Ebook Clinical examinations in cardiology: Part 2

BASIC INVESTIGATIONS
6A. CLINICAL ELECTROCARDIOGRAPHY
22. Introduction and basic concepts

459

23. The normal electrocardiogram

474

24. Abnormal P, T and U waves

490

25. Ventricular hypertrophy

500

26. Intraventricular conduction defects

516

27. Myocardial infarction and ischemia

533

28. Pericarditis and myocarditis

560

29. Drug effects and electrolyte abnormalities

568

30. Arrhythmias

580


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INTRODUCTION
INTRODUCTION
BASIC CONCEPTS
a) Electrophysiology of the Heart
b) Electrocardiographic Instrument,
Recording Electrodes and Lead

AND
459
461
461

CHAPTER 22

BASIC CONCEPTS

c) Precautions to be Taken for

Recording an ECG
REFERENCES

472
473

466

INTRODUCTION
The electrocardiogram (ECG) is a graphic record of the electrical potentials produced
during heart beat. ECG of today is the product of a series of technological and physiological advances occurred over the past two centuries.
●

●

●

The existence of electricity in the animal (“animal electricity”) was first suggested by
Edward Bancroft (1769, in torpedo fish)1 and substantiated by John Walsh (1773 in
eel)2 and Luigi Galvani (1780 in dissected frog) (see Table 22.1).
However; it was in 1842, when Carlo Matteucci, Professor of Physics at the University
of Pisa first showed that an electric current accompanies each heart beat in a dissected
frog,3 which was later confirmed by Rudolph von Koelliker and Heinrich Muller
in 1856.4
First successful attempt to record an ECG in humans was made by Alexander Muirhead,
a Telegraph engineer in 1869 at St. Bartholomew’s hospital, London, using Thomson
Siphon recorder.
Table 22.1 History of development of ECG
Discovery/invention

Scientist

1. Animal electricity

Bancroft (1769), Walsh (1773)
and Galvani (1780)
Matteucci (1842), Koelliker and
Muller (1856)
Gabriel Lippmann (1872)
Willem Einthoven (1901)
Alexander Muirhead (1869)
Augustus D Waller (1887)
Willem Einthoven (1895)

2. Electric current accompanies each
heart beat (frog)
3. Capillary electrometer
4. String galvanometer
5. Attempt to record ECG in humans
6. Recorded first human ECG
7. Naming of deflections in ECG as “PQRST”


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BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY
●

●

●

●

●

●

French Physicist Gabriel Lippmann invented (1872) capillary electrometer, a glass tube
with a column of mercury beneath the sulphuric acid, for which he was awarded
a Nobel Prize in 1908.
British Physiologists John Burden Sanderson and Frederick Page in 1878 first recorded
the heart’s electric current with a capillary electrometer which consisted of two phases
from the ventricle of a frog.5
But it was in 1887 when Augutus D Waller, British Physiologist, at St. Mary’s Medical
school, London, recorded the first human ECG with a Lippmann’s capillary electrometer and labeled the deflections as ‘V1’, ‘V2’ and the third wave which was later
discovered as ‘A’.6
After witnessing the Waller’s demonstration in 1889, the Dutch Physiologist
Willem Einthoven recorded ECG with an improved Lippmann’s electrometer
in 1895 and named the deflections as “ABCD” and with a correction formula
as “PQRST”7 as per the mathematical convention derived from the French
Philosopher Descartes points on the curves (1662).8 His invention of string galvanometer later in 1901 provided a reliable and direct method for recording ECG,
and by 1910 the string galvanometer emerged from the research laboratory in the
clinic.9
Subsequent improvement of the instrument and better understanding of the ECG
resulted in the wide use of ECG and has become an invaluable clinical tool for the
detection and diagnosis of a broad range of cardiac conditions.
Though at present not a sine qua non for the diagnosis of the heart diseases, it continues even 100 yrs after its inception to be the most commonly used cardiologic
test
– For the diagnosis of the cause of chest pain

– As a reliable tool for the diagnosis of acute myocardial infarction and dictates the
timely administration of life saving thrombolytic therapy
– For the diagnosis and the management of cardiac arrhythmias
– Can help with the diagnosis of the cause of breathlessness
– For the diagnosis of pericarditis and
– For assessing the electrolyte disorders, drug effects and toxicity (see Table 22.2).

A patient with an organic heart disorder may have a normal ECG and a perfectly
normal individual may show non-specific ECG abnormalities. Hence, a patient
should not be given an unwarranted assurance of the absence of heart disease solely on
the basis of a normal ECG.

Table 22.2 Utility of ECG in the current era
Diagnosis

Management

Assessment

1.
2.
3.
4.

1. Acute myocardial infarction
2. Cardiac arrhythmias

1. Electrolyte disorders
2. Drug effects and toxicity

Chest pain
Acute myocardial infarction
Pericarditis
Cardiac arrhythmias


INTRODUCTION AND BASIC CONCEPTS

461

BASIC CONCEPTS
The basic concepts are described as follows:
●
●
●

Electrophysiology of the heart
Electrocardiographic instruments, recording electrodes and leads
Precautions to be taken for recording an ECG.

a) Electrophysiology of the Heart
1) The Conduction System of the Heart
See Part-1: Basic anatomy and physiology: chapter 6.
2) The Contractile or Working Myocardial Cell
See Part-1: Basic anatomy and physiology, chapter 7:
a)
b)
c)
d)
e)

Sarcolemma—see p57
Intercalated discs—see p58
Sarcotubular system—see p59
Diadic cleft—see p60
Contractile proteins—see p61

3) Electrical Activity of the Heart
a) Properties of the transmembrane potentials: see Part-1: Basic anatomy and physiology, chapter 8
b) Recording of the electrical potentials (electrogram) produced by the normal
cardiac cell:
(i) Resting cell: In a resting cardiac muscle cell, molecules dissociate into positively
charged ions on the outer surface and negatively charged ions on the inner surface of
the cell membrane, and the cell is in an electrically balanced or polarized resting state.
If an electrode is placed on the surface of the resting cell, no deflection is recorded by
the galvanometer as entire cell surface has zero potential due to high impedance of the
cell membrane (see Fig. 22.1).
(ii) Depolarization: When the cell is stimulated (S) by an excitatory electrical wave,
the negative ions migrate to the outer surface of the cell and positively charged ions
pass into the cell, this reversal of polarity is called depolarization.
●

●

●

If an electrode is placed so that the depolarization wave flows toward the electrode,
a galvanometer will record a positive or an upward deflection.
When a depolarization current is directed away from an electrode, a negative or
downward deflection is recorded.

If an electrode (E) overlies the mid portion of the cell (muscle strip), the deflection
will be diphasic. The initial deflection is upward due to an advancing positive charge,
while the second deflection is downward due to the effect of passing negative charge
(see Fig. 22.2).


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BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

ϩ
Ϫ

ϩ
Ϫ

ϩ
Ϫ

Ϫ
ϩ

Ϫ
ϩ

Ϫ
ϩ

Ϫ
ϩ

Ϫ
ϩ

Ϫ
ϩ

ϩ
Ϫ

ϩ
Ϫ

ϩ Ϫ

Ϫ ϩ

Ϫ ϩ

Polarized resting state
no deflection

ϩ Ϫ

ϩ
Ϫ

Fig. 22.1

Electrical activity

Depolarization
positive redeflection

| Electrical activity in resting cell and effect of depolarization.
Ϫ

Ϫ

ϩ

Ϫ
E

Ϫ

ϩ

E

Upward deflection
S
Current flow towards the electrode

Downward deflection
S
Current flow away from the electrode

Ϫ

E

ϩ

Diphasic deflection
S
Electrode overlying the mid portion of a cell

Fig. 22.2

| Depolarization wave in a single cell. E: electrode, S: stimulation.
ϩ

Ϫ

Ϫ

E

ϩ
E

S
Two muscle strips of equal size

Fig. 22.3

●

●

| Depolarization wave in two cells of equal size. E: electrode, S: stimulation.

If two cells (muscle strips) of approximately equal size are stimulated at a central point,
a positive of equal magnitude is recorded at either end (see Fig. 22.3).
If two cells (muscle strips) of different sizes (e.g. RV and LV) are stimulated at a central
point, a large positive deflection is recorded over the large cell (muscle mass) and a small
positive deflection followed by a deep negative deflection or entirely negative deflection
is recorded over the smaller cell surface (muscle mass) (see Fig. 22.4).


INTRODUCTION AND BASIC CONCEPTS

Ϫ
ϩ

463

ϩ

Ϫ
E

OR

S
Two muscle strips of different sizes

Fig. 22.4

| Depolarization wave in two cells of unequal size. E: electrode, S: stimulation.

Ϫ

ϩ

E

Ϫ
E

S
Depolarization towards the electrode

Fig. 22.5

E

Repolarization in the opposite direction

| Repolarization in the opposite direction of depolarization. E: electrode, S: stimulation.

Ϫ
E

ϩ

ϩ
E

S
Depolarization towards the electrode

Fig. 22.6

ϩ

E

E

Ϫ
E

Repolarization in the same direction

| Repolarization in the same direction of depolarization. E: electrode, S: stimulation.
(iii) Repolarization: During recovery period, positively charged ions return to the
outer surface and negatively charged ions move into the cell. The electrical balance of the
cell is restored; this process of return of the stimulated cell to the resting state is known
as repolarization.
●

●

If the repolarization occurs in a direction opposite to that of depolarization, the deflection will be in the same direction as that produced by depolarization (see Fig. 22.5).
If the repolarization occurs in the same direction as that of depolarization, the
deflection will be opposite to that of depolarization (see Fig. 22.6).

c) Intracellular and extracellular ion concentrations: see Part-1: Basic anatomy

and physiology, chapter 8.


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BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY
●

●

●

The transfer of the Naϩ and Kϩ ions across the cell membrane plays an important
role in generating cardiac electrical activity.
Intracellular concentration of Kϩ is 30 times greater than extracellular Kϩ. Naϩ
concentration is 30 times less inside the cell as compared to outside.
Because of this ionic composition, membrane of the resting cardiac fiber is in an
electrically balanced or polarized state.

d) Origin and sequence of cardiac activation: see Part-1: Basic anatomy and
physiology, chapter 8.
e) Phases of cardiac action potential: see Part-1: Basic anatomy and physiology,
chapter 8.
f) The modifying transmission factors: These factors affect transmission of electrical
activity of the heart throughout the body and are broadly grouped into four categories:
(i) Cellular factors determine the intensity of the current flow. They include:
●
●

Intracellular and extracellular resistance

Intracellular and extracellular ions: Lower ion concentrations reduce the intensity
of the current flow by reducing the movement of the ions and by lowering the extracellular potentials.

(ii) Cardiac factors affect the transmission of current from one cardiac cell to another.
These include:
●

●

Anisotropy: It is the property of the cardiac tissue to propagate more rapidly along the
length of the fiber than transversely. Hence, the recording electrodes oriented along
the long axis of a cardiac fiber register larger potentials than the electrodes oriented
perpendicular to the long axis.
Connective tissue between the cardiac fibers: It disrupts the effective electrical coupling between adjacent fibers. The waveforms recorded from fibers with little or no
intervening connective tissue are narrow and smooth in contour, whereas those recorded from the fibers with abundant connective tissue (fibrosis) are prolonged and
fractionated.10

(iii) Extracardiac factors include all tissues and structures that lie between the region
of cardiac electrical activity and the body surface. These tissues alter the electrical activity due to differences in electrical resistances of the adjacent tissues i.e. electrical inhomogeneities within the torso. e.g. intracardiac blood has lower resistance of 162 ⍀-cm
than the lungs (2150 ⍀-cm)
●
●
●
●
●
●
●

Ventricular walls
Intracardiac and intrathoracic blood volume

Pericardium
Lungs
Skeletal muscles
Subcutaneous fat and
Skin.


INTRODUCTION AND BASIC CONCEPTS

465

Table 22.3 Factors modifying transmission of action potential
Modifying factors
1.
2.
3.
4.
5.
6.
7.

Intracellular and
extracellular
resistance

Intracellular and extracellular resistance
Intracellular and extracellular ions
Anisotrophy
Connective tissue between the cardiac fibers
Electrical in-homogeneities within the torso

Distance between the heart and recording electrode
Eccentric location of the heart

Intracellular and
extracellular ions

Cellular factors

Eccentric location
of the heart

Cardiac action
potential

Cardiac factors

Anisotrophy

Connective
tissue between
cardiac fibers

Fig. 22.7

Connective tissue
between heart and
recording electrode

Physical factors

Extacardiac factors

1. Ventricular walls
2. Pericardium

Intracardiac and
intrathoracic
blood volume

1. Subcutaneous fat
2. Skin

1. Lungs
2. Skeletal muscles

| Factors modifying cardiac action potential.
(iv) Physical factors which affect the electrical activity are:
●

●

The distance between the heart and recording electrode is governed by ‘inverse square
law’ i.e. amplitude of the electrical potential decreases in proportion to the square of
the distance. All electrodes placed at a distance Ͼ15 cm from the heart may be considered to be equidistant from the heart in electrical sense as the amplitude of the
electrical potentials recorded will be the same in all electrodes.
Eccentric location of the heart i.e. the heart is located eccentrically more anteriorly
so that the RV and anteroseptal portion of the LV are located closer to the anterior
of the chest than other parts of the LV and atria. Hence, the ECG potentials and
wave forms generated by the anterior regions of the heart are higher and greater than
those generated by the posterior ventricular regions and atria.

As a result of all these factors, body surface potentials have amplitude of only 1% of the
amplitude of transmembrane potentials (see Table 22.3 and Fig. 22.7).


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BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 22.4 Methods of ECG recording
Methods
1.
2.
3.
4.

Standard method
ECG monitoring
Ambulatory ECG
Telemetry

b) Electrocardiographic Instrument, Recording Electrodes and Lead
1) Electrocardiographic Instrument
The two main types of apparatus used are:
●
●

String galvanometer
Radio amplifier

String galvanometer records on the photographic paper which has to be developed.
It requires experience to operate so as not to damage the valuable string.
Radio amplifier is compact, light, easy to operate and has a direct writer. Many modern machines record multiple leads simultaneously. Other methods utilized clinically
are (see Table 22.4):
●

●

●

●

Oscilloscopic viewing of the ECG i.e. ECG monitoring in coronary and intensive care
units. This produces a constant ECG on a fluorescent screen with a facility to obtain
the ECG tracing.
Ambulatory ECG recording: A small ECG tape recorder is attached to the patient
for continuous recordings for 24 hrs while the patient is ambulatory which can be
reviewed later by the attending physician for arrhythmias or myocardial ischemia.
Telemetry ECG: ECGs can be transmitted via telephone lines, for constant or temporary monitoring and interpretation by a physician many miles away from the patient.
Computer facilities are available not only for ECG interpretation but also for the
recognition and quantitation of arrhythmias.

2) Recording Electrodes and Leads
These are as follows:
●
●
●
●
●
●

●
●

Bipolar standard or limb leads
Bipolar chest leads
Unipolar augmented limb leads
Unipolar precordial or chest leads
Monitor leads
Unipolar esophageal leads
The Mason-Liker modified standard leads
Unipolar intracardiac leads.

The standard clinical ECG consists of 12 leads: 3 bipolar limb leads (I, II, III), 3 augmented limb leads (aVR, aVL, aVF) and 6 unipolar precordial leads (V1–V6). The bipolar


INTRODUCTION AND BASIC CONCEPTS

467

Connected to ECG
Ϫ I
ϩ

RA lead

LA lead
II

RA lead
Ϫ

Connected to ECG II
ϩ
LL lead

Fig. 22.8

III

LA lead
Ϫ
III Connected to ECG
ϩ
LL lead

| Bipolar standard leads (I, II, III).

and augmented limb leads are oriented in the frontal or coronal plane of the body,
while the precordial leads are oriented in horizontal or transverse plane of the body.
(1) Bipolar standard or limb leads: These were introduced by Einthoven.11 These
leads record the potential difference between the two limbs and consists of three leads:
I, II and III with four electrodes: LA (left arm electrode), RA (right arm electrode), LL
(left leg electrode), and RL (right leg electrode) which serves as a ground connection.
The electrodes are usually placed just above the wrists and ankles or to the stump in the
amputated limb.
●

●

●

Lead I represents the potential difference between LA (positive electrode) and RA
(negative electrode) (LA-RA). This lead with aVL is oriented to the left lateral wall.
Lead II represents the potential difference between LL (positive electrode) and RA
(negative electrode) (LL-RA).
Lead III represents the potential difference between LL (positive electrode) and LA
(negative electrode) (LL-LA). Leads II and III with aVF are oriented to the inferior
surface of the heart (see Fig. 22.8).

The relation between these three leads is expressed algebraically by Einthoven’s equation
or equilateral traiangle:11
Lead II ‫ ؍‬Lead I ؉ Lead III i.e. electrical potential recorded in Lead II equals the
sum of electrical potentials recorded in Leads I and III.
This equation is based on Kirchhoff ’s Law i.e. the algebraic sum of all potential
differences in a closed circuit equals zero. Hence IϪII ϩ III ϭ 0 or II ϭ I ϩ III.
(2) Bipolar chest leads: Presently, a special bipolar chest lead (Lewis lead) is sometimes used to amplify the atrial activity and thereby to clarify the mechanism of an
atrial arrhythmia.
The RA electrode is placed in the 2nd intercostal (IC) space to right of the sternum,
the LA electrode is placed in the 4th IC space to right of the sternum, and tracing is
recorded on lead I.


468

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

(3) Unipolar augmented limb leads: The unipolar leads (limb leads: VR, VL, VF;
multiple chest leads: V and esophageal leads E) were introduced by Wilson.12
● The unipolar leads represent the potentials in a given lead and not the differences in
potentials as in bipolar leads.
● The unipolar lead system consists of a Wilson’s central terminal or indifferent lead and

an exploring lead. The central terminal is formed by joining electrodes (RA, LA, and
LL) together to 5000 ⍀ resistor which is attached to negative terminal of the machine.
● In unipolar limb leads, the central terminal is connected to the RA electrode of the
machine (which acts as negative terminal) and exploring lead (positive terminal) is
connected to the LA electrode of the machine and the tracing is recorded on lead I.
Although technically this system has two electrodes i.e. bipolar leads, it represents a
unipolar lead since one of the potentials is zero (central terminal has zero potential).
● At present, only augmented limb leads (aVR, aVL and aVF, introduced by Emanuel
Goldberger in 1942) are in vogue as the amplitude of the deflections is 50% more
than the non-augmented leads (VR, VL and VF).
● To record aVR (a ϭ augmented, VR ϭ vector of right arm), the LA electrode (exploring
lead) of the machine is placed on the right arm, while RA electrode of the machine
(indifferent lead/central terminal through 5000 ⍀ resistor) is placed on the left arm
and left leg. This lead is oriented to the cavity of the heart and hence all deflections
(P, QRS, and T) are normally negative.
● To record aVL (a ϭ augmented, VL ϭ vector of left arm), the LA electrode of the
machine is placed on the left arm, while RA electrode of the machine (indifferent
lead through 5000 ⍀ resistor) is placed on the right arm and left leg. This lead is oriented to the anterolateral or superior surface of LV.
● To record aVF (a ϭ augmented, VF ϭ vector for left leg), the LA electrode of the
machine is placed on the left leg, while the RA electrode (indifferent lead through
5000 ⍀ resistor) of the machine is placed on the right arm and left arms. This lead
is oriented to inferior surface of the heart (see Fig. 22.9).
The unipolar limb leads bear a definite mathematical relationship to the standard bipolar
leads. This relationship is derived from Einthoven’s formula: VR ϩ VL ϩ VF ϭ 0.
I ϭ 2/3 (aVLϪaVR) aVR ϭ ϪI ϩ II/2
II ϭ 2/3 (aVFϪaVR) aVL ϭ I Ϫ III/2
III ϭ 2/3 (aVFϪaVL) aVF ϭ II ϩ III/2
Bipolar and unipolar leads are not of equal lead strength. An augmented lead is 87%
of the lead strength of a bipolar lead. Therefore, the above equations must be corrected.
When the strength (voltage) of an augmented unipolar lead is determined from the

bipolar lead values, it is corrected by multiplying by 0.87, and when the strength (voltage) of a bipolar lead is determined from an augmented lead values, it is corrected by
multiplying by 1.15 (100/87) (see Fig. 22.10).
Hence, I ϭ 2/3 (aVLϪaVR) (1.15)
aVR ϭ ϪIϩII/2 (0.87)
II ϭ 2/3 (aVFϪaVR) (1.15)
aVL ϭ IϪIII/2 (0.87)
III ϭ 2/3 (aVFϪaVL) (1.15)
aVF ϭ IIϩIII/2 (0.87)
To determine voltage of R waves in augmented leads from the actual measurements of
R waves from standard leads from illustration Fig. 22.10.


INTRODUCTION AND BASIC CONCEPTS

T

LA lead
RA lead

aVR

LA lead
ead
RA l

aVL

ECG
Recording on
lead l

T

469

ECG
Recording on
lead l

LL lead
LL lead

Unattached

Unattached

T

aVF

RA lead

ECG

LA lead
Recording on
lead l
LL lead
Unattached

Fig. 22.9

| Augmented limb leads—aVR, aVL, aVF.
1ϩ11
aVR = Ϫ
2
Ϫ1.3

I = 2/3 (aVL Ϫ aVR)

I ϪIII
2

aVL =

ϩ10

Ϫ3.5

ϩ1.7
ϩ1
Ϫ11.3
aVR

ϩ3

0

I

Ϫ
Ϫ

ϩ
Ϫ

ϩ16

ϩ0.5
aVL

ϩ6
ϩ5

ϩ2

ϩ1

ϩ2
III

11

II = 2/3 (aVF Ϫ aVR)

ϩ ϩ
+9.6

III = 2/3 (aVF Ϫ aVL)

+1.3
+3
aVF

aVF =

Fig. 22.10

II ϩ III
2

| Relationship between unipolar and bipolar limb leads.

aVR ϭ [10 ϩ 16/2] (0.87) ϭ Ϫ11.3
aVL ϭ [10 Ϫ 6/2] (0.87) ϭ ϩ1.7
aVF ϭ [16 ϩ 6/2] (0.87) ϭ ϩ9.6
Similar method is to used to determine voltages of P and T waves.
To determine voltage of R waves in standard leads from the actual measurements of
R waves from augmented leads from illustration Fig. 22.10.


470

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I ϭ 2/3(1.7 ϩ 11.3) (1.15) ϭ ϩ10
II ϭ 2/3(9.6 ϩ 11.3) (1.15) ϭ ϩ16
III ϭ 2/3(9.6 Ϫ 1.7) (1.15) ϭ ϩ6
Similarly, same equation is used for P and T waves.
(4) Unipolar precordial (chest) leads also consist of a Wilson’s central terminal or

indifferent lead, the negative terminal of which is attached to RA lead of the machine,
while one end of the exploring electrode is attached to LA lead of the machine, and
the other end is applied to the desired chest positions, producing multiple unipolar
chest leads i.e. V lead (V1 to V6 in standard lead system and from V1 to V9, V3RϪ9R in
extended lead system). The common precordial positions of the chest leads as per AHA
recommendations 193813 and 1992,14 are as follows:
th
● V : 4
intercostal space (ICS) at the right of the sternal border
1
th
● V : 4
ICS at the left of the sternal border
2
● V : Equidistant between V and V
3
2
4
th
● V : 5
ICS in left mid-clavicular line. All subsequent leads (V5–V9) are taken in the
4
same horizontal plane as V4 i.e. in the 5th ICS
● V : Anterior axillary line
5
● V : Mid-axillary line
6
● V : Posterior axillary line
7
● V : Posterior scapular line

8
● V : Left border of the spine
9
● V
3R-9R: Taken on the right side of the chest in the same location as the left sided leads
V3–V9 (see Fig. 22.11).
However, the usual routine ECG consists of only 12 leads: I, II, III, aVR, aVL, aVF,
and V1–V6. The precordial leads are arbitrarily subdivided into: anterior leads: V1, V2,
anteroseptal leads: V3–V4, lateral or apical leads: V5 and V6. Leads V1 and V2 tend to
be oriented to RV, while leads V4–V6 tend to be oriented to LV.
(5) Monitor leads: In coronary care unit, modified bipolar chest leads are used.
For rhythm evaluation the positive electrode is placed in usual V1 position (modified
CL1), the negative electrode is placed near the left shoulder, and a third electrode which
serves as a ground electrode is placed at a more remote area of the chest (see Fig. 22.12).
● For monitoring ST-T changes (due to ischemia), the positive electrode is placed in
V4 or V5 position.
(6) Unipolar esophageal leads are useful in recording atrial complexes, which are greatly
magnified at this location for exploring the posterior surface of the LV (see Fig. 22.13).
Esophageal lead (E) is passed into the esophagus through the nares and is attached to
V (chest) lead of the machine. The nomenclature of the lead is derived from the distance
in cm from the tip of the nares to the electrode in the esophagus. e.g. E50: represents
the esophageal lead at a distance of 50 cm from the nares. For more accurate localization
of the position of the esophageal leads, fluoroscopy may be used.
●

●
●
●

Leads E15–25: These reflect the atria.

Leads E25–35: These reflect the region of AV groove.
Leads E40–50: These reflect the posterior surface of LV.


INTRODUCTION AND BASIC CONCEPTS

471

Midclavicular line
Anterior axillary
line
Midaxillary line

Horizontal
plane of V4–6

V1 V2 V3V4 V5V6

V7

V8 V9

V9R V8R V7R

V6RV5RV4RV3R V2R V1R

Fig. 22.11

| Location of unipolar precordial leads.

E20
E30
E50
3

Fig. 22.12

1

| Monitoring leads.

2

Fig. 22.13

| Unipolar esophageal leads.

(7) Unipolar intracardiac leads: An electrode contained in a cardiac catheter is
attached to the V (chest) lead. Care must be taken as currents as low as 10 ␮A can
induce ventricular fibrillation. They are used for:
● Clarification of an arrhythmia by amplifications of the waves of the atrial activity.
● Localization of the catheter tip when a floating pacemaker is inserted without fluoroscopic guidance at bed side in intensive care units. The nature of P waves and
QRS complexes will identify the location of the catheter tip.
● Pericardiocentesis without fluoroscopic guidance, by attaching V lead to a pericardiocentesis needle under sterile conditions. When the needle strikes the epicardium,
ST elevation will be recorded, which is an indication for withdrawal of the needle.


472

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

1 small square represents
0.04 s (40 ms)

1 large square represents
0.2 s (200 ms)

R–R interval:
5 large squares represent 1 s

Fig. 22.14

●
●

●
●
●
●
●
●
●

| Relationship between the squares on the ECG paper and time.

Recording bundle of His potentials with special catheter electrodes in cardiac laboratory.
Multiple intracardiac recordings with programmed stimulation in specialized electrophysiological laboratories which are of value in determining the site of ectopic
activity, efficacy of the drug therapy and for identification of the accessory pathways.
Orientatation of leads in routine ECG:
Leads I and aVL are oriented to left lateral wall
Leads II, III and aVF are oriented to inferior surface of the heart

Leads V1 and V2 are oriented to RV
Leads V4–V6 are oriented to LV
Leads V1–V4 are considered to be anteroseptal leads
Leads V5 and V6 are considered to be apical or lateral leads
There is no lead which is oriented directly to the posterior wall of the heart.

3) The Electrocardiographic Grid
The electrocardiographic paper on which ECG is recorded is a graph paper with horizontal and vertical lines present at 1 mm intervals. A heavier line is present at every
5 mm (large square).
● Time is measured along the horizontal lines: 1 mm ϭ 0.04 s, 5 mm ϭ 0.20 s, every
15th large square (a 3 s period) is marked by a vertical line on the upper border for
quick assessment of heart rate (see Fig. 22.14).
● Voltage is measured along the vertical lines: 10 mm ϭ 1 mV.
● For routine ECG, the recording speed is 25 mm/s with usual standardization producing
1 cm or 10 mm deflection with 1 mV signal.
c) Precautions to be Taken for Recording an ECG
For good ECG record, following precautions should be taken:
● The procedure should be explained to the patient before hand in order to allay any fears
or anxieties and ECG should be recorded in a comfortable bed/couch and patient must
be completely relaxed as any muscular motions or twitchings can alter the record.
● There should be good contact between the skin and the electrode.


INTRODUCTION AND BASIC CONCEPTS

473

Table 22.5 Precautions to be observed for recording ECG
1.
2.

3.
4.
5.

●

●

●

Prior procedural explanation
Good skin and electrode contact
Proper grounding of the patient and equipment
Proper standardization of the equipment
All electronic equipment should be away from the equipment

The patient and the machine must be properly grounded to avoid alternating current
interference.
The machine must be properly standardized so that 1 mV will produce a deflection
of 1 cm. Incorrect standardization will produce inaccurate voltage of the ECG complexes
which leads to faulty interpretation.
Any electronic equipment such as electrically regulated infusion pump can produce
artifacts in the ECG; hence they should not come in contact with the patient
(see Table 22.5).

REFERENCES
1. Bancroft E. An essay on the natural history of Guiana, London: T Becket and PA de Hondt, 1769.
2. Walsh J. On the electric property of Torpedo: in a letter to Ben Franklin. Phil Trans Royal Soc 1773;
63:478–489.
3. Matteucci C. Sur un phenomena physiologique produit par les muscles en contraction. Ann Chim

Phys 1842;6:339–341.
4. von Koelhker A, Muller H. Nachwels der negation Schwankung des Murkelstroms am naturlich sich
Kontrahierenden Herzen, Verhand lungen der Physikalisch-Medizinischen Gesellschaft in Wurzberg
1856:528–533.
5. Burdon Sanderson J. Experimental results relating to the rhythmical and excitatory motions of the
ventricle of the frog. Proc R Soc Lond 1878;27:410–411.
6. Waller AD. A demonstration on man of electromotive changes accompanying the heart’s beat.
J Physiol (Lond) 1887;8:229–234.
7. Einthoven W. Ueber die Form des menschlichen Electrocardiograms. Arch fd Ges Physiol 1895;60:
102–123.
8. Descartes R. De Homine (Treatise of Man). 1662: Moyardum & Leffen, Leiden.
9. Einthoven W. Un nouveau Galvanometre. Arch Necri Sc Ex Nat 1901;6:625–633.
10. Spach MS, Dolber PC. Relating extracellular potentials and their derivatives to anisotrophic propagation at a microsopic level in human cardiac muscle. Circ Res 1986;58:356–371.
11. Einthoven W. The different forms of the human electrocardiogram and their significance. Lancet
1912(1):853–861.
12. Wilson NF, Johnston FE, Macleod AG et al. Electrocardiograms that represent the potential variation
of a simple electrode. Am Heart J 1934;9:447–458.
13. Barnes AR, Pardee HEB, White PD et al. Standardization of precordial lead. Am Heart J 1938;15:
235–239.
14. Schlant RC, Adolph RJ, DiMarco JP et al. Guidelines for electrocardiography. A report of the
American Collage of Cardiology/American Heart Association Task Force on Assessment of Diagnostic
and Therapeutic Cardiovascular Procedures (Committee on Electrcardiography). J Am Coll Cardiol
1992;19:473–481.


■ ■ ■ CHAPTER 23

T HE N ORMAL E LECTROCARDIOGRAM
WAVES
474

1. P Wave
474
2. Q(q) Wave
476
3. R(r) Wave
476
4. S(s) Wave
477
5. RЈ(rЈ) Wave
477
6. T Wave
477
7. U Wave
478
8. Ta Wave
478
INTERVALS
479
SEGMENTS
480
THE ELECTRICAL AXIS
481
1. The Hexaxial Reference System 481
2. Methods of Determination of
Electrical Axis
482

EFFECT OF HEART POSITION ON ECG
1. Electrical Rotation of the Heart
in Frontal Plane on

Anteroposterior Axis
2. Electrical Rotation of the Heart
in Horizontal Plane on Long Axis
NORMAL ECG VARIANTS
1. Normal ECG in Infants and
Children
2. Juvenile Pattern
3. Early Repolarization
4. Anxiety and Hyperventilation
5. Postprandial Response
6. Effect of Deep Respiration
REFERENCES

484

484
485
486
486
487
487
489
489
489
489

The normal ECG consists of waves, intervals and segments (see Table 23.1). Capital
letters (Q, R, S) are used for large waves of Ͼ5 mm, and small letters (q, r, s) refer to
smaller waves of Ͻ5 mm in size (see Figs 23.1 and 23.2).

WAVES
1. P Wave
It is the first deflection of the ECG which is small, smooth and rounded.
i) The initial portion is due to RA depolarization and the late portion is due to LA
depolarization. The duration of RA depolarization is 0.02–0.04 s and that of LA
is 0.05–0.06 s.
ii) The normal duration of P wave is Ͻ0.12 s (120 ms) and its amplitude is not
Ͼ2.5 mm or 25% of the normal R wave in normal individuals, especially in limb
leads.
iii) It is best seen in lead II, but usually studied in lead V1 as initial and terminal components are clearly identifiable, in which it is normally diphasic. The terminal


THE NORMAL ELECTROCARDIOGRAM

475

R

Isoelectric line: horizontal
level between cardiac cycles

ST segment

PR

T wave
P

P
QRS

V = Vulnerable
period

1

Phase

2

0

3
Phase 4
QT

Fig. 23.1

| Phases of action potential and normal ECG.
I

aVL

V1

V4

II

aVI

V2

V5

III

aVF

V3

V6

Fig. 23.2

| Normal ECG.
Table 23.1 Composition of normal ECG
Waves

Intervals

Segments

1.
2.
3.
4.
5.
6.
7.

RR
PP
PR
QRS
QT
VAT

PR
ST
J junction

P
Q (q)
R (r)
S (s)
RЈ(rЈ)
T
U

negative deflection should not exceed 0.03 s in duration and 1 mm in depth (see
Table 23.2).
iv) As the normal P wave is oriented to the left, inferiorly in frontal planes (I, II, III,
aVR, aVL and aVF), left and slightly anteriorly in horizontal planes (V1–V6).


476

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 23.2 Characteristics of normal P waves

Features

Findings

1.
2.
3.
4.
5.

Ͻ0.12 s (RA: 0.02–0.04 s, LA: 0.05–0.06 s)
Ͻ2.5 mm
Ͻ0.03 mm-s
0Њ to ϩ90Њ
II and V1 leads

Duration
Amplitude
Terminal Ϫve deflection in V1
Frontal plane axis
Best seen

Table 23.3 Characteristics of normal q waves
Features

Findings

1. Duration
2. Depth

Ͻ0.04 s
Ͻ3 mm, Ͻ25 % of the R wave amplitude
in the same QRS complex
Normal

3. QS in V1

●

●
●

It is upright in leads I, II, aVF, and V3ϪV6 with P axis in frontal plane between
0Њ and ϩ90Њ.
Inverted in a VR and frequently in V1 and sometimes in V2.
Upright, diphasic or inverted in leads III and aVL.
– P wave is upright in lead III if P axis is Ͼ ϩ30Њ, and inverted if Ͻϩ30Њ.
– P wave is upright in lead aVL if P axis is Ͻ ϩ60Њ, and inverted if Ͼϩ60Њ.

2. Q(q) Wave
All the three waves of the QRS complex are due to ventricular depolarization.
i) This wave is the initial negative deflection which is due to the initial depolarization of mid portion of left side of the interventricular septum from left to right
and hence it is oriented rightwards and anteriorly.
ii) It is a small wave of Ͻ0.04 s in duration and Ͻ3 mm deep i.e. Ͻ25% of the height
of R wave in the same QRS complex in leads I, II, aVF and V4–V6 (see Table 23.3).
● A larger Q wave (Ն0.04 s in duration or Ͼ25% of the R wave) may normally
be seen alone in lead III (for diagnostic significance, abnormal Q must also be
present in lead aVF) or aVL (for diagnostic significance, abnormal Q must also
be present in lead I or in precordial leads).
iii) A QS complex (entirely negative) is often a normal finding in V1 and occasionally

in V2.
3. R(r) Wave
It is the first positive deflection during ventricular depolarization.
i) After activation of the mid portion of the septum, anteroseptal region of the RV
is depolarized which is oriented rightwards, anteriorly and either superiorly or


THE NORMAL ELECTROCARDIOGRAM

477

inferiorly which results in r wave in V1–V2 (right precordial leads) and q wave in
I, V5 and V6, with a duration of Ͻ0.03 s.
ii) Then the major activation of both ventricles (major muscle mass) which is oriented
to the left, inferiorly and posteriorly results in a large dominant R wave in leads I,
II, and V4–V6 with a duration of 0.03–0.05 s.
The upper limit of R wave amplitude is 1.5 mV in lead I, 1.0 mV in lead aVL, 1.9 mV
in leads II, III and aVF, and 0.6 mV in V1. Among the precordial leads, the tallest R wave
is commonly seen in V4.
● Lead aVF will record R wave when frontal mean axis is 0Њ to ϩ90Њ, RS or rs complex if
mean axis is 0Њ and a negative deflection (S) if the mean axis is between 0Њ and Ϫ30Њ.
● Lead aVL will record R wave when frontal mean axis is between Ϫ30Њ and ϩ60Њ, and
a negative deflection (S) if the mean axis is ϩ60Њ to ϩ90Њ.
● Lead III will record R wave when frontal mean axis is between ϩ30Њ and ϩ90Њ, and
a negative deflection (S) if the mean axis is between ϩ30Њ and Ϫ30Њ.
4. S(s) Wave
It is the negative deflection of ventricular depolarization that follows the first positive
deflection (R), with duration of 0.01–0.02 s.
i) It is due to the activation of last portion of the ventricular mass (posterior basal
portion of LV, pulmonary conus and uppermost portion of the interventricular

septum). In leads I and V5–V6 , s is small as it is oriented rightwards.
ii) S wave may be due to major activation of ventricles and may be due to a dominant wave in leads.
● aVR: S is most prominent and always dominant, and a maximum amplitude
upto 1.6 mV may be seen. It is deepest in V2 lead among the precordial leads.
● aVF when the frontal mean axis is between 0Њ and Ϫ30Њ.
● aVL when the frontal mean axis is ϩ60Њ to ϩ90Њ.
● III when the frontal mean axis is between ϩ30Њ and Ϫ30Њ.
5. R؅(r؅) Wave
It is the second positive deflection that may occur during ventricular depolarization
following S wave.
●

●

If the activation of the last portion of the ventricular mass is oriented anteriorly,
a small positive deflection rЈ is recorded in leads V1–V2.
The negative deflection which may occur following rЈ is termed as the sЈ wave.

6. T Wave
It is the deflection produced by ventricular repolarization and coincides with the closure
of the semilunar valves.
●
●

The T wave is usually asymmetrical.
Its orientation is to the left and inferiorly with a mean frontal axis between 0Њ and
ϩ90Њ. However, it may normally be oriented slightly superiorly with mean axis
between 0Њ and Ϫ30Њ, with similar QRS orientation.

478

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY
●

●
●

It should be at least one tenth or 10% of the R wave amplitude in the same complex.
Normally, its amplitude is Ͻ6 mm in limb leads with tallest T wave in lead II, and
Ͻ10 mm in precordial leads with tallest T wave in leads V2 and V3.
It is upright in leads I, II, aVF, and V2–V6 and inverted in aVR.
It may be upright, diphasic or inverted in leads III, aVL (analogous to P wave) and V1
(occasionally in V2). It is inverted in V1 in approximately 50% of women and in
Ͻ33% of men (see Table 23.4).

7. U Wave
●
●

●

●

●

●

It follows T wave preceding the next P wave.
It is normally smaller than T wave, and usually Ͻ0.2 mV or approximately 10%

of T wave in amplitude and 0.08 s in duration, with same polarity as the preceding
T wave (see Table 23.5).
The interval from the end of the T wave to the apex of the U wave is 90–110 ms,
and the interval from the end of the T wave to the end of the U wave is 160–200 ms.
Sometimes, a notch in the T wave may be mistaken for U wave. However, the interval
between the apices of a notched T wave is usually Ͻ0.15 s, while the interval between
the apices of the T and U waves is usually Ͼ0.15 s.1
It is best seen in leads V2–V4 and II as a “hump on a camel’s back” (Ͼ prominent in
precordial leads).
It is due to slow repolarization of the Purkinje fibers.2 More recently, U wave is
thought to be due to ‘M’ cells in deep subepicardium (also for J or Osborne wave of
hypothermia).3

8. Ta Wave
It is usually a small negative deflection following P wave due to atrial repolarization
which is not usually seen in a standard 12-lead ECG.
Table 23.4 Characteristics of normal T waves
Features

Findings

1. Amplitude

1/10th of R wave in the same QRS complex, Ͻ6 mm
in limb leads and Ͻ10 mm in precordial leads
III, aVF, V1
0Њ to ϩ90Њ

2. Upright/diphasic/inverted
3. Frontal axis

Table 23.5 Characteristics of U waves
Features

Findings

1.
2.
3.
4.

10% of T wave of the same complex (Ͻ0.2 mV)
0.08 s
ϩ60Њ
V2–V4 and II leads

Amplitude
Duration
Mean frontal axis
Best seen


THE NORMAL ELECTROCARDIOGRAM
1 small square represents
0.04 s (40 ms)
QT 0.40 s PR 0.20 s

479

1 large square represents

0.2 s (200 ms)
QRS 0.10 s

R–R interval:
5 large squares represent 1 s

Fig. 23.3

| ECG intervals (PR and QRS).

INTERVALS
1. RR interval is the distance between the two consecutive R waves.
● In regular sinus rhythm, the RR interval in seconds divided by 60 will give the
heart rate/min.
● In irregular rhythm, the number of R waves in a given period of time (e.g. 10 s)
converted into the number per minute will give the ventricular rate/min.
2. PP interval is the distance between the two consecutive P waves. The heart rate can be
calculated in regular sinus rhythm similar to RR interval. However, in irregular
rhythm atrial rate per minute is computed similar to the ventricular rate.
3. PR interval is measured from the onset of P wave to the beginning of QRS complex.
It measures the AV conduction time from the onset of atrial depolarization to the
onset of ventricular depolarization which includes:
●
●
●

Depolarization of both atria,
AV node conduction including normal conduction delay in AV node (about 0.07 s),
And passage of impulse through the bundle of His and bundle branches.

The normal PR interval is 0.12–0.20 s.4 However, it must be correlated with heart rate
as slower the heart rate, longer the PR interval.
4. QRS interval (duration of QRS complex) is measured from the onset of Q (q) wave or
R (r) wave (if Q/q wave is not seen) to the termination of S wave (see Fig. 23.3).
● It measures the total ventricular depolarization time.
● The normal duration of QRS complex is Ͻ0.12 s, which is slightly longer in
males and large and tall subjects than in females and small and short subjects.5
5. QT interval is measured from the onset of Q wave to the end of T wave. It measures
the total duration of ventricular depolarization and repolarization which corresponds
to the duration of ventricular action potential.


480

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 23.6 ECG intervals
Features

Findings

1.
2.
3.
4.

Ͼ0.12–0.20 s
Ͻ0.12 s
Յ0.42 s in men, Յ0.43 s in women
Ͻ0.03 s in V1–V2

Ͻ0.05 s in V5–V6

PR interval
QRS duration
QTc interval
VAT

Intrinsic deflection
(VAT)
–

+
E

S

Fig. 23.4

| Ventricular activation time (VAT).

i) Corrected QT interval (QTc ): As the QT interval varies with the heart rate i.e.
QT interval decreases as the heart rate increases, it should always be corrected by
Bazett (1920) formula6:
QTc ϭ QT/(R–R)
where QTc is corrected QT interval, QT is the measured QT interval, RR is the
measured RR interval.
● The QT is Յ0.42 s in men and Յ0.43 s in women.
c
● The QT interval is slightly longer in the evening and at night during sleep due
to influence of the autonomic nervous system.7

ii) QU interval: When the end of T wave overlaps the beginning of U wave especially in metabolic abnormalities, QT is designated as QT (U) or QU interval.
iii) QT interval dispersion: The QT interval also varies from lead to lead, maximum
in mid precordial leads (V2–V3) and normally the difference between the longest
and shortest intervals in the leads should not be more than 0.05 s. This variation
in QT interval duration from lead to lead is known as QT interval dispersion and
increased QT interval dispersion indicates electrical instability and risk of occurrence of ventricular arrhythmias8 (see Table 23.6).
6. Ventricular activation time (VAT) is the time that the impulse takes to traverse the
myocardium from endocardium to epicardial surface (see Fig. 23.4). It reflects the intrinsicoid deflection and is measured from the beginning of the Q wave to the peak of
R wave. Normally, it should not exceed 0.03 s in V1–V2 leads and 0.05 s in V5–V6 leads.

SEGMENTS
1. PR segment is the portion of the ECG tracing from the end of the P wave to the
onset of QRS complex and normally it is isoelectric.


THE NORMAL ELECTROCARDIOGRAM

481

2. ST segment is the portion of the ECG tracing that lies between the end of the QRS
complex and the beginning of the T wave.
● It represents the period when all parts of the ventricles are in depolarized state.
But early repolarization may encroach on the ST segment to a variable degree.
● The point at which QRS complex ends and ST segment begins is the J or junction
point. The ST segment from J point to the beginning of T wave is usually isoelectric, but may vary from Ϫ0.5 (depression) to ϩ1 mm (elevation) in precordial leads.

THE ELECTRICAL AXIS
The electrical axis may be defined as a vector or an electromotive force originating in the
center of Einthoven’s equilateral triangle which has magnitude, direction and polarity.9,10
The mathematical symbol expressed is an arrow pointing in the direction of the net

potential (positive or negative), while its length indicates the magnitude of the electrical
force. The electrical axis is usually determined in the frontal plane from the limb leads by
using the hexaxial reference system, derived from Einthoven’s equilateral triangle.
1. The Hexaxial Reference System
It is composed of lead axis of six frontal plane limb leads. The lead axis of these leads
is rearranged so that their centers overlay one another and these axes divide the plane
into 12 segments, each subtending 30Њ (see Fig. 23.5).
●
●
●
●
●
●

The postive pole of lead I is designated as 0Њ, and the negative pole as Ϯ180Њ
The positive pole of aVF is designated as ϩ90Њ, and the negative pole as Ϫ90Њ
The positive pole of lead II is designated as ϩ60Њ, and negative pole as Ϫ120Њ
The positive pole of lead III is designated as ϩ120Њ and negative pole as Ϫ60Њ
The positive pole of aVR is designated as Ϫ150Њ and negative pole as ϩ30Њ
The positive pole of aVL is designated as Ϫ30Њ and negative pole as ϩ150Њ
Superior
–120o
–150o

–90o
–60o
–30o

aV
R

L
aV

I

Right

+120o

aVF
+90o
Inferior

Fig. 23.5

| The hexaxial reference system.

II

+150o

III

±180o

+60o

0o

+30o
Left