ELECTROCARDIOGRAM

It is a graphic recording of changes of total electromotive

force of heart (a sum vector) during spreading excitation wave
in the heart

Functions of myocardium that can be

evaluated by the electrocardiography:

functions of automaticity, conductibility, excitability.

But not myocardial contractility!

AUTOMATICITY

It is ability of heart to initiate electric impulses in the absence

of exogenous irritants.

Pacemakers:
1. Pacemaker of the first order – sinoatrial node (60-80 electric impulses per minute)
2. Pacemaker of the second order – atrioventricular joint (march between AV node
and initial part of His bundle) (40-60 electric impulses per minute)
3. Pacemaker of the third order – finite part of His bundle, its branches and
hemifascicles (25-40 electric impulses per minute)

In health only pacemaker is sinoatrial node which suppresses

activity of the rest of ectopic pacemakers!
CONDUCTIBILITY

It is ability of specialized conducting tissue and ordinary

muscles to conduct the activation.

Ordinary muscles conduct impulses at a velocity much lower than

intraventricular specialized conducting tissue (the His-Purkinje system),
but considerably faster than AV node.
EXCITABILITY

It is ability of specialized conducting tissue cells and ordinary

muscle fibers to become excited under the influence
exogenous electric impulses.

Ordinary muscles conduct impulses at a velocity much lower than

intraventricular specialized conducting tissue (the His-Purkinje system),
but considerably faster than AV node.
BASICS ELECTROCARDIOGRAPHY
An extracellular cardiac electrical field is
generated by ion fluxes across cell
membranes and between adjacent cells.
These ion currents are synchronized by
cardiac activation and recovery sequences
to generate a cardiac electrical field in and
around the heart that varies with time during
the cardiac cycle. As each site is activated,
the polarity of the transmembrane potential
is converted from negative to positive.
Activation of each fiber creates a dipole
oriented in the direction of activation. The
net effect of all the dipoles in this wave front
is a single dipole equal to the (vector) sum
of the effects of all the simultaneously active
component dipoles. Thus, an activation front
propagating through the heart can be
represented by a single dipole that projects
positive potentials ahead of it and negative
potentials behind it.
Isopotential lines of the heart’s
electromotive force on the body surface
THE CONDUCTION SYSTEM OF THE HEART
1 – sinoatrial node;
2 – anterior internodal tract;
3 – Bachmann's bundle;
4 – medial internodal tracts;
5 – Kent’s bundle;
6 – trunk of His’ bundle;
7 – left bundle branch;
8 – posterior hemifascicle;
9 – anterior hemifascicle;
10 – Purkinje fibers;
11 – right bundle branch;
12 – Mahaim fibers;
13 – James tract;
14 – atrioventricular node;
15 – posterior internodal tract.
THE HIS-PURKINJE CONDUCTION SYSTEM
Atrial activation begins with
impulse generation in the
sinoatrial (SA) node. Once the
impulse leaves this pacemaker
site, atrial activation spreads in
the right atrium and
simultaneously impulse
spreads along the atrial
internodal tracts toward the left
atrium and atrioventricular (AV)
node. Upon exiting the AV
node, the impulse traverses
the bundle of His to enter the
bundle branches (right and left)
and then Purkinje fibers to
finally activate working muscle
fibers. Sequence of ventricular
activation: interventricular
septum, lateral walls of the left
and right ventricles (from
endocardium to epicardium),
the basal areas of the
ventricles are the last to be
activated.
 WAVE OF DEPOLARISATION

Shape of QRS complex in any lead depends on orientation of

that lead to vector of depolarisation.

An electrode senses positive potentials when an activation

front is moving toward it and negative potentials when the
activation front is moving away from it.
 COMPONENTS USED IN THE RECORDING AND
PROCESSING OF AN ELECTROCARDIOGRAM

A modern electrocardiograph includes the following parts: (1) the sensitive elements,
electrodes, which are attached to the body of the patient to pick up the potential
differences that arise during excitation of the heart muscle, and lead wires; (2) amplifiers,
which amplify the minutest voltage of e.m.f. (1-2 mV) to the level that can be recorded;
(3) a galvanometer to measure the voltage; (4) a recording instrument, including a
traction mechanism and a time marker; and (5) a power unit (the instrument is supplied
either from the AC mains or a battery).
 OPERATING PRINCIPLES
The ECG is recorded on to standard
paper travelling at a rate of 50 mm/s.
The paper is divided into large
squares, each measuring 5 mm wide
and equivalent to 0.1 s. Each large
square is five small squares in width,
and each small square is 1 mm wide
and equivalent to 0.02 s.

The electrical activity detected by

If an electrocardiogram is recorded at a
speed of 25 mm/s, each millimeter of
the curve corresponds to 0.04 second.
the electrocardiogram machine is
measured in millivolts. Machines are
calibrated so that a signal with an
amplitude of 1 mV moves the
recording stylus vertically 1 cm. The
amplitude of waveforms is
expressed as:
0.1 mV = 1 mm = 1 small square.
CLINICAL ELECTROCARDIOGRAPHIC
LEAD SYSTEMS
BIPOLAR LIMB LEADS

Lead POSITIVE NEGATIVE

INPUT INPUT
LEAD I Left arm Right arm

LEAD II Left leg Right arm

LEAD III Left leg Left arm

 EINTHOVEN'S LAW

I + III = II

The heart vector H and

its projections on the
lead axes of leads I and
III. Voltages recorded in
lead I will be positive
whereas potentials in
lead III will be negative
 AUGMENTED UNIPOLAR LIMB LEADS

Dotted lines indicate connections to generate the reference electrode potential

Lead POSITIVE INPUT NEGATIVE INPUT

aVR Right arm Left arm + left leg
aVL Left arm Right arm + left leg
aVF Left leg Left arm + left arm
 HEXAXIAL DIAGRAM

Projection of six leads in vertical plane showing each lead's view of the heart.
The Bayley hexaxial reference system composed of the lead axes of the six frontal
plane leads. The lead axes of the six frontal plane leads have been rearranged so
that their centers overlay one another. These axes divide the plane into 12
segments, each subtending 30 degrees. Positive ends of each axis are labeled with
the name of the lead.
POSITION OF THE SIX CHEST ELECTRODES

V1: right sternal edge, 4th intercostal space;

V2: left sternal edge, 4th intercostal space;
V3: between V2 and V4;
V4: mid-clavicular line, 5th space;
V5: anterior axillary line, horizontally in line with V4;
V6: mid-axillary line, horizontally in line with V4
 LEAD VECTORS

The three bipolar limb leads, the three augmented unipolar limb leads (left),
and the six unipolar precordial leads (right).
 ANATOMICAL RELATIONS OF LEADS IN A
STANDARD 12 LEAD ELECTROCARDIOGRAM
Lead I: lateral wall of left ventricle
Lead II: a sum potential of heart on longitudinal axis
Lead III: right ventricle and posterodiaphragmatic (inferior) surface of left
ventricle
aVR: a sum potential of heart on longitudinal axis (the heart vector is oriented
from this electrode, therefore Р wave, maximal wave of QRS complex and Т
wave are negative);
aVL: high areas of lateral wall of left ventricle
aVF: right ventricle and posterodiaphragmatic (inferior) surface of left ventricle
V1 and V2: anterior wall of heart

V3: anterior area of the interventricular septum

V4: heart apex

V5: anterolateral wall of left ventricle

 MAKING A RECORDING

1. The patient must lie down and relax (to prevent muscle
tremor)
2. Connect up the limb electrodes, making certain that they
are applied to the correct limb
3. Calibrate the record with the 1 mV signal
4. Record the six standard leads – three or four complexes
are sufficient for each
5. Record the six V leads.
 THE NORMAL ELECTROCARDIOGRAM

The P wave is generated by activation of the atria,

the PR segment represents the duration of atrioventricular (AV) conduction,
the QRS complex is produced by activation of both ventricles,
the ST-T wave reflects ventricular recovery.
 THE ECG WAVES
R

T
P

Q
S

The P wave represents the electrical activation (depolarization) of both atria;

the Q wave corresponds to excitation of the interventricular septum (beginning
of ventricular depolarization);
the R wave displays the subsequent spreading of excitation of right and left
ventricular myocardium;
the S wave represents the completion of ventricular depolarisation (excitation
of the basal areas of interventricular septum);
the T wave corresponds to the process of rapid late repolarization of the
ventricular myocardium.
 THE ECG INTERVALS
RR

PQ QT TP

The PQ interval represents the time required for impulse to pass from SA node
through the atrial internodal tracts, atrioventricular node, His’ bundle, bundle
branches, Purkinje fibers to the working muscle fibers (normal duration of PQ
interval is 0.12-0.20 sec);
the RR interval represents the duration of one cardiac cycle;
the QT interval shows the duration of electric systole of ventricles;
the interval TP displays the duration electric diastole of ventricles.
CHARACTERISTICS OF THE P WAVE

•Positive in leads I and II

•Best seen in leads II and V1
•Commonly biphasic in lead V1
•< 0.1 sec in duration
•< 2.5 mm in amplitude
 ABNORMAL P WAVE

Normal P wave P mitrale P pulmonale

•inverted (i.e. negative in the leads in which it is usually positive). This
indicates depolarization of the atria in an unusual direction, and that the
pacemaker is not in the sinus node, but is situated either elsewhere in the
atrium, in the AV node or below this; or there is dextrocardia
•broadened and notched, due to delayed depolarization of the left atrium
•when this chamber is enlarged (P mitrale). In V1, the P wave is then usually
biphasic with a small positive wave preceding a deep and broad negative one
•tall and peaked, exceeding 3 mm, as a result of right atrial enlargement (P
pulmonale)
•absent or invisible due to the presence of junctional rhythm or sinoatrial block
•replaced by flutter or fibrillation waves.
CHARACTERISTICS OF THE QRS COMPLEX

• The R wave is any positive (upward) deflection of the QRS. If there is more than
one R wave, the second is denoted R’; an R wave of small voltage may be
denoted r.
• A negative (downward) deflection preceding an R wave is termed Q.
• A negative deflection following an R wave is termed S.
• If the ventricular complex is entirely negative (i.e. there is no R wave), the
complex is termed QS.
• The whole complex is often referred to as the QRS complex irrespective of
whether one or two of its components are absent.
 GENESIS OF THE QRS COMPLEX

The first phase, directed from left to right across the The QRS complex represents
septum, produces a Q wave in V6 and an R wave in the electrical forces
V1. The second phase, due mainly to depolarization of generated by ventricular
the left ventricle from endocardium to epicardium, depolarisation. The duration
results in a tall R wave in V6 and a deep S wave in V1. of the QRS complex is
Finally, depolarization of the basal parts of the measured in the lead with the
ventricles may produce a terminal S wave in V6 and a widest complex and should
terminal R wave in V1. not exceed 0.10 sec.
 MORPHOLOGY OF THE QRS COMPLEX IN
THE PRECORDIAL LEADS

In the precordial leads, QRS morphology changes depending on whether the

depolarisation forces are moving towards or away from a lead. The forces generated by
the free wall of the left ventricle predominate, and therefore in lead V1 a small R wave
is followed by a large negative deflection (S wave). The R wave in the precordial leads
steadily increases in amplitude from lead V1 to V6, with a corresponding decrease in S
wave depth, culminating in a predominantly positive complex in V6. Thus, the QRS
complex gradually changes from being predominantly negative in lead V1 to being
predominantly positive in lead V6. The lead with an equiphasic QRS complex is located
over the transition zone; this lies between leads V3 and V4, but shifts towards the left
with age.
 CHARACTERISTICS OF THE Q WAVE

When the wave of septal depolarisation travels away from the recording
electrode, the first deflection inscribed is negative. Thus small "septal" Q waves
are often present in the lateral leads, usually leads I, aVL, V5, and V6.
These non-pathological Q waves are less than 2 mm and less than one 0.03 sec
wide, and should be <25% of the amplitude of the corresponding R wave.
‘Normal’ Q wave in lead III diminishes or disappears on deep inspiration because
of an alteration in the position of the heart, whilst the ‘pathological’ Q wave of
infarction persists.
CHARACTERISTICS OF THE R WAVE

The height of the R wave is variable and increases progressively

across the precordial leads; it is usually <27 mm in leads V5 and V6.
The R wave in lead V6, however, is often smaller than the R wave in
V5, since the V6 electrode is further from the left ventricle.
CHARACTERISTICS OF THE S WAVE

The S wave is deepest in the right precordial leads; it decreases in

amplitude across the precordium, and is often absent in leads V5 and
V6. The depth of the S wave should not exceed 30 mm in a normal
individual, although S waves and R waves >30 mm are occasionally
recorded in normal young male adults.
 CHARACTERISTICS OF THE T WAVE

The normal T wave is asymmetrical, the first half having a more gradual slope than
the second half.
The T wave should generally be at least 1/8 but less than 2/3 of the amplitude of the
corresponding R wave; T wave amplitude rarely exceeds 10 mm.
T wave orientation usually corresponds with that of the QRS complex, and thus is
inverted in lead aVR, and may be inverted in lead III. T wave inversion in lead V1 is
also common. It is occasionally accompanied by T wave inversion in lead V2, though
isolated T wave inversion in lead V2 is abnormal.
CHARACTERISTICS OF THE ST SEGMENT

The QRS complex terminates at the J point or ST junction. The ST segment

lies between the J point and the beginning of the T wave, and represents the
period between the end of ventricular depolarisation and the beginning of
repolarisation.
The ST segment should be in the same horizontal plane as the TP segment;
the J point is the point of inflection between the S wave and ST segment.
CHANGE IN ST SEGMENT MORPHOLOGY ACROSS THE
PRECORDIAL LEADS

In leads V1 to V3 the rapidly ascending S wave merges directly with the T

wave, making the J point indistinct and the ST segment difficult to identify.
This produces elevation of the ST segment, and this is known as "high take-
off."
Non-pathological elevation of the ST segment is also associated with
benign early repolarisation, which is particularly common in young men,
athletes, and black people.
 NORMAL AND ABNORMAL ST SEGMENTS AND T WAVES

(A) Normal ST segment with J point. (B) Horizontal ST depression in myocardial ischaemia. (C) ST
segment sloping upwards in sinus tachycardia. (D) ST sagging in digitalis therapy. (E) Asymmetrical
T wave inversion associated with ventricular hypertrophy. (F) Similar pattern sometimes seen
without voltage changes in hypertrophy – ‘strain’. (G) ST sagging and prominent U waves of
hypokalaemia. (H) Symmetrically inverted T wave of myocardial ischaemia or infarction. (I) ST
elevation in acute myocardial infarction. (J) ST elevation in acute pericarditis. (K) Peaked T wave in
hyperkalaemia.
 QT INTERVAL

The QT interval is measured from the beginning of the QRS complex to the end of the T
wave and represents the total time taken for depolarisation and repolarisation of the
ventricles.
The QT interval lengthens as the heart rate slows, and thus when measuring the QT
interval the rate must be taken into account. As a general guide the QT interval should
be 0.35-0.45 sec, and should not be more than half of the interval between adjacent R
waves (R-R interval). The QT interval increases slightly with age and tends to be longer
in women than in men. Bazett's correction is used to calculate the QT interval corrected
for heart rate (QTc): QTc = QT/√ R-R (seconds).
 THE ORDER ECG INTERPRETATION

• Regularity of heart beats (regular, irregular)

• Rhythm (sinus or other)
• Heart rate
• Cardiac axis
• A description of the P wave
• Conduction intervals
• A description of the QRS complexes
• A description of the ST segments and T waves
• A description of the QT interval
• ECG report.
 THE ECG REPORT

1. Rhythm (sinus or other)

2. Regularity of cardiac rhythm (regular, irregular)
3. Heart rate
4. Cardiac axis
5. ECG abnormalities of:
- rhythm
- conduction
- hypertrophy of myocardium of ventricles or atria
- myocardial damage (ischaemia, injury, necrosis, scar)
 THE RHYTHM OF THE HEART

As known, electrical activation of the heart can sometimes begin in places other
than the SA node. The word ‘rhythm’ is used to refer to the part of the heart
which is controlling the activation sequence. The normal heart rhythm, with
electrical activation beginning in the SA node, is called ‘sinus rhythm’.
CARDINAL FEATURES OF SINUS RHYTHM

• The P wave appears before each QRS complex

• The P wave has the permanent identical contour in
the same lead
• The P wave is upright in leads I and II
• Each P wave is followed by a QRS complex
• The heart rate is 60-89 beats/min
 REGULARITY OF CARDIAC RHYTHM

Regular rhythm

• The RR intervals should be equal.

• Its fluctuations normally do not exceed 0.1 sec or ±10%.

Irregular rhythm

• Greater variations in the length of the RR intervals

indicate disordered cardiac rhythm.
 CALCULATION OF HEART RATE IN
REGULAR RHYTHM (1)
Duration of one cardiac cycle (the RR interval) and the number of such
cycles in one minute length should be determined.

If the ECG is recorded on to paper travelling at a rate of 50 mm/s:

60sec 60
Heart Rate = =
RRsec 0.02 × RRmm
or

3000
Heart Rate =
RRmm
 CALCULATION OF HEART RATE IN
REGULAR RHYTHM (2)

If the ECG is recorded on to paper travelling at a rate of 25 mm/s:

60sec 60
Heart Rate = =
RRsec 0.04 × RRmm

or

1500
Heart Rate =
RRmm
 CALCULATION OF HEART RATE IN
IRREGULAR RHYTHM (1)
The length of five or ten RR intervals is determined, the mean, maximum
and minimum RR interval found, and the cardiac rate is finally determined as
for regular cardiac rhythm.

If the ECG is recorded on to paper travelling at a rate of 50 mm/s:

60 3000
Heart Ratemean = =
0.02 × RRmm ( mean ) RRmm ( mean )

60 3000
Heart Ratemax = =
0.02 × RRmm (min) RRmm (min)

60 3000
Heart Ratemin = =
0.02 × RRmm (max) RRmm (max)
 CALCULATION OF HEART RATE IN
IRREGULAR RHYTHM (2)
The number of RR intervals is determined for certain time, e.g. for 3
seconds. This result is multiplied by 20 in this case because:

60 sec ÷ 3 sec = 20

Heart Ratemean = RRnumber for 3 sec × 20

 THE ELECTRICAL AXIS

Calculation of the mean electrical axis during the QRS complex from the areas under the
QRS complex in leads I and III. Magnitudes of the areas of the two leads are plotted as
vectors on the appropriate lead axes, and the mean QRS axis is the sum of these two
vectors.
 THE ELECTRICAL AXIS AND α ANGLE

The electrical axis of the heart (ventricles) is a projection of a sum electromotive force
vector of ventricular depolarization in the frontal plane.
The α angle is the angle formed by a horizontal line, which is parallel to the axis of lead I,
and the electrical axis of the heart.
 POSITIONS OF THE ELECTRICAL AXIS OF THE
HEART
Normal positions:
vertical position: α angle = +70-+90°,
normal one: α angle = +40-+69°,
horizontal position: α angle = 0-+39°.

Pathological positions:
left axis deviation: α angle <0°;
right axis deviation: α angle > +90°.
NORMAL POSITION OF THE ELECTRICAL AXIS

∠α = +40°… + 69°

R II > R I > R III

R III > S III
S aVL ≈ R aVL
VERTICAL POSITION OF THE ELECTRICAL AXIS

∠α = + 90° ∠α = +70°… + 90°

R II = R III > R I R II > R III > R I
RI = SI RI > SI
R aVF max > R I and R II S aVL ≥ R aVL
HORIZONTAL POSITION OF THE ELECTRICAL AXIS

∠α = 0°… + 30° ∠α = 0°

R I > R II > R III R I > R II > R III

S III > R III S III > R III
R aVF > S aVF R aVF = S aVF
 LEFT AXIS DEVIATION

∠α = 0°… − 30° ∠α = − 30° ∠α < − 30°

R I > R II > R III R I > R II > R III R I > R II > R

R II > S II R II = S II III
S III > R III S III > R III S II > R II
S avF > R avF S avF > R avF S III > R III
S avF > R avF
R avR ≥ Q(S)
 RIGHT AXIS DEVIATION

∠α ≥ +120°
∠α > + 90°
R III > R II > R I
R III > R II > R I SI > RI
SI > RI R aVR ≥ Q (S) aVR
CALCULATION OF ELECTRICAL AXIS POSITION

Algebraic sum QRS complex

Algebraic sum QRS complex
in lead I in lead III

Lead I Lead III

Table
DISORDERS OF CARDIAC RHYTHM (ARRYTHMIAS)

Arrhythmia – any abnormality in the rate, regularity, or sequence of

cardiac activation

Types

1. Abnormalities of heart rate (more or less than normal range)

2. Irregular rhythm of any origin
3. Any non-sinus rhythm (abnormal location of impulse formation –
ectopic pacemaker)
4. Disorders of impulse conduction
 DISORDERS OF IMPULSE FORMATION

A. Disorders of automaticity of sinoatrial node (nomotopic arrythmias):

2. Sinus bradycardia
3. Sinus tachycardia
4. Sinus arrhythmia
B. Ectopic rhythm due to predominance of automaticity of ectopic centre
C. Ectopic rhythm without disorders of automaticity (re-entry mechanism)
• Extrasystole (atrial, atrioventricular, ventricular)
8. Paroxismal tachycardia (atrial, atrioventricular, ventricular)
9. Atrial flutter
10.Atrial fibrillation
11.Ventricular fibrillation
DISORDERS OF IMPULSE CONDUCTION

1. Sinoatrial blocks
2. Intraatrial blocks
3. Atrioventricular blocks:
a) first degree block
b) Mobitz type I of second degree block
c) Mobitz type II of second degree block
d) third-degree (complete) block
4. Intraventricular block (His bundle branch blocks):
a) monofascicular heart block
b) bifascicular heart block
c) trifascicular heart block
 ECG CRITERIA OF SINUS BRADYCARDIA

• Sinus rhythm features are present in each cardiac cycle (the P

waves before each QRS complex, they have the permanent
identical contour in the same lead, upright P wave in lead II, the PR
interval is at least 0.12 s);
• impulse formation beginning in the sinus node is slowed down (most
often 40-59 beats/min);
• the RR interval is enlarged due to electric diastole TP.

1.20 sec
 CAUSES OF SINUS BRADYCARDIA

Physiological

•During sleep in normal individuals

•High vagal tone ( athletes and young healthy adults)

Pathological

•Acute myocardial infarction

•Drugs for example, β-blockers, digoxin, amiodarone
•Obstructive jaundice
•Raised intracranial pressure
•Sick sinus syndrome
•Hypothermia
•Hypothyroidism
ECG CRITERIA OF SINUS TACHYCARDIA
• Sinus rhythm features are present in each cardiac cycle
(see above);
• Impulse formation beginning in the sinus node is
accelerated (between 91 and 160 (180) beats/min,);
• The RR interval is shortened due to electric diastole TP.

0.4 sec

The rate rarely exceeds 200 beats/min in adults. The rate increases
gradually and may show beat to beat variation. With a fast tachycardia
the P wave may become lost in the preceding T wave. ST segment
may be sloping upwards in fast sinus tachycardia.
 CAUSES OF SINUS TACHYCARDIA

• Physiological
Exertion, anxiety, pain

• Pathological
Fever, anaemia, hypovolaemia, hypoxia, heart failure

• Endocrine
Thyrotoxicosis, pregnancy, pheochromocytoma

• Pharmacological
Adrenaline as a result of phaeochromocytoma;
salbutamol; alcohol, caffeine
 ECG CRITERIA OF SINUS ARRHYTHMIA
• Sinus rhythm features are present in each cardiac cycle (see
above);
• Impulse formation beginning in the sinus node is irregular;
• The RR intervals vary in length: the difference between maximum
RR interval and minimum RR interval exceeds 0.12 sec or
fluctuations of RR interval duration exceed 10 per cent.

RRmax − RRmin
× 100 > 10%
RRmax

inspiration expiration

s s 0 s s s s
 CAUSES OF SINUS ARRHYTHMIA

It is present in most healthy young persons at rest; it consists of a

quickening of the heart rate during inspiration and a slowing during
expiration, tends to be intensified by deep breathing, and tends to
disappear when the breath is held or when the heart rate is
increased by exercise or fever.
It has no pathological significance.
 ATRIAL FIBRILLATION

Chaotic, disorganized excitation and contractions of separate atrial fibers

(rapid irregular twitchings ) at a rate of 350 to 600 beats/min (without
effective atrial contraction), the ventricles respond to the dysrhythmic
bombardment from the atria irregularly (absolute arrhythmia of ventricular
contractions).

Clinical forms of atrial fibrillation

• tachyarrhythmic, in which ventricles contract at a rate from 90 to 180 per min,

bradyarrhythmic, in which the heart rate does not exceed 60 per min,
normosystolic, in which the ventricles contract at a rate of 60-90 per min.
• paroxismal;
persistent.
 MECHANISM OF ATRIAL FIBRILLATION

Atrial fibrillation is caused by multiple re-entrant circuits or "wavelets" of activation

sweeping around the atrial myocardium. These are often triggered by rapid firing foci.
The direction of excitation wave varies permanently in atrial fibrillation due to unequal
duration of the refractory period of separate muscular fibres. There is a chaotic
excitation and their contraction with frequency of 350-600 per a minute.
Conduction of atrial impulses to the ventricles is variable and unpredictable.
CAUSES OF ATRIAL FIBRILLATION
•Ischaemic heart disease
•Myocardial infarction
•Hypertensive heart disease
•Rheumatic heart disease (mitral valve disorders)
•Myocarditis
•Thyrotoxicosis
•Alcohol misuse (acute or chronic)
•Cardiomyopathy (dilated or hypertrophic)
•Sick sinus syndrome
•Post-cardiac surgery
•Chronic pulmonary disease
•Idiopathic (lone)
CLINICAL FEATURES OF ATRIAL FIBRILLATION

Complaints:
• palpitations and/or intermissions in heartbeats

Physical examination:
• irregular apex beat is revealed by inspection and palpation;
• pulse is irregular and unequal; pulse deficit is possible;
• the following findings may be revealed by auscultation of heart: heart
sounds are irregularly irregular, variation in intensity of the first heart
sound if difference in duration of RR intervals is significant (loud S1
and quiet S2 are heard after short diastole, and vice versa quiet S1
and loud S2 are heard after long diastole).
 ECG CRITERIA OF ATRIAL FIBRILLATION
• P waves is absent in all leads;
• multiple oscillating baseline waves ‘f’ (fibrillation) of various
amplitude and shape are recorded instead of P waves (usually
best seen in the leads II, III, aVF, V1 and V2);
• RR intervals are of various duration (irregular ventricular rhythm);
• QRS complexes are not changed.
 ATRIAL FLUTTER

Rapid regular coordinated ectopic atrial rhythm at a rate of 220 to 350

beats/min, accompanied by regular or irregular ventricular contractions
of various frequency.

As a rule, not all atrial impulses are conducted to the ventricles. Each other, third
or fourth impulse, is only conducted to the ventricles since partial (incomplete)
atrioventricular block develops simultaneously. Conduction of the AV node
sometimes constantly changes: each other impulse is now conducted; then the
rhythm changes to conduction of each third impulse, and the ventricles contract
arrhythmically.
Patients with accelerated heart rate (high conduction of the AV node) complain of
palpitation. Examination reveals tachycardia that does not depend on the posture
of the patient, exercise or psychic strain, since the SA node does not function as
the pacemaker in atrial flutter.
 MECHANISM AND CAUSES OF ATRIAL FLUTTER

Atrial flutter is usually the result of a single re-entrant circuit in the right atrium with
secondary activation of the left atrium.
The causes of atrial flutter are similar to those of atrial fibrillation, although idiopathic
atrial flutter is uncommon. It may convert into atrial fibrillation over time or, after
administration of drugs such as digoxin.
 ECG CRITERIA OF ATRIAL FLUTTER

• the P wave is absent in all leads;

• regular multiple high equiform waves ‘F’ (flutter) are recorded
instead of P waves (undulating saw-toothed baseline waves
usually best seen in the leads II, III, aVF, V1, V2);
• QRS complex is not changed;
• ST segment and T wave are deformed due to superposition of
F waves;
• RR intervals are equal in duration (in the regular type of atrial
flutter) or in different duration (in the irregular type of atrial
flutter).
 EXTRASYSTOLE
Extrasystole is a premature activation of all heart or its parts (only
atriums or only ventricles) that breaks correct sequence of cardiac
contractions.

Compensatory pause – the pause following an extrasystole, when

the pause is long enough to compensate for the prematurity of the
extrasystole; the short cycle ending with the extrasystole plus the
pause following the extrasystole together equal two of the regular
cycles.

Coupling interval – the interval, usually expressed in hundredths

of a second, between a normal sinus beat and the ensuing
premature beat.
 COMPENSATORY PAUSE
Compensatory pause is called fully if the RR interval produced by the two
sinus-initiated QRS complexes on either side of the premature complex
equals twice the normally conducted RR interval: RRse+RRes=2RRs

Rs Rs Re Rs Rs Rs

Noncompensatory pause: RRse+Rres<2RRs

Rs Rs Re Rs Rs Rs
 MECHANISMS OF EXTRASYSTOLE

Three common mechanisms exist for extrasystoles, (1) automaticity, (2)

reentry, and (3) triggered activity, as follows:

• Automaticity: the development of a new site of depolarization in non-nodal

ventricular tissue, which can lead to an extrasystole. Increased automaticity
could be due to electrolyte abnormalities or ischemic myocardium.
• Re-entry circuit: return of the same impulse into a zone of heart muscle that it
has recently activated; re-entry typically occurs when slow-conducting tissue
(e.g., infarcted myocardium) is present adjacent to normal tissue (the re-entry
circuits that support ventricular extrasystole can be "micro" or "macro" in
scale).
• Triggered activity: afterdepolarizations triggered by a preceding impulse can
lead to premature activation if the threshold is reached, and this can cause a
extrasystole. Afterdepolarization can occur either during (early) or after (late)
completion of repolarization.
 TYPES OF EXTRASYSTOLES (1)

a – atrial; b – nodal; c – ventricular; d – polytopic. Extrasystoles are

marked by the arrows.
 TYPES OF EXTRASYSTOLE (2)
Interpolated extrasystole – a extrasystole which, instead of being followed by a
compensatory pause, is sandwiched between two consecutive sinus cycles.
s s

Premature extrasystole – initial wave of extrasystole collides with previous T wave.

Ex

Group extrasystoles – a normal contraction follows by several extrasystoles at a run.

These are 3 and more extrasystoles follows one after another.
 ECG CRITERIA OF ATRIAL EXTRASYSTOLE
• Inter-beat TP (RR) interval between preceding and extrasystolic beat
is shortened (premature appearance of the cardiac complex);
• the P wave appears before the QRS complex of extrasystole;
• alteration of extrasystolic P wave (flat, biphasic or negative wave);
• extrasystolic PQ interval is shortened;
• extrasystolic QRS complex is not changed (normal shape);
• noncompensatory pause occurs after premature beat.
ECG CRITERIA OF ATRIOVENTRICULAR (NODAL)
EXTRASYSTOLE
• Inter-beat RR interval between preceding and extrasystolic beat is
shortened;
• depending on location of impulse generation from AV node ("upper
nodal", "midnodal", "lower nodal" extrasystoles) negative P wave
precedes extrasystolic QRS complex, is lost in it or follows it;
• as a rule QRST complex of premature beat is not changed;
• noncompensatory pause occurs after extrasystolic beat.

a – "upper nodal“ extrasystole

b – “lower nodal“ extrasystole

ECG CRITERIA OF VENTRICULAR EXTRASYSTOLE

• Inter-beat RR interval between preceding and extrasystole is

shortened;
• the extrasystolic QRS complex is not preceded by a P wave (but can
be preceded by a nonconducted sinus P wave occurring at its
expected time);
• extrasystolic QRS complex is deformed (abnormal in shape) due to
increased amplitude and duration (> 0.10 sec);
• ST segment and T wave (commonly large) are opposite in direction to
the major deflection of the QRS complex (discordance);
• the fully compensatory pause follows premature beat.
LEFT-VENTRICULAR EXTRASYSTOLE

• high R wave in the standard lead

III and the deep S wave in the
standard lead I;
• high R wave in the right chest
leads (V1-V2) and a broad or
deep S wave in the left chest
leads (V5-V6).
RIGHT-VENTRICULAR EXTRASYSTOLE

• high R wave in the standard

lead I, and a deep S wave in the
standard lead III;
• the deep S wave in the right
chest leads (V1-V2) and a high
R wave in the left chest leads
(V5-V6).
MULTIFOCAL VENTRICULAR EXTRASYSTOLE

If excitability of the myocardium is high, several (rather than one)

ectopic foci may exist. Extrasystoles generated in various heart
chambers and can have different contours and are often called
multifocal or polytopic extrasystole. More properly they should be called
“multiform,” “polymorphic,” or “pleomorphic” since it is not known
whether multiple foci are discharging or whether conduction of the
impulse originating from one site is merely changing.
Extrasystoles are described as "monomorphic" when their QRS
complexes have the same general appearance in the same lead.

Monomorphic extrasystoles Polymorphic extrasystoles

 ALLORHYTHMIA
Allorhythmia – an irregularity in the cardiac rhythm that repeats itself any
number of times.

Variants
Bigeminy – that cardiac rhythm when each beat of the dominant rhythm (sinus or
other) is followed by a premature beat, with the result that the heartbeats occur in
pairs.

Trigeminy – a cardiac arrhythmia in which the beats are grouped in trios, usually
composed of a sinus beat followed by two extrasystoles.

Quadrigeminy – a cardiac arrhythmia in which the heartbeats are grouped in fours,

each usually composed of one sinus beat followed by three extrasystoles, but a
repetitive group of four of any composition is quadrigeminal.
 CLINICAL FEATURES OF EXTRASYSTOLES

Complaints:
palpitations and/or intermissions in heartbeats

Physical examination:
• the presence of a premature beat followed by a pause that is longer
than normal;
• irregular and unequal pulse, premature pulse waves of small volume
and so decreased or absent peripheral (e.g., radial) pulse;
• irregular heartbeats in auscultation, decrease in intensity of the heart
sounds, often with auscultation of just the first heart sound, which can
be sharp and snapping (loud).
SCHEME OF CONDUCTIBILITY DISORDERS

Heart block is a disturbance

of impulse conduction that
can be permanent or
transient depending on the
anatomical or functional
impairment.

1. Sinoatrial blocks.
2. Intraatrial blocks.
3. Atrioventricular blocks.
4. Left bundle branch block.
5. Right bundle branch
block.
 ECG CRITERIA OF SINOATRIAL BLOCK

Sinoatrial block is characterised by a transient failure of impulse

conduction to the atrial myocardium, resulting in periodic missing
of the heart complex in the presence of a regular sinus rhythm
(neither P wave nor the QRST complex are recorded); the duration
of long pause between two next P (or R) wave depends on amount
of blocked ("missed") sinus impulses: if one sinus impulse is
blocked the length of diastole doubles, if two successive sinus
impulses are blocked the length of pause is equal to sum of three
usual RR intervals of sinus rhythm.
 ECG CRITERIA OF INTRAATRIAL BLOCK
Intraatrial block is impaired conduction through the atria, manifested by the
following:
the P wave duration increases more than 0.12 second;
it may be notched P wave in all cardiac cycles.

notched P
wave

> 0.12 sec

 CAUSES OF ATRIOVENTRICULAR BLOCK

Atrioventricular block is partial or complete block of electric impulses

originating in the atrium or sinus node preventing them from reaching the
atrioventricular node and ventricles.

• Myocardial ischaemia or infarction

• Degeneration of the His-Purkinje system
• Infection for example, Lyme disease, diphtheria
• Immunological disorders for example, systemic lupus erythematosus
• Surgery
• Congenital disorders
 ATRIOVENTRICULAR BLOCK I DEGREE

In first degree block there is a delay in conduction of the atrial impulse to

the ventricles, usually at the level of the atrioventricular node.
This results in prolongation of the PQ interval to more than 0.20 sec (up
to 0.36-0.40 sec), but all impulses are conducted and every QRST
complex is preceded by a P wave and the PQ interval remains constant.

Speed = 25 mm/sec
ATRIOVENTRICULAR BLOCK II DEGREE MOBITZ
TYPE I, WENCKEBACH TYPE

In second degree block there is intermittent failure of conduction

between the atria and ventricles. Some P waves are not followed by a
QRS complex. There are two types of second degree block.
ECG shows progressive lengthening of the PQ interval until an impulse
is not conducted to ventricles and and the P wave is not followed by a
QRST complex (“unreciprocated” P wave). After this pause which is
equal in duration to one cardiac cycle the first PQ interval becomes short
again, and the cycle repeats (Wenckebach period).
ATRIOVENTRICULAR BLOCK II DEGREE MOBITZ
TYPE II
There is intermittent failure of conduction of P waves:
“unreciprocated” P waves (QRST complexes do not follow them) are
recorded on ECG without prior measurable lengthening of PQ interval; loss
of QRST complexes may be regular (repetitive) or chaotic.
The more impulses are blocked, the less rate of ventricular contractions is.
High degree atrioventricular block, which occurs when a QRS complex is
seen only after every three, four, or more P waves, may progress to
complete third degree atrioventricular block.
 ATRIOVENTRICULAR BLOCK III DEGREE
In third degree block there is complete failure of conduction between the atria
and ventricles, with complete independence of atrial and ventricular
contractions. The P waves bear no relation to the QRS complexes and
usually proceed at a faster rate.
The ECG demonstrates two independent rhythms (the independence of P
waves and QRST complexes):
atrial rhythm (P waves are sinus or ectopic with a rate of 60-80 beat/min and
more) and ventricular rhythm (QRST complexes are rhythmical, their rate
slows down less than 60-30 beat/min depending on the position of
pacemaker in the conduction system).
 BUNDLE BRANCH BLOCK
Bundle branch blocks result from
conduction delay or block in any of
several sites in the intraventricular
conduction system, including the
main bundle branches, in the
fascicles, or less commonly, within
the fibers of the bundle of His.
The intrinsicoid deflection
time (J) is the time up to that
moment the activation front
has reached the subjacent
muscle (from the beginning
of QRS complex to the peak
of its maximum positivity).
RIGHT BUNDLE BRANCH BLOCK (RBBB)
In this disorder, the right branch of the
bundle is blocked, but the septum is
activated from left to right, as in the
normal heart. The left ventricular q
wave is preserved, as is the initial r
wave over right chest leads. The left
ventricle is then depolarized, producing
an S wave in right chest leads and an
R wave in left chest leads. Finally,
depolarization reaches the right
ventricle, and so produces an R in the
right chest leads and a deep broad S
wave in the left chest leads. An M
pattern is thus seen in the right chest
leads, such as V1. It is also common to
see T wave abnormalities in leads V2
and V3.
ECG CRITERIA OF COMPLETE RBBB

• The major deflection of the QRS complex

is directed positively (R wave), it is
notched or split in right precordial leads
(V1 and V2);
• intrinsicoid deflection time is prolonged
(>60 msec) in V1 and V2;
• ST segment and T wave are discordant to
the major deflection of the QRS complex
in the right precordial leads;
• QRS complex is broad >0.12 sec;
• S wave is wide and deep in leads V5-V6
and lead I, sometimes in leads II and
aVL;
• electrical axis tends to deviation to the
right.
CONDITIONS ASSOCIATED WITH RBBB

• Rheumatic heart disease

• Cor pulmonale/right ventricular hypertrophy
• Myocarditis or cardiomyopathy
• Ischaemic heart disease
• Degenerative disease of the conduction
system
• Pulmonary embolus
• Congenital heart disease for example, in
atrial septal defects
LEFT BUNDLE BRANCH BLOCK (LBBB)
When the left branch of the bundle is
blocked, the interventricular septum is
activated from the right instead of from the
left side and the initial vector (phase 1) is
directed to the left. Because of this, the
normal initial q wave in the left ventricular
leads is lost, being replaced by a small r
wave. Right ventricular depolarization,
which follows, produces an r in V1 and an s
in V6. The left ventricle is finally
depolarized resulting in an R in V6 and a
broad S in V1. The QRS duration is
increased to 0.12 s or more. The abnormal
left ventricular depolarization sequence in
left bundle branch block causes secondary
repolarization changes. Consequently, the
ST segment and T wave are abnormal.
ECG CRITERIA OF COMPLETE LBBB
• The major deflection of the QRS
complex is directed positively (R wave),
it is notched or split in lateral precordial
leads (V5 and V6) and usually leads I
and aVL;
• intrinsicoid deflection time is prolonged
(>60 msec) in V5 and V6;
• ST segment and T wave are discordant
to the major deflection of the QRS
complex;
• QRS complex is broad >0.12 sec;
• electrical axis tends to deviation to the
left.