Respiratory system, physiology of respiratory system and neural control

ANATOMY OF RESPIRATORY
SYSTEM
ZISHAN AKHTAR

Organs of the Respiratory system
 Nose
 Pharynx
 Larynx
 Trachea
 Bronchi
 Lungs –
alveoli

 Gas exchange: Oxygen enters blood and carbon
dioxide leaves
 Regulation of blood pH: Altered by changing
blood carbon dioxide levels
 Voice production: Movement of air past vocal
folds makes sound and speech
 Olfaction: Smell occurs when airborne
molecules drawn into nasal cavity
 Protection: Against microorganisms by
preventing entry and removing them

 Upper tract
 Nose, pharynx
and associated
structures
 Lower tract
 Larynx, trachea,
bronchi, lungs

 Nose
 External nose
 Nasal cavity
 Functions
 Passageway for air
 Cleans the air
 Humidifies, warms air
 Smell
 Along with paranasal
sinuses are resonating
chambers for speech
 Pharynx
 Common opening for
digestive and
respiratory systems
 Three regions
 Nasopharynx
 Oropharynx
 Laryngopharynx

 Functions
 Maintain an open passageway for air movement
 Epiglottis and vestibular folds prevent swallowed material
from moving into larynx
 Vocal folds are primary source of sound production

 Windpipe
 Divides to form
 Primary bronchi
 Carina: Cough reflex

 Conducting zone
 Trachea to terminal bronchioles which is ciliated for
removal of debris
 Passageway for air movement
 Cartilage holds tube system open and smooth muscle
controls tube diameter
 Respiratory zone
 Respiratory bronchioles to alveoli
 Site for gas exchange

Trachea (Windpipe)
Slide
 Connects larynx with bronchi
 Lined with ciliated mucosa
Beat continuously in the opposite direction of
incoming air
Expel mucus loaded with dust and other
debris away from lungs
 Walls are reinforced with C-shaped
hyaline cartilage

Primary Bronchi
Slide
 Formed by division of the trachea
 Enters the lung at the hilus
(medial depression)
 Right bronchus is wider, shorter,
and straighter than left
 Bronchi subdivide into smaller
and smaller branches

Lungs
Slide
 Occupy most of the thoracic cavity
Apex is near the clavicle (superior portion)
Base rests on the diaphragm (inferior
portion)
Each lung is divided into lobes by fissures
Left lung – two lobes
Right lung – three lobes

Coverings of the Lungs
Slide
 Pulmonary (visceral)
pleura covers the
lung surface
 Parietal pleura lines
the walls of the
thoracic cavity
 Pleural fluid fills the
area between layers
of pleura to allow
gliding

Respiratory Tree Divisions
Slide
 Primary bronchi
 Secondary bronchi
 Tertiary bronchi
 Bronchioli
 Terminal bronchioli

Bronchioles
Slide
 Smallest
branches of
the bronchi
 All but the smallest
branches have
reinforcing cartilage

Bronchioles
Slide
 Terminal
bronchioles
end in alveoli

Alveoli
Slide
 Structure of alveoli
Alveolar duct
Alveolar sac
Alveolus
Gas exchange occurs here.

Respiratory Membrane
(Air-Blood Barrier)
Slide
 Thin squamous epithelial layer lining
alveolar walls
 Pulmonary capillaries cover external
surfaces of alveoli
 The blood–air barrier (alveolar–
capillary barrier or membrane) exists in
the gas exchanging region of the lungs.
It exists to prevent air bubbles from
forming in the blood, and from blood
entering the alveoli.

Respiratory Membrane
(Air-Blood Barrier)
Slide

Events of Respiration
Slide
Pulmonary ventilation: O2 into lungs from inspired
air; CO2 out of lungs from expired air.
External respiration: Gas exchange between
alveoli and the capillaries.
Respiratory gas transport: Gasses are transported
in blood (via vessels) to tissues.
Internal respiration: Gas exchange between blood
and tissue cells in systemic capillaries
Cellular respiration.

Mechanics of Breathing
(Pulmonary Ventilation)
Slide
 Two phases
Inspiration – flow of air into lung
Expiration – air leaving lung

 Trachea lies in midline of neck
 Extends from vertebral level C6 in the lower
neck to vertebral level T4 in the mediastium
where it bifurcates into a right and left main
bronchus.

 Each lung is conical in shape
 It has:-
 APEX
 BASE
 THREE BORDERS
 TWO SURFACES

 APEX- it lies above the level of first rib. It
reaches 2-5 cm above the medial one third of
clavicle, just medial to supraclavicular fossa.
 BASE- rest on the diaphgram which seperates
the right lung from the right lobe of the liver
and the left lung from the left lobe of the liver,
fundus of stomach and the spleen.

 BORDERS
 ANTERIOR BORDER- right lung continues
running downwards till the 6th costochondral
junction.
 ANTERIOR BORDER- left lung continues
running downwards till the 4th costal cartilage
then curves laterally ½ inch forming the cardiac
notch then descends downwards till the 6th
costochondral junction.

 INFERIOR BORDER- Is sharp and seperates
the base from costal surface.
 POSTERIOR BORDER-Is rounded, thick and
lies beside the vertebral column.

SURFACES
 COASTAL SURFACE- lies immediately adjacent to the
ribs and intercostal spaces of the thoracic wall
 MEDIAL SURFACE- It is divided into two parts:
a) Anterior(mediastinal part): Contains a HILUM in the
middle(depression in which bronchi,vessels and nerves
forming the root of lungs.
b) Posterior(vertebral part): It is related to:
-bodies of thoracic vertebrae, IV discs, posterior
intercostal vessels.
 DIAPHRAGMATIC SURFACE

 LOBES
 The right lung have 3 lobes-
Upper, Middle and lower lobes
 The left lung have 2 lobes-
Upper and Lower lobes

 FISSURES
 OBLIQUE FISSURE: (right and left lung)
It starts at the 3rd thoracic spine while the arms
are elevated, decends downwards, laterally
and anteriorly along the medial border of the
scapula touching the inferior angle of scapula
cutting the midaxillary line in the 5th rib and
ending the 6th costal cartilage 3 inches from the
midline.

 HORIZONTAL FISSURES( right lung)
It follows the 4th intercostal space from the
sternum until it meets the oblique fissure as it
crosses the 5th rib.

 Completely mechanical process
 Depends on volume changes in the
thoracic cavity
 Volume changes lead to pressure
changes, which lead to the flow of
gases to equalize pressure

 Two phases
Inspiration – flow of air into lung
Expiration – air leaving lung

Inspiration
 Diaphragm and intercostals muscles
contract
 The size of the thoracic cavity increases
 External air is pulled into the lungs due to
an increase in intrapulmonary volume

1.
Sternocleidomast
oid muscles,
which lift upward
on the sternum
2. Anterior serrati,
which lift many of
the ribs
3. Scaleni, which lift
the first two ribs.

Exhalation
 Largely a passive process which depends
on natural lung elasticity
 As muscles relax, air is pushed out of the
lungs
 Forced expiration can occur mostly by
abdominal recti, which have the powerful
effect of pulling downward on the lower
ribs and internal intercostal muscles
depress the rib cage

Lung recoil It is due to Elastic recoil and surface tension.
Elastic recoil:
Elastic forces of the lung tissue it is determined mainly by
elastin and collagen fibers.
Surface tension:
It is the elastic tendency of a fluid surface which makes it
acquire the least surface area possible.
As the air inside the lungs is moist, there is considerable
surface tension within the tissue of the lungs. Because
the alveoli are highly elastic, they do not resist surface
tension on their own, which allows the force of that
deflate the alveoli as air is forced out during exhalation
by the contraction of the pleural cavity.

.
Surfactant: Reduces tendency of lungs to collapse
It is secreted by special surfactant-secreting
epithelial cells called type II alveolar epithelial
cells

Pleural fluid produced by pleural membranes
Acts as lubricant
Helps hold parietal and visceral pleural membranes together

The difference between the alveolar pressure and
the pleural pressure, this is called the
transpulmonary pressure.
 TPP can be measured by performing
oesophageal manometry
# Pneumothorax : In this an abnormal collection
of air in the pleural space between the lung and
the chest wall. https://www.hamilton-
medical.com/en_IN/Solutions/Transpulmona
ry-pressure-measurement.html
https://www.hamilton-medical.com/en_IN/Solutions/Transpulmonary-pressure-measurement.html

Measure of the ease with which lungs and
thorax expand
A lower-than-normal compliance means the lungs and
thorax are harder to expand

 Tidal volume : Volume of air inspired or expired
during a normal inspiration or expiration , Usually
500 millilitres in the adult male
 Inspiratory reserve volume: Amount of air
inspired forcefully after inspiration of normal tidal
volume , It is usually equal to about 3000 millilitres
• Expiratory reserve volume: Amount of air forcefully
expired after expiration of normal tidal volume It is
usually 1100 milliliters
• Residual volume: Volume of air remaining in
respiratory passages and lungs after the most
forceful expiration. It is usually 1200 milliliters.

All pulmonary volumes and capacities are about 20 to 25
percent less in women than in men, and they are greater in
large and athletic people than in small and asthenic
people.

 Inspiratory capacity: Tidal volume plus
inspiratory reserve volume (about 3500
milliliters)
 Functional residual capacity: Expiratory reserve
volume plus the residual volume (about 2300
milliliters)
 Vital capacity: Sum of inspiratory reserve
volume, tidal volume, and expiratory reserve
volume (about 4600 milliliters)
 Total lung capacity: Sum of all volume (about
5800 milliliters)

 Minute ventilation:Total amount of air moved into
and out of respiratory system per minute
 Respiratory rate or frequency: Number of breaths
taken per minute. It is about 12 breaths per
minute.
 Anatomic dead space: It is the total volume of
the conducting airways from the nose or mouth
down to the level of the terminal bronchioles,
and is about 150 ml on the average in humans.
 Alveolar ventilation: How much air per minute
enters the parts of the respiratory system in which
gas exchange takes place

One of the most important
problems in all the respiratory
passageways is to keep them
open and allow easy
passage of air to and from the
alveoli.
multiple cartilage rings
less extensive curved cartilage
plates
The bronchioles are not prevented
from collapsing by the rigidity of
their walls. Instead, they are kept
expanded mainly by the same
transpulmonary pressures that
expand the alveoli

In addition to keeping the surfaces
moist, the mucus traps small
particles out of the inspired air and
keeps most of these from ever
reaching the alveoli. These particles
are either swallowed or coughed to
the exterior.
200 cilia on each epithelial cell
Cilia beat continually at a rate of 10 to 20 times per
secondcilia in the lungs beat upward, whereas those in the nose beat
downward.

 The bronchi and trachea are so sensitive to light touch
that very slight amounts of foreign matter or other
causes of irritation initiate the cough reflex
Sneeze Reflex
The sneeze reflex is like the cough reflex, except that
it applies to the nasal passageways instead of the
lower respiratory passages. The initiating stimulus of
the sneeze reflex is irritation in the nasal
passageways.

 In respiratory physiology, one deals with
mixtures of gases, mainly of oxygen, nitrogen,
and carbon dioxide.
 The rate of diffusion of each of these gases is
directly proportional to the pressure caused by
that gas alone, which is called the partial
pressure of that gas.

 Diffusion of gases through the respiratory membrane
 Depends on membrane’s thickness,
 the diffusion coefficient of gas,
 surface areas of membrane,
 partial pressure of gases in alveoli and blood
 Relationship between ventilation and pulmonary capillary
flow
 Increased ventilation or increased pulmonary capillary
blood flow increases gas exchange
 Physiologic shunt is deoxygenated blood returning from
lungs

Oxygen is transported by hemoglobin (98.5%)
and is dissolved in plasma (1.5%)
Oxygen-hemoglobin dissociation curve shows
that hemoglobin is almost completely saturated
when P02 is 80 mm Hg or above. At lower
partial pressures, the hemoglobin releases
oxygen.
A shift of the curve to the left because of an
increase in pH, a decrease in carbon dioxide, or
a decrease in temperature results in an increase
in the ability of hemoglobin to hold oxygen

The substance 2.3-bisphosphoglycerate
increases the ability of hemoglobin to

In lung capillaries, bicarbonate ions and
hydrogen ions move into RBCs and
chloride ions move out. Bicarbonate ions
combine with hydrogen ions to form
carbonic acid. The carbonic acid is
converted to carbon dioxide and water.
The carbon dioxide diffuses out of the
RBCs.
Increased plasma carbon dioxide lowers
blood pH. The respiratory system
regulates blood pH by regulating plasma
carbon dioxide levels

 Normal rate of respiration in adults is 12-16/min
,with tidal volume of 500ml.This rate and depth
of respiration i.e total pulmonary ventilation can
be adjusted to the requirements of the body.
 The size of thorax is altered by the action of the
respiratory muscles ,which contract as a result of
nerve impulses transmitted to them from centers
in the brain and relax in absence of nerve
impulses.
 These nerve impulses are sent from clusters of
neurons located bilaterally in the medulla
oblongata and pons of the brain stem .This
widely dispersed group of neurons collectively
called the respiratory center .

 This rhythmic discharge from the brain that
produces spontaneous respiration is regulated
by 2 mechanisms:-
1) NERVOUS REGULATORY MECHANISM
2) CHEMICAL REGULATORY MECHANISM

 TWO SYSTEM:-
 AUTOMATIC CONTROL :Medullary
rhythmicity area in the medulla oblongata.
 Pneumotaxic area in pons.
 Apneustic area in pons .
 VOLUNTARY CONTROL : via cerebral cortex .

 Composed of neurons in medullary rhythmic
area(MRA)in medulla oblongata, pneumatoxic
& apneustic area in pons.
 MRA (Medullary rhythmic area) located in
ventrolateral medulla overlying olivary
nucleus .There are two types of respiratory
neuron I and E neuron.

Function of MRA to control basic rhythm of
respiration .
Inspiratory & expiratory area within MRA
During quiet breathing inhalation lasts for about 2sec
and exhalation for about 3 sec .
Nerve impluse generated in inspiratory area
Establish basic rhythm of breathing
Active insp. area generate nerve impluse for about 2
sec .
Impluse propogated to ext IC muscles via IC nerve
and diagram via phrenic nerve

 When nerve impluse reach diaphragm and ext
IC muscles muscle contract and inhalation
occur .
 At the end of 2sec insp. area become inactive
nerve impulse ceases with no impulse
arriving daiphragm and ext.IC muscles relax for
about 3 sec ,allowing passive elastic recoil of lung
,thoracic wall and the cycle repeats .

 Neurons in exp. Area remain inactive during
quiet breathing .However during forceful
breathing nerve impulse from insp.area
activate the exp.area.
 Impulses from the exp. area cause contarction
of int.IC muscle and abdominal muscle which
decrease size of thoracic cavity and causes
forceful exhalation .

 Help to coordinate transition between inhalaton
and exhalation ( in upper pons ) .Transmit
inhibitory impulses to inspiratory area.These
impulses shorten the duration of inhalation .When
the pneumotaxic area is more active ,breathing rate
is more rapid.
APNEUSTIC AREA
 This is in lower pons. This sends stimulatory
impulses to the inspiratory area that activate and
prolong inhalation .The result is long deep
inhalation.
 When pneumotaxic area is active ,it overrides
signal from the apneustic area.

 Cerebral cortex has connections with respiratory
center, we can voluntarily alter our pattern of
breathing .We can refuse to breathe for short
period of time.
 Voluntary control is protective as it enables us to
prevent water or irritating gases entering from
lungs.This ability to not to breathe is limited by the
build up of CO₂ and H⁺ in the body.
 When Pco₂ and H⁺ conc. Increase to a certain level ,the
inspiratory area is strongly stimulated , nerve impluses
are sent along phrenic and IC nerves to respiratory
muscles ,and breathing resumes.

 Some chemical stimuli modulate how quickly
and deeply we breathe.The respiratory system
functions to maintain proper levels of CO₂ and
O₂ and is very responsive to changes in the levels of
these gases in body fluids .
 There are some sensory neurons that are
responsive to chemicals called chemoreceptors
.Chemoreceptors in 2 locations monitor levels of
CO₂,H⁺,O₂ and provide input to respiratory center .

 2 types of chemoreceptors :-
 CENTRAL CHEMORECEPTORS :-Are located
near medulla oblongata in CNS.They respond
to changes in H⁺ conc. Or pCO₂ or both in CSF .
 PERIPHERAL CHEMORECEPTORS :-Are located in the
aortic bodies( clusters of chemoreceptors located in
the wall of the arch of aorta ) and cartoid bodies
(oval nodules in the wall of the left and right
common carotid arteries .These are part of PNS and
are sensitive to changes in Po₂,H⁺,Pco₂ in blood .
 Axons of sensory neurons from the aortic bodies
are part of the vagus nerve and those of carotid
bodies are part of right and left glosdopharyngeal
nerves.

 Normally ,Pco₂ in arterial blood is 40 mmHg .Slight
increase in it cause condition called hypercarbia or
hypercapina. Central chemoreceptors are
stimulated by both high Pco₂ and the rise in H ⁺.
 When Po₂ in arterial blood falls from normal level of
100mmHg but is still above 50mmHg ,peripheral
chemoreceptors are stimulated .Deficiency of O₂
depresses activity of central chemoreceptors and
inspiratory area which then don’t respond to any input
and send fewer impulses to muscles of inhalation .As a
result breathing rate decreases.

 Chemoreceptors participate in a negative feedback
that regulates level of CO₂,O₂ and H⁺in blood ,as a
result of increased H⁺ ,Pco₂ input from the central and
peripheral chemoreceptor causes inspiratory area to
become highly active .Rate and depth of breathing
increases called hyperventilation, allows the inhalation
of more O₂ and exhalation of more CO₂ until level of
Pco₂ and H⁺ are lowered to normal.
 If arterial Pco₂ is lower than 40mmHg – hypocapnia
and hypocarbia, both the chemoreceptor are not
stimulated therefore impulses are not sent to
inspiratory area.As a result the area sets to it own pace
until CO₂ accumulates and rises above 40 mmHg .The
inspiratory area is stimulated more strongly when Pco₂
level rises above normal and Po₂ fall below normal.

 EXERCISE rate and depth of breathing ,even
before changes in Po₂,Pco₂,H⁺level occur.
 Main stimulus for these changes is input from
propiroceptors which mointor movement of joint
and musles nerve impulse from propiroceptors
stimulate inspiratory area of the medulla oblongata.
 At same time axon collateral of UMN that originate
in primary motor cortex also feed exctitatory
response to inspiratory area.

 Recent advances have clarified how the brain
detects CO₂to regulate breathing (central respiratory
chemoreception ).These mechanism are reviewed and
their significance is presented in the general context of
CO₂/pH homeostasis via breathing .
 At rest resp. chemoreflexes initiated at peripheral and
central sites mediate rapid stabilization of arterial
PCO₂and PH .
 Specific brainstem neurons ( retrotrapezoid
nucleus,serotonergic ) are activated by PCO₂ and
stimulate breathing .

 RTN neurons detect CO₂via intrinsic proton
receptors ,synaptic input from peripheral
chemoreceptors and signals from astrocytes .
 Respiratory chemoreflexes are arousal state
dependent whereas chemoreceptor stimulation
produces arousal .
 When abnormal these interactions lead to sleep
disorderd breathing .During exercise ,” central
command “ and reflexes from exercising muscles
produce the breathing stimulation required to
maintain arterial PCO₂ and ph despite elevated
metabolic activity .

 New advances in the neural control of
breathing.
 This issue contain 3 review articles based on
talks given as part of a symposium entitled
“New Advances in the neural control of
breathing “ took place during the 1st pan
American congress of Physiological sciences
on 3 aug 2014 by Brazilian society of
physiology and sponsored by “The Journal of
Physiology “.

 AIM: To discuss cellular and molecular
mechanism by which the brain control
breathing .
 TOPIC: Includes:-
 Network basis of respiratory rhythmogenesis
by pre botzinger complex.
 Role of purinergic signalling in central and
peripheral chemoreception .
 Role of serotonergic raphe neurons in control
of breathing .

 The next caudal segment of the VRC, the Bötzinger
complex, contains GABAergic expiratory neurons which
modulate respiratory rhythm . The next most rostral region
is the pre-BötC; neurons in this region form the core
respiratory rhythm-generating circuit and relay this
inspiratory drive to more rostral premotor populations that
control breathing. Finally, the rostral and caudal segments
of the VRG contain premotor neurons dedicated to the
control of inspiratory and expiratory activities, respectively.
 The authors propose that respiratory rhythm generation by
the pre-BötC is not dependent on intrinsic pacemaker
.Specifically, they suggest that pre-inspiratory ‘burstlets’
produced by the convergent activity of a few neurons can
produce a subthreshold rhythm that is translated into an
inspiratory burst by a recurrently connected network of
excitatory preBötC neurons. These exciting new insights
will enhance our understanding of mechanisms underlying
respiratory rhythmogenesis, and in a broader context, may
provide useful insight into the complex underpinnings of
other rhythmic microcircuits.

 The review by Moreira and colleagues entitled
‘Independent purinergic mechanisms of central and
peripheral chemoreception in the rostral ventrolateral
medulla.’ describes the role of purinergic signalling at
the level of the ventrolateral medulla in coordinating
cardiorespiratory responses to hypoxia and
hypercapnia by activating RTN chemoreceptors and
presympathetic neurons. In the context of central
chemoreception, evidence suggests that RTN astrocytes
respond to high CO₂ by releasing ATP via 26
hemichannels . This purinergic signal up-regulates the
activity of local RTN chemoreceptors and contributes
to the ventilatory response to CO₂. The authors also
describe the contribution of purinergic signalling to
peripheral chemoreceptor modulation of breathing and
blood pressure by a P2Y1-receptor-dependent
mechanism.

The review by Mulk and colleagues entitled
‘Molecular underpinnings of ventral surface
chemoreceptor function: focus on KCNQ channels’
describes key regulators of intrinsic excitability of
RTN chemoreceptors .They summarize evidence
suggesting that KCNQ channels regulate the activity
of RTN chemoreceptors. They also put forth a model
where KCNQ and TASK-2 channels work together to
limit activity under control conditions and during
activation by high CO2/H+. Considering that
respiratory failure is thought to be an underlying
cause of sudden unexplained death in epilepsy
(SUDEP), and since KCNQ channels regulate the
activity of neurons that control breathing and loss of
function mutations in certain KCNQ channels can
cause certain types of epilepsy, the authors propose
that KCNQ channels represent a common substrate
for epilepsy and respiratory problems.

•Pulmonary function tests are a
group of tests that measure how
well the lung works i.e., how well
your lungs take in and release air
and how well they move oxygen
into the blood.

 Compare your lung function with known standards
that show how well your lungs should be working.
 Measure the effect of chronic diseases like asthma,
chronic obstructive pulmonary disease (COPD), or
cystic fibrosis on lung function.
 Identify early changes in lung function that might show
a need for a change in treatment.
 Detect narrowing in the airways.
 Decide if a medicine (such as a bronchodilator) could be
helpful to use.
 Show whether exposure to substances in your home or
workplace have harmed your lungs.
 Determine your ability to tolerate surgery and medical
procedures.

 Pediatric neuromuscular disorder such
as Duchenne muscular Dystrophy.
 Musculoskeletal deformities such as
kyphoscoliosis (contribute to restrictive lung
disease)
 Chronic dyspnoea
 Asthma
 Chronic obstructive pulmonary disease (COPD)
 Restrictive lung disease
 Preoperative testing

 Recent eye surgery
 Thoracic , abdominal and cerebral aneurysms
 Active hemoptysis
 Pneumothorax
 Unstable angina/ recent MI within 1 month

Standard PFTs include:
 Spirometry
 Lung volumes
 Diffusion capacity

 Spirometry (meaning the measuring of breath) is the most
common of the pulmonary function tests (PFTs),
measuring lung function, specifically the amount
(volume) and/or speed (flow) of air that can be inhaled
and exhaled.
 The most common parameters measured in spirometry
are
1. Vital capacity (VC),
2. Forced vital capacity (FVC),
3. Forced expiratory volume (FEV) at timed intervals of 0.5,
1.0 (FEV1), 2.0, and 3.0 seconds,
4. Forced expiratory flow 25–75% (FEF 25–75) and
5. Maximal voluntary ventilation (MVV)

• In a spirometry test, you breathe into a mouthpiece
that is connected to an instrument called a spirometer.
The spirometer records the amount and the rate of air
that you breathe in and out over a period of time. The
primary signal measured in spirometry may be volume
or flow.
• The test effort can be presented as a ‘flow-volume
loop’ or as a ‘volume-time curve’.
 Normal values vary and depend on:
 height – directly proportional
 age – inversely proportional
 gender
 ethnicity

1. No coughing: especially during first second of FVC
2. Good start of test: <5% of FVC exhaled prior to a
max expiratory effort. (<5% extrapolation)
3. No early termination of expiration: exhalation time
of six seconds or a plateau of 2 seconds
4. No variable flows: flow rate should be consistent
and as fast as possible throughout exhaled VC
5. Good reproducibility or consistency of efforts: 2
best FVC's and 2 best FEV1's should agree within
5% or 100 ml (whichever is greatest)

 Place the nose clip.
 Have patient seated comfortably
 Have patient take a deep breath (inspiration) as
fast as possible.
 Place the spirometer on mouth (should be
sealed within the lips),blow out as hard as they
can until you tell them to stop.(expiration)

 Flow volume loops provide a graphical
illustration of a patient's spirometric efforts.
Flow is plotted against volume to display a
continuous loop from inspiration to expiration.
The overall shape of the flow volume loop is
important in interpreting spirometric results

(A) Normal. Inspiratory limb
of loop is symmetric and
convex. Expiratory limb is
linear. Flow rates at the
midpoint of the inspiratory
and expiratory capacity are
often measured. Maximal
inspiratory flow at 50% of
forced vital capacity (MIF
50%FVC) is greater than
maximal expiratory flow at
50% FVC (MEF 50%FVC)
because dynamic compression
of the airways occurs during
exhalation.

(B) Obstructive disease
(e.g, emphysema,
asthma). Although all
flow rates are diminished,
expiratory prolongation
predominates, and MEF <
MIF. Peak expiratory flow
is sometimes used to
estimate degree of
airway obstruction but is
dependent on patient
effort.

(C) Restrictive disease (eg,
interstitial lung disease,
kyphoscoliosis). The loop is
narrowed because of
diminished lung volumes, but
the shape is generally the
same as in normal volume.
Flow rates are greater than
normal at comparable lung
volumes because the
increased elastic recoil of
lungs holds the airways open.

(D) Fixed obstruction of
the upper airway (eg,
tracheal stenosis). The
top and bottom of the
loops are flattened so
that the configuration
approaches that of a
rectangle. Fixed
obstruction limits flow
equally during
inspiration and
expiration, and MEF =
MIF.

(E) Variable extrathoracic
obstruction (eg, unilateral
vocal cord paralysis, vocal
cord dysfunction).
When a single vocal cord is
paralyzed, it moves
passively with pressure
gradients across the glottis.
During forced inspiration, it
is drawn inward, resulting in
a plateau of decreased
inspiratory flow. During
forced
expiration, it is passively
blown aside, and expiratory
flow is unimpaired.
Therefore, MIF 50%FVC <
MEF 50%FVC.
Expiratory
flow
unimpaire
d

 Asthma and COPD have many similarities and can
occur together in the same patient.
 The major difference between asthma and COPD is
that airflow obstruction is largely reversible in
asthma, but in COPD it is largely irreversible.
 When spirometry shows an obstructive pattern, it
is important to establish whether the obstruction is
reversible.
 In order to establish the diagnosis, reversibility
should be tested with both short- acting
bronchodilators and corticosteroids (when FEV1 is
less than 60% of the predicted value).

 The reversibility test is as follows:
 Spirometry test ( with at least two reproducible
flow-volume loops)
 Intake of a fast acting bronchodilator (often
salbutamol) thorough inhalation.
 15 minutes pause.
 A second spirometry test (with at least two
reproducible flow-volume loops)
 A positive response is demonstrated by:
 FVC increase >10%
 FEV1 increase of 200ml or 15% over baseline

FEV1 FVC FEV1/ FVC
NORMAL > 80% of predicted > 80% of predicted >70% of predicted
OBSTRUCTUVE Decreased:
•Close to 80
Borderline
•65-79 Mild
•50-64 Moderate
•< 50 severe
Normal Decreased (<70%)
RESTRICTIVE Normal or
decreased
Decreased:
•Close to 80
Borderline
•65-79 Mild
•50-64 Moderate
•< 50 severe
Normal or increased

 The diffusing capacity of the lungs (DL)
estimates the transfer of oxygen from alveolar
gas to red blood cells.

 The amount of oxygen transferred is largely
determined by three factors:
 One factor is the area (A) of the alveolar–capillary
membrane, which consists of the alveolar and capillary
walls. The greater the area, the greater the rate of
transfer and the higher the DL. Area is influenced by
the number of blood-containing capillaries in the
alveolar wall.
 The second factor is the thickness (T) of the membrane.
The thicker the membrane, the lower the DL.
 The third factor is the driving pressure, that is, the
difference in oxygen tension between the alveolar gas
and the venous blood (∆PO2). Alveolar oxygen tension
is higher than that in the deoxygenated venous blood
of the pulmonary artery. The greater this difference
(∆PO2), the more oxygen transferred.

 Measuring the diffusing capacity of carbon
monoxide (DLCO) provides a valid reflection of
the diffusion of oxygen.
 The subject exhales to residual volume and then
inhales a gas mixture containing a very low
concentration of carbon monoxide (CO) plus an
inert gas, usually helium. After a maximal
inhalation, the patient holds his or her breath for
10 seconds and then exhales completely. During
the breath hold, CO is absorbed while helium is
equilibrating with alveolar gas. A sample of
exhaled alveolar gas is collected and analyzed.

 LOW DLCO (<80% predicted)
Causes:
EMPHYSEMA ,
INTERSTITIAL LUNG DISEASE ,
PULMONARY HYPERTENSION ,
PULMONARY EMBOLISM ,
PULMONARY EDEMA ,
RIGHT TO LEFT SHUNT TOF,
ANAEMIA .
 HIGH DLCO( >120-140%
predicted)
Causes:
ASTHMA,
POLYCYTHEMIA ,
LEFT TO RIGHT SHUNT:
Ventricular septal defect (VSD)
Patent ductus arteriosus (PDA)
Atrial septal defect (ASD),
OBESITY,
PULMONARY HEMORRHAGE .

 Lung volumes can be measured by:
 Helium dilution method
 Nitrogen washout method
 Body plethysmography

 Nitrogen washout (or
Fowler’s method) is a test
to measure the anatomic
dead space in the lung
during a respiratory
cycle, as well as some
other parameters related
to closure of airways.
 A nitrogen washout can
be performed with a
single nitrogen breath, or
multiple ones. Both tests
can estimated the
functional residual
capacity (FRC)

 The subject breathes 100% oxygen, and all the
nitrogen in the lungs is washed out.
 The exhaled volume and the nitrogen concentration
in that volume are measured by analyzer.
 The difference in nitrogen volume at the initial
concentration and at the final exhaled concentration
allows a calculation of intrathoracic volume, usually
FRC.
 Most people with normal distribution of airway
resistances will reduce their expired end-tidal
nitrogen concentrations to less than 2.5% within
seven minutes.

• The helium dilution technique is a way to measure
the functional residual capacity (FRC) of the lungs.
• This technique is a closed circuit system where a
spirometer is filled with a mixture of helium and
oxygen. The amount of helium in the spirometer is
known at the beginning of the test.
(concentration x volume = amount)
• The subject is asked to breathe (normal breaths) in
the mixture starting from FRC, which is the gas
volume in the lung after a normal breath out.

 The spirometer measures the helium concentration.
 Because there is no leak of substances in the system,
the amount of helium remains constant during the
test, and the FRC is calculated using the following
equation:
C1 x V1 = C2 x V2
C1 x V1 = C2 x (V1+FRC)
FRC= ((C1 x V1)/C2) – V1
Where, V2= total gas volume (FRC+ volume of
spirometer)
V1= volume of gas in spirometer
C1= initial (unknown) concentration of helium
C2= final concentration of helium (measured by spirometer).

 Body plethysmography is a test to find out how much air is
in your lungs after you take in a deep breath, and how much
air is left in your lungs after breathing out as much as you
can.
 Based on principle of BOYLE’S LAW(P*V=k)
 Principle advantage over other two method is it quantifies
non‐ communicating gas volumes.

 The subject is placed inside a sealed chamber with a
single mouthpiece.
 At the end of normal expiration, the mouthpiece is
closed. The subject is then asked to make an inspiratory
effort.
 As the subject tries to inhale, the lungs expand,
decreasing pressure within the lungs and increasing lung
volume.
 This, in turn, increases the pressure within the box since
it is a closed system and the volume of the box
compartment has decreased to accommodate the new
volume.
 Boyles law is used to calculate the unknown volume
within the lungs.

It is a diagnostic procedure in which a blood is obtained from an
artery directly by an arterial puncture or accessed by a way of
indwelling arterial catheter.

 ABG analysis is one of the first tests ordered to assess
respiratory status because it helps evaluate gas
exchange in the lungs.
 An ABG test can measure how well the person's lungs and
kidneys are working and how well the body is using
energy.
 It measures the acidity (pH) and the levels of oxygen
and carbon dioxide in the blood from an artery. This test
is used to check how well your lungs are able to move
oxygen into the blood and remove carbon dioxide from
the blood.

 Respiratory failure - in acute and chronic states.
 Any severe illness which may lead to a metabolic acidosis
- for example:
 Cardiac failure.
 Liver failure.
 Renal failure.
 Hyperglycaemic states associated with diabetes
mellitus.
 Multiorgan failure.
 Sepsis.
 Burns.
 Poisons/toxins.
 Ventilated patients.
 Sleep studies.

 An arterial blood gas (ABG) test is done to:
 Check for severe breathing problems and lung
diseases, such as asthma, cystic fibrosis, or chronic
obstructive pulmonary disease (COPD).
 See how well treatment for lung diseases is working.
 Find out if you need extra oxygen or help with
breathing (mechanical ventilation).
 Find out if you are receiving the right amount of
oxygen when you are using oxygen in the hospital.
 Measure the acid-base level in the blood of people
who have heart failure, kidney failure,
uncontrolled diabetes, sleep disorders, severe
infections, or after a drug overdose.

 Overlying infection or burn at insertion site.
 Absence of collateral circulation.
 Synthetic graft.
SITES
 Preferred site-Radial and femoral artery.
 Less common-Dorsalis pedis and post tibial artery.
 Avoid – artery without collateral supply.

Arterial blood can be obtained by direct arterial puncture most usually at
the wrist (radial artery) as it is easy to palpate and has a good collateral
presentation. Alternatives to the radial artery include the femoral and
brachial artery. It is important to ensure good collateral circulation as
there is a theoretical risk of thrombus occlusion.
 If the radial artery is to be used, perform Allen's test to confirm
collateral blood flow to the hand.
 Allen's test
 Elevate the hand and make a fist for approximately 30 seconds.
 Apply pressure over the ulnar and the radial arteries occluding both
(keep the hand elevated).
 Open the hand which will be blanched.
 Release pressure on the ulnar artery and look for perfusion of the
hand (this takes under eight seconds).
 If there is any delay then it may not be safe to perform radial artery
puncture.

 The patient's arm is placed palm-up on a flat
surface, with the wrist dorsiflexed at 45°. A towel
may be placed under the wrist for support. The
puncture site should be cleaned with alcohol or
iodine, and a local anaesthetic should be infiltrated.
 Local anaesthetic makes arterial puncture less
painful for the patient. The radial artery should be
palpated for a pulse, and a pre-heparinised syringe
with a 23 or 25 gauge needle should be inserted at
an angle just distal to the palpated pulse.A small
quantity of blood is sufficient. If repeated arterial
blood gas analysis is required, it is advisable to use a
different site (such as the other radial artery) or
insert an arterial line.

 Bleeding at the puncture site.
 Blood flow problems at puncture site (rare).
 Bruising at the puncture site.
 Delayed bleeding at the puncture site.
 Fainting or feeling light-headed.
 Hematoma (blood accumulating under the skin).
 Infection (a slight risk any time the skin is broken).

 PH:
measures hydrogen ion concentration in the blood, it shows
blood’ acidity or alkalinity
 PCO2 :
It is the partial pressure of CO2 that is carried by the blood
for excretion by the lungs, known as respiratory parameter
 PO2:
It is the partial pressure of O2 that is dissolved in the blood ,
it reflects the body ability to pick up oxygen from the lungs
 HCO3 :
known as the metabolic parameter, it reflects the kidney’s
ability to retain and excrete bicarbonate

 PH = 7.35 – 7.45
 PCO2 = 35 – 45 mmhg
 PO2 = 80 – 100 mmhg
 HCO3 = 22 – 26 meq/L

 The following indices should be looked at in the following
order :
 Blood pH - high indicates alkalosis, low indicates acidosis
and normal indicates either normal, mixed defect or a
compensated defect.
 PaCO2 level - is it a respiratory problem? If not, look at
the bicarbonate level. High PaCO2 with an acidosis
indicates a respiratory problem. If the PaCO2 is normal
or low it indicates compensation.
 Bicarbonate - if the bicarbonate fits with the pH it
suggests a primary metabolic problem. If not, it
indicates compensatory changes.
 Look for any compensation - eg, low PaCO2 in severe
metabolic acidosis.
 Anion gap in metabolic acidosis
 O2 level - is hypoxaemia present?

 It is possible to have a mixed respiratory and
metabolic disorder that makes interpretation of an
arterial blood gas result difficult. As a general rule,
when a normal pH is accompanied by an abnormal
PaCO2 or HCO3ˉ then a mixed metabolic-
respiratory disorder exists. (Table) provides some
common clinical examples of mixed respiratory and
metabolic disturbances.

Disorder Characteristics Selected situations
Respiratory acidosis with
metabolic acidosis
↓in pH
↓ in HCO3
↑ in PaCO2
•Cardiac arrest
•Intoxications
•Multi-organ failure
Respiratory alkalosis with
metabolic alkalosis
↑in pH
↑ in HCO3-
↓ in PaCO2
•Cirrhosis with diuretics
•Pregnancy with vomiting
•Over ventilation of COPD
Respiratory acidosis with
metabolic alkalosis
pH in normal range
↑ in PaCO2,
↑ in HCO3-
•COPD with diuretics, vomiting, NG suction
•Severe hypokalemia
Respiratory alkalosis with
metabolic acidosis
pH in normal range
↓ in PaCO2
↓ in HCO3
•Sepsis
•Salicylate toxicity
•Renal failure with CHF or pneumonia
•Advanced liver disease
Metabolic acidosis with
metabolic alkalosis
pH in normal range
HCO3- normal
•Uremia or ketoacidosis with vomiting, NG
suction, diuretics, etc.

 Alveolar-arterial oxygen gradient - (A-a)pO2;
difference in oxygen partial pressures between the
alveolar and arterial side.It provides a measure of
oxygen diffusion across the alveoli into the blood.
Thus, will be impaired in lung disease such as
COPD. Raised (A-a)pO2 may also represent the
presence of an intrapulmonary shunt, ie a lung that
is perfused but not ventilated - for example,
pneumonia.

 The anion gap is the difference in the
measured cations (positively charged ions) and the
measured anions (negatively charged ions)
in serum, plasma, or urine.
 Anion gap can be classified as either high, normal or, in
rare cases, low.
 A high anion gap indicates acidosis.
 A low anion gap is frequently caused by hypoalbuminemia.
 Usually done when primary metabolic acidosis is
suspected. Anion gap helps determine the etiology of
the metabolic acidosis.
 Normal=10-18mmol/L

Respiratory system, physiology of respiratory system and neural control

Respiratory system, physiology of respiratory system and neural control

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