RESPIRATORY

SYSTEM
 Pulmonary ventilation
 Pulmonary ventilation, or breathing, is the flow
of air into and out of the lungs. In pulmonary
ventilation, air flows between the atmosphere and
the alveoli of the lungs because of alternating
pressure differences created by contraction and
relaxation of respiratory muscles. The rate of
airflow and the amount of effort needed for
breathing are also influenced by alveolar surface
tension, compliance of the lungs, and airway
resistance.
 Pressure Changes during Pulmonary
Ventilation
 Air moves into the lungs when the air pressure
inside the lungs is less than the air pressure in
the atmosphere. Air moves out of the lungs when
the air pressure inside the lungs is greater than
the air pressure in the atmosphere.
 Inhalation
Breathing in is called inhalation (inspiration). Just before each
inhalation, the air pressure inside the lungs is equal to the air pressure
of the atmosphere, which at sea level is about 760 millimeters of
mercury (mmHg), or 1 atmosphere (atm). For air
to flow into the lungs, the pressure inside the alveoli must become
lower than the atmospheric pressure. This condition is achieved by
increasing the size of the lungs.
Differences in pressure caused by changes in lung volume force
air into our lungs when we inhale and out when we exhale. For
inhalation to occur, the lungs must expand, which increases lung
volume and thus decreases the pressure in the lungs to below
atmospheric pressure. The first step in expanding the lungs
during normal quiet inhalation involves contraction of the main
muscle of inhalation, the diaphragm, with resistance from
external intercostals
 (c) During
inhalation, the
lower ribs (7–
10) move
(a) Muscles of inhalation (left); upward and
muscles of exhalation (right); outward like
arrows indicate the direction of the handle on
muscle contraction a bucket
The most important muscle of inhalation is the diaphragm, the
dome-shaped skeletal muscle that forms the floor of the thoracic
cavity. It is innervated by fibers of the phrenic nerves, which emerge
from the spinal cord at cervical levels 3, 4, and 5. Contraction of the
diaphragm causes it to flatten, lowering its dome. This increases the
vertical diameter of the thoracic cavity. During normal quiet inhalation,
the diaphragm descends about 1 cm (0.4 in.), producing a pressure
difference of 1–3 mmHg and the inhalation of about 500 mL of
air. In strenuous breathing, the diaphragm may descend 10 cm
(4 in.), which produces a pressure diff erence of 100 mmHg and
the inhalation of 2–3 liters of air. Contraction of the diaphragm is
responsible for about
75% of the air that enters the lungs during quiet breathing.
Advanced pregnancy, excessive obesity, or confining abdominal
clothing can prevent complete descent of the diaphragm.
The next most important muscles of inhalation are the external
intercostals. When these muscles contract, they elevate the ribs. As a result,
there is an increase in the anteroposterior and lateral diameters of the chest
cavity. Contraction of the external intercostals is responsible for about 25%
of the air that enters the lungs during normal quiet breathing.
Intrapleural pressure is the pressure within the pleural cavity.
Intrapleural pressure is always a negative pressure ranging from
754–756 mmHg during normal quiet breathing. Because the pleural
cavity has a negative pressure, it essentially functions as a vacuum.
The suction of this vacuum attaches the visceral pleura to the chest
wall. Thus, if the thoracic cavity increases or decrease in size, the
lungs also expand or recoil. As the diaphragm and external
intercostals contract and the overall size of the thoracic cavity
increases, the volume of the pleural cavity also increases, which
causes intrapleural pressure to decrease to about 754 mmHg. As the
thoracic cavity expands, the parietal pleura lining the cavity is pulled
outward in all directions, and the visceral pleura and lungs and pulled
along with it.
As the volume of the lungs increases in this way, the pressure of
air within the alveoli of the lungs, called the alveolar (intrapul monic)
pressure, drops from 760 to 758 mmHg. A pressure diff erence is thus
established between the atmosphere and the alveoli and inhalation takes
place. During deep, forceful inhalations, accessory muscles of
inspiration also participate
in increasing the size of the thoracic cavity. The muscles are so
named because they make little, if any, contribution during normal
quiet inhalation, but during exercise or forced breathing they may
contract vigorously. The accessory muscles of inhalation include
the sternocleidomastoid muscles, which elevate the sternum; the
scalene muscles, which elevate the first two ribs; and the
pectoralis minor muscles, which elevate the third through fifth
ribs. Because both normal quiet inhalation and inhalation during
exercise or forced breathing involve muscular contraction, the
process of inhalation is said to be active.
 Exhalation
Breathing out, called exhalation (expiration), is also due to a pressure gradient, but in
this case the gradient is in the opposite direction.
Exhalation starts when the inspiratory muscles relax. As the diaphragm relaxes,
its dome moves superiorly owing to its elasticity. As the external intercostals
relax, the ribs are depressed. These movements decrease the vertical, lateral,
and anteroposterior diameters of the thoracic cavity, which decreases lung
volume. In turn, the alveolar
pressure increases to about 762 mmHg. Air then flows from the area of higher
pressure in the alveoli to the area of lower pressure in the atmosphere.
Exhalation becomes active only during forceful breathing, as occurs while
playing a wind instrument or during exercise. During these times, muscles of
exhalation—the abdominal and internal intercostals—contract, which increases
pressure in the abdominal region and thorax. Contraction of the abdominal
muscles moves the inferior ribs downward and compresses the abdominal
viscera, thereby forcing the diaphragm superiorly. Contraction of the internal
intercostals, which extend inferiorly and posteriorly between adjacent ribs, pulls
the ribs inferiorly. Although intrapleural pressure is always less than alveolar
pressure, it may briefly exceed atmospheric pressure during a forceful
exhalation, such as during a cough.
Breathing Patterns and Modified
Breathing Movements
Changes in partial
pressures of oxygen
and carbon dioxide
(in mmHg) during
external and
internal
respiration.
Gases diffuse from
areas of higher
partial pressure to
areas of lower
partial pressure
Transport of oxygen (O2)
and carbon dioxide
(CO2) in the blood.
Most O2 is transported by
hemoglobin as
oxyhemoglobin (Hb–O2)
within red blood cells;
most CO2 is transported in
blood plasma as
bicarbonate ions (HCO3
−).
 Oxygen Transport
Oxygen does not dissolve easily in water, so only about 1.5% of inhaled O 2 is dissolved in blood
plasma, which is mostly water. About 98.5% of blood O2 is bound to hemoglobin in red
blood cells .
Each 100 mL of oxygenated blood contains the equivalent of 20 mL of gaseous O2.
Using the percentages just given, the amount dissolved in the plasma is 0.3 mL and the
amount bound to hemoglobin is 19.7 mL.
The heme portion of hemoglobin contains four atoms of iron, each capable of binding to
a molecule of O2 .Oxygen and hemoglobin bind in an easily reversible reaction to form
oxyhemoglobin:

The 98.5% of the O2 that is bound to hemoglobin is trapped inside RBCs, so only the dissolved O 2
(1.5%) can diff use out of tissue capillaries into tissue cells. Thus, it is important to understand
the factors that promote O2 binding to and dissociation (separation) from hemoglobin.
 The Relationship between Hemoglobin and Oxygen
Partial Pressure
The most important factor that determines how much O 2 binds to hemoglobin is the PO2; the
higher the PO2, the more O2 combines with Hb. When reduced hemoglobin (Hb) is
completely converted to oxyhemoglobin (Hb–O2), the hemoglobin is said to be fully saturated;
when hemoglobin consists of a mixture of Hb and Hb–O 2, it is partially saturated. The percent
saturation of hemoglobin expresses
the average saturation of hemoglobin with
oxygen. For instance, if each hemoglobin
molecule has bound two O2 molecules,
then the hemoglobin is 50% saturated
because each Hb can bind a maximum of
four O2. The relationship between the
percent saturation of hemoglobin and PO2 is
illustrated in the oxygen–hemoglobin
dissociation curve
Note that when the PO2 is high, hemoglobin binds with large amounts of O2 and is almost
100% saturated. When PO2 is low, hemoglobin is only partially saturated. In other words, the
greater the PO2, the more O2 will bind to hemoglobin, until all the available hemoglobin
molecules are saturated. Therefore, in pulmonary capillaries, where PO2 is high, a lot of O2
binds to hemoglobin. In tissue capillaries, where the P O2 is lower, hemoglobin does not hold as
much O2, and the dissolved O2 is unloaded via diff usion into tissue cells.

Other Factors Affecting the Affinity of Hemoglobin for Oxygen

several other factors influence the tightness
or aff inity with which hemoglobin
binds O2.
1. Acidity (pH).--As acidity increases
(pH decreases), the affinity of
hemoglobin for O2 decreases, and O2
dissociates more readily from
hemoglobin, i.e. increasing acidity
enhances the unloading of oxygen
from hemoglobin
Partial pressure of carbon dioxide—
CO2 also can bind to hemoglobin, and the effect is similar to that of H+ (shifting the
curve to the right). As PCO2 rises, hemoglobin releases O2 more readily
Thus, an increased PCO2 produces a more acidic environment, which helps release O2
from hemoglobin. During exercise, lactic acid—a by-product of anaerobic metabolism
within muscles—also decreases blood pH. Decreased PCO2 (and elevated pH) shift s
the saturation curve to the left .
Temperature.
Within limits, as temperature increases, so does the amount of O2 released from
hemoglobin
 Regulation of respiration
Respiration is a reflex process. But it can be controlled voluntarily
for a short period of about 40 seconds. However, by practice,
breathing can be withheld for a long period. At the end of that
period, the person is forced to breathe.
Normally, quiet regular breathing occurs because of two regulatory
mechanisms:
1. Nervous or neural mechanism.
2. Chemical mechanism.
NERVOUS MECHANISM
Nervous mechanism that regulates the respiration
includes:
1. Respiratory centers.
2. Afferent nerves
3. Efferent nerves.
 RESPIRATORY CENTERS
Respiratory centers are group of
neurons, which control the rate,
rhythm and force of respiration.
These centers are bilaterally situated
in reticular formation of the
brainstem.
Depending upon the situation in
brainstem, the respiratory centers
are classified into two groups:
A. Medullary centers consisting of
1. Dorsal respiratory group of
neurons
2. Ventral respiratory group of
neurons
B. Pontine centers
1. Apneustic center
2. Pneumotaxic center.

Nervous regulation of respiration.

Solid green line = Stimulation, Dotted red
line = Inhibition.
 MEDULLARY CENTERS
1. Dorsal Respiratory Group of Neurons
Situation
Dorsal respiratory group of neurons are diffusely situated in the nucleus of tractus
solitarius present in the upper part of the medulla oblongata. Usually, these neurons are
collectively called inspiratory center.
2. Ventral Respiratory Group of
Neurons
Situation
present in nucleus ambiguous
and nucleus retroambiguous.
Ventral respiratory group has both
inspiratory and expiratory
neurons. Inspiratory neurons
are found in the central area of
the group. Expiratory neurons are
in the caudal and rostral areas of
the group.

Function
Normally, ventral group neurons are inactive during quiet breathing and
become active during forced breathing. During forced breathing, these
neurons stimulate both inspiratory muscles and expiratory muscles.
 PONTINE CENTERS
Apneustic Center
Situation
Apneustic center is situated in the reticular formation of lower
pons.
Function
Apneustic center increases depth of inspiration by acting
directly on dorsal group neurons.
 Pneumotaxic Center
Situation
Pneumotaxic center is situated in the dorsolateral part of reticular
formation in upper pons. It is formed by neurons of medial
parabrachial and subparabrachial
nuclei. Subparabrachial nucleus is also called ventral parabrachial or
Kölliker-Fuse nucleus.
Function
Primary function of pneumotaxic center is to control the medullary
respiratory centers, particularly the dorsal group neurons. It acts
through apneustic center.
Pneumotaxic center inhibits the apneustic center so that the
dorsal group neurons are inhibited. Because of this, inspiration
stops and expiration starts. Thus, pneumotaxic center influences
the switching between inspiration and expiration.
Pneumotaxic center increases respiratory rate by reducing
the duration of inspiration.
 „ CHEMICAL MECHANISM
Chemical mechanism of regulation of respiration is operated
through the chemoreceptors. Chemoreceptors are the sensory
nerve endings, which give response to changes in chemical
constituents of blood.

Changes in Chemical Constituents of Blood which Stimulate

Chemoreceptors
1. Hypoxia (decreased pO2)
2. Hypercapnea (increased pCO2)
3. Increased hydrogen ion concentration.

Types of Chemoreceptors
Chemoreceptors are classified into two groups:
1. Central chemoreceptors
2. Peripheral chemoreceptors.
„ CENTRAL CHEMORECEPTORS
Central chemoreceptors are the chemoreceptors present in the
brain.
Situation
Central chemoreceptors are situated in deeper part of medulla
oblongata, close to the dorsal respiratory group of neurons. This
area is known as chemosensitive area and the neurons are
called chemoreceptors. Chemo-receptors are in close contact
with blood and cerebrospinal fluid.
Mechanism of Action
Central chemoreceptors are connected with respiratory centers,
particularly the dorsal respiratory group of neurons through
synapses. These chemoreceptors act slowly but effectively.
Central chemoreceptors are responsible for 70% to 80% of
increased ventilation through chemical regulatory mechanism.
Main stimulant for central chemoreceptors is the increased
hydrogen ion concentration. Hydrogen ions stimulate the central
chemoreceptors.
From chemoreceptors, the excitatory impulses are sent to dorsal
respiratory group of neurons, resulting in increased ventilation
(increased rate and force of breathing). Because of this, excess
carbon dioxide is washed out and respiration is brought back to
normal. Lack of oxygen does not have significant effect on
the central chemoreceptors, except that it generally depresses the
overall function of brain. CO2 + H2O → H2CO3 → H+ + HCO3-
PERIPHERAL CHEMORECEPTORS
Peripheral chemoreceptors are the chemoreceptors present in
carotid and aortic region.
Mechanism of Action
Hypoxia is the most potent stimulant for peripheral
chemoreceptors. It is because of the presence of oxygen sensitive
potassium channels in the glomus cells of peripheral
chemoreceptors. Hypoxia causes closure of oxygen sensitive
potassium channels and prevents potassium efflux. This leads to
depolarization of glomus cells (receptor potential) and
generation of action potentials in nerve ending.
These impulses pass through aortic and Hering nerves and excite
the dorsal group of neurons. Dorsal group of neurons in turn, send
excitatory impulses to respiratory muscles, resulting in increased
ventilation. This provides enough oxygen and rectifies the lack of
oxygen.
 Disturbance of respiration
Normal respiratory pattern is called eupnea. Respiratory
pattern is altered by many ways. Altered patterns of respiration are:
1. Tachypnea: Increase in the rate of respiration
2. Bradypnea: Decrease in the rate of respiration
3. Polypnea: Rapid, shallow breathing resembling panting in dogs.
In this type of breathing, only the rate of respiration increases but the
force does not increase significantly.
4. Apnea: Temporary arrest of breathing
5. Hyperpnea: Increase in pulmonary ventilation due to increase in rate
or force of respiration. Increase in rate and force of respiration occurs
after exercise. It also occurs in abnormal conditions like fever or other
disorders.
6. Hyperventilation: Abnormal increase in rate and force of
respiration, which often leads to dizziness and sometimes chest pain.
7. Hypoventilation: Decrease in rate and force of respiration
8. Dyspnea: Difficulty in breathing.
9. Periodic breathing: Abnormal respiratory rhythm.
„ HYPOXIA
„ DEFINITION
Hypoxia is defined as reduced availability of oxygen to the tissues. The
term anoxia refers to absence of oxygen. In olden days, the term anoxia
was in use. Since there is no possibility for total absence of oxygen
in living conditions, use of this term is abandoned.

„ CLASSIFICATION AND CAUSES OF HYPOXIA

Four important factors which leads to hypoxia are:
1. Oxygen tension in arterial blood
2. Oxygen carrying capacity of blood
3. Velocity of blood flow
4. Utilization of oxygen by the cells.
On the basis of above factors, hypoxia is classified into four types:
1. Hypoxic hypoxia
2. Anemic hypoxia
3. Stagnant hypoxia
4. Histotoxic hypoxia.
1. Hypoxic Hypoxia
Hypoxic hypoxia means decreased oxygen content in blood. It is also
called arterial hypoxia.
Causes for hypoxic hypoxia
Hypoxic hypoxia is caused by four factors.
i. Low oxygen tension in inspired (atmospheric) air, which does not
provide enough oxygen.
ii. Respiratory disorders associated with decreased pulmonary
ventilation, which does not allow intake of enough oxygen.
iii. Respiratory disorders associated with inadequate oxygenation in
lungs, which does not allow diffusion of enough oxygen.
iv. Cardiac disorders, in which enough blood is not pumped to
transport oxygen.
2. Anemic Hypoxia
Anemic hypoxia is the condition characterized by the inability of blood to
carry enough amount of oxygen. Oxygen availability is normal. But the
blood is not able to take up sufficient amount of oxygen due to anemic
condition.
Causes for anemic hypoxia
Any condition that causes anemia can cause anemic hypoxia. It is
caused by the following conditions:
i. Decreased number of RBCs
ii. Decreased hemoglobin content in the blood
iii. Formation of altered hemoglobin
iv. Combination of hemoglobin with gases other than oxygen and carbon
dioxide.
 3. Stagnant Hypoxia
Stagnant hypoxia is the hypoxia caused by decreased velocity of blood
flow. It is otherwise called hypokinetic hypoxia.
Causes for stagnant hypoxia
Stagnant hypoxia occurs mainly due to reduction in velocity of blood
flow. Velocity of blood flow decreases in the following conditions:
i. Congestive cardiac failure
ii. Hemorrhage
iii. Surgical shock
iv. Vasospasm
v. Thrombosis
vi. Embolism.
4. Histotoxic Hypoxia
Histotoxic hypoxia is the type of hypoxia produced by the inability of
tissues to utilize oxygen.
Causes for histotoxic hypoxia
Histotoxic hypoxia occurs due to cyanide or sulfide poisoning.
These poisonous substances destroy the cellular oxidative enzymes
and there is a complete paralysis of cytochrome oxidase system. So,
even if oxygen is supplied, the tissues are not in a position to utilize it.
„ EFFECTS OF HYPOXIA
Acute and severe hypoxia leads to unconsciousness. If not treated
immediately, brain death occurs. Chronic hypoxia produces
various symptoms in the body. Effects of hypoxia are of two types:
1. Immediate effects
2. Delayed effects.
1. Immediate effects

i. Effects on blood ii. Effects on cardiovascular system

iii. Effects on respiration iv. Effects on digestive system
v. Effects on kidney vi. Effects on central nervous system
Delayed Effects of Hypoxia
Delayed effects appear depending upon the length and severity of the
exposure to hypoxia. The person becomes highly irritable and develops the
symptoms of mountain sickness, such as nausea, vomiting, depression,
weakness and fatigue.
TREATMENT FOR HYPOXIA – OXYGEN THERAPY
Best treatment for hypoxia is oxygen therapy, i.e. treating the affected
person with oxygen. Pure oxygen or oxygen combined with another gas
is administered.
Oxygen therapy is carried out by two methods:
1. By placing the patient’s head in a ‘tent’ containing oxygen.
2. By allowing the patient to breathe oxygen either from a mask or an
intranasal tube.
Depending upon the situation, oxygen therapy can be given either under
normal atmospheric pressure or under high pressure (hyperbaric
oxygen).
In Normal Atmospheric Pressure
With normal atmospheric pressure, i.e. at one atmosphere
(760 mm Hg), administration of pure oxygen is
well tolerated by the patient for long hours. However,
after 8 hours or more, lung tissues show fluid effusion
and edema. Other tissues are not affected very much
because of hemoglobin-oxygen buffer system.
In High Atmospheric Pressure –
Hyperbaric Oxygen
Hyperbaric oxygen is the pure oxygen with high atmospheric
pressure of 2 or more than 2 atmosphere.
Hyperbaric oxygen therapy with 2 to 3 atmosphere is tolerated by the
patient for about 5 hours.
Types of Hypoxia
Oxygen therapy is the best treatment for hypoxia. But it is not
effective equally in all types of hypoxia. Value of oxygen therapy
depends upon the type of hypoxia. So, before deciding the oxygen
therapy, one should recall the physiological basis of different types
of hypoxia. In hypoxic hypoxia, the oxygen therapy is 100%
useful. In anemic hypoxia, oxygen therapy is moderately
effective to about 70%. In stagnant hypoxia, the effectiveness of
oxygen therapy is less than 50%. In histotoxic hypoxia, the oxygen
therapy is not useful at all. It is because, even if oxygen is
delivered, the cells cannot utilize oxygen
„ ASPHYXIA
„ DEFINITION
Asphyxia is the condition characterized by combination of
hypoxia and hypercapnea, due to obstruction of air passage.
„
CONDITIONS WHEN ASPHYXIA OCCURS
Axphyxia develops in conditions characterized by acute
obstruction of air passage such as:
1. Strangulation
2. Hanging
3. Drowning, etc.
„ EFFECTS OF ASPHYXIA
Effects of asphyxia develop in three stages:
1. Stage of hyperpnea
2. Stage of convulsions
3. Stage of collapse.
1. Stage of Hyperpnea
Hyperpnea is the first stage of asphyxia. It extends for about 1
minute. In this stage, breathing becomes deep and rapid. It is due
to the powerful stimulation of respiratory centers by excess of
carbon dioxide. Hyperpnea is followed by dyspnea and
cyanosis. Eyes become more prominent.
2. Stage of Convulsions
Stage of convulsions is characterized mainly by convulsions.
Duration of this stage is less than 1 minute. Hypercapnea
acts on brain and produces the following effects:
i. Violent expiratory efforts
ii. Generalized convulsions
iii. Increase in heart rate
iv. Increase in arterial blood pressure
v. Loss of consciousness.
3. Stage of Collapse
Stage of collapse lasts for about 3 minutes. Severe hypoxia
produces the following effects during this stage:
i. Depression of centers in brain and disappearance
of convulsions
ii. Development of respiratory gasping occurs.
During respiratory gasping, there is stretching
of the body with opening of mouth, as if gasping
for breath.
iii. Dilatation of pupils
iv. Decrease in heart rate
v. Loss of all reflexes.
 Artificial respiration
CONDITIONS WHEN ARTIFICIAL RESPIRATION IS REQUIRED
Artificial respiration is required whenever there is an arrest of breathing,
without cardiac failure. Arrest of breathing occurs in the following
conditions:
1. Accidents
2. Drowning
3. Gas poisoning
4. Electric shock
5. Anesthesia.
Stoppage of oxygen supply for 5 minutes causes irreversible changes
in tissues of brain, particularly tissues of cerebral cortex. So, artificial
respiration (resuscitation) must be started quickly without any
delay, before the development of cardiac failure. Purpose of artificial
respiration is to ventilate the alveoli and to stimulate the respiratory
centers.
METHODS OF ARTIFICIAL RESPIRATION
Methods of artificial respiration are of two types:
1. Manual methods
2. Mechanical methods.
„ MANUAL METHODS
Manual methods of resuscitation can be applied quickly without
waiting for the availability of any mechanical aids. Affected person must
be provided with clear air. Clothes around neck and chest regions must
be loosened. Mouth, face and throat should be cleared of mucus,
saliva, foreign particles, etc. Tongue must be drawn forward and it must
be prevented from falling posteriorly, which may cause airway
obstruction.
Manual methods are of two types:
i. Mouth-to-mouth method
ii. Holger Nielsen method.
Mouth-to-mouth Method
The subject is kept in supine position and the resuscitator (person
who give resuscitation) kneels at the side of the subject. By keeping
the thumb on subject’s mouth, the lower jaw is pulled downwards.
Nostrils of the subject are closed with thumb and index finger of the
other hand. Resuscitator then takes a deep breath and exhales
into the subject’s mouth forcefully. Volume of exhaled air must be twice
the normal tidal volume. This expands the subject’s lungs. Then, the
resuscitator removes his mouth from that of the subject. Now, a passive
expiration occurs in the subject due to elastic recoil of the lungs. This
procedure is repeated at a rate of 12 to 14 times a minute, till normal
respiration is restored. Mouth-to-mouth method is the most effective
manual method because,
carbon dioxide in expired air of
the resuscitator can directly
stimulate the respiratory
centers and facilitate the
onset of respiration.
Holger Nielsen Method or Back
Pressure Arm Lift Method
Subject is placed in prone position
with head turned to one side. Hands
are placed under the cheeks with
flexion at elbow joint and abduction of
arms at the shoulders. Resuscitator
kneels beside the head of the subject. By placing the palm of the hands
over the back of the subject, the resuscitator bends forward with straight
arms (without flexion at elbow) and applies pressure on the back of the
subject. Weight of the resuscitator and pressure on back of the subject
compresses his chest and expels air from the lungs. Later, the
resuscitator leans back. At the same time, he draws the subject’s arm
forward by holding it just above elbow. This procedure causes
expansion of thoracic cage and flow of air into the lungs. The
movements are repeated at the rate of 12 per minute, till the normal
respiration is restored.
„ MECHANICAL METHODS
Mechanical methods of artificial respiration become necessary
when the subject needs artificial respiration for long periods. It is
essential during the respiratory failure due to paralysis of
respiratory muscles or any other cause.
Mechanical methods are of two types:
i. Drinker method
ii. Ventilation method
i. Drinker method
The machine used in this
method is called iron lung
chamber or tank
respirator. The equipment
has an airtight chamber,
made of iron or steel. Subject is placed inside this chamber with the
head outside the chamber. By means of some pumps, the pressure
inside the chamber is made positive and negative alternately.By using
tank respirator, the patient can survive for
a longer time, even up to the period of one year till the
natural respiratory functions are restored.
Ventilation Method
A rubber tube is introduced into the trachea of the patient through the
mouth. By using a pump, air or oxygen is pumped into the lungs with
pressure intermittently. When air is pumped, inflation of lungs and
inspiration occur. When it is stopped, expiration occurs and the cycle is
repeated. Apparatus used for ventilation is
called ventilator and it is mostly used to treat acute
respiratory failure. Ventilator is of two types:
a. Volume ventilator
b. Pressure ventilator.
Volume ventilator
By volume ventilator, a
constant volume
of air is pumped into the
lungs of patients intermittently
with minimum pressure.
Pressure ventilator
By pressure ventilator, air is
Pumped into the lungs of
subject with constant high pressure
 „ MEASUREMENT OF LUNG VOLUMES AND CAPACITIES
Spirometry is the method to measure lung volumes and capacities.
Simple instrument used for this purpose is called spirometer. Modified
spirometer is known as respirometer. Nowadays plethysmograph
is also used to measure lung volumes and capacities. Volume, which
cannot be measured by
spirometry, is the residual
volume. Capacities, which
include residual volume also
cannot be measured.
Capacities that include
residual volume are
functional residual capacity
and total lung capacity.

During expiration, the air enters the spirometer

from lungs. Inverted drum moves up and the pen
draws a downward curve on the recording drum.
„ FORCED EXPIRATORY VOLUME OR TIMED VITAL CAPACITY
„ DEFINITION
Forced expiratory volume (FEV) is the volume of air, which can be
expired forcefully in a given unit of time (after a deep inspiration). It is
also called timed vital capacity or forced expiratory vital capacity
(FEVC). It is a dynamic lung volume.
FEV1 = Volume of air expired forcefully in 1 second
FEV2 = Volume of air expired forcefully in 2 seconds
FEV3 = Volume of air expired forcefully in 3 seconds
„ NORMAL VALUES
Forced expiratory volume in persons with normal
respiratory functions is as follows:
FEV1 = 83% of total vital capacity
FEV2 = 94% of total vital capacity
FEV3 = 97% of total vital capacity
After 3rd second = 100% of total vital capacity.
„ SIGNIFICANCE OF DETERMINING FEV
Vital capacity may be almost normal in some of the respiratory diseases.
However, the FEV has great diagnostic value, as it is decreased
significantly in some respiratory diseases. It is very much decreased in
obstructive diseases like asthma and emphysema. It is slightly reduced
in some restrictive respiratory diseases like fibrosis of
Lungs.
„ PEAK EXPIRATORY FLOW RATE
„ DEFINITION
Peak expiratory flow rate (PEFR) is the maximum rate
at which the air can be expired after a deep inspiration.
„ NORMAL VALUE
In normal persons, it is 400 L/minute.
„ MEASUREMENT
Peak expiratory flow rate is measured by using Wright
peak flow meter or a mini peak flow meter.
„
SIGNIFICANCE OF DETERMINING PEFR
Determination of PEFR rate is useful for assessing the respiratory
diseases especially to differentiate the obstructive and restrictive
diseases. Generally, PEFR is reduced in all type of respiratory
disease. However, reduction is more significant in the obstructive
diseases than in the restrictive diseases.
Thus, in restrictive diseases, the PEFR is 200 L/minute
and in obstructive diseases, it is only 100 L/minute.