GULU UNIVERSITY

FACULTY OF MEDICINE

DEPARTMENT OF PHYSIOLOGY

COURSE UNIT: PHYSIOLOGY (PHYS 1011)

EXPERIMENT: EXAMINATION OF BLOOD

DATE OF PRACTICAL:

DATE OF SUBMISSION: 18TH APRIL 2024

TECHNICIAN: Mr. Okello Joseph

STUDENT’S NAME REGISTRATION SIGNATURE

NUMBER
1. OJAMBO JOSHUA HAMIRIE 23/U/3962/GUM/PS
2. ASINDE JENIPHER 23/U/3287/GUM
3. BWAMBALE EMMANUEL 23/U/0020/GUM
4. OKELLO DENISH 23/U/3295/GUM
5. MUNDUA GLORIA 23/U/3312/GUM
6. KOBUGABE EDGAR 23/U/3309/GUM
7. MUYINDA KIIRYA DAVID 23/U/0061/GUM
8. ALUMA DAN HENRY 23/U/3978/GUM
9. OPIO ZACHARY 22/U/1740/GUM/PS
10. OWEKA INNOCENT 23/U/0096/GUM

SUPERVISOR: Dr. Muzaale Francis

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 REPORT ON THE STUDY OF THE ELECTRICAL ACTIVITY OF THE
HEART USING ELECTROCARDIOGRAPHY

OBJECTIVES

 Determination of Heart rate

 Determination of the rhythm
 Determination of the Cardiac Axis
 Determination of waves forms and intervals

BACKGROUND

The cardiac conduction system is made of specialized conduction tissue and

consists of; Sino Atrial node, sometimes called the heart’s natural pacemaker. It is
located in the junction of Superior vena cava and right atrium, supplied by branch
from the coronary artery or the left circumflex artery. It consists of special atrial
cells that are under the influence of autonomic nervous system and circulating
cetacholamines. The SA node has the fastest rate automaticity.

The SA node is responsible for the fundamental physiological property

rhythmicity. Rhythmicity is the ability of a tissue to produce its own impulses
regularly. This feature accounts for the uniformly paced alternating periods of
contraction and relaxation.

When the cardiac impulse passes through the heart, electrical current also spreads
from the heart into the adjacent tissues surrounding the heart. Conductive system
of the heart is formed by the modified cardiac muscle fibers. These fibers are the
specialized cells, which conduct the impulses rapidly from SA node to the
ventricles. Conductive tissues of the heart are also called the junctional tissues.

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Components of Conductive System in Human Heart include; AV node, Bundle of
His, Right and left bundle branches and finally Purkinje fibers.

SA node is situated in right atrium, just below the opening of superior vena cava.
AV node is situated in right posterior portion of intra-atrial septum. Impulses from
SA node are conducted throughout right and left atria. Impulses also reach the AV
node via some specialized fibers called internodal fibers. There are three types of
internodal fibers:

 Anterior internodal tract: Begins at the anterior margin of the SA node

and curves anteriorly around the SVC to enter the abterior band called the
Bachmann bundle. This band continues to the left atrium with the anterior
internodal pathway entering the superior margin of AV node.
 Middle internodal tract: Begins at the superior margins of the sinus node,
travels behind the SVC to the crest of the interatrial septum, and descends in
the interatrial septum to the superior margin of the AV node.
 Posterior internodal tract: Starts at the posterior margin of the sinus node,
where it joins the superior margin of the AVN

All these fibers from SA node converge on AV node and interdigitate with fibers
of AV node. From AV node, the bundle of His arises. It divides into right and left
branches, which run on either side of the interventricular septum. From each
branch of bundle of His, many Purkinje fibers arise and spread all over the
ventricular myocardium

When depolarization reaches the contractile cardiac muscle cells, they contract –
this mechanical event is called systole. After repolarization, cells relax, which is
called diastole. Thus, the rhythmic change in electrical activity leads to the

3
mechanical pumping action of the heart, providing the driving force for circulating
blood.

However, the entire myocardium is not depolarized at once: The atria depolarize
before the ventricles; the ventricles depolarize in a specific sequence; the atria
repolarize while the ventricles are depolarizing; and the ventricles repolarize in a
specific sequence. As a result of the sequence and the timing of the spread of
depolarization and repolarization in the myocardium, potential differences are
established between different portions of the heart, and also a small portion of the
current spreads all the way to the surface of the body, which can be detected by
electrodes placed on the body surface and recorded. the recording is known as an
electrocardiogram (ECG).

The electrocardiogram is a graphic record of electrical activity of the heart

generated during each cardiac cycle and is recorded by an electrocardiography.

The electrical activation of the heart muscle cell leads to action potentials, which
consists of depolarization and repolarisation process. The ECG records the
depolarization and repolarization potentials generated by the working atria and
ventricular myocardial fibres. This sets up an electrical current which is detected
by surface electrodes, amplified and displayed on a monitor as the ECG.

The convectional ECG is recorded using 12 leads applied to arms, legs and chest.
These leads represent the difference in electrical potentials in frontal and horizontal
planes of the body.

The 12-lead ECG is generated from chest and limb electrodes. These are 4 limb
electrodes and 6 chest leads V1-V6 from electrodes placed on the anterior and
lateral side of over the heart. The electrode are fixed on the skin with jelly.
4
The Lead system

A lead is a pair of electrodes consisting of exploring electrodes and an indifferent

electrode. The potential difference between these 2 electrodes is recorded. The
average vector of ventricular depolarisation is known as cardiac axis. Normal axis
is between -30 and +90.

There are three types of lead system i.e.

1. Standard bipolar limb leads

2. Augmented/Unipolar limb leads
3. Precordial leads/Unipolar chest leads)

Standard bipolar limb leads

These measure potential differences between 2 limbs

 Exploring electrode is the positive lead

 Indifferent electrode is the negative lead

The position is as follows

 Lead I: Left arm (+ve) Right arm (-ve)

 Lead II: Left leg (+ve), Right arm (-ve)
 Lead III: Left leg (+ve), Left arm (-ve)

These three leads record electrical activity along three different axes in the frontal
plane.

The right leg electrode acts as an earthing electrode

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The Einthoven’s Triangle: This is an imaginary formation of three limb leads in a
triangle used in the electrocardiography, formed by the two shoulders and pubis.
The shape forms an inverted equilateral triangle with the heart at the centre. It was
named after Willem Einthoven who theorized its existence.

Einthoven law states that the voltage in lead I plus the voltage in lead III is equal to
the voltage in lead II.

Unipolar Limb leads

Unipolar limb leads VR, VL and VF denotes the position of exploring electrodes
when placed on right arm, left arm or left foot respectively. They produce low
amplitude potentials which are augmented by suitable mechanism and termed as
aVR aVL and aVF. Record electrical activity between limb electrode and modified
central terminal.

For example;

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  Lead aVL records signals between left arm and central negative terminal
formed by connecting right arm and left leg electrodes. These leads also
record electrical activity in frontal plane.
 Lead aVR records signals between left arm and central negative terminal
formed by connecting left arm and left leg electrodes
 Lead aVF records signals between left arm and central negative terminal
formed by connecting right arm and left arm electrodes

Precordial Leads (Unipolar Chest leads)

Indifferent electrode is connected to the central terminal while exploring electrode

is placed at various points on chest wall. These are: V1-V6

 V1: 4TH intercostal space near the right sternal border

 V2: 4th intercostal space near the left sternal border
 V3: Between V2 and V4
 V4: 5th intercostal space midclavicular line
 V5: 5th intercostal space at anterior axillary line
 V6: 5TH intercostal space at mid axillary line

Lead V1 and V2 lie over the right ventricle

Lead V3 and V4 lie over the interventricular septum

Lead V5 and V6 lie over the left ventricle

Because of the 3 bipolar leads, 3 augmented unipolar leads and 6 precordial

unipolar leads, a term 12 lead ECG is obtained.

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Normal ECG waves

 P Wave- Electrical depolarization of both the atria (best seen in LI and V1)
 Q Wave- Excitation of interventricular septum-beginning of ventricular
depolarization
 R Wave- Displays spreading of excitation of right and left ventricular
myocardium
 S Wave-Completion of ventricular depolarisation-excitation of base of the
interventricular septum
 QRS complex- Ventricular depolarization
 T Wave- Repolarization of ventricles

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 A table of normal physiological measurements obtained from the ECG
recording.

Heart P-R Q-T Wave Amplitu Duration Polari

rate interval(sec interval(sec de (mV) (seconds) ty
(beats onds) ond) (millivol (s)
per (s) (s) ts)
minute)
(bpm)
Norm 60 - 90 0.12 – 0.20 0.4 - 0.42 or P 0.1 – 0.1 +
al ≤ 0.44 0.12
ECG QRS 1.0 0.08 - +
0.10
T 0.3 0.2 +

Clinical significance of P wave

Variation in the duration, amplitude and morphology of ‘P’ wave helps in the
diagnosis of several cardiac problems such as:
 Right atrial hypertrophy: ‘P’ wave is tall (more than 2.5 mm) in lead II. It is
usually pointed
 Left atrial dilatation or hypertrophy: It is tall and broad based or M shaped
 Atrial extra systole: Small and shapeless ‘P’ wave, followed by a small
compensatory pause
 Hyperkalemia: ‘P’ wave is absent or small
 Atrial fibrillation: ‘P’ wave is absent

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  Middle AV nodal rhythm: ‘P’ wave is absent
 Sinoatrial block: ‘P’ wave is inverted or absent
 Atrial paroxysmal tachycardia: ‘P’ wave is inverted
 Lower AV nodal rhythm: ‘P’ wave appears after QRS complex.
Clinical significance of PR interval
Variation in the duration of ‘P-R’ intervals helps in the diagnosis of several cardiac
problems such as:
 It is prolonged in bradycardia and first degree heart block
 It is shortened in tachycardia, Wolf-Parkinson-White syndrome, Lown-
Ganong-Levine syndrome, Duchenne muscular dystrophy and type II
glycogen storage disease
Clinical Significance of QRS complex
Variation in the duration, amplitude and morphology of ‘QRS’ complex helps in
the diagnosis of several cardiac problems such as:
 Bundle branch block: QRS is prolonged or deformed
 Hyperkalemia: QRS is prolonged.
Clinical Significance of QT interval
 ‘Q-T’ interval is prolonged in long ‘Q-T’ syndrome, myocardial infarction,
myocarditis, hypocalcemia and hypothyroidism
 ‘Q-T’ interval is shortened in short ‘Q-T’ syndrome and hypercalcemia

Clinical Significance of ST segment

 Elevation of ‘S-T’ segment occurs in anterior or inferior myocardial

infarction, left bundle branch block and acute pericarditis. In athletes, ‘S-T’
segment is usually elevated

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  Depression of ‘S-T’ segment occurs in acute myocardial ischemia, posterior
myocardial infarction, ventricular hypertrophy and hypokalemia
 S-T’ segment is prolonged in hypocalcemia
 S-T’ segment is shortened in hypercalcemia

R-R’ interval
‘R-R’ interval is the time interval between two consecutive ‘R’ waves.
‘R-R’ interval signifies the duration of one cardiac cycle.
Duration: 0.86 seconds
Significance of Measuring ‘R-R’ Interval
Measurement of ‘R-R’ interval helps to calculate:
 1. Heart rate
 2. Heart rate variability.

Cardiac axis

The electrical axis of the heart is the mean direction of the action potential
traveling through the ventricles during ventricular activation (depolarisation), i.e.
major direction of the overall electrical activity of the heart. The QRS complex,
which represents ventricular depolarisation is used for the determination of the
electrical heart axis.

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 Illustration

Clinical applications of ecg

The ECG can be used for determining;
Rate and rhythm of heartbeats,

Size and position of the heart chambers,

The effects of cardiac drugs,

The function of implanted pacemakers.

The presence of any damage to the heart's muscle cells or conduction system,
Others, including;

SINUS RHYTHMS/ARRHYTHMIAS: Sinus rhythm, Sinus tachycardia, Sinus

bradycardia, Sinus arrhythmia, Sinus arrest or pause, 2nd Degree Sinoatrial exit
block.

OTHER SV ARRHYTHMIAS: PAC's (nonconducted), PAC's (conducted

normally), PAC's (conducted with aberration), Ectopic atrial rhythm or tachycardia

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(unifocal), Multifocal atrial rhythm or tachycardia, Atrial fibrillation, Atrial flutter,
Junctional premature beats, Junctional escapes or rhythms, Accelerated Junctional
rhythms, Junctional tachycardia, PSVT’s: AVNRT and AVRT

VENTRICULAR ARRHYTHMIAS: PVC's, Ventricular escapes or rhythm,

Accelerated ventricular rhythm, Ventricular tachycardia (uniform), Ventricular
tachycardia (polymorphic or torsade), Ventricular fibrillation

AV CONDUCTION: 1st degree AV block, Type I 2nd degree AV block

(Wenckebach), Type II 2nd degree AV block (Mobitz), AV block, advanced (high
grade), 3rd degree AV block (Junctional escape rhythm), 3rd degree AV block
(ventricular escape rhythm), AV dissociation (default), AV dissociation
(usurpation), AV dissociation (AV block)

INTRAVENTRICULAR CONDUCTION: Complete LBBB (fixed or

intermittent), Incomplete LBBB, Complete RBBB (fixed or intermittent),
Incomplete RBBB, Left anterior fascicular block (LAFB), Left posterior fascicular
block (LPFB), Nonspecific IV conduction delay (IVCD), WPW pre-excitation
patterns

QRS AXIS AND VOLTAGE: Right axis deviation (+90 to +180), Left axis
deviation (-30 to -90), Bizarre NW Quadrant axis (-90 to -180), Indeterminate axis
(all small, isoelectric QRS), Low QRS voltage frontal plane (all QRS <0.5 mV),
Low QRS voltage precordial (all QRS <1.0 mV)
HYPERTROPHY/ENLARGEMENTS: Left, Right, and bi-atrial enlargement,
Left ventricular hypertrophy, Right ventricular hypertrophy, Biventricular
hypertrophy

ST-T AND U ABNORMALITIES: Early repolarization (normal variant),

Nonspecific ST-T abnormalities, ST changes secondary to hypertrophy, ST

13
elevation (pericarditis pattern), Symmetrical T wave inversion, Hyperacute T
waves, Prominent upright U waves, U wave inversion, Prolonged QT interval,
Brugada patterns

MI PATTERNS (acute, recent, old): ST-T changes due to ischemia, Acute

current of injury, ST elevation MI, Non-ST elevation MI, Q-wave myocardial
infarction, Abnormal Q waves not due to MI, Time course of ECG in MI, ECG
localization of MI

CLINICAL DISORDERS: Chronic pulmonary disease pattern, Hypokalemia,

Hyperkalemia, Hypocalcemia, Hypercalcemia, ASD (primum and secundum),
Dextrocardia, Mitral stenosis, Suggests CNS disease, Hypothermia, Drug effects
(digoxin, tricyclics, etc.)

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EQUIPMENTS USED

1. Ecg machine
2. Power cable
3. ECG paper
4. Chest electrodes
5. Limb Clamp electrodes

15
PRECAUTIONS

1. Areas such as the chest where the adhesive electrodes will be placed may
need to be shaved first, and then skin is cleaned.

2. Avoid oily or greasy skin creams and lotions the day of the test. They
interfere with the electrode-skin contact.

3. The subject should be at rest.

4. The subject should not receive any medication.

5. The subject should remove all the jewelries and wear a hospital gown

6. Wear a shirt that can easily be removed to place the leads on the chest.

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PROCEDURES
1. A subject was prepared, the procedure was explained to him and we ensured
he was comfortable. He was asked to remove any jewelry, clothing, or
accessories that may interfere with the test.
2. The subject was allowed lie down on a table in supine position, and remain
as still as possible during the test.
3. The electrodes were placed on the subject's chest, arms, and legs; red to the
right arm, yellow to the left arm, green to the right leg and finally black to
the left leg, for limb electrodes.

Electrode Electrode placement

label
RA (red) On the right arm, avoiding thick muscle.
LA (yellow) In the same location where RA was placed, but on the left arm.

RL (green) On the right leg, lateral calf muscle.

LL (black) In the same location where RL was placed, but on the left leg.

Placement of chest electrodes

 V1: 4TH intercostal space near the right sternal border

 V2: 4th intercostal space near the left sternal border
 V3: Between V2 and V4
 V4: 5th intercostal space midclavicular line
 V5: 5th intercostal space at anterior axillary line
 V6: 5TH intercostal space at mid axillary line.

17
4. The ECG machine was turned on to ensure it is properly calibrated and
functioning correctly.
5. The ECG recording was started by pressing the appropriate buttons on the
machine. The ECG machine ran for a few seconds to a few minutes,
capturing the electrical activity of the heart.
6. The subject was monitored for any signs of discomfort or distress.
7. Upon the ECG completion, the results were reviewed as we looked for any
abnormalities or irregularities in the heart's electrical activity of the subject.
8. The electrodes were carefully removed from the subject's skin, being gentle
to avoid causing any discomfort or skin irritation.
9. The ECG machine was cleaned thoroughly and the electrodes disinfected
according to the manufacturer's instructions to prepare for future use.

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19
 SUBJECT DETAILS

NAME OF SUBJECT: OWEKA INNOCENT

DATE OF BIRTH: 19/DEC/2002

AGE: 21YRS

HOSPITAL: GULU REFFERAL HOSPITAL

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 RESULTS

DETERMINATION OF HEART RATE

Method 1:

Number of small squares dividing by 1500

Lead Used: Lead II

Number of large squares between R waves: 21

Heart Rate: 1500/21 =71

Method 2:

Number of large squares dividing by 300

Lead used: Lead 11

Heart Rate: 300/4 = 75

Method 3:

Lead Used: Lead II

RR interval: 21

Duration: 0.84s

Heart Rate: 0.84*60 = 71

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DETERMINATION OF THE RHYTHM

Method:

Inspecting the rhythm strips for consistency in p-p intervals

Rhythm: Normal Sinus Rhythm

The P waves in leads I and II is upright (positive). This means that the rhythm is
coming from the sinus node.

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DETERMINATION OF CARDIAC AXIS

Method 1: Quadrant method

-900

+180 00 Lead I

+90
aVF

Cardiac Axis: +90-0

Normal Axis

Method 2:

Biphasic lead: aVL

Lead perpendicular to aVL: Lead II

Direction of Lead II QRS complex: Positive

Cardiac axis: Between +90-0

Normal Axis

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 RESULTS

Measurements

S/O PARAMETER VALUE UNITS

1 Heart rate 68 Beats per minute (bpm)
2 PR interval - Microseconds (ms)
3 QRS complex 106 Microseconds (ms)
4 QT interval 388 Microseconds (ms)
5 QTc 406 Microseconds (ms)

WAVE DESCRIPTION OF RESULTS

Heart P-R Q-T Wav Amplitude Duration Polari

rate(bpm interval(s interval(s e (mV) (s) ty
) ) ) (millivolts) (seconds)
Lead I 71 0.16 0.4 P 0.1 0.08 +
QRS 0.6 0.06 +
T 0.3 0.16 +
Lead 71 0.16 0.32 P 0.1 0.08 +
II QRS 1.4 0.06 +
T 0.3 0.12 +
Lead 71 0.16 0.32 P 0.1 0.08 +
III QRS 1.4 0.06 +
T 0.2 0.20 +
aVR 68 0.16 0.36 P 0.1 0.08 -
QRS 0.7 0.06 -

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 T 0.2 0.12 -
aVL 68 0.12 P +
QRS 0.4 0.06 +
T +
aVF 68 0.12 0.36 P 0.1 0.08 +
QRS 0.9 0.06 +
T 0.3 0.16 +

V1 68 0.12 0.32 P 0.1 0.08 +

QRS 0.5 0.08 -

T 0.2 0.12 +

V2 68 0.12 0.32 P 0.1 0.08 +

QRS 0.8 0.08 -
T 0.7 0.2 +
V3 868 0.12 0.36 P 0.1 0.08 +
QRS 0.9 0.08 +
T 0.7 0.2 -
V4 71 0.12 0..36 P 0.1 0.08 +
QRS 3.1 0.08 +
T 0.6 0.02 +
V5 71 0.12 0.4 P 0.1 0.08 +
QRS 2.4 0.08 +
T 0.5 0.12 +
V6 71 0.12 0.32 P 0.1 0.08 +

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 QRS 1.3 0.08 +
T 0.4 0.16 +

S AND V WAVE FORMS

Lead V1

S wave: 22mm

R wave: 3mm

Lead V5

S wave: 6mm

R wave: 17mm

Lead V6

S wave: 1mm

R wave: 12mm

DISCUSSION

Rhythm

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In our investigation, we focused on analyzing the rhythm of the subject's cardiac
activity, with particular attention to identifying any deviations from the normal
sinus rhythm. The sinus rhythm is considered the normal rhythm of the heart,
characterized by the initiation of electrical impulses from the sinoatrial (SA) node,
followed by the orderly propagation of these impulses through the atria,
atrioventricular (AV) node, bundle of His, and Purkinje fibers, resulting in
coordinated atrial and ventricular contraction.
Our findings revealed that the subject exhibited a normal sinus rhythm. This
signifies that the heart's electrical activity originates from the SA node, with a
regular rhythm and rate within the typical range of 60 to 100 beats per minute for
adults. The presence of a normal sinus rhythm indicates the absence of significant
conduction abnormalities or arrhythmias, reflecting the healthy functioning of the
heart's intrinsic pacemaker.
The normal sinus rhythm is characterized by several key features:
Regular rhythm: The intervals between consecutive heartbeats are consistent,
demonstrating regularity in the cardiac cycle. This regularity ensures efficient
cardiac output and effective tissue perfusion.

The P wave proceeding each QRS complex: In a normal sinus rhythm, each QRS
complex on the electrocardiogram (ECG) is preceded by a P wave, indicating the
depolarization of the atria before ventricular contraction. This sequential activation
ensures synchronized atrial and ventricular function.
Normal P wave morphology: The P waves exhibit normal morphology, indicating
uniform atrial depolarization. Abnormalities in P wave morphology may suggest
atrial enlargement or conduction abnormalities.

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Consistent PR interval: The PR interval, representing the time between atrial
depolarization and ventricular depolarization, remains within the normal range of
0.12 to 0.20 seconds. A consistent PR interval ensures proper coordination
between atrial and ventricular contractions.
Normal QRS duration: The duration of the QRS complex reflects the time taken
for ventricular depolarization. In a normal sinus rhythm, the QRS complex
duration falls within the normal range (typically < 0.12 seconds), indicating
effective ventricular conduction.

Normal Heart rate: The heart rate, determined by the frequency of sinus node
depolarization, falls within the normal range for the subject's age and physiological
condition.
A normal sinus rhythm is indicative of a healthy cardiovascular system, with
effective coordination of electrical impulses and mechanical cardiac function.
However, it is essential to recognize that certain factors, such as medication use,
electrolyte imbalances, and autonomic nervous system activity, can transiently
affect the sinus node function and rhythm. Therefore, ongoing monitoring and
clinical assessment are necessary to ensure the maintenance of a normal sinus
rhythm and to promptly identify any deviations or abnormalities that may arise.

Wave form analysis in Bipolar leads

Bipolar leads in electrocardiography (ECG) provide critical insights into the

electrical activity of the heart. They consist of two electrodes measuring the

28
potential difference between specific points on the body, enabling visualization of
cardiac depolarization and repolarization events. Proper lead placement determines
the orientation and direction of the electrical vectors recorded.

Our observations in Lead I, Lead II, and Lead III revealed normal waveforms,
including the P wave, QRS complex, and T wave. Notably, with a QRS complex
duration of 0.06 seconds, these waveforms demonstrated:

The P wave signifies atrial depolarization, initiating atrial contraction. Across all
bipolar leads, the P wave exhibited consistent morphology with amplitude between
0.08mV-0.1mV and duration between 0.08-0.12seconds, indicating normal atrial
electrical activity.

The QRS complex, with a duration of 0.06 seconds, represents ventricular

depolarization, leading to ventricular contraction. Despite its short duration, the
QRS complex displayed uniform amplitude and morphology in Lead I, II, and III,
suggesting synchronized ventricular activation.

The T wave corresponds to ventricular repolarization, marking the recovery phase

of the ventricles. In our observations, the T wave in Lead I, II, and III exhibited
normal morphology and timing relative to the QRS complex, indicating effective
ventricular repolarization.

Clinical significance of a normal wave form

The presence of normal waveforms in bipolar leads indicates a healthy cardiac

electrical system. Clinically, this suggests normal atrial and ventricular conduction,
absence of significant structural abnormalities, and effective myocardial
repolarization. These findings are crucial for diagnosing conditions such as
arrhythmias, conduction disturbances, and myocardial ischemia.

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Right atrial hypertrophy presents with a tall, pointed p-wave. Left atrial
hypertrophy presents an m shaped p-wave; a condition called p_mitrale. Other
conditions like Sino-atrial block and atrial extra-systole are diagnosable from the
p-wave. 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 hyperkalaemia are also diagnosed by prolonged
QRS complexes.
The subject’s T-wave had a duration of 0.16s, magnitude of 0.3mV 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 PR interval holds significant importance in electrocardiography as it reflects
the duration of conduction through the atrioventricular (AV) node, known as AV
nodal conduction delay. This delay allows for coordinated ventricular contraction
to occur slightly after atrial contraction, facilitating optimal ventricular filling
before ejection of blood. A prolonged PR interval is often indicative of first-degree
heart block and certain bradycardic conditions. Conversely, it is shortened in
instances of tachycardia and conditions involving alternative conduction pathways
from the atria to the ventricles.

30
Similarly, the QT interval's isoelectric line represents the period during which the
ventricles undergo complete depolarization. An elongated QT interval is frequently
observed in pathological states such as myocardial infarction, myocarditis,
hypercalcemia, and hypothyroidism. Conversely, it is shortened in conditions like
QT syndrome and hypocalcemia. Understanding the significance of both the PR
and QT intervals aids in diagnosing various cardiac abnormalities and guiding
appropriate clinical management.

Wave form Analysis in Unipolar Leads

With aVR, atrial depolarization, ventricular depolarization, and ventricular

repolarization move away from the exploring electrode. The P wave and T wave
and QRS complex produced negative deflection.

For leads aVL and aVF which view the ventricles, the deflections are positive
(aVF) or biphasic (aVL) and the aVR Lead being negative from the isoelectric line
(They are all similar to the standard limb lead recordings, except that the recording
from the aVR lead is inverted)

The P wave is absent in lead aVL:

This is because Lead aVL is oriented away to the flow of current through the
atrium.
In leads V1 and V2, the QRS recordings of the normal heart are mainly negative
because the chest electrode in these leads is nearer to the base of the heart than to
the apex, and the base of the heart is the direction of electronegativity during most
of the ventricular depolarization process. Conversely, the QRS complexes in leads
V4, V5, and V6 are mainly positive because the chest electrode in these leads is
nearer the heart apex, which is the direction of electro-positivity during most of
depolarization.

31
Cardiac Axis

The cardiac axis is a crucial parameter in the assessment of cardiac health and
function. It represents the overall direction of electrical activity within the heart
during the cardiac cycle. Determining the cardiac axis aids in diagnosing various
cardiac abnormalities and guiding clinical decisions. In this experiment, we
explored the concept of cardiac axis and its implications in a clinical setting.

In our study, we observed a normal cardiac axis in the subject under investigation.
A normal cardiac axis typically falls within the range of -30° to +90°. This
indicates that the overall electrical activity within the heart is proceeding in a
physiologically expected direction.

A normal cardiac axis suggests the absence of significant structural or functional

abnormalities within the heart. It indicates that the electrical impulses generated
during the cardiac cycle are following the typical conduction pathways, originating
from the sinoatrial (SA) node and propagating through the atria, atrioventricular
(AV) node, bundle of His, and Purkinje fibers, ultimately leading to coordinated
ventricular contraction.

Several factors contribute to maintaining a normal cardiac axis. These include the
integrity of the conduction system, proper functioning of the cardiac chambers, and
absence of significant anatomical abnormalities such as hypertrophy or dilation.
Additionally, factors such as body habitus and electrode placement can influence
the recorded axis.

While a normal cardiac axis is reassuring, it is important to note that deviations

from the normal range may indicate underlying cardiac pathology. For instance, a
leftward deviation (left axis deviation) may be indicative of conditions such as left
ventricular hypertrophy, myocardial infarction involving the inferior wall, or

32
conduction abnormalities. Conversely, a rightward deviation (right axis deviation)
may suggest right ventricular hypertrophy, chronic lung disease, or conduction
disturbances.

R and V wave forms

The R and V wave forms are within the normal range which is indicative of normal
ventricles.

Summation of the R in V1 and the S in V5 or V6 is less than 10.5mm. Above

10.5mm indicates right ventricular hypertrophy and given that the cardiac axis is
normal confirms that there is no hypertrophy on the right ventricle.

Likewise, left ventricular hypertrophy is absent given that the sum of S wave in V1
and R wave in V5 or V6, 34mm is less than less than 35mm above which is left
ventricular hypertrophy which also agrees with the cardiac axis being normal.

Conclusion

33
The heart recordings obtained from our subject reveal a healthy and properly
functioning myocardium. These results align with the expected values described
in Guyton and Hall Textbook of Medical Physiology, 13th edition, specifically for
a normal electrocardiogram (ECG) when using the same electrodes at consistent
locations.

34
REFERENCES

1. Ganong’s Review of Medical Physiology, 24th Edition, chapter 29. Origin

of Heartbeat and electrical activity of the heart

2. K. Sembulingam & Prema Sembulingam: Essentials of medical physiology,

8th Edition

3. Rema, P. Hemant ,S. (2018). Cardiology A prep Manual, (1 st Ed), Paras

Medical Publisher

4. Guyton & Hall, 11th edition (year 2006): Text Book of Medical Physiology
pg. 131-156. 94.V10.0

5. Frank G. Yanowitz, MD Professor of Medicine (2017-2018); Introduction to

ECG-interpretation
6. Kumar, p., Clark,M. (Eds.). (2020). Kumar and Clark’s Clinical Medicine
(10th ed). Elsevier

35
 GULU UNIVERSITY

FACULTY OF MEDICINE

DEPARTMENT OF PHYSIOLOGY

COURSE UNIT: PHYSIOLOGY (PHYS 1202)

TASK: BLOOD PRESSURE

DATE OF SUBMISSION: 18TH APRIL 2024.

STUDENT’S NAME INITIALS REGISTRATION SIGNATURE

NUMBER
1. OJAMBO JOSHUA HAMIRIE OJH 23/U/3962/GUM/PS

2. ASINDE JENIPHER AJ 23/U/3287/GUM

3. BWAMBALE EMMANUEL BE 23/U/0020/GUM
4. OKELLO DENISH OD 23/U/3295/GUM
5. MUNDUA GLORIA MG 23/U/3312/GUM
6. KOBUGABE EDGAR KE 23/U/3309/GUM
7. MUYINDA KIIRYA DAVID MKD 23/U/0061/GUM
8. ALUMA DAN HENRY ADH 23/U/3978/GUM
9. OWEKA INNOCENT OI 23/U/0096/GUM
10. OPIO ZACHARY OZ 22/U/I740/GUM/PS

SUPERVISOR: Dr. MUZAALE FRANCIS.

TECHNICIAN: MR. OKELLO JOSEPH.

OBJECTIVES OF THE EXPERIMENT.

36
  To determine blood pressure under various normal physiological conditions

BLOOD PRESSURE

Arterial blood pressure is lateral pressure exerted by the column of blood on wall
of arteries. Arterial blood pressure is expressed in four terms that is;

 Systolic blood pressure

 Diastolic pressure
 Pulse pressure
 Mean Arterial Pressure (MAP)

Systolic blood pressure is the maximum pressure exerted in the arteries during
systole of cardiac cycle. The normal is 120mmHg and it ranges between 110 –
140mmHg

Diastolic blood pressure is the minimum pressure exerted in the arteries during
diastole of cardiac cycle. The normal is 80mmHg and ranges between 60 –
80mmHg

Pulse pressure is the difference between systolic pressure and diastolic pressure
and the normal is 40mmHg

Mean Arterial Pressure is the average pressure existing in arteries. Normal MAP is
93mmHg.

All these vary according to the sex, activity, motional condition and posture.

Blood pressure = CO (Cardiac output)*TPR (Total Peripheral Resistance)

Cardiac Output = Stroke Volume (SV)*Heart rate (HR)

Stroke volume is determined by:

37
  Cardiac contractility
 Venous return to the heart (Preload)
 The resistance the left ventricle must overcome to eject blood into the aorta
(afterload)

At least four systems are directly responsible for BP regulation

 Heart, which supplies the pumping pressure

 Blood vessel tone, which determines systemic resistance
 Kidney, which regulates intravascular volume
 Hormones which modulate the functions if the three systems

No matter how high the CO or TPR, renal excretion has the capacity to completely
return BP to normal by reducing intravascular volume. Therefore, the maintenance
of chronic hypertension requires participation in the presence of normally
functioning kidneys, an increase in BP leads to augmented urine volume and
sodium excretion, which then returns the BP to normal.

This process is known as pressure natriuresis, is blunted in the kidneys of

hypertensive patients; thus higher pressures are required to excrete a given sodium
and water load. Current evidence suggests at least two possible reasons or this
blunted response.

1. First, microvascular and tubulointerstitial injury within the kidneys of

hypertensive patients impairs sodium excretion.
2. Second, the defect may lie with hormonal actors critical to appropriate renal
reactions to the sodium and intravascular volume environment. In contrast
to the first possibility, abnormalities of hormonal regulation are amenable
correction with appropriate therapy.

38
Blood pressure is measured using a sphygmomanometer

Uses of sphygmomanometer

 Detect hypertension, hypotension

 Diagnose AR by wide pulse pressure and hills sign
 Diagnose obstructive valvular lesion AS, MS (narrow pulse pressure)
 Detect pulsus paradous and pulsus alternans
 To demonstrate:
o Accoucheur’s hand tetany
o Trousseau’s sign (inflate more than systolic pressure within 3
minutes-develop carpal spasm in tetany)
o Hess test (capillary fragility test) BP cuff inflated more than 90 for
5min. If capillaries are fragile purpuric spots appear distal to
compression. Normally lessthan 15 petechiae appear in a circle of
5cm drawn on forearm. More than 15 indicate capillary fragility.

PHYSIOLOGICAL VARIATIONS BLOOD PRESSURE

Age

39
Arterial blood pressure increases as age advances
Systolic pressure in different age Diastolic pressure in different age

Newborn: 70 mm Hg
After 1 month: 85 mm Hg
After 6 month: 90 mm Hg
After 1 year: 95 mm Hg
At puberty: 120 mm Hg
At 50 years: 140 mm Hg
At 70 years: 160 mm Hg
At 80 years: 180 mm Hg
Newborn: 40 mm Hg
After 1 month: 45 mm Hg
After 6 month: 50 mm Hg
After 1 year: 55 mm Hg
At puberty: 80 mm Hg
At 50 years: 85 mm Hg
At 70 years: 90 mm Hg
At 80 years: 95 mm Hg

Sex
In females, up to the period of menopause, arterial pressure is 5 mm Hg, less than
in males of same age. After menopause, the pressure in females becomes equal to
that in males of same age.
Body Built
Pressure is more in obese persons than in lean persons.
Diurnal Variation
In early morning, the pressure is slightly low. It gradually increases and reaches the
maximum at noon. It becomes low in evening.

After Meals

40
Arterial blood pressure is increased for few hours after meals due to increase in
cardiac output.
During Sleep
Usually, the pressure is reduced up to 15 to 20 mm Hg during deep sleep.
However, it increases slightly during sleep associated with dreams.
Emotional Conditions
During excitement or anxiety, the blood pressure is increased due to release of
adrenaline.
After Exercise
After moderate exercise, systolic pressure increases by 20 to 30 mm Hg above the
basal level due to increase in rate and force of contraction and stroke volume.
Normally, diastolic pressure is not affected by moderate exercise. It is because, the
diastolic pressure depends upon peripheral resistance, which is not altered by
moderate exercise. After severe muscular exercise, systolic pressure rises by 40 to
50 mm Hg above the basal level. But, the diastolic pressure reduces because the
peripheral resistance decreases in severe muscular exercise.

Blood Pressure

Equipment for blood pressure

 Sphygmomanometer

41
  Stethoscope

Stethoscope

Sphygmomanometer

Precautions:
1. Wearing a laboratory coat and closed shoes at all times in the laboratory.

42
 2. Strictly following the standard operating procedures set for the experiment
and the manufacturer’s instructions for each equipment used.
3. Preferably wrap the cuff on a bare arm.
4. Interpret the blood pressure readings in relation to the persons age, physical
condition, medical history and medications being used.
For the subject
5. Avoid heavy exercise like walking or eating prior to the test.
6. Don’t smoke or ingest caffeine before blood pressure measurement.
7. Sit quietly for at least 5 minutes before the test begins.

Procedure:
1. Introduced self to the subject, asked for consent and briefly explained the
procedure to be done.
2. Then asked the subject to sit comfortably and in a relax state for 5 minutes.

43
 3. Wrapped the cuff of the sphygmomanometer around the upper part of the
left arm (at heart’s level, lower edge one inch above the antecubital fossa).
4. Then placed the stethoscope over the brachial artery.
5. Held the rubber bulb and pump the air from into the cuff by repeatedly
squeezing the bulb.
6. Inflated the cuff to a level of 30mmHg higher than the expected systolic
pressure.
7. Then slowly opened the valve of the bulb and release the pressure at a
moderate rate of about 2 or 3 mm Hg per second.
8. Listened to the first sound with the help of a stethoscope and also by
observing the mercury column. Recorded this as the systolic blood pressure.
9. Kept listening to the sound until it disappeared and the pressure dropped and
noted the pressure at which the last sound was heard. Recorded this reading
as the diastolic pressure.
10.Released the pressure from the cuff and unwrapped it from the arm.

BLOOD PRESSURE.

Condition Systolic Diastolic Mean arterial

pressure

44
 Ind 1 Ind Ind Ind Ind 2 Ind Ind Ind 2 Ind 3
2 3 1 3 1
Resting 100 121 128 60 82 80 73.3 95 96
seated
Resting 110 118 125 75 80 80 86.7 92.7 95
supine
Post 120 180 130 80 110 85 133. 82 100
exercise 3
Where Ind represents individual

45
 BLOOD PRESSURE
450

400

350

300

250

200

150

100

50

0
Ind 1 Ind 2 Ind 3 Ind 1 Ind 2 Ind 3 Ind 1 Ind 2 Ind 3
Systolic Diastolic Mean arterial pressure

Resting seated Resting supine Post exercise

46
 DISCUSSION OF RESULTS

BLOOD PRESSURE

Blood pressure readings consist of two numbers, i.e. 120/80 mm Hg. The systolic
pressure represents the force exerted on artery walls when the heart beats.
The diastolic pressure measures the pressure between heartbeats when the heart is
at rest. The unit of measurement is mm Hg (millimeters of mercury).

According to the American Heart Association, the normal blood pressure for adults
is less than 120/80 mm Hg. Hypertension is defined as having a systolic pressure
of 130 mm Hg or higher or a diastolic pressure of 80 mm Hg or higher, most of the
time.

Resting Seated:

Systolic pressures are within the normal range.

Diastolic pressures are also normal.

Mean arterial pressure falls within the expected values.

Resting Supine

Systolic pressures remain normal.

Diastolic pressures are within the acceptable range.

47
Mean arterial pressure is consistent.

Post Exercise

Systolic pressures show variability, with some values exceeding the normal range.

Diastolic pressures are elevated.

Mean arterial pressure is notably high.

Clinical Implications

Elevated post-exercise systolic pressures may indicate cardiovascular stress.

Diastolic pressures above normal require medical attention.

Monitoring the trends in blood pressure over time is very important for early detection
of hypertension.

Recommendations

 For individuals with high post-exercise systolic pressures, further evaluation is

necessary.
 Lifestyle modifications (such as exercise, diet, and stress management) can help
maintain healthy blood pressure.
 Regular check-ups and communication with healthcare providers are essential.

48
CONCLUSION

The blood pressure results for the three individuals exhibit variability across
different conditions. While most values fall within the normal range, certain post-
exercise systolic pressures need medical attention. Diastolic pressures, although
not alarmingly high, should be monitored. Individual assessments are required for
accurate interpretation and management.

49
REFERENCES

1. K Sembulingam and Sembulingam. (2012). Essentials of Medical

Physiology. Jaypee Brothers Medical Publishers (P) Ltd.

2. Rema, P. Hemant ,S. (2018). Cardiology A prep Manual, (1 st Ed), Paras

Medical Publisher

3. Whelton, P. K., Carey, R. M., Aronow, W. S., et al. (2018). 2017

ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA
Guideline for the Prevention, Detection, Evaluation, and Management of
High Blood Pressure in Adults: A Report of the American College of
Cardiology/American Heart Association Task Force on Clinical Practice
Guidelines. Journal of the American College of Cardiology, 71, e127-e248

4. Kumar, p., Clark,M. (Eds.). (2020). Kumar and Clark’s Clinical Medicine
(10th ed). Elsevier
5. Hall, J.E., & Guyton, A.C. (2011). Guyton and Hall textbook of medical
physiology. Philadelphia, PA: Saunders Elsevier, pp 492

50
 GULU UNIVERSITY

FACULTY OF MEDICINE

DEPARTMENT OF PHYSIOLOGY

COURSE UNIT: PHYSIOLOGY (PHYS 1202)

TASK: BLOOD PRESSURE

DATE OF SUBMISSION: 18TH APRIL 2024.

STUDENT’S NAME INITIALS REGISTRATION SIGNATURE

NUMBER
11. OJAMBO JOSHUA HAMIRIE OJH 23/U/3962/GUM/PS

12. ASINDE JENIPHER AJ 23/U/3287/GUM

13. BWAMBALE EMMANUEL BE 23/U/0020/GUM
14. OKELLO DENISH OD 23/U/3295/GUM
15. MUNDUA GLORIA MG 23/U/3312/GUM
16. KOBUGABE EDGAR KE 23/U/3309/GUM
17. MUYINDA KIIRYA DAVID MKD 23/U/0061/GUM
18. ALUMA DAN HENRY ADH 23/U/3978/GUM
19. OWEKA INNOCENT OI 23/U/0096/GUM
20. OPIO ZACHARY OZ 22/U/I740/GUM/PS

SUPERVISOR: Dr. MUZAALE FRANCIS.

TECHNICIAN: MR. OKELLO JOSEPH.

51
OBJECTIVES OF THE EXPERIMENT

 To determine Pulse rate under different physiological conditions

BACKGROUND

PULSE RATE

The pulse or heart rate, is a vital sign in the study of physiology, offering a window
into the cardiovascular systems functionality. It is the tangible manifestation of the
heartbeat, felt through the walls of various arteries, where the rhythmic expansion
and contraction of the artery occurs in response to the heart’s pumping action.

Each pulse wave corresponds to a heartbeat where the heart muscle contracts,
propelling blood through the circulatory system. This rhythmic ejection of blood is
essential for the delivery of oxygen and nutrients to tissues and removal of
metabolic wastes. The rate, rhythm and strength of pulse can reveal much about an
individual’s cardiac health and overall physiological state.

The generation of pulse begins in the heart’s sinoatrial node, the natural
pacemaker, which initiates the electrical impulses that trigger cardiac contraction.
These impulses travel through the heart muscle, leading to coordinated
contractions that eject muscle leading to coordinated contractions that eject blood
into the arteries. The arterial walls being elastic, absorb some of the force of the
ejected blood, creating the pulse wave palpable at various points.

52
 Diagram of a normal arterial pulse tracing

A-The upstroke is the percussion wave/the limb/anarcrotic limb. It is produced by

ventricular systole/ ventricular ejection.

B-Peak systole (maximum pressure generated during ventricular systole)

C-The tidal wave is the decreasing pressure during systole (Rapid decline in
arterial pressure as the ventricular contraction comes to an end)

D-Dicrotic notch is the beginning of diastole (produced immediately before the

aortic valve closure; it is due to sharp fall in pressure due to back flow of blood
into ventricle as it starts relaxing)

E- Dicrotic wave/diastole (rapid decline in arterial pressure as the ventricular

contraction comes to an end)

53
Description of Pulse

It is describe in the following order

1. Rate
2. Rhythm
3. Volume
4. Character
5. Condition of the vessel wall
6. Peripheral pulses
7. Radial femoral delay
8. Pulse deficit if there is AF

54
Peripheral Arteries palpated and where to palpate

Radial pulse is the pressure changes transmitted in form of waves through radial
artery wall from the heart to periphery. The normal radial pulse ranges within 60 –
55
100 beats per minute in adult

Examination of radial pulse rate is valuable clinical procedure that represents the
heartbeat. By examining radial pulse important information regarding cardiac
function such as rate of contraction, rhythmicity can be obtained.

Radial pulse is obtained by putting over thumb side of the wrist between tendons
of the brachioradialis and Flexor Carpi radialis on radial artery.

56
 PULSE RATE

Equipment for pulse rate.

 Stop watch

57
Precautions
a. Wash and dry your hands before measuring the pulse.
b. Do not use your thumb for sensing the pulse because you may feel a pulse
coming from an artery in the thumb itself.
c. Avoid heavy exercise, walking or eating prior to the test.
d. Sit quietly for at least 5 minutes before the test begins.

58
Procedure
1. Introduced self to the subject, asked for consent and briefly explained the
procedure to be done.
2. Then asked the subject to sit comfortably and in a relax state for 5 minutes.
3. Placed the tip of the index and middle finger on the radial artery of the
opposite wrist just below the base of thumb and pressed gently.
4. When a normal and strong pulse was identified, we measured it for 30
seconds. Doubled the number to give pulse per minute (36 pulse beats in
30 seconds means 72 beats in 1 minute).
5. Repeated the procedure when the subject was in resting position in, supine,
sitting, standing, after an exercise.
6. Recorded the details in the notebook.
7. Washed and dried hands.

59
RESULTS

RIGHT RADIAL PULSE

B0DY PULSE RATE

POSTURE/ACTIVIT Ind Ind 2 Ind 3 Ind 4
Y 1
SUPINE 69 65 65 85
SITTING 72 66 65 89
STANDING 76 71 70 97
AFTER EXERCISE 84 98 76 116

60
 PULSE RATE
140

120
116

100 98 97
89
84 85
80
76 76
72 71 70
69
66
65 65
60

40

20

0
Ind 1 Ind 2 Ind 3 Ind 4
PULSE RATE

SUPINE SITTING STANDING AFTER EXERCISE

61
DISCUSSION OF RESULTS

Heart rate and pulse rate are often used interchangeably, however they have
distinct meanings: Heart rate measures the number of heart beats per minute while
pulse rate reflects the increase in blood pressure due to the heartbeat and can be
measured by counting the pulses at various locations per minute i.e at the wrist and
neck.

Experimental Findings

The pulse rates of all individuals were within the normal range for each condition:

Supine Position:

When lying flat on your back, the heart rate tends to be at its lowest. This is
the resting heart rate. The normal range typically falls between 60 to 100 beats per
minute. When transitioning from a reclining position to standing, your heart rate
may increase by 10 to 15 beats per minute. However, it settles back down
within 15 to 20 seconds after standing up.

Sitting Position

While in the sitting position, the pulse rates were consistent with what we expect at
rest. The sympathetic nervous system which is responsible for increasing heart rate
and the parasympathetic nervous system which slows down the heartbeat maintain
a balance.

Standing Position
When an individual stood up, the pulse rate is increased slightly. There is an
increase in pulse rate when the individuals were standing because on standing there
is peripheral pooling of blood in lower parts of the body which leads to lowering of

62
venous return to the heart. This in turn leads to a decrease in cardiac output hence
decrease in systolic blood pressure, which elicits an immediate baroreceptor reflex
thereby resulting in strong sympathetic discharge throughout the body leading to
an increase in total peripheral resistance due to vasoconstriction ultimately leading
to an increase in arterial pressure, thereby increasing the pulse rate. (Guyton and
hall textbook of medical physiology 12th edition, chapter 18, pg 207-208)

After Exercise

There is an increase in pulse rate after an exercise because of the increased demand
for oxygen and nutrients. As you exercise, muscles require more oxygen to
produce energy. The chemoreceptors in the aortic arch and carotid arteries detect
the decreased level of oxygen and low pH of blood caused by the high levels of
carbon dioxide. These receptors send signals to the brainstem which then increase
heart rate to enhance oxygen delivery to tissues and consequently leading to an
increase in pulse rate.

Interpretation

All individuals’ pulse rates fell within the normal range which indicates healthy
cardiovascular function. Our bodies can adapt to changes in position and activity
level, maintaining homeostasis. While normal ranges exist, individual variations
are expected. Factors like fitness level, age, and overall health influence pulse
rates.

63
Recommendations

 A normal resting heart rate for adults falls between 60 and 100 beats per
minute. If your resting heart rate is within this range, it’s considered healthy.
Visit a trained health personnel if the resting heart rate is above normal.
 During moderately intense activities, aim for a heart rate that is about 50-69%
of your maximum heart rate.
 Engage in hard physical activity to elevate your heart rate to improve
cardiovascular health and endurance.
 Factors like stress, anxiety, hormones, and physical fitness can influence heart
rate. Athletes or highly active individuals may have a resting heart rate as low
as 40 bpm

64
CONCLUSION

The experiment demonstrates the dynamic nature of pulse rates. Whether sitting,
standing, or exercising, our cardiovascular system responds appropriately to meet
the body’s demands. It is important to understand these variations to helps us
appreciate how the hearts beats efficiently.

65
REFERENCES

1. K Sembulingam and Sembulingam. (2012). Essentials of Medical

Physiology. Jaypee Brothers Medical Publishers (P) Ltd.

2. Rema, P. Hemant ,S. (2018). Cardiology A prep Manual, (1 st Ed), Paras

Medical Publisher

3. Kumar, p., Clark,M. (Eds.). (2020). Kumar and Clark’s Clinical Medicine
(10th ed). Elsevier
4. Hall, J.E., & Guyton, A.C. (2011). Guyton and Hall textbook of medical
physiology. Philadelphia, PA: Saunders Elsevier, pp 492

66