RESPIRATORY SYSTEM MECHANICS

Measuring Respiratory Volumes and Calculating Capacities

Created by:

GROUP 5

Ikhsan Nurhaliq Hanafi Gabrina Miranti

(04011181722013) (04011281722089)
Rizqi Ilma Mutiarani Dienda Alya Zafira
(04011181722019) (04011281722113)
Lia Wulandari Tria Monica N
(04011181722027) (04011281722115)
Indah Sitta Ramadhani Arini Jati Fiviatika
(04011181722055) (04011281722131)
Andi Pranata Leo Medianto Faziqin
(04011281722071) (04011281722135)
Fahrina Azzahra Haidar Ali Hamzah
(04011281722081) (04011281722137)
M. Bibit Bagus Rama Pasca Jody Putra Wijaya
(04011281722083) (04011281722147)
Arina Puspitaningrum Jatmiko
(04011281722087)

FACULTY OF MEDICINE

SRIWIJAYA UNIVERSITY

2018
 PREFACE

First of all, the writer would like to express the deepest gratitude to Allah SWT.
The Most Gracious and Merciful for His countless blessings the writer could finish this
paper. The title of this paper is: “Respiratory System Mechanics: Measuring
Respiratory Volumes and Calculating Capacities” is written to fulfill group assignment
in reporting the results of the lab.
In this opportunity, the writer would also like to express the greatest
appreciation to the greatest teachers, dr. Budi Santoso, M.Kes and dr. Minerva Riani
Kadir, Sp.A., M.Kes who have given the writer their guidance and assistance.
At last but not least, the writer realizes this paper has many mistakes. Therefore, the
writer would be very happy to welcome any comments, critics, and suggestions from
everyone for making this paper better. The writer hopes this paper will be useful for
us.

Palembang, 15th of March 2018

Writers

(Group 5)

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 TABLE OF CONTENT

PREFACE ............................................................................................................. ii

TABLE OF CONTENT ........................................................................................ iii

CHAPTER I : INTRODUCTION ......................................................................... 1

A. Background ............................................................................................... 1
B. Purpose ...................................................................................................... 5
C. Hypotheses ................................................................................................ 6

CHAPTER II : Methods ........................................................................................ 7

CHAPTER III : Results ......................................................................................... 8

CHAPTER IV : Discussion ................................................................................... 13

A. Interpretation of Data ................................................................................ 14

B. Limitations ................................................................................................ 17

CHAPTER V : Conclusion ................................................................................... 18

REFERENCES ...................................................................................................... 19

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 CHAPTER I

INTRODUCTION

A. Background

The physiological function of the respiratory system is essential to life. If the

problems develop in most other physiological systems, we can survive for some time
without addressing them. But if a persistent problem develops within the respiratory
system (or the circulatory system), death can occur in minutes.

The primary role of the respiratory system is to distribute oxygen to, and
remove carbon dioxide from, all the cells of the body. The respiratory system works
together with the circulatory system to achieve this. Respirations includes ventilation,
or the movement of the air into and out of the lungs (breathing), and the transport (via
blood) of oxygen and carbon dioxide between the lungs and body cells (view Figure
7.1) the heart pumps deoxygenated blood to pulmonary capillaries, where gas exchange
occurs between blood and alveoli (air sacs in the lungs). Thus oxygenating the blood.
The heart pumps the oxygenated blood to body tissues, where oxygen is used for cell
metabolism. At the same time, carbon dioxide (a waste product of metabolism) from
body tissues diffuses into the blood. This carbon dioxide-enriched, oxygen-reduced
blood then returns to the heart, completing the circuit.

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 Figure 7.1

Ventilation is the result of skeletal muscle contraction (view figure 7.2). When
the diaphragm-a dome-shaped muscle contract, the volume in the thoracic and
abdominal cavities-and the external intercostal muscles contract, the volume in the
thoracic cavity increases. This increase in thoracic volume reduces the pressure in the
thoracic cavity, allowing atmospheric gas to enter the lungs (a process called
inspiration). When the diaphragm and the external intercostals relax, the pressure in
the thoracic cavity increases as the volume decreases. Forcing air out of the lungs (a
process called expiration). Inspiration is considered an active process because muscle
contraction requires the use ATP, whereas expiration is usually considered a passive
process because the muscle relax, rather than contract. When a person is running,
however, expiration becomes an active process, resulting from the contraction of
internal intercostal muscles and abdominal muscles. In this case, both inspiration and
expiration are considered active processes because muscle contraction is needed for
both.

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 Figure 7.2: Inspiration and Expiration

The amount of air that flows into and out of the lungs in 1 minute is pulmonary
minute ventilation, which is calculated by multiplying the frequency of breathing by
the volume of each breath (the tidal volume). Ventilation must be regulated at all times
maintain oxygen in arterial blood and carbon dioxide in venous blood at sea level, the
total pressure is 760 mmHg. Oxygen makes up 21% of the total atmosphere and,
therefore, has a partial pressure (PO2) of 160 mmHg (760 mmHg x 0,21).

Oxygen and carbon dioxide diffuse down their partial pressure gradients, from
high partial pressure to low partial pressures. Oxygen diffuses from the alveoli of the
lungs into the blood, where it can dissolve in plasma and attach to hemoglobin, and
then diffuses from the blood into the tissues. Carbon dioxide (produced by the
metabolic reactions of the tissues) diffuses from the tissues into the blood and then
diffuses from the blood into the alveoli for export from the body.

In this exercise you will investigate the basic mechanics and regulation of the
respiratory system. The concepts you will explore with a simulated lung will help you
understand the operation of the human respiratory system in better detail.

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 The two phases of ventilation, or breathing, are (1) inspiration, during which
air is taken into the lungs, and (2) expiration, during which air is expelled from the
lungs. Inspiration occurs as the external intercostal muscles and the diaphragm
contract. The diaphragm, normally a dome-shaped muscle, flattens as it moves
inferiorly while the external intercostal muscles, situated between the ribs, lift the rib
cage (view Figure 7.2). These cooperative actions increase the thoracic volume. Air
rushes into the lungs because this increase in thoracic volume creates a partial vacuum.

During quite expiration, the inspiratory muscles relax, causing the diaphragm
to rise superiorly and the chest wall to move inward. Thus, the thorax returns to its
normal shape because of the elastic properties of the lung and thoracic wall. As in a
deflating balloon, the pressure in the lungs rises, forcing air out of the lungs and
airways. Although expiration is normally a passive process, abdominal-wall muscles
and the internal intercostal muscles can also contract during expiration to force
additional air from the lungs. Such forced expiration occurs, for example, when you
exercise, blow up a balloon, cough, or sneeze.

Normal, quite breathing moves about 500 ml (0,5 liter) of air (the tidal volume)
into and out of the lungs with each breath, but this amount can vary due to a person’s
size, sex, age, physical condition, and immediate respiratory needs. In this activity you
will measure the following respiratory volumes (the values given for the normal adult
male and female approximate).

 Tidal volume (TV): amount of air inspired and then expired with each
breath under resting conditions (500 ml)
 Inspiratory reserve volume (IRV): Amount of air that can be forcefully
inspired after a normal tidal volume inspiration (male, 3100 ml; female,
1900 ml)
 Expiratory reserve volume (ERV): amount of air that can be forcefully
expired after a normal tidal volume expiration (male 1200 ml; female
700 ml)
 Residual volume (RV): Amount of air remaining in the lungs after
forceful and complete expiration (male, 1200 ml; female,1100 ml)

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 Respiratory capacities are calculated from the respiratory volumes. In this
activity you will calculate the following respiratory capacities.

 Total lung capacity (TLC): Maximum amount of air contained in lungs

after a maximum inspiratory effort: TLC = TV + IRV + ERV + RV
(male, 6000 ml; female 4200 ml)
 Vital capacity (VC): Maximum amount of air that can be inspired and
then expired with maximal effort: VC = TV + IRV + ERV (male, 4800
ml; female 3100 ml)

You will also perform two pulmonary function tests in this activity.

 Forced vital capacity (FVC): Amount of air that can be expelled when
the subject takes the deepest possible inspiration and forcefully expires
as completely and rapidly as possible.
 Forced expiratory volume (FEV1): measures the amount of the vital
capacity that is expired during the first second of the FVC test (normally
75% – 85% of the vital capacity).

B. PURPOSE

1. To understand the use of the terms ventilation, inspiration, expiration,

diaphragm, external intercostal, internal intercostal, abdominal-wall muscles,
expiratory reserve volume (ERV), forced vital capacity (FVC), tidal volume
(TV), inspiratory reserve volume (IRV), residual volume (RV), and forced
expiratory volume in one second (FEV1)
2. To understand the roles of skeletal muscles in the mechanics of breathing.
3. To understand the volume and pressure changes in the thoracic cavity during
ventilation of the lungs.
4. To understand the effects of airway radius and, thus, resistance on airflow.

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C. HYPOTHESES

Lung diseases are often classified as obstructive or restrictive. An obstructive

disease affects airflow, and a restrictive disease usually reduces volumes and
capacities. Although they are not diagnostic, pulmonary function tests such as forced
expiratory volume (FEV1) can help a clinician determine the difference between
obstructive and restrictive diseases. Specifically, an FEV1 is the forced volume expired
in 1 second. In obstructive diseases such as chronic bronchitis and asthma, airway
radius is decreased. Thus, FEV1 will decrease proportionately.

6
 CHAPTER II

METHODS

The basic setup to measured respiratory volumes and calculating capacities was
similar to the usual balloon model of respiration. The simulated lungs are suspended in
a glass jar, and a rubber diaphragm at the bottom of the jar is used to adjust the volume
and pressure of the cavity surrounding the lungs. In this experiment, we investigated
the effect of airway radius on respiratory parameters such as tidal volume (TV) and
forced expiratory volume in 1 second (FEV1).
The first step of the experiment was set the airway radius 5.00 mm before the
simulated lung breathed in normal pattern and established the baseline respiratory
volumes. Observed the spirogram on the oscilloscope and noted that the simulated
lungs was breathed a tidal volume.
The next step is to measured the respiratory volumes and determined the
respiratory capacities. The forced expiration would happened after the expiratory
reserved volume pushed out by the contraction of the internal intercostal muscles and
abdominal-wall muscles. The forced vital capacity would be known by observed the
lungs that would first inspired maximally and then expired fully.
The vital capacity and total lung capacity were calculated from the addition of
tidal volume, expiratory reserve volume, inspiratory reserve volume, and residual
volume. Minute ventilation was the amount of air that flowed into and then out of the
lung in a minute. Minute ventilation would be known by this following mathematic
equation:

Minute ventilation (ml/min) = TV (ml/breath) x BPM (breath/min)

We would know the effect changing of the airway radius on the pulmonary
function by decreased the airway radius, 0,5 mm, from 5,00 mm until 3,00 mm. FEV1
would be known by matemathic equation below:

FEV1 (%) = ( FEV1 / FVC volume) x 100%

7
 CHAPTER III

RESULTS

A total of six experiments were done, giving some various data in this study
(table 1). The experiment was calculated and based on the radius airway which
started with 5 mm to 3 mm radius airway. Each experiment represented broad range
of respiratory parameters (tidal volume, expiratory reserve volume, inspiratory
reserve volume, residual volume, vital capacity, forced expiratory volume at the
first one second/FEV1, and total lung capacity) with no difference between the
breath rates.
Radius Flow TV ERV IRV RV VC FEV1 TLC Breath
(ml/min) Rate
5.00 7485 499 - - - - - - 15

5.00 7500 500 1200 3091 1200 4791 3541 5991 15

4.50 4920 328 787 2028 1613 3143 2303 4756 15

4.00 3075 205 492 1266 1908 1962 1422 3871 15

3.50 1800 120 288 742 2112 1150 822 3262 15

3.00 975 65 156 401 2244 621 436 2865 15

Table 1. TV: Tidal volume, ERV: expiratory reserve volume, IRV: Inspiratory reserve volume,
RV: Residual volume, VC: Vital capacity, FEV1: Forced expiratory volume in one second, TLC:
Total lung capacity

Table 1: Experiment Data

As shown in the table above, the pulmonary minute ventilation, the TV, the
ERV, the IRV, the RV, the VC, the FEV1, and the TLC all went way down as the
airway radius decreased, except for the RV. Compared with the higher airway
radius, the experiment with lower airway radius would have lower recorded data.
The examples were written as following. The experiment with narrower airway
radius would flow the air into the lungs in smaller amount per minute. For instance,
the experiment which initiated in airway radius of 5 mm would flow 7500 ml/min
amount of the air while the experiment started in airway radius of 3 mm would only
send 975 ml/min amount of the air. The smaller flow happened in smaller airway
radius because of the smaller produce of tidal volume in it. In the airway radius of

8
5 mm, the tidal volume was 500 ml/min while in the airway radius of 3 mm, the
tidal volume decreased, becoming only 65 ml/min. Compared with the ERV in
airway radius of 5 mm, the ERV in airway radius of 3 mm was recorded way much
smaller, with the ratio 1200:156 ml. Compared with the IRV in airway radius of 5
mm, the IRV in airway radius of 3mm would be recorded lower in data, with the
ratio 3091:401 ml. A different occurrence was found in the residual volume (RV)
data. Compared with the RV in airway radius of 5 mm, the RV in airway radius of
3 mm was higher, with the ratio 1200:2244. Compared with the VC in airway radius
of 5 mm, the VC in airway radius of 3 mm would have lower data, with the ratio
4791:621. Compared with the FEV1 airway radius of 5mm, the FEV1 in airway
radius of 3mm was lower, with the ratio 3541:436. Compared with the TLC airway
radius of 5 mm, the TLC in airway radius of 3 mm was lower, with the ratio
5991:2885. These experiments were applied with various range of the radius
airway, but the breath rates were the same: 15 breath rates per minute.

Multivariate analysis of respiratory parameters depended on the radius

airway applied.

Chart 1: normal breathing patterns Chart 2: respiratory values measured in the airway
radius of 5 mm

As shown in chart 1 (first experiment), the spirogram on the oscilloscope

showed the tidal volume or a normal breathing patterns when the person breath
moves about 499 ml (table 1) of air into (inspired) and out of the lungs (expired)
with each breath under resting conditions. This amount due to the person’s size,
sex, age, physical condition, and immediate respiratory needs.

9
 Chart 2, the second experiment, showed the respiratory volumes (TV, IRV,
ERV, and RV) and the respiratory capacities (TLC and VC). As the contraction and
relaxation of diaphragm, the TV was 500 ml. The pulmonary minute ventilation
(flow) could be measured by multiplying the TV (500 ml) and BPM (15x) together,
resulting 7500 ml/min. In addition to the TV, the ERV, IRV, and RV were
measured. 10 seconds after the experiment was initiated, the ERV was 1200 ml. In
the next a few seconds, the RV was 1200 ml and the IRV was 3091 ml. The VC
was calculated by summing up the TV (500 ml), ERV (1200 ml), IRV (3091 ml)
and resulting 4791 ml. The TLC was measured by summing up the VC (4791 ml)
and RV (1200), and the result is 5991 ml. Then, the FVC was measured in the next
10 seconds or 20th second after the experiment was initiated and was equal to VC,
showing 4791 ml. The FEV1 would appear, showing 3541 ml in the graph and data
grid (note that FEV1 is the data measured at the first second of FVC).

Chart 3: respiratory values measured in the airway Chart 4: respiratory values measured in the airway
radius of 4.5 mm radius of 4 mm

Chart 3, the third experiment, showed that the TV was 4920 ml. The
pulmonary minute ventilation (flow) could be calculated by multiplying the TV
(328 ml) and BPM (15x) together, resulting 4920 mm/min. Ten seconds after the
experiment was initiated, the ERV was 787 ml. In the next a few seconds, the RV
was 1613 ml and the IRV was 2028 ml. The VC was calculated by summing up the
TV (328 ml), ERV (787 ml), IRV (2028 ml) and resulting 3143 ml. The TLC was
measured by summing up the VC (3143 ml) and RV (1613), and the result is 4756
ml. Then, the FVC was measured in the next 10 seconds or 20 th second after the

10
 experiment was initiated and was equal to VC, showing 3143 ml. The FEV1 would
appear, showing 2303 ml in the graph and data grid.

The fourth experiment result (Chart 4) explained that the TV was 205 ml as
the contraction and relaxation of diaphragm. By multiplying the TV (3075 ml) and
BPM (15x), you had gotten the pulmonary minute ventilation (flow) which the
result is 3075 ml/min. Ten seconds after the experiment was initiated, the ERV was
492 ml. Then, the IRV was 1266 ml and the RV was 1908 ml in a few seconds after
experiment was initiated. The VC and TLC could be calculated from those volumes.
The VC was calculated by using the sums of TV, ERV, and IRV, resulting 1962
ml. The TLC was measured by summing up the VC and RV, resulting 3871 ml. The
FVC was measured in the next 10 seconds or 20th second after the experiment was
initiated and was equal to VC, showing 1962 ml. The FEV1 would appear, showing
1422 ml in the graph and data grid.

Chart 5: respiratory values measured in the airway Chart 6: respiratory values measured in the airway
radius of 3.5 mm radius of 3 mm

The result in fifth experiment (Chart 5) will be explained as followings. As

the contraction and relaxation of diaphragm, the TV was 120 ml. The pulmonary
minute ventilation (flow) could be measured by multiplying the TV and BPM
together, resulting 1800 ml/min. In addition to the TV, the ERV, IRV, and RV were
measured. 10 seconds after the experiment was initiated, the ERV was 288 ml. In
the next a few seconds, the RV was 2112 ml and the IRV was 742 ml. The VC and
TLC could be calculated from those volumes. According to it, the VC was 1150 ml
and the TLC was 3262 ml. The FVC could be measured in the next 10 seconds (at
20th second after the experiment was initiated) and was equal to VC, showing 1150

11
ml. The FEV1 would appear, showing 822 ml in the graph and data grid (note that
FEV1 is the data measured at the first second of FVC) .

The result in sixth experiment (Chart 6) will be explained as followings. As

the contraction and relaxation of diapraghm, the TV was 65 ml. The pulmonary
minute ventilation (flow) could be measured by multiplying the TV and BPM
together, resulting 975 ml/min. In addition to the TV, the ERV, IRV, and RV were
measured. 10 seconds after the experiment was initiated, the ERV was 156 ml. In
the next a few seconds, it was recorded that the RV was 2244 ml and the IRV was
401 ml. The VC and TLC could be calculated from those volumes. According to it,
the VC was 621 ml and the TLC was 2865 ml. The FVC could be measured in the
next 10 seconds (at 20th second after the experiment was initiated) and was equal to
VC, showing 621 ml. The FEV1 would appear, showing 436 ml in the graph and
data grid (note that FEV1 is the data measured at the first second of FVC).

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 CHAPTER IV

DISCUSSION

Air moves from a region of higher pressure to one of lower pressure.

Therefore, for air to be moved into or out of the lungs, a pressure difference between
the atmosphere and the alveoli must be established. If there is no pressure gradient,
no airflow will occur. Under normal circumstances, inspiration is accomplished by
causing alveolar pressure to fall below atmospheric pressure. When the mechanics
of breathing are being discussed, atmospheric pressure is conventionally referred to
as 0 cm H2O, so lowering alveolar pressure below atmospheric pressure is known
as negative pressure breathing. As soon as a pressure gradient sufficient to
overcome the resistance to airflow offered by the conducting airways is established
between the atmosphere and the alveoli, air flows into the lungs. It is also possible
to cause air to flow into the lungs by raising the pressure at the nose and mouth
above alveolar pressure. This positive-pressure ventilation is generally used on
patients unable to generate a sufficient pressure gradient between the atmosphere
and the alveoli by normal negative-pressure breathing. Air flows out of the lungs
when alveolar pressure is sufficiently greater than atmospheric pressure to
overcome the resistance to airflow offered by the conducting airways. (Levitzsky,
2007)

The alveoli are not capable of expanding themselves. They only expand
passively in response to an increased distending pressure across the alveolar wall.
This increased transmural pressure gradient, generated by the muscles of
inspiration, further opens the highly distensible alveoli and thus lowers the alveolar
pressure. The transmural pressure gradient is conventionally calculated by
subtracting the outside pressure (in this case, the intrapleural pressure) from the
inside pressure (in this case, the alveolar pressure). (Levitzsky, 2007)

The pressure in the thin space between the visceral and parietal pleura is
normally slightly subatmospheric, even when no inspiratory muscles are
contracting. This negative intrapleural pressure (sometimes also referred to as
negative intrathoracic pressure) is mainly caused by the mechanical interaction
between the lung and the chest wall. At the end of expiration, when all the

13
respiratory muscles are relaxed, the lung and the chest wall are acting on each other
in opposite directions. The lung is tending to decrease its volume because of the
inward elastic recoil of the distended alveolar walls; the chest wall is tending to
increase its volume because of its outward elastic recoil. Thus the chest wall is
acting to hold the alveoli open in opposition to their elastic recoil. Similarly, the
lung is acting by its elastic recoil to hold the chest wall in. (Sherwood, 2010)

Because of this interaction, the pressure is negative at the surface of the very
thin, fluid-filled pleural space. There is normally no gas in the intrapleural space,
and the lung is held against the chest wall by the thin layer of serous intrapleural
liquid, estimated to have a total volume of about 15 to 25 mL in the average adult.
Initially, before any airflow occurs, the pressure inside the alveoli is the same as
atmospheric pressure—by convention 0 cm H2O. Alveolar pressure is greater than
intrapleural pressure because it represents the sum of the intrapleural pressure plus
the alveolar elastic recoil pressure:

Alveolar pressure = intrapleural pressure + alveolar elastic recoil pressure

INTERPRETATION OF DATA

The basic setup to measured respiratory volumes and calculating capacities

was similar to the usual balloon model of respiration. The experiment investigated
the effect of airway radius on respiratory parameters such as tidal volume (TV)
and forced expiratory volume in 1 second (FEV1).
Airway resistance is the opposition to flow caused by the forces of friction.
It is defined as the ratio of driving pressure to the rate of air flow. Resistance to
flow in the airways depends on whether the flow is laminar or turbulent, on the
dimensions of the airway, and on the viscosity of the gas. (Levitzsky, 2007)

For laminar flow, resistance is quite low. That is, a relatively small driving
pressure is needed to produce a certain flow rate. Resistance during laminar flow
may be calculated via a rearrangement of Poiseuille's Law :

14
 The most important variable here is the radius, which, by virtue of its
elevation to the fourth power, has a tremendous impact on the resistance. The effect
of airway radius and resistance on airflow is if the airway radius is smaller than it
should, the resistance will be increased so the air flow will be decreased. If the
airway radius is bigger than it should, the resistance will be decreased so the air
flow will be increased too. The resistance to airflow cannot be measured directly
but must be calculated from the pressure gradient and airflow during a breath.
(Guyton & Hall, 2016)

Thus, if the diameter of a tube is doubled, resistance will drop by a factor of

sixteen. Airway resistance decreases as lung volume increases because the airways
distend as the lungs inflate, and wider airways have lower resistance. Thus, the
airway resistance is highly dependent on airway radius which also affects airway
flow that directly express volume (such tidal volume, ERV, IRV, etc.) and flow
discharge.

Radius Flow TV ERV IRV RV VC FEV1 TLC Breath

(ml/min) Rate
5.00 7485 499 - - - - - - 15

5.00 7500 500 1200 3091 1200 4791 3541 5991 15

4.50 4920 328 787 2028 1613 3143 2303 4756 15

4.00 3075 205 492 1266 1908 1962 1422 3871 15

3.50 1800 120 288 742 2112 1150 822 3262 15

3.00 975 65 156 401 2244 621 436 2865 15

The results table shows that changes in the radius greatly affect the flow and
volume. Airway radius affect the airway resistance that causes the airflow to bear.
This affects the speed of filling the volume of air in the lung cavity.
The first experiment describes the baseline graph. In this graph uses radius
5.00 made flow 7485 L/min and tidal volume exactly 499 ml. This indicates that
tidal volume or volume when breathing normally is 499 ml. Baseline is important
as comparison subject for other experiment.

15
 After the baseline was obtained, the next experiment was to test TV, ERV,
IRV, RV, VC, FEV1, and TLC. In this experiment we focus on the comparison of
FEV1 and VC (This case VC same with FVC). FEV1 (%) = (FEV1 / FVC volume)
x 100%.
The experiment was set airway radius in 5.00 mm. The experimental results
have been in the results sheet, with the data found, the comparison FEV 1/VC is
3541/4791 or about 73,90%.
Third experiment was set airway radius in 4.50 mm. The result shows all
volume decreased as the flow decreased. Comparing FEV1/VC is 2303/3143 or
about 73,48%. Fourth experiment set radius downward to 4.00 mm. Similar with
third experiment, all volume decreased because of flow. FEV 1/VC shows
1422/1962 or about 72,47%. Fifth experiment was set airway radius to 3.50 mm.
For the percentage FEV1 is 822/1150 or about 71,47%. Flow and other volume
decreased sharply with just small changing in radius. Airway radius was set to 3.00
mm in last experiment. All result from this experiment drastically decreased if we
compare to the first experiment. Percentage FEV1 is 436/621 or about 70%.
From the result above, airway radius affects airflow and volume greatly. As
the radius decreased, it makes the airway resistance increased. It increased, air flow
will be decreased. Thus, all volume from air changing will be decreased as well
because flow are not enough to fulfill the lungs optimally. Also, the percentage of
FEV1 was decreased from 73,90% in 5.00 mm to 70% in 3.00 although it doesn’t
show any major changes. Changes in airway radius indirectly also alter the ability
to collect air volume. Forced vital capacity (FVC) is the amount of water that can
be inspired by the deepest possible inspiration and forcefully expires as possible, so
it does not depend with time. But FEV1 depends on the time, because it's measured
in one second. The change in the radius causes the airflow that comes out rather
stifled slightly because there is airway resistance. In addition, from the FEV 1
percentage it was concluded that the subject had a percentage below normal. The
normal data percentage of FEV1 is 75% -85%. Subjects may experience obstructive
disease.

16
LIMITATIONS
In this experiment we used the simulated lungs that were suspended
in a glass jar and a rubber diaphragm at the bottom of the jar was used to adjust the
volume and pressure of the cavity surrounding the lungs. In this experiment, we
investigated the effect of airway radius on respiratory parameters such as tidal
volume (TV) and forced expiratory volume in 1 second (FEV 1). The experiment’s
data would be more accurate if we knew the person’s size, sex, age, physical
condition, and immediate respiratory needs. Because that things could influence the
respiratory volume and capacities.

17
 CHAPTER V

CONCLUSION

According to result and discussion, we can conclude that:

1. Ventilation consist of (a) inspiration, during which air is taken into the
lungs, and (b) expiration, during which air is expelled from the lungs.
2. Ventilation is the result of skeletal muscle contraction. Respiratory muscles
are diaphragm-a dome-shape muscle, external intercostal muscle, internal
intercostal muscle, abdominal muscles, etc.
3. Airway radius influences the airflow into or out of the lungs and the
pulmonary function.
4. The respiratory volumes and capacities can vary due to a person’s size , sex,
age, physical condition, and immediate respiratory needs.

18
 REFERENCES

Airway Resistance. (n.d.). Retrieved from Johns Hopkins University:

http://oac.med.jhmi.edu/res_phys/Encyclopedia/AirwayResistance/Airway
Resistance.HTML
Guyton, Arthur C and John E Hall. 2016. Textbook of Medical Physiology. 13th
edition.
Levitzsky, Michael G. 2007. Pulmonary Physiology. 7th edition.
Sherwood, Lauralee. 2010. Human Physiology from Cells to Systems. 7th edition.

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