Cardiovascular Laboratory

Study sources for lab work and the pre-lab examination

1. Lectures (hemodynamics and heart mechanics)
2. R.M. Berne, M.N. Levy, B.M. Koeppen, B.A. Stanton Physiology , Mosby
5th Ed pp. 265-267, 313-318, 341-366
6th Ed. Pp. 289-291, 321-326, 330-343

Instructions for the lab report

The following parts should be included in the lab report:
a. Give brief answers to all the questions that appear in the protocol (numbered 1-16).
b. Attach the printouts and graphs you are requested to produce in the protocol.
Lab objectives
1. Blood pressure measurement.
2. Reviewing the cardiac cycle and studying the time relationship between electrical and
mechanical events in the heart.
3. Learning the factors that determine blood pressure (computer imaging).
Introduction
In this lab, we will learn the technique for measuring blood pressure; we will discuss the main
events occurring during the entire cardiac cycle; we will clarify the relationship between cardiac
output, arterial blood vessels resistance (and their elastic properties) and the systolic and
diastolic blood pressure.

Exercise 1 - Blood pressure measurement by a sphygmomanometer and a stethoscope

Instrumentation
The sphygmomanometer is a wide cuff that is wrapped around the arm and inflated with a
manual rubber pump, while the pressure in the cuff is read by mercury manometer. A suitable
screw permits pressure release at a controlled rate. The pressure in the cuff (the one that is read
by the manometer) is the pressure acting radially on the brachial artery of the arm. The
stethoscope enables you to hear sounds connected with the periodic opening and closing of the
brachial artery. These sounds are called Korotkoff sounds.

The blood pressure measurement method (as recommended by the American Heart
Association (1988)

1.
2.
3.
4.
5.

6.
7.
8.

9.
10.
11.
12.
13.
14.
15.

Make sure that the subject did not smoke or eat for at least 30 minutes before the test.
Ensure that the subject is sitting comfortably and relaxing for at least 10 minutes before the
test.
Expose the subjects arm. (Applying additional pressure through the shirt sleeve may cause
an inaccurate evaluation).
Find the auscultation point by sensing the brachial pulse at the cubital fossa.
Provide support for the elbow of the tested arm and make sure that the auscultation point is
placed on the level of the subjects heart. (Measuring the pressure while the arm is not
located at the level of the heart will add or reduce hydrostatic pressure leading to inaccurate
evaluation).
Place the manometer at your eye level to insure comfortable reading.
Wrap the cuff around the arm tightly but without pressure. The lower edge of the cuff should
be at least 2 cm above the auscultation point.
Inflate the cuff while feeling the brachial (or radial) pulse manually; observe the pressure at
which the brachial (or radial) pulse disappears - this pressure is close to the systolic
pressure. Inflate the cuff 10-30 mm Hg above the pressure where the pulse disappeared.
Put the stethoscope head on the auscultation point, while avoiding application of additional
pressure on it. Do not insert it under the cuff.
Reduce the pressure slowly (2 to 3 mm Hg per second ).
When you hear Korotkoff sounds in the stethoscope for the first time, the pressure in the
cuff equals the systolic pressure.
Continue reducing the pressure slowly. When the sounds disappear you have reached the
diastolic pressure.
Before repeating the test release the pressure from the cuff completely. Wait at least 2
minutes and allow the blood to drain from the veins in the tested arm.
Write the blood pressure as the mean value of the two measurements. Indicate the subjects
position (sitting or lying) and the arm on which the blood pressure was measured.
Repeat the blood pressure measurement on the other arm as well.

** In case there are difficulties with hearing the Korotkoff sounds, ask the subject to raise his
hand before and during the inflation of the cuff and to lower it back immediately when the
release of the pressure starts. You can try to measure the pressure on the other arm as well.
Korotkoff sounds appear when the value of the pressure applied by the sphygmomanometer cuff
on the artery is between the maximal blood pressure (the systolic) value and the minimal (the
diastolic) value.
The following diagram describes how these sounds are created:
1. When the air pressure in the cuff is higher than the systolic pressure in the blood vessel - the
blood vessel is blocked, so blood does not flow and no Korotkoff sounds are heard.
'
0 80 120140 120 80 0

2. When he air pressure in the cuff is lower than the systolic pressure but higher than the
diastolic pressure, blood passes in units (partial or not homogeneous blood flow) and causes
the flutter phenomenon and turbulent flow. As long as blood continues to pass in units,
Korotkoff sounds are heard.
'

40

80

Korotkoff sounds

100
80 40 0

Flutter

In this situation, a pressure wave reaches the blocked artery and opens it. As long as the pressure
in the blood vessel is higher than the pressure applied to the cuff, the vessel will remain open.
The force of the pressure wave is applied to the unit of blood that is passing while the blood
' and the flow
vessel is open. Due to the effect of this force, the unit of blood is accelerated

becomes turbulent. At a high speed, the kinetic component of the

Flutter
40 80 10 8

blood pressure increases strongly at the expense of the lateral component of the pressure
(Bernoulli effect). In this situation, the artery walls collapse internally. After the portion of blood
has passed, the elastic walls of the artery return to their previous state. These repeated
movements of the artery wall, called "flutter," and the turbulent flow of the blood generate
sounds, which were first described by Korotkoff in 1905.
The force that accelerates the unit of blood and the quantity of blood passing along the artery
changes during blood pressure measurement. All this affects the acoustical characteristics of the
Korotkoff sounds: the sounds change in intensity and frequency during the test. Five types of
Korotkoff sounds, which change during blood pressure measurement, can be distinguished:
Type 1 Tapping sounds that appear when the pressure in the cuff equals the systolic pressure.
These sounds are weak, but distinct, and their intensity increases as air pressure in the cuff
decreases.
Type 2 - Murmuring sounds, which appear immediately after the end of the Type 1 Korotkoff
sounds.
Type 3 - The strongest and most distinct sounds that can be heard during blood pressure
measurement.
Type 4 - Muffled whistling or blowing sounds.
Type 5 - Sounds appearing when the pressure in the cuff equals the diastolic pressure.
As mentioned above, the appearance of sounds indicates the value of the systolic pressure, and
marks the moment that the pressure wave reaches the blocked artery.
3. When the air pressure in the cuff is lower than the diastolic pressure in the blood vessel blood flows freely, no sounds.
'
0 20 40 60

20 0

1). For your lab report please prepare distribution histograms for:
a. Systolic blood pressure
b. Diastolic blood pressure
c. Mean blood pressure
Use the data from your lab class. Do your curves fit the distribution curves in general
population? Explain why?
2). Why should the subjects position during the test be stated? Is it also important to
report how long before the test the subject changed his position? Explain.

Additional references regarding blood pressure measurement:

1. Anderson F.D., Cunningham S.G., Maloney J.P. Indirect blood pressure measurement:
a need to reassess Am J Crit Care 1993 2(4):272-9.
2. Bates B., Bickley L.S., Hoekelman R.A. Bates' Guide to Physical Examination and
History Taking
1998 7th edition Lippincott Williams & Wilkins Publishers.
3. Croft P.R. Standardizing blood pressure measurement in everyday practice: whats
the gold standard? J Hum Hypertens 1999 13(2):85-6.
4. Frohlich E.D., Grim C., Labarthe D.R. et al Recommendations for human blood
pressure determination by sphygmomanoneters Ann Intern Med 1988 109(8):612.
5. Haynes R.B., Lacourciere Y., Rabkin S.W. et al Diagnosis of hypertension in adults
CMAJ 1993 149(4):409-18.
6. McKay D.W., Campbell N.R., Parab L.S. et al Clinical assessment of blood pressure
J Hum Hypertens 1990 4(6):639-45.
7. Pickering T.G. Blood pressure measurement and detection of hypertension Lancet
1994 344(8914):31-5
8. Roche V., OMalley K., OBrien E. How scientific is blood pressure measurement in
leading medical journals? J Hypertens 1990 8(12):1167-8.

Exercise B Reviewing the cardiac cycle

In order to understand the sequence of the events during the cardiac cycle, we will record the
followings physiological parameters:
1. ECG The electrical activity of the heart (Ch. 3)
2. Heart sounds - will be recorded using a microphone. These sounds represent the mechanical
activity of the heart valves (Ch. 5).
3. Volume pulse - will be recorded by a photoelectric transducer fastened on the finger (Ch. 2).
4. Pressure in a sphygmomanometer - cuff will be measured by a transducer connected to the
cuff inflation tubule (Ch. 1).
5. Korotkoff sounds - will be recorded using a microphone placed above the brachial artery
(Ch. 4)
Work procedure
The experiment will be carried with the help of an instructor.
Select the cardiovascular laboratory in the lab menu, and press Start. The screen will
show recordings from the five channels, arranged one above the other on the same time
axis.
Clarify which signal is recorded on each channel, and which transducer is used for each
signal.
A subject (volunteer from the group) is connected to the measuring instruments.

1)

Make sure that a clear recording is obtained on every channel. Note the shape of the
signals and their mutual timing.
When everything is clear, start the procedure.
Inflate the cuff until the volume pulse in the finger disappears (approx. 150 mm Hg).
Release the pressure gradually. While releasing the pressure, note the appearance of
Korotkoff sounds and their subsequent disappearance.
Stop recording and save the data file.
Print the experiment graph and mark on the printout:
a. First and second heart sound on the microphone channel. Which cardiac cycle event
may cause these sounds?
b. On the ECG channel, mark the P-wave, the QRS complex and the T-wave. Which
electrical event does each of the waves represent?
c. On the photoelectric channel, note the point where the volume starts to increase and
the peak of the positive slope of the volume wave. Which part of the cardiac cycle is
represented by these parts of the volume wave?
d. Mark and measure the duration of the following intervals: RR interval, PR interval,
duration of QRS complex, QT interval. Compare the values to reference normal
values. If the results deviate from normal values, what could be the reasons?
e. On the microphone channel of the sphygmomanometer cuff, mark a Korotkoff sound
wave.

2) During one cardiac cycle, mark the time when the following events occur: peak of the
QRS complex, end of the T wave, 1st sound, 2nd sound and peak of the volume wave.
Sequence these events and describe their integration in the cardiac cycle.
3) Measure the time intervals between:
1). The QRS complex and the beginning of a Korotkoff sound.
2). The QRS complex and the appearance of the volume wave in the finger.
3). The 2nd sound and the end of the volume wave.
What may affect the above time intervals?

Exercise 3 - Imaging of the arterial system

The blood pressure and the cardiac output (CO) are interconnected. This exercise is focused on
the relationship between the cardiac output, the heart rate and the blood pressure in the systemic
blood circulation.
The systolic pressure is an expression of the volume of blood present in the aorta during
contraction of the myocardium. The blood volume in the aorta depends on the quantity of blood
entering the aorta from the left ventricle, relative to the quantity of blood exiting to the peripheral
blood vessels. It is important to point out that, during the systole, most of the stroke volume of
the left ventricle accumulates in the aorta under tension. Only a small amount (approx. 20%, the
quantity depends on the response of the aorta) of the stroke volume escapes to the peripheral
blood vessels. Indeed, an increased stroke volume will cause an increase in the value of the
systolic pressure. A change in the stroke volume will have a smaller effect on the diastolic
pressure.
The diastolic pressure is an expression of the volume of blood present in the aorta during
relaxation of the myocardium. This blood volume flows to peripheral blood vessels. The lower
the resistance of the peripheral blood vessels, the lower the generated pressure (the diastolic
pressure). The longer the time interval between the systole (injection) and the diastole, the more
time will the blood that has accumulated in the aorta have to flow to the periphery. This means
that the lower the heart rate, the lower the diastolic pressure.
Formulas required for the test:
1. The stroke volume as a function of cardiac output and heart rate: SV = CO / HR.
2. The systemic vascular resistance SVR = (Pmean-Pra) / CO (Pmean - mean arterial blood pressure,
Pra - mean blood pressure in the right atrium, SVR - systemic vascular resistance (TPVR)).
As a rule, flow resistance is defined as R = P/Q (Ohm's law), where Q is the output at the
entrance to the vessel system and P is the difference between upstream and downstream
pressures.
The software:
The SimBioSys Physiology Labs" software is imaging software that simulates the
functioning of the human body; it is supplied along with a textbook and tests in various
physiological fields. All known physiological parameters and their interactions are fed into the
software. Any change in a physiological index or variable leads to a chain of reactions. A
detailed explanation on how to operate the software will be given in class.
a.
Systemic vascular resistance
In the systemic blood vessel system, the main resistance occurs in the arterioles, particularly in
those having a diameter of less than 100 m. In the systemic blood circulation, the upstream
pressure is Pmean and the downstream pressure is the pressure in the large veins. Since there are no
valves separating the right atrium from the large veins, Pra (right atrium pressure) equals the
venous pressure, and normally it is used to describe the downstream pressure of the systemic
circulation. The arterial pressure is determined by the cardiac output (CO), the systemic vascular
resistance (SVR) and the pressure in the right atrium (Pra). In practice, the pressure in the right

atrium is very low compared with the arterial pressure, and, consequently, it can be ignored in
the equation. Thus, the arterial pressure is very close to the product of CO and SVR.
In this exercise, two windows appear: Monitor = a window for recording the arterial and venous
blood pressures (right atrium pressure), and Physiological Data = a window with a table of
physiological values.
1.

It is often stated that the mean blood pressure can be evaluated from the following equation:
Pmean = Pdia + 1/3PP
PP (pulse pressure) = Psys - Pdia

Record the following variables from the data window and then check the correctness of the
following formula:
Pdia

Psys

Mean blood pressure appearing on the computer

Calculated mean blood pressure

1) In your opinion, what is the difference (if any) between the mean blood pressure value
that you calculated and the pressure that is displayed in the table window?
To better illustrate the blood pressure change, change the time axis. Select the time axis,
right click on the mouse -> axis, and set the horizontal axis endpoint maximum at 30.
2.

Record the arterial pressure, the pressure in the right atrium, the cardiac output, the heart
rate and SVR in the baseline column of the table. Calculate the SVR by using the recorded
pressure and the flow data, and compare the result with the displayed value.
nitroprusside

phenylephrine

baseline
Pdia
Psys
Pmean
Pra
HR
SV
CO
SVR
Calculated SVR

3.

Start infusion of phenylephrine. (Phenylephrine activates 1 receptors and causes contraction

of the smooth muscle in the blood vessel walls.) For the purpose of infusion, select the Drug
and Fluid Infuser line in the Tools window, press + to add a medication, add phenylephrine
by continuous IV, and set the infusion rate at 10 g/kg/min, by using the left arrow. Start
infusion by pressing the red circle until you reach 1000 g/kg. Stop simulation, by pressing
Simulation -> Set Simulation Speed -> Paused, and record the data obtained in the table.
2) How did Phenylephrine affect the systemic vascular resistance (SVR)?
3) How did Phenylephrine affect the arterial blood pressure (Pmean) and the cardiac
output?

4.

Reset the conditions, by pressing Simulation -> Reset Physiological State, and start infusion
of Nitroprusside at a rate of 10 g/kg/min up to 1000 g/kg. (Nitroprusside causes relaxation
of the smooth muscle in the blood vessel walls by releasing NO.) Stop simulation and record
the new values obtained in the table.

4) How did Nitroprusside affect the systemic vascular resistance?

5) How did Nitroprusside affect arterial pressure and cardiac output? What caused the
change in cardiac output?
6) From the above experiments, how does the diameter of the blood vessels affect the
systemic vascular resistance? Can you estimate this relationship mathematically?

b. Effect of the cardiac output on the blood pressure values

The heart rate is one of the variables that affect the cardiac output, and as such it also affects the
blood pressure. When the heart rate increases, the time interval between two heartbeats (= the
diastole) is shortened. This shortening of the diastole has a number of affects: the time required
for the aorta to be emptied (and for the pressure that has built up in it to be lowered), and the
time required for the left ventricle to be filled is also reduced. In this exercise, the interactions
between the heart rate and the blood pressure values are demonstrated. For a better
demonstration, change the time axis to 10 seconds.

40/mi
n

50/mi
n

70/mi
n

90/mi
n

110/m
in

130/m 150/m
in
in
Pdia
Psys
Pmean
Pulse pressure
(PP)
Stroke volume
(SV)
Cardiac output
(CO)
Pra

1.

2.

In order to change the heart rate, the automatic heart rate (the rate of the SA node
pacemaker) must be changed. Select the Sinus Rate line in the Physiological Data window,
and press the lock to open it. Change the sinus rate to the values in the table, starting with
the fast heart rate. Wait a few seconds each time, for stabilization. Pause the simulation. Fill
in the values in the table. There is no need to reset the simulation each time.
Plot the following graphs (the graphs must be submitted together with the lab report):
a. Stroke volume vs. heart rate
b. Cardiac output vs. heart rate
c. Systolic and diastolic pressures, mean pressure and pulse pressure as functions of
the heart rate

7) Explain the graphs obtained. In your opinion, what is the physiological mechanism of
the relationship between these values and the heart rate?

10

c. Shape and nature of the pulse wave

During the systole, blood is injected into the arteries. The blood vessel wall is stretched and
stores part of the pressure energy. During the diastole, this energy is returned and generates blood
flow in the period when the ventricles dont cause any blood flow. This ability of the arteries to
expand, and to store blood and energy, is due to the response of the arterial system. The overall
effect of the arterial response is that fluctuations in blood pressure between heartbeats are
reduced, and the blood flows almost continuously in the capillaries.
To start this test, load a new physiological state, by pressing: File -> Load Physiology State ->
Waveform.sim. A warning that the existing windows will be deleted appears on the screen. Press
Yes.
Two new windows should appear on the screen: a window for recording the pulse wave in
different areas, and a window with a table for physiological values.
4 mmHg

2 mmHg

Baseline
(-4mmHg)
Psys
Pdia
Pmean
Pulse pressure
(PP)
Stroke volume
(SV)
Pra

1.
2.

3.
4.

Fill in the baseline column in the table, from the window of physiological values.
To reduce the stroke volume, increase the extracardiac pressure to 2 mm Hg. To increase the
pressure, select the Extracardiac Pressure line, and change the value of the variable by
means of the scale on the right-hand side. Wait about one minute for stabilization. Record
the new values, as obtained above, in the table.
Increase the pressure to 4 mm Hg; wait for stabilization and record the values obtained.
Close the lock again, and wait for stabilization.
Based on the data obtained, plot a graph of pulse pressure - systolic, diastolic and mean
pressures vs. the stroke volume.
8) How did the reduction in stroke volume affect the systolic and diastolic pressure, the
mean pressure and the pulse pressure?
9) From the graph of pulse pressure vs. stroke volume that you plotted, can you think of a
way to estimate changes in cardiac output according to vital signs (blood pressure,
pulse)?

11

5.

Increase the size of the Aortic and Femoral Pressure window, in order to see in detail the
pressure in the aorta and the femoral artery.

Note that the shape of the wave in the aorta shows a deep dicrotic notch, while the femoral artery
shows only a deflection point, which reflects closing of the semi-lunar valve. Print the recording,
by selecting the window and pressing the printer icon.
- On the printed sheets, mark the dicrotic notch, systolic pressure and diastolic pressure.
Note that there is a time difference between pressure build-up in the aorta and pressure build-up
in the femoral artery. By reducing the time axis (select time axis, make a right click and set the
desired time period), try to estimate the magnitude of this time difference.
10) What is the time difference between the appearance of the pressure wave in the aorta
and the appearance of the pressure wave in the femoral artery? In your opinion, what is
the cause of these time differences?
11) How do the structures of the pressure wave and the pulse pressure change, when we
move towards the periphery? Which parameter hardly changes? (To explain this, use
the printout of blood pressure in the aorta and in the femoral artery).

12

Appendix 1
Patho-physiology of hypertension
Today, hypertension is considered one of the major diseases in developed countries. People who suffer
from hypertension for long periods of time, without being treated, will develop many complications,
including sclerotic processes in the arteries, cardiac insufficiency, kidney insufficiency, strokes and
damage to the retina. Untreated hypertension reduces life expectancy by 10 to 20 years.
One of the problems in identification of the disease is that, in most cases, the condition is
nonsymptomatic and most often a diagnosis is only made during routine blood pressure tests.
Hypertension is defined as a diastolic pressure above 80 mm Hg and/or a systolic pressure above
120 mm Hg. Different degrees of severity are distinguished, and these serve to determine the treatment.
Category
Normal
Prehypertension
Hypertension stage 1
Hypertension stage 2

SBP (mm HG)

120 >
120-139
140-159
160 <

DBP (mm HG)

80 >
80-89
90-99
> 100

)From JNC 7)

The mean blood pressure is determined by two variables: the cardiac output and the general peripheral
resistance:
Pmean =CO*TPVR
The main resistance and pressure drop in the arterial system is located in the arterioles. The extent of
contraction of the smooth muscle in the walls of the arterioles determines the diameter of the blood
vessels and the resistance to flow through them. Vasodilators are substances that reduce the extent of
contraction of the smooth muscle in the blood vessel wall, and, as a result, they expand the blood vessels.
Vasoconstrictors cause contraction of the smooth muscle, increase in the resistance of the blood vessel,
and increase in TPVR. The cardiac output is determined by two variables: the stroke volume and the
heart rate:
CO = SV*HR.
A change in any of the above variables will cause a corresponding change in blood pressure.
In spite of significant developments in understanding the causes of hypertension, the cause is not yet
known in about 90 to 95% of the cases (primary hypertension). Primary hypertension probably involves
a number of diverse factors, exhibited in the general clinical picture. The disease has a multitude of
causes and is influenced by many factors, such as heredity, environment, nutrition (consumption of salt,
alcohol), obesity, socioeconomic status.
The cause of hypertension is known in only about 5% of the cases. This type of hypertension is called
secondary hypertension, because it is caused by other diseases, such as renal artery hypertension.
Stenosis of the kidney artery reduces perfusion of the kidney tissue. The kidney has a sensing system that
is able to sense reduction in perfusion. This system is connected with a hormonal system, responsible for
control of the salt content and the extracellular fluid volume - the Renin-Angiotensin-Aldosterone system.
Activation of the system causes an increase in blood pressure, in two ways:
1. The Angiotensin II hormone causes vasoconstriction of the peripheral arterioles TPVR
Pmean.

13

2.

Angiotensin II stimulates the adrenal cortex to discharge aldosterone discharge of sodium in the
kidney preservation of fluids in the kidney extracellular volume plasma volume
preload CO Pmean.

14

Endocrinous hypertension
Primary aldosteronism - uncontrolled, excessive discharge of aldosterone from a tumor of the adrenal
cortex. High levels of aldosterone cause hypertension due to retention of the body fluid volume in the
kidney.
Pheochromocytoma - a rare tumor of the medulla cells of the adrenal cortex. The tumor discharges large
quantities of epinephrine and norepinephrine, which cause excessive stimulation of adrenergic receptors
in blood vessels and in the myocardium. Blood pressure increases, due to the effect of two variables that
determine the blood pressure:
1. Peripheral vasoconstriction by activation of -adrenergic receptors in the muscular wall of the
arterioles TPVR Pmean.
2. Stimulation of the myocardium (by activating -adrenergic receptors in the heart) HR (positive
chronotropic effect) and SV (positive inotropic effect) => CO Pmean.
Hypertension caused by use of contraceptive pills and preparations containing estrogen: contraceptive
pills containing estrogen were, until a few years ago, a common cause of endocrinous hypertension. In the
last few years, the problem has become less significant, as new pills with low estrogen content came on
the market.
The mechanism that causes hypertension when the pills are used probably derives from activation of the
Renin-Angiotensin-Aldosterone system. The estrogenic factor in the pill initiates production of
angiotensinogen - the renin substrate - in the liver.

Additional literature references concerning hypertension:

1.

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure (JNC 7)

2.

Kaplan N.M. Systemic hypertension: mechanisms and diagnosis (in Braunwalds Heart Disease) 5th ed.
W.B. Saunders Company.
Williams G.H. in Harrisons principles of internal medicine. (Fauci A.S., Braunwald E., Isselbacher K.J.
et al (editors). pp. 1380-1394, 14th ed. McGraw-Hill.

3.

15

Appendix 2
Basics of ECG (electrocardiography) interpretation
The theoretical background of heart activity recording will be discussed later, within the scope of the
course on physiology of the body systems. The purpose of this appendix is to familiarize the student with
ECG recordings made in this laboratory.
Electrocardiography is a procedure for recording on paper the electrical activity of the myocardium.
Like any electrically-charged body, the myocardium has an electric field. Although the heart is hidden
deep in the thorax, its field expands and can be identified and sampled from a distance. ECG measures
and records the myocardiums electric field as projected on the bodys skin surface.
The myocardium cells have a rest potential of -80-(-90) mV. The activity potential of the myocardium
reaches a peak of +30-(+40) mV. At any given moment of the heart activity cycle, part of the myocardium
is contracted while the remaining part is relaxed1. The contracted cells are positively charged relative to
the relaxed cells and, consequently, the myocardium can be represented as an electric dipole having a
given electric field.

The electric field of the dipole not only has an absolute value, but also a direction, and it can be
represented by a vector. Since ECG only constitutes a scalar (numerical) measurement and recording of
the dipole electric field that represents the myocardium, sampling and measurement of the field is
required at a number of points, in order to obtain a vector of the dipole electric field.
It is agreed that the electric field of the heart is measured in the center of a triangle, the vertices of which
are the right shoulder, the left shoulder and the pubic symphysis. The triangle vertices can be moved to
the left arm, the right arm and the left leg, accordingly.

By sampling the dipole electric field with the ECG apparatus at the triangle vertices, the direction of
expansion of depolarization (contraction) and repolarization (relaxation) in the myocardium can be
established. The ECG apparatus is a standard voltmeter. The signal measured by the voltmeter is
amplified by means of amplifiers for the purpose of recording.

Since the duration of the twitch of the myocardium cells is similar to that of the action potential, the cell is in a 1
.state of depolarization at maximum contraction

16

It is agreed that the electric signal, which is positive with respect to a reference point 2, is recorded as a
positive deviation from the baseline3. Every deviation (also called a wave), whether positive or
negative, is marked with a letter, beginning with the letter P.

In electrocardiography, two kinds of reference points are used; they will be explained in the 2
.relevant lectures
The ECG baseline is called the isoelectric point. The isoelectric point is plotted on paper 3
when there is no potential difference between the positive and negative poles of the terminals of
.the ECG apparatus
17

The first ECG wave, wave P, indicates depolarization expansion in the heart atria, which is parallel to contraction of
the atria.

The Q, R and S waves indicate expansion of the depolarization (parallel to contraction) in the ventricles.
The complex of waves Q, R and S, also called the QRS complex, is the most conspicuous ECG
complex because the muscular mass of the ventricles is very large, relative to the atria.

The interval between the start of the P wave and the start of the QRS complex is the time period required
for passage of the electric signal from the sinoatrial node (SAN) to the atrioventricular node (AVN). The
SAN is located in the upper part of the right atrium, and the AVN is located in the lower part of the right
atrium (to be exact, at the partition between the atria and the ventricles).
ECG permits characterization of not only the expansion of depolarization in the myocardium, but also the
repolarization. Repolarization of the atria is usually hidden in the QRS complex and, consequently,
cannot be identified. Repolarization of the ventricles creates a T wave. The repolarization process is slow,
as compared with depolarization and, therefore, the T wave amplitude is smaller than the amplitude of the
QRS complex.
Additional literature references regarding ECG:

18

1. Goldberger A.L. in Harrisons principles of internal medicine. (Fauci A.S., Braunwald E., Isselbacher K.J.
(editors)). et al. pp. 1231-1237, 14th ed. McGraw-Hill.
2. Huang P. Introduction to electrocardiography. W.B. Saunders Company.
3. Schamroth L. An introduction to electrocardiography. (C. Schamroth (editor)) 7th ed. Blackwell Science.

19

Appendix 3
Cardiac cycle
The attached graph describes the time relationships
between the various events that make up the cardiac cycle.
Note the division into stages,
as shown at the top of the illustration.
Source:
Berne R.M., Levy, M.N., Physiology;
Fourth edition

20