MBARARA UNIVERSITY OF SCIENCE AND TECHNOLOGY

FACULTY OF MEDICINE

DEPARTMENT OF PHYSIOLOGY

THE CARDIOVASCULAR SYSTEM

DATE OF PRACTICAL: 7TH MARCH 2022

DATE OF SUBMISSION: 21ST MARCH 2022

GROUP 6
1. EKEJU ABRAHAM 2021/PHS/028/PS EA

2. ANDIMA NOBERT 2021/MLC/002/PS AN

3. OGWAL SOLOMON 2021/MLS/141/PS OS

4. SSERUFUNGO TONY BLAIR 2021/MLS/169/PS STB

5. AKANKWATSA MICHELLE 2021/MLS/189.PS AM

6. KAIGWA MUBARAKA 2021MLS/200/PS KM

7. MOHAMED C SAIDA 2021/MLC/008/PS MCS

8. KAYIIWA NOOH 2021/MLS/071/PS KN

9. ABAMWESIGWA ALBERT 2021/MLS/012.PS AA

LECTURER
DR. MIGISHA RICHARD

TECHNICIANS

1. MRS. HOPE MBABAZI RUKUNDO

2. MR. MWEBAZE HERBERT

3. MR. MWESIGWA GEOFFREY

4. MR. TWINORUSA JOHN

5. MR. NSABIMANA GILBERT

 INTRODUCTION
The cardiovascular system is a closed system of branching tubules used to transport
substances all over the body. It’s composed of the heart and the blood vessels. The heart
basically is a modified blood vessel which functions as a double pump, therefore when its
contracts, it generates the pressure which drives blood through the systemic and pulmonary
circulations. It has three types of myocardium; atrial muscle, ventricular muscle, specialized
excitatory and conductive fibres. The atrial and ventricular muscles are similar to the skeletal
muscles, but differ in their excitation-contraction coupling mechanisms and their duration of
contraction. Also, the excitatory fibres exhibit auto rhythmicity, thus discharge action
potentials which are conducted by the conductive fibres through the heart, therefore
providing the excitatory system which controls the rhythmic beating of the heart.
The heart rate and blood pressure are often used to determine the state of health of the heart,
which fluctuates as the heart conditions changes. The heart rate can be obtained by counting
the number of arterial pulsations felt per minute at a palpated artery e.g. the radial artery is
easily palpated with the tips of the fingers just above the wrist. The normal heart rate is
within 60 to 100 beats per minute and values outside this range are associated with either
bradycardia (abnormally slow heart rate) or tachycardia (faster heart rate than normal). Blood
pressure is usually represented by arterial systolic pressure over arterial diastolic pressure.
It’s measured using a sphygmomanometer in palpation method (measures systolic blood
pressure only) and auscultation method (measures both systolic and diastolic blood
pressures).
The electrocardiograph measures the heart’s electrical activity. This is possible because the
impulse conduction through the heart can be detected at the surface of the body and the
fluctuations in action potentials of myocardial fibres can be recorded extracellularly,
therefore the recordings of the electrical changes that accompany each cardiac cycle is called
electrocardiogram (ECG).
In a volume conductor, the sum of the potentials at the points of an equilateral triangle with
the heart at its centre as a current source (Einthoven’s triangle) is zero at all times. The
triangle is approximated by placing electrodes on both arms and on the left leg (the three
standard limb leads). The electrodes are connected to an indifferent electrode that stays near
zero potential. Depolarization moving toward an active (+ve) electrode in a volume
conductor produces a positive deflection (upward deflection on the ECG) while
depolarization moving in the opposite direction produces a negative deflection (downward
deflection on the ECG). The Augmented unipolar limb leads have two limbs connected
through electrical resistances to the negative terminal of the electrocardiograph, with the third
limb connected to the positive terminal. With the positive terminal on the right arm, the lead
is the aVR lead; when on the left arm, the aVL lead; and when on the left leg, the aVF lead.
The basic ECG comprises the P wave produced by atrial depolarization, the QRS complex by
ventricular depolarization, and the T wave by ventricular repolarization. The U wave, an
inconstant finding, is attributed to slow repolarization of the papillary muscles.
Electrocardiograms of the unipolar chest leads are recorded with electrodes placed on the
anterior surface of the chest directly over the heart at conventional points. The six standard
chest leads V1, V2, V3, V4, V5, and V6 allow relatively minute abnormalities in the
ventricles to be detected, as heart surfaces are close to the chest wall. Each chest lead records
the electrical potential of the myocardium immediately beneath the electrode. Myocardial
defects cause changes in the electrocardiograms recorded from these chest leads.
OBJECTIVES OF THE PRACTICAL
o To determine the human Electrocardiogram
o To determine the effects of exercise on the heart via the Electrocardiogram
o To determine the human arterial blood pressure
 o To determine the effect of posture on the arterial blood pressure
o To determine the human heart rate by pulse pressure
METHODOLOGY
EXPERIMENT 1: THE ELECTROCARDIOGRAM
Materials and apparatus
o Electrocardiograph machine o ECG gel
o Tissue paper o Coach bed
PROCEDURES
One student acted as the subject and each student took a turn as ECG operator.
The subject sat relaxed and breathed quietly.
Coated non-hairy skin on both wrists and both ankles thinly with salts enriched electrodes
jelly and then placed metal electrodes firmly on the skin with rubber traps.
Connected the multiple leads to the appropriate electrodes, white to the right arm, black to the
left arm, green to the right arm and left leg.
Located the intercoastal space on the chest and smeared the spots with ECG electrode jelly.
Put in place the six chest electrodes by use of the suction pressure created by pressing the
bulb.
Turned on the instrument to warm up the amplifier for a few minutes.
With the lead selector at standardised switch to Un and inserted a 1mV calibration for 1
second. This gave a1cm deflection. And quickly turned the switch back to 0N to stop the
recording paper.
Took sample records of only 4-6 beats with each of the three bipolar leads and each of the
three unipolar leads switched to start. Used a pen to label each record as it was completed.
Tried the following procedure on the subject.
➢ Investigating cardiovascular reflexes: for carotid sinus reflex the subject lied
completely relaxed on his back. Felt the pulsation of carotid artery deep to the anterior
edge sternomastoid muscle, the bifurcation and sinus at the upper border of the
thyroid cartilage. Started the ECG with standard lead II connections after a few
seconds of control recording, compressed the artery firmly with three fingers against
the vertebral bodies for a few seconds only and looked for subsequent slowing and
then recovery of the heart rate during 10 seconds following the compressions. Marked
the period of compression on the record by depressing the marked button. Measured
the interval between beats to slowing.
➢ Effect of position of the heart: took 5 inspiration records with the three standard
bipolar leads while the subject held his breath in the deepest possible inspiration.
➢ Investigating the effects of exercise: subject in the relaxed, seated position, recorded
a control segment with lead II and stopped. Subject immediately started making some
exercise. When the task was done, subject lied down and recording started
immediately.
➢ Valsalva manoeuvre: subject lied down, breathing normally. After a control
recording subject closed his glottis and exerted strong exhalation movement without
letting the air out. Kept the pressure on for 15 seconds and marked the onset and the
release of the pressure and continued recording for 30 seconds.
EXPERIMENT 2: MEASUREMENT OF PULSE IN MAN
Materials used - Timer
PROCEDURE
o The subject is let to sit comfortably and rest for some minutes.
o The radial artery is palpated at the wrist with the tips of the fingers.
o The timer is started and the pulse per minute is counted.
o The results are then recorded.
EXPERIMENT 3: SYSTOLIC PRESSURE BY PALPATION
Materials used
Mercury sphygmomanometer
PROCEDURE
Lying position
o The subject was let to lie supine with arm unclothed and the person to take
measurement sat near the subjects left hip. The cuff was wrapped around the subjects
left upper arm placing the centre of the arm as it would go.it was wrapped tightly but
snugly that it would not slip down the arm and very neatly to support the distended
pneumatic pad uniformly feel the radial pulse. The pressure of the cuff was raised to
200mmhg. The valve was opened a little to allow the mercury to fall steadily until the
first beat of the returning pulse was felt and we noted this reading.
Standing position
o The subject stands upright with arm unclothed, the cuff wrapped around his arm
tightly and snugly that it would not slip down the arm and very neatly to support the
distended pneumatic pad uniformly feel the radial pulse. Pressure of the cuff was
raised to 200mmhg, the valve was opened slowly to allow the Mercury fall steadily
until the first beat of the returning pulse was felt an we noted the reading.
Sitting position
o The subject sat properly with his arm unclothed, the cuff was wrapped around his arm
tightly and snugly that it would not slip down the arm and very neatly to support the
distended pneumatic pad uniformly feel the radial pulse, pressure of the cuff was
raised to 200mmhg, the valve was opened a little to allow the Mercury fall steadily
until the first beat of the returning pulse was felt and we noted the reading.
EXPERIMENT 4: AUSCULTATION METHOD
Materials Used
 Stethoscope  Mercury sphygmomanometer
PROCEDURE
o The subject’s elbow was brought to rest upon the knees while the relaxed forearm
kept fully extended by its own weight.
o The position of the bronchial pulsation was located, and the bell of the stethoscope
was then pressed over the pulsation.
o The dull thud of the first pulsation to pass gave us the reading of the systolic blood
pressure. And as the mercury column fell, the sound became louder. The point of
disappearance of the sound was then recorded as the diastolic blood pressure.
o The experiment was done for the supine, standing and sitting positions and their
respective results recorded appropriately.
RESULTS
EXPERIMENT 1: THE ELECTROCARDIOGRAM
Artefacts Heat P-R Q-T Amplitude Duration (s) Polarity
rate interval interval (mV)
(Bpm)
Normal None 72 0.12 0.4- P 0.10- P 0.10 P +
ECG 0.42 0.12
QRS 0.50 QRS 0.08- QRS +
0.10
T 0.30 T 0.20 T +
Lead I None 80 0.10 0.32 P 0.10 P 0.12 P +
QRS 0.40 QRS 0.08 QRS +
T 0.20 T 0.16 T +
 Lead II None 70 0.10 0.4 P 0.10 P 0.08 P +
QRS 0.54 QRS 0.05 QRS +
T 0.28 T 0.18 T +
Lead None 60 0.12 0.4 P 0.08 P 0.10 P +
III QRS 0.12 QRS 0.10 QRS +
T 0.12 T 0.12 T +
aVR None 80 0.08 0.42 P 0.10 P 0.12 P -
QRS 0.52 QRS 0.12 QRS -
T 0.36 T 0.14 T -
aVL None 60 0.06 0.36 P 0.08 P 0.60 P -
QRS 0.30 QRS 0.04 QRS +
T 0.20 T 0.08 T +
aVF None 60 0.10 0.4 P 0.26 P 0.08 P +
QRS 0.48 QRS 0.06 QRS +
T 0.30 T 0.12 T +

EXPERIMENT 2: Heart Rate = 63 Beats per minute

EXPERIMENT 3: BLOOD PRESSURE BY PALPATION

Position Systolic blood pressure (mmHg)
Lying 120
Standing 105
Sitting 112

EXPERIMENT 4: BLOOD PRESSURE BY AUSCULTATION

Position Blood pressure in mmHg
Lying 130/79
Standing 128/76
Sitting 124/72

DISCUSSION OF THE RESULTS

THE ELECTROCARDIOGRAM
In unipolar recordings, an active electrode is connected with indifferent electrode at zero
potential. Bipolar recording involves two active electrodes on opposite sides of the heart.
For the standard bipolar limb leads, electrodes are placed on both arms and on the left leg.
Einthoven’s law dictates that, in a triangle approximated about the heart (Einthoven’s
triangle) by the standard bipolar limb leads, the sum of the potentials of the leads I and III is
equal to that of lead II. Lead II gives the largest amplitude of the QRS complex and P wave
as it contains the largest component of the mean vector of depolarization of the heart.
With aVR, atrial depolarization, ventricular depolarization, and ventricular repolarization
move away from the exploring electrode. The P wave, QRS complex, and T wave produce
negative (downward) deflections. For leads aVL and aVF which view the ventricles, the
deflections are positive (aVF) or biphasic (aVL)
In an ECG, the P wave is produced by atrial depolarization, the QRS complex by ventricular
depolarization, and the T wave by ventricular repolarization. A U wave is an inconstant
finding, believed to be due to slow repolarization of the papillary muscles.
Lead II gives the largest deflections of The P wave, QRS complex and T wave as it contains
the largest component of the mean direction vector of depolarization and repolarization of the
heart. Atrial depolarization is almost parallel to lead II, defects in atrial depolarisation are
best noted from this lead.
The subject’s P-wave lies within the normal ranges of magnitude (0.08mV-0.1mV) and
duration (0.8s-0.12s) as seen from lead II. Variations in P wave morphology, amplitude and
duration are used in diagnosis of atrial cardiac anomalies. Right atrial hypertrophy presents
with a tall, pointed p-wave. Left atrial hypertrophy presents an m shaped p-wave. Other
conditions like Sino-atrial block and atrial extra-systole are diagnosable from the p-wave.
The QRS complex consists of the Q, R and S-waves. The Q-wave is a small negative
deflection due to depolarisation of the inter-ventricular septum. The R-wave is a positive
deflection due to depolarisation of ventricular muscle. The S-wave is a small negative
deflection due to depolarisation of the basal portion of the ventricles, near the fibrous
annulus. The subject’s QRS complex by lead II was close to the normal ranges of duration
(0.08s-0.1s) and magnitude (about 0.5mV).
Variations in QRS complex morphology, amplitude and duration are used in diagnosis of
ventricular anomalies. Ventricular hypertrophy presents a prolonged QRS complex due to
prolonged impulse conduction through the ventricle. Bundle branch block and hyperkalemia
are also diagnosed by prolonged QRS complexes.
The subjects T-wave had a duration of 0.22s, magnitude of 0.28mV which fall near the
normal figures. Analysis of the T-wave helps in diagnosis of acute myocardial ischemia
which presents shortened depolarisation of cardiac muscle due to current flow through the
potassium channels, giving a hyper-acute T wave. Hyperventilation, pericarditis and
infraction present a small tall and tented T wave.
Overdoses of drugs like digitalis that have a positive inotropic effect may cause increased
durations of ventricular depolarisation in one part of the ventricle, relative to other parts. This
may bring about non-specific changes like T-wave inversion or a bi-phasic T-wave.
The iso-electric line of the PR interval is the period of conduction through the atrioventricular
node (A.V. Nodal silence). This period of conduction delay causes ventricular contraction a
few seconds after atrial contraction. This allows the atria to completely fill the ventricles
before they pump blood. A prolonged P-R interval is associated with first degree heart block
and certain bradycardia. It is shortened in tachycardia and conditions of secondary
conduction pathways from atria to ventricles.
The isoelectric line of the Q-T interval presents the period at which the ventricles are
completely depolarized. It is prolonged in conditions like myocardial infraction, myocarditis,
hypercalcemia hypothyroidism, etc. It is shortened in conditions like Q-T syndrome and
hypocalcemia.
In the Unipolar chest leads, the active electrode connects to the positive terminal of the
electrocardiograph, and the indifferent electrode is connected through equal electrical
resistances to the right arm, left arm, and left leg all at the same time.
In Leads V1 and V2, the QRS recordings of the heart are mainly negative because, the chest
electrode is nearer to the base of the heart than to the apex. The base of the heart is the
direction of electronegativity during most of the ventricular depolarization process.
QRS complexes in leads V4, V5, and V6 are mainly positive because the chest electrode is
nearer to the heart apex, the direction of electro-positivity during most of depolarization.
Valsalva manoeuvre;
During the Valsalva manoeuvre, there is increased intra-thoracic pressure which compresses
the central veins, reducing venous return, as well as increased peripheral venous pressure due
to accumulation blood in peripheral veins. Reduced venous return and compression of heart
chambers reduce heart filling and preload, decreasing the cardiac output (Frank-sterling
mechanism).
Cardiovascular reflexes;
There is an increase in arterial pressure detected by baroreceptor cells at the carotid sinus that
stimulate firing of the glossopharyngeal nerve that signals nucleus tractus solitarius in the
medulla, causing inhibition of the vasoconstrictor centre and increased parasympathetic
stimulation of the hear via the vagus nerve, lowering the heart rate and cardiac output.
Vasodilation of peripheral vessels leads to lowered peripheral resistance.
Deep inspiration and expiration have no effect on the amplitude of the recorded waves in the
ECG. Deep inspiration increases the heart rate while deep expiration decreases it, affecting
the R-R intervals. Increased intra-thoracic pressure during expiration causes compression of
the central veins, reducing venous return, preload and cardiac output via the Frank-sterling
mechanism. Reducing cardiac output in turn lowers the heart rate.
During deep expiration, decreasing intra-thoracic pressure causes increased venous return,
preload and cardiac output by the Frank-sterling mechanism. Increased stretch of atrial walls
also triggers a reflex tachycardia as a compensatory mechanism. All this act to increase the
heart rate.
Effect of exercise;
Increased muscle action during exercise demands more oxygen (O2) and increases partial
pressures of carbon dioxide (CO2) and lowers blood pH. Changes in partial pressures of O2,
CO2 and pH are detected by peripheral chemoreceptors (Glomus cells) at the carotid and
aortic body. These induce impulses that are sent to the brain, increasing sympathetic action at
the heart to increase the heart rate and blood pressure. There is also stimulation of respiratory
muscle, inducing hyperventilation to get rid of excess CO2. With our subject, this presents as
a decrease in the R-R interval, with major changes in P-wave amplitude and morphology. The
QRS complex is slightly shortened, with a shortened QT interval and an up-sloping ST
segment. The distance between P and T waves is also shortened.
BLOOD PRESSURE
Blood pressure was measured by palpation and auscultation. In palpation, the cuff is inflated
rapidly to a pressure above the point at which the radial pulse disappears. It is then slowly
deflated until the radial pulse returns and the approximate systolic blood pressure is recorded.
Auscultation bases on turbulent flow that occurs with partial constriction of the artery,
vibrating the arterial walls and producing sounds. These sounds, heard by use of a
stethoscope are known as Korotkoff sounds. Turbulent flow occurs when cuff pressure is
greater than diastolic pressure and less than systolic pressure. The first sound to be heard
indicated systolic pressure, while the point at which they disappeared indicated the diastolic
pressure. Values obtained for arterial pressure lie around normal values, 120/80.
The systolic blood pressure of an individual was recorded in different positions; supine
position, sitting position and standing position. The highest systolic blood pressure was seen
when in supine position(120mm/Hg) and the lowest was in standing position(105mm/Hg).
The change in blood pressure observed with position can be attributed to the effects of
gravity on venous return. When standing, there is decreased cardiac output due to reduced
venous return thus low systolic blood pressure while lying down, there is increased cardiac
output due to increase in venous return thus high systolic blood pressure.
MEASUREMENT OF PULSE
The Heart Rate is measured by arterial pulsations per minute. Pressure changes during
ventricular systole eject blood into the aorta with great force, causing distention of the blood
vessel. A pressure wave is produced and conducted through the elastic walls of the arteries,
which can be felt by palpation of arteries in certain anatomical regions. It can therefore show
ventricular activity over a period of time. The normal range of the heart rate is from 60-100
Bpm (beats per minute). Values above this range are associated with Tachycardia of varying
severities. Values below this range are associated with Bradycardia of varying severities. Our
subject had a heart rate within the normal range.
 CONCLUSION
The recordings collected about our subjects indicate that there are no defects in the
myocardium and the heart is healthy and properly functioning
REFERENCES
1. GUYTON AND HALL (2006) the textbook of Medical physiology 11th edition
Elsevier Saunders
2. K Sembulingam and P Sembulingam (2012) Essentials of Medical Physiology,6th
Edition, JP medical ltd
3. Physiology practical by Kiguli James Mukasa, Twinomugisha John, Tumwesigye
Herbert (2015 August) department of physiology faculty of medicine Mbarara
University of Science and Technology
4. Review of Medical Physiology by William F, Gangnong,22nd edition,2005

AUTHORS’ CONTRIBUTIONS
 AN did the methodology for measurement of pulse in man
 AM did the methodology for blood pressure by palpation
 OS did the introduction
 EA did the discussion for blood pressure by palpation
 MCS did the discussion of auscultation method
 STB did the methodology for electrocardiogram
 KN & AA did the discussion for the electrocardiogram
 KM did the methodology for blood pressure by auscultation