heart lesion is identified.
NB: Remember the following points:
Before interpreting an ECG, one must know details about the ECG paper, standardization and different waves in ECG, etc. It is a matter of experience and pattern interpretation, which requires a method of systematic ECG analysis.
During interpretation, look at the following points carefully:
  1. Standardization (see in the beginning)—like this
    which is 10 mm (1 mV).
  2. Paper speed—25 mm/second.
  3. Rhythm—by looking at RR interval (LII is usually called rhythm lead), see regular or irregular.
  4. Count the heart rate.
  5. Different waves:
    • P—whether normal, small or tall, inverted, wide, notched, bifid, variable configuration, etc.
    • PR interval—normal or prolonged or short.
    • Q—normal or pathological.
    • R—normal or tall or short, notched or M pattern.
    • QRS—normal or wide, high or low voltage, variable or change of shape.
    • ST segment—elevated or depressed.
    • T—normal or tall or small or inverted.
    • U wave—normal or small.
    • QT—short or prolonged.
  6. Axis—whether normal or right or left axis deviation.
  7. Abnormalities—any arrhythmia, infarction, hypertrophy, etc.
One must have some basic idea about the ECG paper, normal ECG tracing, limits of normal value, duration, rhythm, etc.
  • Q. What are the diseases diagnosed by looking at an ECG?
Ans. As follows:
  • Tachycardia or bradycardia.
  • Chamber enlargement.
  • Myocardial infarction.
  • Arrhythmias.
  • Block (First degree block, SA block, AV block, bundle branch block).
  • Drug effect (such as digoxin).
  • Extracardiac abnormalities—electrolyte imbalance (such as hypokalemia or hyperkalemia), hypo- or hypercalcemia, low voltage tracing (in myxedema, hypothermia, emphysema).
  • Exercise ECG to see coronary artery disease.
ECG paper shows small and large squares. In each small square, thin horizontal and vertical lines are present in 1 mm interval. A heavier thick line is present in every 5 mm (5 small squares) interval. Time is measured horizontally and voltage / height is measured vertically.
  1. One small square:
    • Height = 1 mm.
    • Horizontal (in time) = 0.04 second.
  2. One big square (5 small squares):
    • Height = 5 mm.
    • Horizontal (in time) = 0.04 × 5 sec = 0.2 second.
    So, 0.2 second = 5 mm.
    • 1 second = 5/0.2 = 25 mm.
    So, recording speed is 25 mm/sec. (i.e. 1500 mm/min).
    A faster recording speed (50 mm/sec) is occasionally used to visualize wave deflection.
  3. Isoelectric line: It is the base line in ECG paper. Waves are measured either above (positive deflection) or below (negative deflection).
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ECG Paper
In any ECG, before telling low voltage or high voltage, see the normal standardization (i.e. 10 mm in height).
  • In standard limb leads—QRS < 5 mm (mainly R wave).
  • In chest leads—QRS < 10 mm (mainly R wave).
  • Incorrect standardization (i.e. if < 10 mm).
  • Obesity.
  • Pericardial effusion.
  • Chronic constrictive pericarditis.
  • Myxedema.
  • Emphysema.
  • Hypothermia.
  • Q. What is depolarization and repolarization?
Ans. As follows:
  • Depolarization: Means initial spread of stimulus through the muscle, causing activation or contraction.
  • Repolarization: Means return of stimulated muscle to the resting state (recovery from activation or contraction).
  • Normal ECG recording consists of P wave (atrial beat), followed by QRS, ST and T wave (ventricular beat).
  • Capital letter P, Q, R, S, T—indicates large wave (> 5 mm).
  • Small letter p, q, r, s, t—indicates small wave (< 5 mm).
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• P
Deflection produced by atrial depolarization.
Deflection produced by ventricular depolarization.
• Q (q)
First negative deflection produced by ventricular depolarization. It precedes R wave.
• R(r)
First positive deflection produced by ventricular depolarization.
• S(s)
Negative deflection after R wave produced by ventricular depolarization.
• T
Indicates ventricular repolarization.
• J
At the beginning of ST segment.
• U
Not always seen. When present, it follows T wave, preceding the next P wave. It indicates repolarization of interventricular septum or slow repolarization of the ventricles.
• PR interval
Distance between the beginning of P to beginning of QRS (Q), ideally called PQ interval.
• PP interval
Distance between two successive P waves. In sinus rhythm, P-P interval is regular.
• RR interval
Distance between two successive R waves. In sinus rhythm, R-R interval is regular.
• QT interval
Distance interval between the beginning of Q wave and the end of T wave.
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ST—Distance from the end of QRS complex to the beginning of T wave. It indicates the beginning of ventricular repolarization. Normally, it is in isoelectric line, but may vary from − 0.5 to + 2 mm in chest leads.
NB: Remember the following points:
Characters of Normal P Wave
  • P wave results from spread of electrical activity through the atria.
  • Width or duration (in time, horizontally) − 0.10 sec (2.5 small sq.).
  • Height − 2.5 mm (2.5 small sq.).
    (Height × Duration = 2.5 × 2.5 small squares).
  • P wave is better seen in LII, as atrial depolarization is towards LII (also seen in V1), because the impulse spread from right to left atrium.
  • P wave is upright in all leads, mainly LI, LII and aVF (except aVR). (P is inverted in aVR and occasionally in aVL).
  • P wave in V1 may be biphasic (equal upward and downward deflection), notched and wide. (Activation of right atrium produces positive component and activation of left atrium produces negative component).
  • Normal P is rounded, neither peaked nor notched.
Abnormalities of P Wave
P wave may be:
  • Absent.
  • Tall or small.
  • Wide, notched, biphasic.
  • Inverted.
  • Variable and multiple.
Causes of absent P wave
  • Atrial fibrillation (P is absent or replaced by fibrillary f wave).
  • Atrial flutter (P is replaced by flutter wave, which shows saw-tooth appearance).
  • SA block or sinus arrest.
  • Nodal rhythm (usually abnormal, small P wave).
  • Ventricular ectopic and ventricular tachycardia.
  • Supraventricular tachycardia (P is hidden within QRS, due to tachycardia).
  • Hyperkalemia.
  • Idioventricular rhythm.
Causes of tall P wave
  • Tall P is called P pulmonale (height > 2.5 mm, i.e. > 2.5 small squares).
  • It is due to right atrial hypertrophy or enlargement.
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P4 mm (tall)
Causes of small P wave
  • Atrial tachycardia.
  • Atrial ectopic.
  • Nodal rhythm (high nodal).
  • Nodal ectopic (high nodal).
Causes of wide P wave
  • Broad and notched P is called P mitrale (duration > 0.11 sec, or > 2.5 small squares).
  • It is due to left atrial hypertrophy or enlargement.
  • In V1, P wave may be biphasic with a small positive wave preceding a deep and broad negative wave (indicates left atrial enlargement or hypertrophy).
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Causes of inverted P wave (negative in LI, LII and aVF)
  • Incorrectly placed leads (reversed arm electrodes).
  • Dextrocardia.
  • Nodal rhythm with retrograde conduction.
  • Low atrial and high nodal ectopic beats.
Causes of variable P waves
Presence of variable P waves indicates wandering pacemaker.
Causes of multiple P waves (consecutive 2 or more)
  • A-V block (either partial or complete heart block).
  • SVT with AV block.
Characters of Normal P-R Interval
  • It is the distance between the onset of P wave to the beginning of Q wave (if Q wave is absent, then measure up to the onset of R wave).
  • It is the time required for the impulse to travel from SA node to the ventricular muscle. (The impulse is transmitted to ventricle via AV node).
  • P-R interval varies with age and heart rate. (P-R interval is short, if the heart rate is increased and long, if heart rate is decreased).
  • Normal PR interval—0.12 to 0.20 sec (maximum 5 small squares).
    • In children, upper limit is 0.16 sec.
    • In adolescent, upper limit is 0.18 sec.
    • In adult, upper limit is 0.22 sec.
  • P-R is short, if it is < 0.10 sec and long, if it is > 0.22 sec.
Abnormalities of P-R Interval
PR interval may be:
  • Prolonged.
  • Short.
  • Variable.
Prolonged P-R interval (> 0.2 second): It is due to first degree heart block. Causes are:
  • Ischemic heart disease (occasionally, inferior MI).
  • Acute rheumatic carditis.
  • Myocarditis (due to any cause).
  • Atrial dilatation or hypertrophy.
  • Hypokalemia.
  • Drugs—digitalis toxicity, quinidine, occasionally β-blocker, calcium channel blocker (verapamil).
Short P-R interval (< 0.12 second): Causes are:
  • Wolff-Parkinson-White (WPW) syndrome. In this case, there is delta wave.
  • Lown-Ganong-Levine (LGL) syndrome. In this case, there is no delta wave.
  • Nodal rhythm.
  • Nodal ectopic (high nodal).
  • Occasionally, if dissociated beat is present and also in infant, steroid therapy.
Variable P-R interval: Causes are:
  • Wenckebach's phenomenon (Mobitz type I): There is progressive lengthening of P-R interval followed by a drop beat.
  • Partial heart block (Mobitz type II): PR interval is fixed and normal, but sometimes P is not followed by QRS.
  • 2:1 AV block: Alternate P wave is not followed by QRS.
  • Complete AV block: No relation between P and QRS.
  • Wandering pacemaker: Variable configuration of P.
Characters of Normal Q Wave
  • Q wave is usually absent in most of the leads. However, small q wave may be present in I, II, aVL, V5 and V6. This is due to septal depolarization.
  • Small q may be present in LIII (which disappears with inspiration).
  • Depth—< 2 mm (2 small squares).
  • Width—1 small square.
  • It is 25% or less in amplitude of the following R wave in the same lead.
Characters of Pathological Q Wave
  • Deep > 2 mm (2 small squares).
  • Wide > 0.04 sec or more (> 1 mm or 1 small square).
  • Should be present in more than one lead.
  • Associated with loss of height of R wave.
  • Q wave should be > 25% of the following R wave of the same lead.
Causes of Pathological Q Wave
  • Myocardial infarction (commonest cause).
  • Ventricular hypertrophy (left or right).
  • Cardiomyopathy.
  • LBBB.
  • Emphysema (due to axis change or cardiac rotation).
  • Q only in LIII is associated with pulmonary embolism (SI, QIII and TIII pattern).
NB: Remember the following points:
Characters of Normal R Wave
  • It is the first positive (upward) deflection, due to ventricular depolarization.
  • Duration < 0.01 sec.
  • R wave usually small (< 1 mm) in V1 and V2. It increases progressively in height in V3 to V6 (tall in V5 and V6), i.e. R is small in V1 and V2, tall in V5 and V6.
Normal Height of R Wave
  • aVL < 13 mm.
  • aVF < 20 mm.
  • V5 and V6 < 25 mm.
(If R wave is > 25 mm, it is always pathological).
Abnormalities of R Wave
R wave may be:
  • Tall.
  • Small.
  • Poor progression.
Causes of tall R wave
  1. Left ventricular hypertrophy (in V5 or V6 > 25 mm, aVL >13 mm, aVF > 20 mm).
  2. In V1, tall R may be due to:
    • Normal variant.
    • Right ventricular hypertrophy (RVH).
    • True posterior myocardial infarction.
    • WPW syndrome (type A).
    • Right bundle branch block.
    • Dextrocardia.
Causes of small R wave: Looks like low voltage tracing.
  • Incorrect ECG calibration (standardization).
  • Obesity.
  • Emphysema.
  • Pericardial effusion.
  • Hypothyroidism.
  • Hypothermia.
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Small R wave
R wave progression: The height of R wave gradually increases from V1 to V6. This phenomenom is called R wave progression.
Poor progression of R wave: Normally, amplitude of R wave is tall in V5 and V6. In poor R wave progression, amplitude of R wave is progressively reduced in V5 and V6.
Causes are:
  • Anterior or anteroseptal myocardial infarction.
  • Left bundle branch block.
  • Left ventricular hypertrophy (though R is tall in most cases).
  • Dextrocardia.
  • Cardiomyopathy.
  • COPD.
  • Left sided pneumothorax.
  • Left sided pleural effusion (massive).
  • Marked clockwise rotation.
  • Chest electrodes placed incorrectly.
  • Deformity of the chest wall.
  • Normal variation.
Characters of Normal S Wave
  • It is the negative deflection after R wave (1/3rd of R wave).
  • Normally, deep in V1 and V2 as impulse is going to the muscles of left ventricle then to the right ventricle.
  • Progressively diminished from V1 to V6 (small S wave may be present in V5 and V6).
  • In V3, R and S waves are almost equal (corresponds with interventricular septum).
Characters of Normal QRS Complex
  • QRS complex represents depolarization of ventricular muscles.
  • Depolarization of left ventricle contributes to main QRS (as the left ventricle has 2 to 3 times mass of right ventricle).
  • QRS is predominantly positive in leads that look at the heart from left side—L1, aVL, V5 and V6.
  • It is negative in leads that look at the heart from the right side—aVR, V1 and V2.
  • In V1, S is greater than R.
  • In V5 and V6, R is tall.
  • QRS appears biphasic (part above and part below the base line) in V3 and V4.
  • Normal duration of QRS is 0.08 to 0.11 second (< 3 small squares) and height < 25 mm.
Various Forms and Components of QRS Complex
  • Q wave: Initial downward deflection.
  • R wave: Initial upward deflection.
  • S wave: Downward deflection after R wave.
  • rS complex: Small initial r wave, followed by large S wave.
  • RS complex: A complex with R and S wave of equal amplitude.
  • Rs complex: A large R wave followed by a small s wave.
  • qRS complex: Small initial downward deflection, followed by a tall R which is followed by a large S.
  • Qr complex: Large Q, followed by a small r.
  • QS complex: Complex with complete negative deflection (no separate Q and S).
  • rSr complex: Small r, then deep S, followed by small r.
  • RSR complex: Tall R, then deep S, followed by tall R.
  • RR complex: When deflection is completely positive and notched (M pattern).
Abnormalities of QRS Complex
QRS may be:
  • High voltage.
  • Low voltage.
  • Wide.
  • Change in shape.
  • Variable.
Causes of high voltage QRS
  • Incorrect calibration.
  • Thin chest wall.
  • Ventricular hypertrophy (right or left or both).
  • WPW syndrome.
  • True posterior myocardial infarction (in V1 and V2).
Causes of low voltage QRS (< 5 mm in LI, LII, LIII and < 10 mm in chest leads)
  • Incorrect calibration.
  • Thick chest wall or obesity.
  • Hypothyroidism.
  • Pericardial effusion.
  • Emphysema.
  • Chronic constrictive pericarditis.
  • Hypothermia.
Causes of wide QRS (> 0.12 second, 3 small squares)
  • Bundle branch block (LBBB or RBBB).
  • Ventricular ectopics.
  • Ventricular tachycardia.
  • Idioventricular rhythm.
  • Ventricular hypertrophy.
  • Hyperkalemia.
  • WPW syndrome.
  • Pacemaker (looks like LBBB with spike).
  • Drugs (quinidine, procainamide, phenothiazine, tricyclic antidepressants).
Causes of changes in shape of QRS
  • Right or left bundle branch block (slurred or M pattern).
  • Ventricular tachycardia.
  • Ventricular fibrillation.
  • Hyperkalemia.
  • WPW syndrome.
Causes of variable QRS
  • Multifocal ventricular ectopics.
  • Torsades de pointes.
  • Ventricular fibrillation.
Characters of Normal ST Segment
  • Measured from the end of S to the beginning of T wave. It represents beginning of ventricular repolarization.
  • Normally, it is in isoelectric line (lies at same level of ECG baseline).
  • ST elevation is normal up to 1 mm in limb leads and 2 mm in chest leads (mainly V1 to V3).
  • In Negroes, ST elevation of 4 mm may be normal, which disappears on exercise.
  • Normally, ST segment may be depressed, < 1mm.
Abnormalities of ST Segment
ST segment may be:
  • Elevated.
  • Depressed.
Causes of ST elevation (> 2 mm)
  • Recent myocardial infarction (ST elevation with convexity upward).
  • Acute pericarditis (ST elevation with concavity upward, chair shaped or saddle shaped).
  • Prinzmetal's angina (ST elevation with tall T).
  • Ventricular aneurysm (persistent ST elevation).
  • Early repolarization (high take off).
  • Normal variant in Africans and Asians.
  • May be in hyperkalemia.
Causes of ST depression (below the isoelectric line)
  • Acute myocardial ischemia (horizontal or down slope ST depression with sharp angle ST-T junction).
  • Ventricular hypertrophy with strain (ST depression with convexity upward and asymmetric T inversion).
  • Digoxin toxicity (sagging of ST depression—like thumb impression, also called reverse tick).
  • Acute true posterior myocardial infarction (in V1 and V2), associated with dominant R and tall upright T wave.
Early repolarization (high take-off)
  • It is a benign, normal finding in young healthy person, more in black males.
  • It is seen in chest leads, commonly V4 to V6 (rarely, in other chest lead).
  • ST elevation is usually associated with J point elevation.
  • It is not associated with inversion of T wave or abnormal Q wave.
NB: Remember the following points:
Characters of Normal T Wave
  • It indicates ventricular repolarization.
  • Follows S wave and ST segment.
  • Upright in all leads, except aVR.
  • Usually, more than 2 mm in height.
  • May be normally inverted in V1 and V2.
  • Normally, not more than 5 mm in standard leads and 10 mm in chest leads.
  • Minimum 1/4th of R wave of the same lead.
  • Tip of T is smooth (rounded).
Abnormalities of T Wave
T wave may be:
  • Inverted.
  • Tall peaked, tented.
Causes of T inversion
  • Myocardial ischemia and infarction.
  • Subendocardial myocardial infarction (non-Q wave myocardial infarction).
  • Ventricular ectopics.
  • Ventricular hypertrophy with strain.
  • Acute pericarditis.
  • Cardiomyopathy.
  • Myxoedema.
  • Bundle branch block.
  • Drugs (digitalis, emetine, phenothiazine).
  • Physiological (smoking, anxiety, anorexia, exercise, after meal or glucose).
Causes of tall peaked T wave
  • Hyperkalemia (tall, tented or peaked).
  • Hyperacute myocardial infarction (tall T wave).
  • Acute true posterior myocardial infarction (tall T in V1 to V2).
  • May be normal in some Africans and Asians.
Causes of small T wave
  • Hypokalemia.
  • Hypothyroidism.
  • Pericardial effusion.
  • Q. What is juvenile T wave pattern?
Ans. It is a disorder in which T is inverted in V1 to V3 (rarely V4 to V6). T inversion is neither symmetrical nor deep. It is common in children and young adults, more in female < 40 years. Frequently, it is associated with sinus arrhythmia and high left ventricular voltage.
Characters of Normal U Wave
  • It follows T wave.
  • It may be present in normal ECG. It is smaller and in the same direction of the preceding T wave.
  • It represents slow repolarization of interventricular septum (Purkinje fibers, but actual genesis of U wave is still controversial).
  • It is better seen in chest leads (V2 to V4).
  • Normal amplitude is 1 mm (2 mm in athlete).
Abnormalities of U Wave
U wave may be:
  • Inverted.
  • Prominent.
Causes of inverted U wave
  • Ischemic heart disease.
  • Left ventricular hypertrophy with strain (hypertensive heart disease).
Causes of prominent U wave
  • May be normally present (usually small).
  • Hypokalemia (commonest).
  • Bradycardia.
  • Ventricular hypertrophy.
  • Hyperthyroidism.
  • Hypercalcemia.
  • Drugs (phenothiazine, quinidine, digitalis).
  • Q. What is the significance of large U wave?
Ans. The patient is prone to develop torsades de pointes tachycardia.
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Characters of Normal QT Interval
  • It is the distance from the beginning of Q wave (or R wave, if there is no Q wave) to the end of T wave. It represents the total time required for both depolarization and repolarization of the ventricles.
  • Normal QT interval is 0.35 to 0.43 seconds.
  • Its duration varies with heart rate, becoming shorter as the heart rate increases and longer as the heart rate decreases. In general, QT interval at heart rate between 60 to 90/minute does not exceed in duration half the preceding RR interval.
  • It is better seen in aVL (because there is no U wave).
  • Corrected formula for real QT is:
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Abnormalities of QT Interval
QT interval may be:
  • Short.
  • Long.
Causes of short QT interval
  • Digoxin effect.
  • Hypercalcemia.
  • Hyperthermia.
  • Tachycardia
Causes of long QT interval
  • Hypocalcemia.
  • Bradycardia.
  • Acute myocarditis.
  • Acute myocardial infarction.
  • Hypothermia.
  • Drug (quinidine, procainamide, flecainide, amiodarone, tricyclic antidepressant, disopyramide, pentamidine).
  • Cerebral injury (head injury, intracerebral hemorrhage).
  • Hypertrophic cardiomyopathy.
  • During sleep.
  • Hereditary syndrome:
    1. Jervell-Lange Nielsen syndrome (congenital deafness, syncope and sudden death).
    2. Romano-Ward syndrome (same as above except deafness).
NB: Prolonged QT interval may be detected in an asymptomatic individual. It may be associated with ventricular arrhythmia. Rarely, it can cause torsades de pointes tachycardia and sudden death.
To see the rhythm—see the successive RR interval.
  • If the RR interval is equal, it is called regular rhythm.
  • If the RR interval is irregular, then it is called irregular rhythm.
Causes of Irregular Rhythm
  1. Physiological: Sinus arrhythmia.
  2. Pathological:
    • Atrial fibrillation.
    • Atrial flutter.
    • Ectopic beat.
    • SA block or sinus arrest.
    • Atrial tachycardia with block.
    • Second degree heart block.
    • Ventricular fibrillation.
Sinus rhythm shows the following 5 characters:
  • P wave is of sinus origin (means characters of normal P wave).
  • P waves and QRS complexes are regular (that means P-P and R-R interval should be constant and identical).
  • Constant P wave configuration in a given lead.
  • P-R interval and QRS interval should be within normal limit.
  • Rate should be between 60 to 100 beats/min (atrial and ventricular rates are identical).
  • Q. What is arrhythmia?
Ans. It is the abnormality in initiation or propagation of cardiac impulse.
NB: Remember the following points:
In any ECG, heart rate should be calculated. Methods vary according to the cardiac rhythm, whether regular or irregular.
Standard speed in ECG paper is 25 mm /second. Heart rate is the number of beats /min.
In the ECG paper:
• 0.04 second
1 small square.
• 0.2 second
5 small squares or 1 large square.
• So, 1 second
25 small squares or 5 large squares.
• So, 1 minute
25 × 60 = 1500 small squares or 5 × 60 = 300 large squares.
Heart rate is determined in the following way:
1. When the cardiac rhythm is regular:
  • Calculate the R-R or P-P interval in small squares or large squares (if the rhythm is sinus, R-R or P-P interval is same).
  • If small square is calculated:
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  • If large square is calculated
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  • Suppose, number of small squares between R-R or P-P is 15.
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  • Suppose number of large squares between to R-R is 5.
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2. When the rhythm is irregular:
  • Count the number of R in 30 large squares (it is equivalent to 6 seconds).
  • Then simply multiply this by 10 (it becomes rate in 1 minute).
  • Suppose, the number of R in 30 large squares is 12.
  • So, the heart rate is 12 × 10 = 120 beats / min.
NB: Remember the following points:
It is the sum of all the depolarization waves as they spread through the ventricles as seen from the front.
Axis Determination
  • Axis can be derived most easily from the amplitude of QRS complex in LI, LII and LIII.
  • The greatest amplitude of R wave in LI or LII or LIII indicates the proximity of cardiac axis to that lead.
  • The axis lies at 90° to the isoelectric complex, i.e. positive and negative deflections are equal in any of the lead LI, LII, LIII, aVL, aVR and aVF.
Normal axis is between −30° to +90°.
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Quick and Simple Way of Determination of Cardiac Axis
  • Positive QRS in both LI and LII means axis is normal.
  • Positive QRS in LI and negative in LIII (tall R in LI and deep S in LIII)—means left axis deviation.
  • Negative QRS in LI and positive in LIII ((tall R in LIII and deep S in LI)—means right axis deviation.
Left Axis Deviation
When the cardiac axis is between −30° to −90°.
Causes are:
  • Normal variant (with increased age).
  • Left ventricular hypertrophy.
  • Left anterior hemiblock.
  • Left bundle branch block.
  • Inferior myocardial infarction.
  • T from apex of left ventricle.
  • WPW syndrome (some).
  • Pacing from the apex of the right or left ventricle (endocardial pacing).
  • Emphysema.
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Left axis deviation
Right Axis Deviation
When the cardiac axis is between +90° to +180°.
Causes are:
  • Normal variant (common in children and young adult).
  • Right ventricular hypertrophy (due to any cause such as—chronic cor pulmonale, pulmonary embolism, congenital heart diseases, i.e. tetralogy of Fallot).
  • Anterolateral myocardial infarction (high lateral MI).
  • Left posterior hemiblock.
  • Dextrocardia.
  • WPW syndrome (type A).
  • Right bundle branch block.
  • Epicardial pacing.
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Right axis deviation
Intermediate Axis
Occurs when QRS lies between +180° and −90°. This term is used when the exact axis can not be determined (all 6 limb leads are biphasic).
In an ECG, occasionally there are certain findings detected which are the normal variants observed in healthy individuals. These are commonly found in young adults and children:
  • Early repolarization syndrome (in young black males).
  • Left ventricular hypertrophy (in children and young adults).
  • Short P-R interval.
  • Right axis deviation (in children and young adults).
  • Sinus arrhythmia with or without wandering pacemaker.
  • Low voltage in obese people.
  • First degree heart block.
  • Wenckebach's phenomenon.
  • Juvenile T wave pattern in children and young adults.
Careful interpretation is essential for the diagnosis. This should not be confused with underlying pathology. Details history and physical findings should be correlated with the ECG findings.
Exercise ECG is a technique used to assess the cardiac response during exercise. Twelve lead ECG is recorded, while the patient walks or runs on a motorized treadmill. The traditional Bruce protocol is followed. The limb leads are placed on the shoulders and hips, rather than wrists and ankles. Blood pressure is recorded, symptoms are assessed such as anginal pain and ST depression or elevation is noted.
The test is positive, if there is anginal pain, blood pressure falls or fails to rise, ST depression > 1 mm (planar or down sloping depression is more important rather than up sloping ST depression which is non-specific). Sometimes, ST elevation may occur, which indicates transmural ischemia due to coronary spasm or critical stenosis.
The patient who can exercise < 6 min., generally have poor prognosis. Sustained fall of blood pressure indicates severe coronary artery disease.
ETT may be false positive (20%), or false negative. It has a specificity of 80% and sensitivity of 70%.
Indications of Exercise Testing
Contraindications of Exercise Testing
NB: False positive exercise test may occur in—Digitalis toxicity, hypokalemia, ventricular hypertrophy, bundle branch block, pre-excitation syndrome (WPW), mitral valve prolapse and female sex.