ELEC4810 Notes-3 PDF

ELEC4810: Introduction to
Biosensors and Bioinstrumentation

Lecture Notes – Set #3
ELEC4810
Textbook: Chapter 4,6

Chapter 2
Biopotentials: the Origin and Measurements
Main Topics:
Electrical Activity at Cellular Level
• bioelectric phenomena at the cellular level
• volume conductor potential distributions
• typical bioelectric sources: heart, brain, muscle, etc.
Recordings of bioelectric signals

• electrocardiogram (ECG)
• electroencephalogram (EEG)
• electromyogram (EMG)
2
2.5 Electrocardiogram (ECG)
• An electrocardiogram (ECG) is a test that records the electrical activity of the heart over
a period of time using electrodes placed on the skin – remote and noninvasive procedure.
ANATOMY AND FUNCTION OF THE HEART

• The heart serves as a four-chambered pump (or two double-stage pumps) for the
circulatory system.
• Every part of your body needs a fresh supply of blood in order to work normally. It's your
heart's job to make sure that this is pumped out regularly.
3
THE Structure of HEART HOW DOES HEART WORK?
4
THE HEART THE HEART AND CIRCULATORY SYSTEM
5
THE HEART
6
• Making of a heart
Cardiac muscle cells (or

cardiomyocytes):
− The muscle cells (myocytes) that

make up the cardiac muscle.
− The foremost function of cardiac

cells is the coordinated
contraction, or the “beating” of
the heart.
− Cells of various groups in a heart are

somewhat different from on another
in anatomy and physiology.
2.5 Electrocardiogram (ECG) Chain of fibers
Cardiac muscle cells (or

cardiomyocytes):
− The muscle cells (myocytes) that

make up the cardiac muscle.
− The foremost function of cardiac A section near an intercalated dish

cells is the coordinated
contraction, or the “beating” of
the heart.
− Cells of various groups in a heart are

somewhat different from on another
in anatomy and physiology.
2.5 Electrocardiogram (ECG) Chain of fibers
A generalized fiber of the heart:

− Many contractile filaments in bundles.
− A double-layered membrane called an

intercalated disk connects one fiber to
another mechanically and electrically.
A section near an intercalated dish
− At various locations in each disk are
“gap junctions”, which are especially
conductive electrically.
− Cardiac cell is rich in mitochondria

which are the major developers of the
ATP.
Cardiac cellular electrochemistry:
Potential of resting cells:
• For a generalized cell of heart, the resting voltage is -50 to -100 millivolts.
• A ventricular cell at rest has typical voltage higher than that of an atrial cell at rest.
• Since the number of ventricular cells definitely outnumber those of atria, the resting
potential for a generalized cell of the heart is set to - 90 mV.
Action potential:
• Cardiac cells are especially fast in producing action potentials repeatedly.
• Certain cells can produce action potential automatically, some can only be
activated by stimulation.
Action potential:
• Cardiac cells are especially fast in producing action potentials
repeatedly.
• Certain cells can produce action potential automatically, some
can only be activated by stimulation.
Action potential:
• Certain cells can produce action potential automatically, some can only be activated by
stimulation.
Electric (circuit) model of the human heart
• A common (electric circuit) model treats the heart as a system composed of a generator
and many conductors.
• The generator is the SA node, and the major conductors are the special paths in the
heart. All components are biologic → nonlinearity.
Conducting system of the heart
Bachmann’s bundle
(interatrial tract) -1
sinoatrial (SA)
node -1
atrioventricular
atrioventricular bundle of His -3
(AV) node - 2
left bundle
branch -4
right bundle
branch -4
Purkinje
network -5
Electric (circuit) model of the human heart
• A common (electric circuit) model treats the heart as a system composed of a generator
and many conductors.
• The generator is the SA node, and the major conductors are the special paths in the
heart. All components are biologic → nonlinearity.
The generator:
• SA node is composed of mass of
specialized cells. At the core of the node
Bachmann’s bundle are P cells that automatically produce
(interatrial tract) -1 action potentials at a rate normally higher
than that of any other cell or group of cells
sinoatrial (SA) in the heart. The SA node is thus the usual
node -1
atrioventricular
pacemaker.
bundle of His -3 • SA node dispatches action potentials at a
atrioventricular rate modified by some nerves and by
(AV) node - 2
left bundle certain substances in the blood. Free-
branch -4 running rate of SA node is higher than its
controlled rate, e.g. the chemical output at
right bundle the ends of the vagal fibers can change the
branch -4
ionic permeability of the cellular
Purkinje membranes and cause a decrease in the
network -5 rate of impulses from the SA node.
Atrial paths of enhanced conduction:

The action potential, or “wave of depolarization”, travels away from the SA node more
quickly through certain paths in the atria than through the other cells or fibers in the heart.
• The depolarization wave speeds along

three intra-atrial conduction paths in the
right atrium from SA node to the
Bachmann’s bundle atrioventricular (AV) node. Cells
(interatrial tract) -1 alongside the paths depolarize as the wave
pass by, and they relay the signal to
sinoatrial (SA) neighboring cells. → atrial contraction
node -1 moves blood to the ventricles.
atrioventricular
atrioventricular bundle of His -3 • Left atrium receive the signal through the
(AV) node - 2 interatrial tract or Bachmann’s bundles.
left bundle → activation of right atrium occurs
branch -4 earlier than left.
right bundle • The estimated speed of the wave in atria is
branch -4 80 - 100 cm/s;
• The time of atrial activation is normally
Purkinje 70-100 ms.
network -5
Another node in the circuit:

• The location of the atrioventricular (AV) node is often divided into three functional
regions: the atrio-nodal (AN), nodal (N) and nodal-His (NH).
• Function of each region: receiving the wave of depolarization, delaying it, and
dispatching it to AV bundle.
• Electrical signal travels slowly: 1-10
Conducting system of the heart cm/s. The speed is lowest in the AN and
highest in the NH. → blood in atria have
Bachmann’s bundle enough time to flow to the ventricles in
(interatrial tract) -1 preparation for the ventricular
contraction.
sinoatrial (SA) • The AN can generate the action potential
node -1 automatically and become the pacemaker
atrioventricular if the SA nose fails. The heart beat in AN
bundle of His -3
atrioventricular pacing is lower that that of SA pacing: 80
(AV) node - 2 beats/min vs. 40 beats/min.
left bundle
branch -4 • NH region of the AV node are fibers
that form the origin of the AV bundle,
right bundle often called the bundle of His. The
branch -4 speed of conduction is approximately
Purkinje 150 cm/s.
network -5
More paths of enhanced conduction:

• After leaving the AV node, AV bundle divides into two serving left and right ventricles.
• The ends of AV bundle touch to the

Conducting system of the heart Purkinje network which consists of
transitional fibers connecting to muscle
fibers.
Bachmann’s bundle
(interatrial tract) -1 • If SA and AV nodes fail, the His-Purkinje
system can assume the role of pacemaker
sinoatrial (SA) and the heart rate would fall to about 20
node -1 beats/min.
atrioventricular
atrioventricular bundle of His -3
(AV) node - 2
left bundle
branch -4
right bundle
branch -4
Purkinje
network -5
Summary:
• Sequence of cardiac excitation: the yellow color denotes areas that are
depolarized.
• the model of main circuit of human heart indicates the normal sequence of
excitation: the SA, atrial tract, AV node, AV bundle (bundle of His), bundle
branches, and Purkinje network.
Quantitative summary of the spread of the cardiac impulse through

the heart:
• Transmission of the cardiac impulse through the heart, showing the time of appearance
(in fractions of a second) of the impulse:
Action potential:
• Certain cells can produce action potential automatically, some can only be activated by
stimulation.
Action potentials of cells of various regions of the heart
ConductionVelocity:
𝐴𝐴 𝑑𝑑2 𝑉𝑉
𝜃𝜃 2 =
2𝑅𝑅𝑅𝑅 𝑑𝑑𝑡𝑡 2
• 𝜃𝜃 - Conduction Velocity
• 𝐴𝐴 - Fiber cross-sectional area
• 𝑅𝑅 - Intercellular resistance
• 𝐼𝐼 - Current required to charge
𝑑𝑑2 𝑉𝑉
• - related to rate of rise
𝑑𝑑𝑡𝑡 2
and amplitude of the action
potential
Action potentials of cells of various regions of the heart
Sequence of Activation:
• SA node: 𝜃𝜃 = 0.05 m/s

• AV node: 𝜃𝜃 = 0.02 - 0.1 m/s
• Intra-atrial conduction paths,
His, BB, Purkinje system: 𝜃𝜃 =
1-4 m/s
• Atrium: 𝜃𝜃 = 0.3-1.0 m/s
• Ventricle: 𝜃𝜃 = 0.3-1 m/s
Animation summary:
• Sequence of cardiac excitation: the SA, atrial tract, AV node, AV bundle
(bundle of His), bundle branches, and Purkinje network.
• ECG: remote monitoring of the sequence of excitation.
Electrocardiographic signals:
• Each action potential of a cell provides important information about the cell.
• A running record of action potentials of a group of cells in part of heart
reflects cardiac health.
• How to obtain the signal?
• How to read electric activity in heart?
𝑃𝑃 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃
𝛷𝛷𝑒𝑒 𝑟𝑟⃑ =
Potential signal from
4𝜋𝜋𝜎𝜎𝑒𝑒 𝑟𝑟 2
an electric dipole
𝑃𝑃 𝑟𝑟̂ � 𝑎𝑎�𝑑𝑑
1 𝑟𝑟⃗ � 𝑃𝑃
𝛷𝛷𝑒𝑒 𝑟𝑟⃑ = � 3
4𝜋𝜋𝜎𝜎𝑒𝑒 𝑟𝑟
1. Attaching the electrode to the heart → thoracic surgery

2. Inserting a sensing catheter to the area of interest, say SA node through the venous system.
→ invasive, involving risk.
3. Lowering a sensing catheter through the nose or mouth to the region of the esophagus
behind the upper portion of the heart. → less risky and with reasonable SNR,
not practical enough.
1. Attaching the electrode to the heart → thoracic surgery
2. Inserting a sensing catheter to the area of interest, say SA node through the venous system.
→ invasive, involving risk.
3. Lowering a sensing catheter through the nose or mouth to the region of the esophagus
behind the upper portion of the heart. → less risky and with reasonable SNR,
not practical enough.
4. Placing electrode on the skin at various locations of body to collect the
signal of differential potentials
 non-invasive, nil risk, practical, indirect measurements,
 not easy to interpret the signals.
Cardiac dipole model
Sequence of Activation: map of potential over the heart
~30ms ~90ms
~180ms ~210ms ~230ms

Sequence of Activation: action potentials
~30ms ~90ms
~180ms ~210ms ~230ms

Sequence of Activation:
~180ms
Cardiac
dipole
Cardiac Dipoles as a function of time:
~30ms ~90ms
~180ms ~210ms ~230ms

Body surface potential map at different time
Remote Measurement of Cardiac Dipole
1 𝑃𝑃 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃
𝛷𝛷𝐴𝐴,𝐵𝐵 𝑟𝑟⃑ = � 2
4𝜋𝜋𝜎𝜎𝑒𝑒 𝑟𝑟1,2
𝑃𝑃 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃1 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃2
𝑽𝑽𝑨𝑨𝑨𝑨 = � 2 − 2
4𝜋𝜋𝜎𝜎Ω 𝑟𝑟1 𝑟𝑟2
Power of the ECG as a Diagnostic Tool

• Non-invasive Detection of
 Sequence of Activation
 Quantity of Active Tissue
 Health of Tissue
 Rhythmicity
Recording of ECG: Einthoven’s triangle

Right Left
shoulder shoulder
abdomen
𝐼𝐼⃗ = 𝑟𝑟⃗1 − 𝑟𝑟⃗2

1 𝑟𝑟𝑖𝑖 � 𝑃𝑃
𝛷𝛷𝑒𝑒 𝑟𝑟𝑖𝑖 = � , 𝑖𝑖 = 1,2,3
𝑟𝑟⃗2 𝑟𝑟⃗1
𝑷𝑷 Lead-I signal:
𝑟𝑟⃗3 𝑉𝑉𝐼𝐼 =𝛷𝛷𝑒𝑒 𝑟𝑟⃗1 − 𝛷𝛷𝑒𝑒 𝑟𝑟⃗2
1 𝑟𝑟⃗1 � 𝑃𝑃 1 𝑟𝑟⃗2 � 𝑃𝑃
= � − �
4𝜋𝜋𝜎𝜎𝑒𝑒 𝑟𝑟 3 4𝜋𝜋𝜎𝜎𝑒𝑒 𝑟𝑟 3
Approximations: 1 𝐼𝐼⃗ � 𝑃𝑃
• Einthoven’s triangle is equilateral = � 𝑟𝑟⃗1 − 𝑟𝑟⃗2 � 𝑃𝑃 =
4𝜋𝜋𝜎𝜎𝑒𝑒 𝑟𝑟 3 4𝜋𝜋𝜎𝜎𝑒𝑒 𝑟𝑟 3
• Heart is located at the center of the
triangle → 𝑟𝑟1 ≈ 𝑟𝑟2 ≈ 𝑟𝑟3 ≈ 𝑟𝑟 𝑃𝑃 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃𝐼𝐼𝐼𝐼
=
𝐼𝐼⃗ = 𝑟𝑟⃗1 − 𝑟𝑟⃗2

1 𝑟𝑟𝑖𝑖 � 𝑃𝑃
𝛷𝛷𝑒𝑒 𝑟𝑟𝑖𝑖 = � , 𝑖𝑖 = 1,2,3
𝑟𝑟⃗2 𝑟𝑟⃗1
𝑷𝑷 Lead-II signal:
𝑟𝑟⃗3 𝑉𝑉𝐼𝐼𝐼𝐼 =𝛷𝛷𝑒𝑒 𝑟𝑟⃗3 − 𝛷𝛷𝑒𝑒 𝑟𝑟⃗2

𝑃𝑃 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃𝐼𝐼𝐼𝐼𝑃𝑃
=
Approximations: Lead-III signal:

• Einthoven’s triangle is equilateral
• Heart is located at the center of the 𝑉𝑉𝐼𝐼𝐼𝐼 =𝛷𝛷𝑒𝑒 𝑟𝑟⃗3 − 𝛷𝛷𝑒𝑒 𝑟𝑟⃗1
triangle → 𝑟𝑟1 ≈ 𝑟𝑟2 ≈ 𝑟𝑟3 ≈ 𝑟𝑟
𝑃𝑃 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃𝐼𝐼𝐼𝐼𝐼𝐼𝑃𝑃
=
The magnitude of the measured Lead signal depends on:
• the orientation of the dipole relative to the recording axis of your electrodes
• the mass off the tissue involved
~30ms
𝑃𝑃 𝑐𝑐𝑐𝑐𝑐𝑐𝜃𝜃𝐼𝐼𝐼𝐼
𝑉𝑉𝐼𝐼 =
𝑉𝑉𝐼𝐼𝐼𝐼 =
𝑉𝑉𝐼𝐼𝐼𝐼𝐼𝐼 =
~90ms
𝑉𝑉𝐼𝐼 =
~180ms
𝑉𝑉𝐼𝐼 =
~210ms
𝑉𝑉𝐼𝐼 =
~230ms
𝑉𝑉𝐼𝐼 =
𝑉𝑉𝐼𝐼 =
• Appearance of ECG in Leads II and III vs. lead I.





Formation of the ECG Signals (a detailed

summary)
• Actual generation of the ECG by taking into
account a realistic progression of the electric
activation of the heart that has begun at the
sinus node.
• As shown in figures, from the sinus node the
vector spreads along the atrial walls. The
resultant vector of the atrial electric activity
is illustrated with a thick yellow arrow. The
projections of this resultant vector on each of
the three limb ECG leads I, II and III is
positive, and therefore, the measured signals
are also positive.

summary)
• After the depolarization has propagated over
the atrial walls, it reaches the AV node. The
propagation through the AV junction is very
slow and involves negligible amount of tissue;
it results in a delay in the progress of
activation. This is a desirable pause which
allows completion of ventricular filling.
• Once activation has reached the ventricles,
propagation proceeds along the Purkinje
fibers to the inner walls of the ventricles.
• The ventricular depolarization starts first
from the left side of the interventricular
septum, and therefore, the resultant dipole
from this activation points to the right.
• This is what causes a negative signal in ECG
leads I and II.

summary)
• In the next phase, depolarization waves
occur on both sides of the septum, and their
electric forces cancel. However, early apical
activation is also occurring, so the resultant
vector points to the apex.

summary)
• After a while, the depolarization front has
propagated through the wall of the right
ventricle; when it first arrives at the
epicardial surface of the right-ventricular free
wall, the event is called breakthrough.
Because the left ventricular wall is thicker,
activation of the left ventricular free wall
continues even after depolarization of a large
part of the right ventricle.
• Because there are no compensating electric
forces on the right, the resultant vector
reaches its maximum in this phase, and it
points leftward.

summary)
• The depolarization front continues
propagation along the left ventricular wall
toward the back. Because its surface area now
continuously decreases, the magnitude of the
resultant vector also decreases until the
whole ventricular muscle is depolarized.

summary)
• The last to depolarize are basal regions of
both left and right ventricles. Because there is
no longer a propagating activation front,
there is no ECG signal either.

summary)
• Ventricular repolarization begins from the
outer side of the ventricles and the
repolarization front "propagates" inward.
This seems paradoxical, but even though the
epicardium is the last to depolarize, its
action potential durations are relatively
short, and it is the first to recover.

summary)
• Although recovery of one cell does not
propagate to neighboring cells, one notices
that recovery generally does move from the
epicardium toward the endocardium. The
inward spread of the repolarization front
generates a signal with the same sign as the
outward depolarization front. Because of the
diffuse form of the repolarization, the
amplitude of the ECG signal is much smaller
than that of the depolarization wave and it
lasts longer.
LEAD II
Wave: any change in voltage that begins and
ends at zero mV.
R-wave: first positive wave of ventricular
depolarization
Q-wave: any negative event that precedes an R-wave
S-wave: any negative event that follows an R-wave
Complex: a series of waves not interrupted by

periods of inactivity.
Segment: a period of time in the ECG that includes

no waves or complexes.
Interval: a period of time in the ECG that includes a

segment and a wave.
Typical ECG durations:
PR interval: 0.12 - 0.2 sec; QRS complex: 0.06 - 0.1(2) sec; T wave duration: 0.1 - 0.25 sec
• P, Q, R, S, and T, is usually recognizable waves.

• Einthoven assigned those letters to the waves. The letters do not have
physiological significance.
Depolarization in
SN: Sinoatrial node
Atria: Right atrium and left atrium
AV node: Atrioventricular node
H: Bundle of His
BB: Bundle branches
P: Purkinje network
V: Right ventricle and left ventricle
Repolarization in
a: Right atrium and left atrium
v: Right ventricle and left ventricle
Electrical signals vs. mechanical responses
LVP: left ventricular pressure

LAP: left atrial pressure
LV: left ventricle volume
Surface electrocardiography:
• Willem Einthoven (21 May 1860 – 29 September

1927) was a Dutch doctor and physiologist. He
invented the first practical electrocardiogram
(ECG or EKG) in 1903 and received the Nobel
Prize in Medicine in 1924 for it.
• Early researchers chose the hands and feet as sites
Saline
for electrodes to obtain ECG signals.
(salt water)
• Figure on the right: Electrocardiographic NaCl.
connections to a patient in 1912
Original Einthoven’s triangle Einthoven’s law:

• Any of the three leads can be
determined from the other two.
Algebraically adding leads I and

III produces lead II:
Right Left Lead-I + Lead-III
shoulder shoulder
= (vL - vR) + (vF – vL)
= (vF - vR)
= Lead II
Lead I + Lead III = Lead II.
abdomen
Kirchhoff's voltage law (KVL)
Simplified Lead-I,II,III
• Lead I:the signal between the left and right hands (arms).
• Lead II: the signal between the left foot (leg) and right hand (arm).
• Lead III: the signal between the left foot (leg) and the left hand (arm).
𝐿𝐿𝐿𝐿𝐿𝐿𝐿𝐿 𝐼𝐼 = 𝑣𝑣𝐿𝐿 − 𝑣𝑣𝑅𝑅 , 𝐿𝐿𝐿𝐿𝐿𝐿𝐿𝐿 𝐼𝐼𝐼𝐼 = 𝑣𝑣𝐹𝐹 − 𝑣𝑣𝑅𝑅 , 𝐿𝐿𝐿𝐿𝐿𝐿𝐿𝐿 𝐼𝐼𝐼𝐼𝐼𝐼 = 𝑣𝑣𝐹𝐹 − 𝑣𝑣𝐿𝐿
where 𝑣𝑣𝐿𝐿 = voltage between left arm and right leg
𝑣𝑣𝑅𝑅 = voltage between right arm and right leg
𝑣𝑣𝐹𝐹 = voltage between left arm and right leg.
• Potential of right leg is taken as reference for voltage amplifier

Augmented leads introduced by Goldberger:

aVR, aVL and aVF
1 1
𝑎𝑎𝑎𝑎𝑎𝑎 = 𝑉𝑉𝑅𝑅 − 𝑉𝑉𝐿𝐿 + 𝑉𝑉𝐹𝐹 = − 𝐼𝐼 + 𝐼𝐼𝐼𝐼
2 2
1 1
𝑎𝑎𝑎𝑎𝐿𝐿 = 𝑉𝑉𝐿𝐿 − 𝑉𝑉𝑅𝑅 + 𝑉𝑉𝐹𝐹 = 𝐼𝐼 − 𝐼𝐼𝐼𝐼𝐼𝐼
2 2
1 1
𝑎𝑎𝑎𝑎𝐹𝐹 = 𝑉𝑉𝐹𝐹 − 𝑉𝑉𝐿𝐿 + 𝑉𝑉𝑅𝑅 = 𝐼𝐼𝐼𝐼 + 𝐼𝐼𝐼𝐼𝐼𝐼
2 2
R L Apply KCL at node M:
𝑉𝑉𝐿𝐿 − 𝑉𝑉𝑀𝑀 𝑉𝑉𝑀𝑀 − 𝑉𝑉𝐹𝐹

=
𝑅𝑅 𝑅𝑅
F 1
𝑉𝑉𝑀𝑀 = 𝑉𝑉 + 𝑉𝑉𝐹𝐹
2 𝐿𝐿
• Connections for augmented leads: (a) aVR. (b) aVL. (c) aVF
• “Viewing angles” of heart from Lead I,II,III and Augmented leads: aVR, aVL and aVF
• But only view the heart activities projected to the plane defined by RA, LA, LL
• “Viewing angles” of heart from Lead I,II,III and Augmented leads: aVR, aVL and aVF
• But only view the heart activities projected to the plane defined by RA, LA, LL
Frontal (Limb Leads) Plane View of Heart
Unipolar (+) chest leads (horizontal plane):

• Leads V1, V2, V3: (Posterior Anterior)
• Leads V4, V5, V6:(Right Left, or lateral)
Unipolar (+) chest leads (horizontal plane):

• Leads V1, V2, V3: (Posterior Anterior)
• Leads V4, V5, V6:(Right Left, or lateral)
Apply KCL at node T:

R L
𝑉𝑉𝑅𝑅 − 𝑉𝑉𝑇𝑇 𝑉𝑉𝐿𝐿 − 𝑉𝑉𝑇𝑇 𝑉𝑉𝑇𝑇 − 𝑉𝑉𝐹𝐹
+ =
𝑅𝑅 𝑅𝑅 𝑅𝑅
1
F 𝑉𝑉𝑇𝑇 = 𝑉𝑉𝑅𝑅 + 𝑉𝑉𝐿𝐿 + 𝑉𝑉𝐹𝐹
3
𝐿𝐿𝐿𝐿𝐿𝐿𝐿𝐿 𝑉𝑉𝑖𝑖 = 𝑉𝑉𝑖𝑖 − 𝑉𝑉𝑇𝑇

T 𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤𝑤 𝑖𝑖 = 1,2,3,4,5,6
Standard electrocardiographic leads for recording 12-lead electrocardiogram
• Orientation of the electrical axis of the standard 12 leads in relationship to the
body surface:
Frontal (Limb Leads) and Horizontal

View (Precordial Leads) of Heart
• Typical waveforms of 12 leads:
• Typical waveforms of 12 leads:
• Characteristics of electrocardiographic signals: amplitudes
P Q R S ST T
No.
No. Min. Max. Mean No. Min. Max. Mean No. Min. Max. Mean No. Min. Max. Mean Case No.
Lead Cases Cases Cases Cases Min. Max. Mean Case Min. Max. Mean
s s
I 475 0 2.5 0.69 505 0 2.0 0.27 505 0.7 19.4 5.51 505 0 6.4 1.27 100 -0.3 0.9 0.11 505 -0.5 5.6 2.20
II 475 0 3.0 1.07 505 0 4.0 0.38 505 0.5 28.0 9.41 505 0 8.2 1.36 100 -1.0 1.0 0.21 505 0 8.0 2.67
III 475 -0.8 2.0 0.56 505 0 4.0 0.48 505 0 22.0 5.56 505 0 13.0 1.29 100 -0.6 0.8 0.04 505 -2.0 5.5 0.77
VR 32 -1.0 -0.5 -0.63 62 0 8.0 2.48 62 0 3.0 0.90 62 0 11.0 3.01 32 0 0 0 62 -4.0 -0.5 -1.65
VL 32 -0.5 0.5 0.07 62 0 1.5 0.16 62 0 7.0 1.21 62 0 7.0 2.01 32 0 0 0 62 -1.0 1.5 0.29
VF 32 0 2.0 0.72 62 0 2.0 0.30 62 0 15.0 6.82 62 0 6.5 0.74 32 0 0 0 62 0 4.6 1.40
aVR 411 -1.5 -0.01 -0.79 552 0 16.8 2.38 552 0 4.1 0.94 552 0 15.7 3.76 — — — — 479 -5.5 -0.2 -2.49
aVL 411 -1.0 1.4 0.51 552 0 3.5 0.27 552 0 10.1 2.61 552 0 11.3 1.35 — — — — 479 -4.0 6.0 -0.73
aVF 411 -1.8 1.7 0.74 552 0 3.0 0.38 552 0 20.0 4.73 552 0 7.1 0.81 — — — — 479 -0.6 5.2 1.85
V1 371 -1.1 2.2 0.57 567 0 0 0 567 0 15.5 3.09 567 0.8 26.2 9.44 33 0 0.5 0.01 512 -4.0 12.2 0.84
V2 371 -0.7 2.0 0.60 594 0 0 0 594 0 23.0 5.96 594 0 39.2 14.09 33 0 1.0 0.09 512 -2.6 18.0 4.70
V3 371 -0.5 2.0 0.61 567 0 1.5 0.01 567 0.7 54.6 8.93 567 0 27.5 9.51 33 0 2.0 0.20 512 -2.0 21.0 5.16
V4 371 -0.2 2.3 0.60 594 0 4.0 0.13 594 1.8 46.0 13.78 594 0 28.8 5.93 33 0 1.0 0.03 512 -0.5 17.0 5.16
V5 371 0 2.4 0.56 567 0 3.4 0.43 567 0.4 33.6 12.01 567 0 16.1 1.96 33 0 0 0 512 0 11.0 3.83
V6 371 0 1.8 0.54 564 0 2.7 0.44 564 2.0 22.6 9.68 564 0 14.3 1.00 33 0 0 0 512 0 6.9 2.80
VE — — — — 30 0 0 0 30 2.0 12.8 5.81 30 0 16.2 6.09 — — — — 30 0.2 52 2.55

• Characteristics of electrocardiographic signals: amplitudes
P Q R S ST T
No.
No. Min. Max. Mean No. Min. Max. Mean No. Min. Max. Mean No. Min. Max. Mean Case No.
Lead Cases Cases Cases Cases Min. Max. Mean Case Min. Max. Mean
s s
I 475 0 2.5 0.69 505 0 2.0 0.27 505 0.7 19.4 5.51 505 0 6.4 1.27 100 -0.3 0.9 0.11 505 -0.5 5.6 2.20
II 475 0 3.0 1.07 505 0 4.0 0.38 505 0.5 28.0 9.41 505 0 8.2 1.36 100 -1.0 1.0 0.21 505 0 8.0 2.67
III 475 -0.8 2.0 0.56 505 0 4.0 0.48 505 0 22.0 5.56 505 0 13.0 1.29 100 -0.6 0.8 0.04 505 -2.0 5.5 0.77
VR 32 -1.0 -0.5 -0.63 62 0 8.0 2.48 62 0 3.0 0.90 62 0 11.0 3.01 32 0 0 0 62 -4.0 -0.5 -1.65
VL 32 -0.5 0.5 0.07 62 0 1.5 0.16 62 0 7.0 1.21 62 0 7.0 2.01 32 0 0 0 62 -1.0 1.5 0.29
VF 32 0 2.0 0.72 62 0 2.0 0.30 62 0 15.0 6.82 62 0 6.5 0.74 32 0 0 0 62 0 4.6 1.40
aVR 411 -1.5 -0.01 -0.79 552 0 16.8 2.38 552 0 4.1 0.94 552 0 15.7 3.76 — — — — 479 -5.5 -0.2 -2.49
aVL 411 -1.0 1.4 0.51 552 0 3.5 0.27 552 0 10.1 2.61 552 0 11.3 1.35 — — — — 479 -4.0 6.0 -0.73
aVF 411 -1.8 1.7 0.74 552 0 3.0 0.38 552 0 20.0 4.73 552 0 7.1 0.81 — — — — 479 -0.6 5.2 1.85
V1 371 -1.1 2.2 0.57 567 0 0 0 567 0 15.5 3.09 567 0.8 26.2 9.44 33 0 0.5 0.01 512 -4.0 12.2 0.84
V2 371 -0.7 2.0 0.60 594 0 0 0 594 0 23.0 5.96 594 0 39.2 14.09 33 0 1.0 0.09 512 -2.6 18.0 4.70
V3 371 -0.5 2.0 0.61 567 0 1.5 0.01 567 0.7 54.6 8.93 567 0 27.5 9.51 33 0 2.0 0.20 512 -2.0 21.0 5.16
V4 371 -0.2 2.3 0.60 594 0 4.0 0.13 594 1.8 46.0 13.78 594 0 28.8 5.93 33 0 1.0 0.03 512 -0.5 17.0 5.16
V5 371 0 2.4 0.56 567 0 3.4 0.43 567 0.4 33.6 12.01 567 0 16.1 1.96 33 0 0 0 512 0 11.0 3.83
V6 371 0 1.8 0.54 564 0 2.7 0.44 564 2.0 22.6 9.68 564 0 14.3 1.00 33 0 0 0 512 0 6.9 2.80
VE — — — — 30 0 0 0 30 2.0 12.8 5.81 30 0 16.2 6.09 — — — — 30 0.2 52 2.55

• Spectra of electrocardiographic signals
25 Hz 150 Hz
• Plot of the overall mean (lower

line) plus two standard deviations
(upper line) spectra from 203 ECG
cycles and 10 subjects.
• This plot was produced by
averaging the 20 lead-averaged
spectra at a series of discrete
frequencies (1.22, 4.88, 10, 20, 30,
40, 50, 60, 70, 80, 90, 100, 110,
120, 150, 200, 250, 300, 400, and
500 Hz).
Alternative placements of chest electrodes:
(a) For signal similar to lead I.
(b) For signal similar to lead II.
(c) For signal similar to lead III.
(d) For lead MCL.
• Esophageal electrocardiography
(a) Connections for simultaneous lead II and bipolar esophageal

electrocardiogram. (b) Typical normal traces. (c) Bipolar esophageal
electrocardiogram showing changes in signal as location of pill is
changed
Noise and artifact
− Non-cardiac muscles → electromyographic (EMG) signals.

− Power line frequency
− Baseline wandering.
Electromyographic
(EMG) artifact
Line frequency (50-hertz)

artifact.
Electromyographic and line

frequency artifact and some
baseline wander
• Diagnosis of heart diseases
Atrioventricular block
a) Complete heart block. Cells in the

AV node are dead and activity
cannot pass from atria to
ventricles. Atria and ventricles beat
independently, ventricles being
driven by an ectopic (other-than-
normal) pacemaker.
b) AV block wherein the node is
diseased (examples include
rheumatic heart disease and viral
infections of the heart). Although
each wave from the atria reaches
the ventricles, the AV nodal delay
is greatly increased. This is first-
degree heart block.
78
Premature ventricular contraction (PVC)
Normal ECG followed by an ectopic

beat. An irritable focus, or ectopic
pacemaker, within the ventricle or
specialized conduction system may
discharge, producing an extra beat, or
extrasystole, that interrupts the
normal rhythm. This extrasystole is
also referred to as a premature
ventricular contraction (PVC).
79
Paroxysmal tachycardia and Atrial flutter
(a) Paroxysmal tachycardia. An

ectopic focus may repetitively
discharge at a rapid regular rate
for minutes, hours, or even days.
(b) Atrial flutter. The atria begin a
very rapid, perfectly regular
‘‘flapping’’ movement, beating at
rates of 200 to 300 bpm.
80
Atrial and Ventricular fibrillation

(a) Atrial fibrillation. The atria stop
their regular beat and begin a
feeble, uncoordinated twitching.
Concomitantly, low-amplitude,
irregular waves appear in the
ECG, as shown. This type of
recording can be clearly
distinguished from the very
regular ECG waveform
containing atrial flutter.
(b) Ventricular fibrillation.
Mechanically the ventricles
twitch in a feeble, uncoordinated
fashion with no blood being
pumped from the heart. The
ECG is likewise very
uncoordinated, as shown.
81
Defibrillation and defibrillators
• Defibrillation is a common treatment for life-threatening cardiac dysrhythmias and
ventricular fibrillation.
• Defibrillation consists of delivering a therapeutic dose of electrical current to the heart
with a device called a defibrillator. This depolarizes a critical mass of the heart muscle,
terminates the dysrhythmia and allows normal sinus rhythm to be reestablished by the
body's natural pacemaker, in the sinoatrial node of the heart.
82

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ELEC4810: Introduction to

Biosensors and Bioinstrumentation

Textbook: Chapter 4,6

Recordings of bioelectric signals

ANATOMY AND FUNCTION OF THE HEART

THE Structure of HEART HOW DOES HEART WORK?

Cardiac muscle cells (or

− The muscle cells (myocytes) that

− The foremost function of cardiac

− Cells of various groups in a heart are

Cardiac muscle cells (or

− The muscle cells (myocytes) that

− The foremost function of cardiac A section near an intercalated dish

− Cells of various groups in a heart are

A generalized fiber of the heart:

− A double-layered membrane called an

− Cardiac cell is rich in mitochondria

Conducting system of the heart

Atrial paths of enhanced conduction:

• The depolarization wave speeds along

Another node in the circuit:

More paths of enhanced conduction:

• The ends of AV bundle touch to the

Quantitative summary of the spread of the cardiac impulse through

Action potentials of cells of various regions of the heart

Action potentials of cells of various regions of the heart

• SA node: 𝜃𝜃 = 0.05 m/s

1. Attaching the electrode to the heart → thoracic surgery

Cardiac dipole model

Sequence of Activation: map of potential over the heart

~180ms ~210ms ~230ms

Sequence of Activation: action potentials

~180ms ~210ms ~230ms

Cardiac Dipoles as a function of time:

~180ms ~210ms ~230ms

Body surface potential map at different time

Remote Measurement of Cardiac Dipole

Power of the ECG as a Diagnostic Tool

Recording of ECG: Einthoven’s triangle

Recording of ECG: Einthoven’s triangle

Recording of ECG: Einthoven’s triangle

𝐼𝐼⃗ = 𝑟𝑟⃗1 − 𝑟𝑟⃗2

𝑟𝑟⃗3 𝑉𝑉𝐼𝐼 =𝛷𝛷𝑒𝑒 𝑟𝑟⃗1 − 𝛷𝛷𝑒𝑒 𝑟𝑟⃗2

Recording of ECG: Einthoven’s triangle

𝐼𝐼⃗ = 𝑟𝑟⃗1 − 𝑟𝑟⃗2

𝑟𝑟⃗3 𝑉𝑉𝐼𝐼𝐼𝐼 =𝛷𝛷𝑒𝑒 𝑟𝑟⃗3 − 𝛷𝛷𝑒𝑒 𝑟𝑟⃗2

Approximations: Lead-III signal:

• Appearance of ECG in Leads II and III vs. lead I.

• Appearance of ECG in Leads II and III vs. lead I.

• Appearance of ECG in Leads II and III vs. lead I.

• Appearance of ECG in Leads II and III vs. lead I.

• Appearance of ECG in Leads II and III vs. lead I.

Formation of the ECG Signals (a detailed

Formation of the ECG Signals (a detailed

Formation of the ECG Signals (a detailed

Formation of the ECG Signals (a detailed

Formation of the ECG Signals (a detailed

Formation of the ECG Signals (a detailed

Formation of the ECG Signals (a detailed