RSS MODULE

Respiratory system

1 
 Objectives
❖ Describe
✓ Embryological development of tracheobronchial tree & lung
✓ Tracheobronchial tree & pleura (layers, recess, surface &
applied anatomy)
❖ Mention parts of respiratory system.
❖ Mention cells of respiratory epithelium
❖ Describe Histological structure of trachea, bronchi
❖ Enumerate parts of respiratory portion & lining epithelium of
each part.
❖ Compare between type I pneumocyte& type II pneumocyte
❖ Describe blood air barrier, lung macrophage, pleura& fetal lung.
❖ Describe
✓ Lungs (external morphology, lobes, fissures, surface anatomy,
segments& blood and nerve supply)
✓ Diaphragm (attachments, major foramina, nerve supply&
action)
✓ Course& distribution of the two phrenic nerves
❖ Describe functional structure of respiratory system
❖ Describe basic principles of respiratory functions tests
❖ Discuss
- surfactant
- Pneumothorax
- Factors affecting diffusion of respiratory membrane
- Hypoxia& cyanosis
- Mention factors affecting increased barometric pressure

2 
 Index

Topics Page No
Embryological development of tracheobronchial 4
tree & lung
Tracheobronchial Anatomy 5
tree Histology 6
The pleura 11
The lung 13
Diaphragm& the phrenic nerve 20
Respiratory portion 21
Lung function 26
Respiratory pressure 28
Compliance 33
The work of breathing 34
Dead space 35
Respiratory functions of blood 36
Control of respiration 47
Regulation of respiration 50
Hypoxia 57
Cyanosis 61
Effects of increase barometric pressure 62

3 
 Trachea and bronchi

4 
 EMBRYOLOGICAL DEVELOPMENT OF TRACHEOBRONCHIAL TREE AND
LUNGS

➢ The endoderm of the cranial part of foregut forms a groove, which will soon
convert into a tube (laryngotracheal tube) which develops into the lining of the
larynx, trachea and divides caudally into two bronchi
➢ The splanchnic mesoderm around will form vessels, cartilages and connective
tissue of their walls. While the mesoderm of the pharyngeal arches develops
into the muscles of the larynx.
➢ Each bronchus becomes surrounded by splanchnic mesoderm called lung buds
which repeatedly divide to form the lungs. The alveoli start formation at the
last trimester of pregnancy and continues after birth.
Congenital anomalies:
• Agenesis of one or both lungs
• Abnormal lobulation of the lung: due to abnormal branching. It may show
a missing or extra lobes.
• Tracheoesophageal fistula: due to incomplete formation of laryngotracheal
tube.
• Congenital lung cysts: due to incomplete dilatation of some bronchi
TRACHEA

❖ It is 12 cm long and 12 mm in diameter.

❖ It shows C shaped cartilages in its wall to keep it open.
❖ It begins at C6 vertebra and ends at T4 vertebra by dividing into 2 bronchi (Rt
& Lt).

BRONCHI

Rt bronchus Lt bronchus
Short (2.5 cm) Long (5 cm)
Wide Narrow
More vertical More horizontal
Divide into 2 bronchi before entering the
lung
1) Sup lobe (eparterial) bronchus Divide inside the lung
2) Rt main (middle & inf lobe or
hyparterial)
Accordingly, the foreign body is more commonly lodged in Rt than Lt bronchus.

5 
 II- Histology

Respiratory system According to function it is divided into:

Conducting Portion Respiratory Portion
(Transports air) (Gas exchange)
1. Nasal cavity 2. Pharynx 1. Respiratory bronchioles
3. Larynx 4. Trachea 2. Alveolar ducts
5. Bronchi 6. Bronchioles 3. Alveolar sacs & alveoli
7. Terminal bronchioles.

Conducting Portion

This part is lined by respiratory epithelium.

❖ The Respiratory epithelium:
• It is pseudostratified columnar ciliated with goblet cells.
• It lines most of the conductive portion of respiratory system.
• It consists of 5 types of cells.
1-Ciliated columnar cells
• The most abundant type.
• Each cell has about 300 cilia.
• Beneath the cilia, are numerous small mitochondria that supply
ATP for ciliary beating.
• The cilia move the mucus and its trapped particles toward the
nasopharynx.
2-Goblet cells
• The next most abundant cells.
• Form & secrete mucous.
3-Brush cells:
• Columnar cells with numerous microvilli on their apical surface.
• They have afferent nerve endings on their basal surfaces and are
sensory receptors.
4-Basal (short) cells :
• Small pyramidal cells that lie on the basal lamina not reach to surface.
• These cells are stem cells that replace the other cell types.

6 
 1- DNES cells (small granule cells):
• Columnar cells with basal dense granules.
• Belong to the diffuse neuroendocrine system.
• Secrete catecholamine and serotonin.

Ciliated columnar cells

ccolumnared columnar

Goblet cell

Basal cells

❖ Trachea and extrapulmonary (primary) bronchi:

1- Mucosa formed of:
a) The respiratory epithelium.
b) The lamina propria is a thin layer of
connective tissue.
c) Elastic membrane separating the lamina
propria from the submucosa.
2- The submucosa is a connective tissue layer
containing many seromucous glands.
3-C-shaped hyaline cartilage: Smooth muscle
extends between the open ends.
4-The adventitia: A layer of C T.

7 
Extrapulmonary bronchus divides in the lung into intrapulmonary bronchi→
primary bronchioles→ terminal bronchioles→ respiratory bronchioles→
alveolar ducts → alveoli.

P.O.C Extra pulmonary Intrapulmonary bronchus

bronchus
Lumen Wide Folded & narrow
Mucosa:
• Epithelium • pseudostratified • Same but with less
columnar ciliated with goblet cells
many goblet cells
• Elastic membrane • Present • Absent
Submucosa Present Absent
Cartilage C shaped Multiple plates
Smooth ms Between two ends of Spirally arranged under
cartilage mucosa
Mucoserous In submucosa In adventitia
glands& lymph f.

❖ Primary bronchioles
• Primary bronchioles have a diameter of 1 millimeter (mm) or less.
• The wall consists of:
1. Mucosa: simple columnar ciliated with Clara cells. Cilia
gradually decrease as the bronchiole gets smaller.

Clara cells:
• Tall, dome-shaped, nonciliated cells.
• Possess numerous secretory granules whose contents aid in
lowering surface tension of the terminal bronchioles.
• They metabolize airborne toxins.
• Clara cells divide& differentiate to form ciliated cells.
2. Musculosa: circularly arranged smooth muscle.
3. Adventitia: Connective tissue.
❖ Terminal bronchioles
• They have a diameter of less than 0.5 mm.
They are lined by a simple cubical epithelium (some are ciliated) with many
Clara cells.

8 
 •
P.O.C Intrapulmonary bronchus Bronchiole
Types Primary: diameter 1mm or less
Terminal: diameter < 0.5 mm
Mucosa: • pseudostratified columnar • Simple columnar ciliated or
• Epithelium ciliated cubical with Clara cells. Cilia
• few goblet cells gradually decrease as the
bronchiole gets smaller &Clara
cells increase.
• No goblet cells
Musculosa Spirally arranged smooth MS circularly arranged smooth MS
Adventitia
-Cartilage Present Absent
-Mucoserous Present Absent
glands& -lymph Present Absent
follicles

9 
 Pleura

10 
 LUNGS AND PLEURA

PLEURA
Definition: Each pleura is a serous sac covering the lung and lining sites of its extension.
Layers:
1) Visceral (Pulmonary):
• Adherent to the lungs & follow the fissures
• It is absent at the hilum of the lung.
• It is supplied by bronchial vessels and autonomic Ns (insensitive to pain, touch
& temperature)
2) Parietal:
• It lines the sites of lung expansion,
• It is supplied by As of thoracic walls and by somatic Ns (intercostal & phrenic
Ns). Inflammation of pleura (pleurisy) is referred to thoracic and abdominal walls
(intercostal Ns) and tip of shoulder (phrenic N)
• It is subdivided into:
a) Cervical Pleura: covers the apex of lung. It is bounded superiorly by
suprapleural membrane.
b) Costal Pleura: lines the thoracic wall.
c) Mediastinal Pleura: covers the mediastinum.
d) Diaphragmatic Pleura: covers the diaphragm.
Recesses of the pleura
1) Costomediastinal Recess: It is the junction of costal and mediastinal pleura. It
is occupied by anterior border of lungs in deep inspiration.
2) Costodiaphragmatic Recess: It is the junction of costal and diaphragmatic
pleura. It is occupied by inferior border of lung in deep inspiration.
The pleural Cavity: a potential space, between the two layers of the pleura and contains
few drops of synovial fluid.
Applied Anatomy: in some diseases, the pleural cavity may be filled by excess fluid
(hydrothorax), blood (hemothorax), pus (pyothorax) or air (pneumothorax). This will
collapse the lung at the same side and push the mediastinum to the opposite side. Fluids
will obliterate costodiaphragmatic recess and can be drained by a needle, which should pass
along the upper border of a rib to avoid injury of intercostal VAN.
Surface anatomy: see lungs

11 
 Lungs

12 
 LUNGS

RT LT
General
Each lung resembles 1/2 a cone, having an apex, 3 borders & 3 surfaces
features
Apex Project through thoracic inlet to the root of neck

Borders:
Ant Thin, sharp & extends into costomediastinal recess

Post Thick, rounded at the side of vertebral column (paravertebral gutter)

• Ant, lat & post → thin, sharp & extends into costodiaphragmatic recess
Inf
• Med → rounded & related to pericardium

Surfaces:
Inf (base) Concave, rests on copula of diaphragm

Costal
Convex, wide & related to ribs, costal cartilages, intercostals muscles & pleura
surface
Medial
surface
Mediastinal • Related to mediastinum
part • Its post part shows the hilum (containing root of lung)
Vertebral Related to sides of thoracic vertebrae, intervertebral discs, sympathetic chain, post
part intercostals Vs & root of splanchnic Ns

Size Larger Smaller

Length shorter Taller

Width Wider Narrower

Ant border Straight Shows cardiac notch & lingula below it

More concave (higher copula of
Inf surface diaphragm due to presence of Less concave
large liver below)

Fissures 2 (oblique & transverse) 1 (oblique)

Lobes 3 (Sup, middle & inf) 2 (Sup & inf)

13 
 Mediastinal surface of Rt lung Mediastinal surface of Lt lung

14 
 Hilum of the lungs

15 
 RT LT
Mediastinal surface Shows the following impressions (both lungs shows the same impressions but
for different structures. Nost of the impressions of Rt lung are venous, while
most of the impressions of the Lt lung are arterial)
• Pericardial impression (for Rt atrium • Pericardial impression (for Lt
& its pericardium) ventricle (mainly), Lt atrium & its
Ant to hilum • Ascending aorta & thymus sup to pericardium)
pericardial impression • Pulmonary trunk & thymus sup to
pericardial impression
• Horizontal: arch of azygous V • Horizontal: arch of aorta
• Vertical (above arch of azygous, from • Vertical (above arch of aorta, from
ant to post) ant to post)
1) SVC (continued sup as Rt 1) Lt common carotid A
Sup to hilum
brachiocephalic V) + Rt phrenic 2) Lt subclavian A
2) Trachea + Rt vagus + Lt vagus & Lt phrenic Ns between
3) Esophagus them
3) Esophagus + thoracic duct
Post to hilum Azygous V + esophagus Descending aorta
Inf to hilum IVC Esophagus
• Along groove of Rt brachiocephalic & • First between Lt common carotid &
SVC (sup to hilum) Lt subclavian, extending to arch of
Phrenic N • Then along pericardial impression (ant aorta (sup to hilum)
to hilum) • Then along pericardial impression
• Then along IVC (inf to hilum) (ant to hilum)
Hilum Containing the root which is formed of:
2; characterized by plates of cartilage • 1 main bronchus, characterized by
1)Sup lobe (eparterial) bronchus plates of cartilage
Bronchus 2)Rt main (middle & inf lobe or • most post structure in hilum
hyparterial) bronchus (most post
structure in the root)
Post to bronchus Post to bronchus
Bronchial vessels −1A − 2 As
− 2 Vs − 2 Vs
• Branch of pulmonary trunk
Pulmonary A • Carries non oxygenated blood from Rt ventricle to the lung
• Anterosuperior to main bronchus
2; carry oxygenated blood from lung to Lt atrium
Pulmonary V − Sup: most ant structure in the root
− Inf: most inf structure in the root
Lymph nodes Between the structures of the root
Autonomic, for bronchial tree, lung substance & visceral pleura
Pulmonary plexus − Ant: ant part of root
− Post: post part of root

16 
 Segments of the lungs

Surface anatomy of lungs and pleura

17 
 RT LT
Segments Each segment contains a bronchus, branch of pulmonary A. Pulmonary V run in the
intersegmental planes
Direction of Direction of
Segment Segment
bronchus bronchus
Apical Sup Apical Sup
Post Post & lat Post Post & inf
Sup lobe Ant Ant & inf Ant Ant & inf
--- --- Sup lingular Ant & inf
--- --- Inf lingular Ant & inf
Lat Middle lobe --- ---
Middle bronchus passes
lobe Med ant & inf then --- ---
divides
Apical Post
Ant basal Inf & ant
Inf lobe Post basal Inf & post As Rt lung As Rt lung
Lat basal Inf & lat
Med basal Inf & med
• Bronchi of middle lobe are narrow & could be occluded by lymph nodes
Applied
• Postural drainage of fluid in the lungs depends on the direction of segmental bronchi
anatomy
• Segment removal could be performed as a treatment
Surface  1 inch above med 1/3 of clavicle  1 inch above med 1/3 of clavicle
Anatomy of (apex) (apex)
lungs  Sternal angle near midline  Sternal angle near midline
 6th costal cartilage near midline  4th costal cartilage near midline
 6th rib at midclavicular line  6th costal cartilage 1 inch from sternal
 8th rib at midaxillary line side
 10th rib near thoracic spines  6th rib at midclavicular line
 To the 1st point  8th rib at midaxillary line
• Oblique fissure: from  10th rib near thoracic spines
3rd thoracic spine to 6th costal  To the 1st point
cartilage • Oblique fissure: from 3rd
• Transverse fissure: thoracic spine to 6th costal cartilage
level of 4th costal cartilage • No transverse fissure
Surface  1 inch above med 1/3 of clavicle  1 inch above med 1/3 of clavicle
anatomy of  Sternal angle near midline  Sternal angle near midline
pleurae  6th costal cartilage near midline  4th costal cartilage near midline
 8th rib at midclavicular line  6th costal cartilage 1 cm from sternal
 10th rib at midaxillary line side
 12th rib near thoracic spines  8th rib at midclavicular line
 To the 1st point  10th rib at midaxillary line
 12th rib near thoracic spines
 To the 1st point
Applied anatomy: intracardiac injection or
needle insertion into pericardium is performed
within 1 cm to the left of sternum between 4 th
& 6th costal cartilages

18 
 Diaphragm

Phrenic nerve

19 
 DIAPHRAGM

Origin Insertion Action NS

Sternal: back of xiphoid process Central • Inspiration Phrenic
Costal: lower 6 ribs & costal cartilages tendon • Increase N (C3-
Rt crus (stronger): L1-3 vertebrae (bodies) & intervertebral abdominal 5)
discs pressure
Lt crus: L1-2 vertebrae (bodies) & intervertebral discs (cough,
5 arcuate ligaments: between the crurae, L1 transverse vomiting...
processes & last ribs etc.)

Major openings of diaphragm:

Opening Site
Inf vena cava T8, 1 inch to Rt (in central tendon)
Esophagus T10, 1 inch to Lt
Aorta T12 in midline

PHRENIC NERVE
Root value: C3,4,5 ventral rami
Course &Relations (revise mediastinal surface of the lungs):
• Accompanied by pericardiophrenic artery.
Lat: corresponding lung & pleura
Med (from above downwards):
Rt Lt
• Rt brachiocephalic • Between Lt common carotid & Lt subclavian As,
• SVC crossed by Lt vagus
• Rt atrium • Arch of aorta
• IVC • Lt ventricle

Post: corresponding hilum of the lung

Branches:
Motor: to diaphragm (pierces it & supply it from inf surface).
Sensory: pleura, pericardium & the Rt phrenic supplies biliary system (pain due to biliary
causes is referred to Rt shoulder).

20 
 Respiratory Portion (histology)
A- Respiratory bronchioles
• The respiratory bronchioles mark the transition from the conducting
to the respiratory portion of the respiratory system.
• The epithelium is simple cubical epithelium & Clara cells
• Their walls are interrupted by alveoli, the sites where gas exchange
occurs.
B- Alveolar ducts
• Their walls consist of adjacent alveoli, which are separated from one
another by interalveolar septum.
• They are the most distal portion of the respiratory system to contain
smooth muscle, which is present in their walls at the openings of
adjacent alveoli.
• They are lined by simple squamous epithelium.
C- Alveolar sacs are expanded outpouchings of numerous alveoli located at the
distal ends of alveolar ducts.
D- Pulmonary alveoli:
• They are structural & functional unit of the lung.
• There are pores in between lung alveoli that allow communication.
• The alveoli are separated from each other by thin inter alveolar septum.
• The alveoli are lined by two types of cells; pneumocyte type I & type II.
P.O.C Type I Pneumocytes Type II Pneumocytes
% 97 3
LM • flat squamous cells • cuboidal cells
• flat densely stained nuclei • rounded large nuclei with prominent
• Little cytoplasm nucleoli
• Foamy cytoplasm
EM • Few cell organelles • Apical microvilli
• Tight junctions with type I • Rich in Golgi apparatus, rER,
and II to avoid escape of mitochondria
tissue fluids within the • Characteristic multilamellar bodies
alveoli (cytosomes) that contain phospholipids
Function gas exchange 1. secrete pulmonary surfactant
2. Stem cells for both types

Multilamellar
rrar
21 
Clinical note:
Surfactant is only secreted late in pregnancy (9 th month) so premature babies
usually have respiratory distress due to deficiency in production of surfactant.
❖ Interalveolar septum:
Definition : It is the partition present in between the lung alveoli.
Structure: It is formed of a thin layer of a highly vascular C.T. rich in elastic
fibers & reticular fibers which are important for elasticity & support of lung
tissues.
❖ Blood air barrier:
Definition : It is the wall through which gas exchange occur. It is present in
between blood in blood capillaries & air within the lung alveoli.
Fused B.M.
surfactant

Pneumocyte
I
Endothelium B.M. Pneumocyte II

Structure:
1- Thin film of pulmonary surfactant.
2- Cytoplasm of pneumocyte type I.
3- Fused basement membrane of type I pneumocytes & capillary
endothelium.
4- Capillary endothelium.
❖ Alveolar phagocytes:
Definition: They are phagocytic cells which are present in the cavities of lung
alveoli or in inter- alveolar septum.
Function: They can phagocytose bacteria & dust particles (rich in
lysosomes).
Origin: They arise from blood monocytes.
Staining: They are demonstrated by vital stain as trypan blue.
Fate: They may be coughed in sputum, or they may die & remain in the
interalveolar septum or the nearby lymph nodes.
Types:
1- Dust cells: these cells phagocytose dust &carbon particles that appear
as black particles within them.
1- Heart failure cells: they can only be seen in patient suffering from heart
failure. Congestion of blood capillaries will lead to their rupture &
escape of RBCs to alveolar cavities. Macrophages phagocytose HB &
destroy it to red colored haemosiderin granules that appear within them.
22 
 Structural transitions in walls and layers of the passageways from
extrapulmonary passageways to alveoli
Layers become thinner as passageways decrease in
diameter
Epithelium decreases in height from pseudostratified to
simple squamous
Cilia & goblet cells Decrease gradually. Goblet cells are stopped
before cilia.
Lamina propria Decrease gradually in thickness

Serous& mucous glands Decrease gradually and stop at the junction of a

bronchus with a bronchiole.
Cartilage decreases in size, breaks up into plates, and stops
at the junction of a bronchus with a bronchiole
Smooth muscle Trachea: trachealis at the free ends of the C-
shaped cartilage.
Intrapulmonary bronchi: Spirally arranged.
Bronchioles: circularly arranged.
Alveolar ducts: only at alveolar openings
Alveolar sacs and alveoli: completely absent.

The lining epithelium of the bronchial tree

Region Epithelium
Trachea& 1ry bronchi Respiratory epithelium
[pseudostratified col. Ciliated with goblet cells]
2nd (Intrapulmonary) Respiratory with less goblet cells
bronchi
Primary bronchioles Simple columnar ciliated with Clara cells
(No goblet)
Terminal bronchioles Simple cubical some ciliated+ many Clara cells
Respiratory bronchiole Simple cubical + Clara cells
Alveolar duct Simple squamous (smooth muscle)
Alveoli Alveolar epithelium

23 
Pleura:
It is a double layered serous membrane formed of the visceral pleura (covering
the lungs) and the parietal pleura (on the chest wall).
Both visceral and parietal pleurae are formed of a superficial layer of simple
squamous mesothelial cells resting on a layer of connective tissue rich in collagen
and elastic fibres.
Between the visceral pleura and the parietal pleura is a potential pleural space that
is ordinarily filled with a thin film of serous fluid.

Foetal lung:

24 
 • Non-functioning collapsed in the intrauterine life.
• Clear lobes and lobules (thick connective tissue).
• Like glands because branches of bronchiolar tree are like ducts of the
glands and alveoli are like acini.
• Alveoli are collapsed and lined by simple cubical epithelium.
• Bronchi and bronchioles are folded.
• Cartilage plates are present in the walls of the bronchi (characteristic
feature of foetal lung)
• Congested pulmonary blood vessels.

25 
 Lung Functions
1) Respiration
Respiration is divided into external respiration & internal respiration
→External respiration
1- Pulmonary ventilation "V" 2- Pulmonary perfusion "Q"
3-Diffusion: Exchange of gases (oxygen & carbon dioxide)
4-Transport of oxygen & carbon dioxide between lungs & body tissues by blood
5-Exchange of oxygen & carbon dioxide between blood & tissues by diffusion
❖ Air passes from pharynx to trachea to two main bronchi
❖ The bronchi repeatedly subdivide within the lungs, becoming smaller and
changing in structure, until the alveoli are reached after 20 generation
❖ The total area of alveoli in contact of capillaries = 100m2
❖ The airways contain cartilage, which gives their shape & support. They are
surrounded by smooth muscle to allow change In diameter
❖ Stimulation of vagus & histamine leads to bronchoconstriction
❖ Stimulation of sympathetic leads to bronchodilation through β2 receptors

→ Internal respiration
- Use of oxygen within mitochondria to generate ATP by oxidative
phosphorylation & production of CO2 as a waste product
- Use of oxygen within mitochondria to generate ATP by oxidative
phosphorylation & production of CO2 as a waste product
2) Non respiratory functions:
a) Regulation of acid base balance (pH): Through control of CO2 level
b) Défense against pathogens c) H2O & heat loss
d) Increase venous return e) Enhancing vocalization

26 
 Pulmonary Ventilation
❖ Air flows into or out of lungs because of pressure gradient between:
1- Alveoli 2- Atmosphere (outside air) 760 mmHg
❖ Resting respiratory rate → 12-16 cycles/min
❖ Tidal Volume "TV→ 500 cc (Volume of air inspired or expired each cycle
during rest equal)
❖ Pulmonary ventilation = Respiratory rate x TV
= 12 x 500 = 6000 cc
❖ Mechanics of inspiration:
• ↑ Vertical diameter: By Diaphragm
• ↑ A-P diameter: By external intercostal muscles
• ↑ Lateral diameter : By external intercostal muscles

Inspiration
- Air rushes in. - Air forced out.
- It is active process. - It is Passive process: Due to elastic
recoil of -lung
-Chest wall ant end of inspiration
Expiration becomes active: [ie expiratory muscles
contract]

- During forced expiration

- As in conditions of bronchial obstruction eg
bronchial asthma

Increase in: Decrease in:

1- Thorax volume (increase all 1- Thorax volume (decrease all
dimensions) dimensions due to relaxation of
2- Lung volume as it follows the muscles)
thoracic wall 2- Lung volume
Decrease in: Increase in:
- Intra-thoracic pressur (intrapleural): - Intra-thoracic pressure: To
from -4 to -6 mmHg -4 mmHg
- Intra-alveolar pressure to: Become - Intra-alveolar pressure: To
-l mmHg +1 mmHg

27 
Inspiratory muscles are: Expiratory muscles are:
➔ Diaphragm: ➔ Abdominal muscles:
➢ Is the most important inspiratory • When contract it increase intra-
muscle. Supplied by phrenic nerve abdominal pressure → push
rd th
(3 to 5 cervical segment) diaphragm up
➢ When it descends: It increases the ➔ Internal intercostal muscles
vertical diameter. 1- They run obliquely
➢ Responsible for 75% of the change downward and backward
in chest volume from rib to rib.
➔ External intercostal muscles: 2- They pull ribs downward.
➢ They run obliquely downward &
forward from rib to rib
➢ When contract they increases:
1) The lateral diameter: By elevation
of ribs
2) Anteroposterior diameter: By
eversion of ribs
➔ Accessory inspiratory muscles:
Contract only with deep (forced)
inspiration. They are:
1) Sternomastoid → lift the sternum
2) Serratus anterior → lift many ribs
3) Scaleni muscles → lift the first two
ribs

Respiratory pressure

Changes in lung volume, alveolar pressure, pleural pressure & trans pulmonary pressure during
normal breathing

I-Intra-Pleural Pressure (IPP)

➢ Definition: It is the pressure between the two layers of the pleura ie
between the visceral pleura and the parietal pleura.
• Normally the intra-pleural space:
28 
 • Contains few cc of lymph for lubrication of movements
• Does not contain air.
• Normally intra-pleural pressure is: Negative
➢ Causes of negative IPP:
Due to: Continuous tendency of the lungs to recoil inwards Against
Continuous tendency of chest wall to expand outwards
1- Recoil tendency of lung Caused by:
A- Lung elasticity
➢ It account for ⅓ of total recoil tendency elastic
➢ Lung volume at the end of normal expiration: Is 2.5 liter [while lung
relaxation volume (at which, it is neither stretched nor compressed): Is one
liter]. So, it tends to collapse to reach its relaxation volume.
B- Surface tension of fluid lining the alveoli
➢ It account for ⅔ of total recoil tendency of lungs.
➢ Any fluid with direct contact of air has a surface tension (intermolecular
attraction between fluid surface molecules) to decrease the surface area so,
alveoli tend always to collapse
The continuous pull of the lung against the stable chest wall create
negative pressure
2- Expansion tendency of chest wall
➢ At the end of normal expiration:
➢ Chest is compressed
➢ Chest volume at the end of normal
expiration: Is 2.5 liter (while chest
relaxation volume is 5 liter). So, the
chest has a continuous tendency to
expand
❖ Measurement of IPP: by intra-esophageal balloon connected to sensitive
manometer
❖ Normal values of IPP:
1. At end of normal expiration: -4 mmHg
2. At end of normal inspiration: -6 mmHg
3. With deep inspiration: -12 mmHg
(Because with deep inspiration there is maximal expansion of lungs → maximal
recoil tendency → IPP becomes more negative)
29 
 4. During forced inspiration against closed glottis (Muller's experiment):
IPP becomes -30 to- 50 mmHg
5. During forced expiration against closed glottis (Valsalva's
experiment): IPP becomes + 50 mmHg
❖ Functions of IPP:
1. It prevents lung collapse & allows for lung expansion.
2. It helps respiratory movement (pressure inside alveoli is positive while
outside is negative)
3. It helps venous & lymphatic return from extra-thoracic vessels
II- Alveolar Pressure (intra-alveolar pressure)
❖ Definition:
It is the pressure inside the alveoli during respiratory cycle
➢ During normal inspiration: The intra-alveolar pressure decreases:
1. Decreases below atmospheric pressure
2. Becomes -1 mmHg less than atmospheric pressure
3. Due to expansion of chest & lungs, so air rushes in
➢ During normal expiration: The intra-alveolar pressure increases
1. Increases above atmospheric pressure
2. Becomes +1 mmHg more than atmospheric pressure
3. Due to elastic recoil of lung & chest, so air forces out
➢ At end of inspiration or expiration:
❖ The intra-alveolar pressure = 0 mmHg The more the lung

III- Trans-pulmonary pressure (transmural pressure)

expansion

➢ It equals = alveolar pressure minus pleural pressure

➢ It is the distending pressure of the alveoli ie:
1- The more the negativity of the intra-pleural pressure or
2- The more the positivity of the intra-alveolar pressure.
Pneumothorax "PTX
❖ Define→ The presence of air in the intra-pleural space.
❖ Types:
1- External or opened pneumothorax:
Air is introduced from outside e.g. chest wound the negative
intrapleural pressure is lost as it is equilibrated· with
atmospheric pressure

30 
 Normal X-Ray Pneumothorax

2- Internal or closed pneumothorax:

➔ Air is introduced from Inside e.g. rupture of alveoli or
damaging pleural wall by pneumonia
❖ Effects: 1- The lung collapse while the chest wall is
expanded
2-The mediastinum shifts toward the intact side decreasing
the lung volume on the normal side.
3- Decrease venous return and lymphatic return

Surfactant
❖ Definition: It is a surface active agent, which means that when it spread
over the surface of a fluid, it reduces its surface tension.
❖ Chemical nature: It is a complex nature, its components are:
1- Phospholipids: Dipalmitoyl-lecithin
2- Surfactant apoproteins→Allow rapid spread of lecithin over the fluid
surface to function effectively.
3- Calcium ions (Ca++)
❖ Origin: It is secreted by type II alveolar epithelium
❖ Functions: Surfactant decreases the surface tension of fluid lining the
alveoli thus:
1- Facilitates lung expansion:
✓ As it reduces surface tension of fluid lining alveoli
✓ Surfactant forms a layer between fluid lining the alveoli & the air in the
alveoli.
✓ This prevents the development of a water-air interface
NB: Water-air interface has surface tension about 10 times as
much as surfactant air interface.

2- Prevents the collapse of alveoli during expiration:

✓ As the alveolus becomes smaller during expiration, the surfactant
concentration is increased reducing surface tension further.
31 
 3- Prevents pulmonary edema (i.e. it prevents the accumulation of fluid
inside the alveolus):
NB: Surface tension in the alveoli favours the filtration of fluid
from the blood into alveoli. So, surfactant decreases the surface
tension of fluid lining the alveoli thus decreases filtering force
preventing pulmonary edema.

❖ Surfactant deficiency:
➢ Causes:
1- Respiratory distress syndrome (RDS) [Hyaline membrane disease:
✓ It may occur in premature infants (may die at birth from respiration failure)
✓ Due to:
• Increase surface tension & decrease lung compliance &
distensibility resulting in large regions of collapsed alveoli.
• As maturation of surfactant in lungs is increased by cortisol, which
reaches high level in fetal and maternal blood only near term.
✓ Diagnosis:
• Based on: the ratio between lecithin and sphingomyelin in the
amniotic fluid
• in (RDS) it is less than one (<1) at birth
• Normally, it is 2 at 35 weeks of gestation (pregnancy).

2)- Inhalation of 100% oxygen for a long time or at 2 atmospheric pressures

of oxygen: As in cardiac surgery
3)-Heavy smokers: Cigarette smoke inhibits surfactant secretion
4)- Obstruction of one of main pulmonary artery
5)-Hypothyroidism
6)- Hypocorticism: Cortisol accelerates maturation of surfactant
7)-Hyperinsulinism: Insulin inhibits surfactant secretion.

This may explain the increased RDS in infants born to diabetic mothers.

32 
 Compliance

Compliance diagram in a healthy person. This diagram shows compliance of: Lungs alone

Comparison of the compliance diagrams of saline-filled and air-filled lungs when the alveolar
pressure is maintained at atmospheric pressure (0 cm H2O) and pleural pressure is changed

❖ Definition: is a RATIO between change in volume to change in distending

pressure (trans mural pressure)
➢ Transmural pressure= Pressure inside the lungs- pressure outside the
lungs -Intra alveolar pressure (zero)
- Intra pleural pressure (-ve)
-Intra-pleural pressure
➢ Compliance = Change in volume / Change in Trans mural pressure
➢ Compliance is an inverse of elasticity i.e. a lung with high elasticity
(increase elastic recoil tendency & tendency to collapse) has low
compliance as there is difficulty in lung expansion.
➢ Normal standard:
• Compliance of lung alone = 0.2 liter/cm H2O
• The compliance of both lungs = 200ml/cm H2O
➢ Compliance diagram of the lungs: Compliance of excised lung:
✓ The compliance curve is made by measuring change in volume that occurs
with each change of pressure during both inflation & deflation of lungs.

33 
 ✓ It is hysteresis loop (not linear) due to change in distribution of surfactant:
During lung deflation, surfactant becomes close together causing decrease
in surface tension -lung become more compliant
❖ Factors affecting lung compliance:
A)- Decreases in →Anything affect distension of lungs
1- Restrictive lung diseases: As pulmonary congestion & fibrosis
3- Respiratory distress syndrome
B)- Increases in→Anything changes lung elastic properties.
1- Old age
2- Emphysema: Which is a pulmonary disease due to destruction of alveolar
wall & elastic tissue of lung leading to → abnormal collection of air →
enlargement of air spaces distal to terminal bronchi
❖ Compliance of thoracic wall & lung together:
➔ It is called dynamic lung compliance.
➔ It is measured in living subjects
➔ Compliance of the combined lung-thorx system is slightly greater than one
half of the lung alone = 0.11 liter/cm H2O
❖ Factors affecting chest compliance
➔ Decreases in: 1-Skeletal muscle diseases 2Arthritis 3- Obesity
➔ Increases in: Athletes
➔ Increases in: Athletes
The work of breathing
❖ Energy needed for breathing is:
✓ 5% of total energy in normal breathing
✓ 20% of total energy in heavy exercise.
❖ The work of breathing is performed by respiratory muscles during
inspiration & there is kinetic energy stored in muscles & released during
expiration as potential energy
❖ The work of inspiration is divided into:
1- Elastance work (compliance work) 65%
✓ It is required to: Expand lungs against elastic forces
✓ Leads to decrease compliance & increase work
✓ The work breathing is increased if:
I- Increase elasticity: (Decreased is reduced) As in:
A- Surfactant deficiency or
B- Lung fibrosis

34 
 II -Airway resistance is increase As in: bronchial asthma
2- Non Elastance work
1)- Tissue resistance work 15%
✓ It is required to overcome:
A)- Viscosity of lungs B)- Chest cage structure
II- Airway resistance work 20%
✓ It is required to overcome: The resistance of airflow through respiratory
Airway resistance work is inversely proportional to total cross
sectional area of air passages:
- Greatest resistance is in medium size bronchioles.
- Less resistance is in small size small bronchioles [because of their large
number &large surface area]

Dead Space (DS)

❖ Definition:
- Air which does not share in
diffusion (gas exchange)
with blood
- With each respiration: 500 cc
air are taken:
➔ 350 cc enter alveoli (alveolar air) &
undergo gas exchange with blood
➔ While 150 cc remain in DS
❖ Types:
1- Anatomical DS (the conducting zone)
➢ Air passages from: Nose -->Pharynx to→ Trachea to→Bronchi to→
Bronchioles down → Respiratory bronchioles
➢ Because of their thick wall: Normal values: = 150 - 167 ml
= 30% of tidal volume
➢ Vagus: Leads to broncho constriction ie decrease dead space
➢ Sympathetic: Leads to broncho dilatation ie increase DS
2- Alveolar DS: Some alveoli not undergo gas exchange because they have no
blood supply
3- Physiological DS (Anatomical DS + Alveolar DS)
Under normal conditions: Physiological dead space = anatomical DS because
all alveoli are functioning
35 
 ➢ Significance:
1] With each respiration: 500 cc air are taken:
- 350 cc enter alveoli (alveolar air) & undergo gas exchange with blood
- -While 150 cc remain in DS

2] It protects alveoli against damage:

- It warms, filters & moistens the inspired air
- Particles with a diameter:
 More than 10 microns: Are caught in nose hairs, stick to mucus of nose
 2-6 microns: Stick to mucus of trachea & bronchi then expelled by: 1- Cough
2-Sneeze reflexes 3- Movements of cilia
 Less than 2 microns: Are removed by phagocytic cells in alveoli
 Less than 0.3 microns: Remain in air phase in the alveoli & are breathed again
➢ Measurement:1- Fowler method 2-Bohar method
Respiratory functions of blood
Gas exchange between alveolar air & venous blood occurs by simple diffusion.
➢ R: Rate of gas diffusion
➢ Pl- P2: Pressure difference
➢ T: Temperature
➢ A: Surface area of diffusion
➢ M: Square root of molecular size
➢ L: Length of the system
➢ S: Solubility of the gas in the medium
➢ n: Viscosity of the medium
❖ Respiratory membrane:
➢ Measures: 0.2 micron
➢ Formed of the following layers:
A)- Fluid lining alveoli and surfactant
B)- Alveolar epithelium
C)- Epithelium of basement membrane
D)- Interstitial space containing fluid
E)- Capillary basement membrane
F)- Capillary endothelium

Ultrastructure of the alveolar respiratory membrane, shown in cross section

36 
 ❖ Diffusion of gases
- Physical factors which control diffusion:
[A] Diffusion in gaseous media:
- In a gaseous media, the rate of gas diffusion (R) is:
1- Directly proportional with: A)- Pressure difference (Pl- P2)
B)- Temperature (T) c)- Surface area of diffusion(A)
2- Inversely proportional with:
1] Square root of molecular size (M) : O2 has molecular weight less than CO2
2]Length of the system
Rα (Pl- P2) T A
ML
2-In gaseous media: The diffusion rate of O2 is 1.2 times faster than CO2
This is because O2 (oxygen) has molecular weight (MW) less than CO2
[B] Diffusion in aqueous media
→ In the body, the respiratory gases diffuse through aqueous media e.g.:
1- Pulmonary membrane 2- Plasma 3- Erythrocyte wall
→ Two additional factors are considered:
1- Directly proportional with: Solubility of the gas in the medium (S)
CO2 is 24 times more soluble in water than O2
2- Inversely proportional with: Viscosity of the medium (n)
Rα (P1-P2) T A S
M Ln
}C{ In aqueous media:
- The diffusion rate of CO2 is 20 times faster than O2
➔ This is because CO2 is 24 times more soluble in water than O2. Thus, in
lung diseases (eg thickening of pulmonary membrane): Diffusion of O2
across the pulmonary membrane is affected earlier than that of CO2

37 
 ❖ Factors affecting diffusion of gas through the respiratory membrane
[A] Diffusion rate is directly proportional to
1- Pressure gradient of gases across the respiratory membrane:
i.e. between alveolar air (= arterial blood) & venous blood (= tissue)
Normally: Alveoli Venous blood Pressure
(Arterial blood) (tissue) gradient
PO2 100 40 60mmHg
PCO2 40 46 6 mmHg
So, O2 diffuses from alveoli to tissue & CO2 diffuses from tissue to alveoli
2- Surface area of pulmonary membrane:
➔ Normally: It is 100 m2 (square meter)
➔ Increases in Muscular exercise due to:
1- More expansion of alveoli
2- Opening of closed capillaries
3- Dilatation of the already opened capillaries
➔ Decreases in:1- Old age 2- Emphysema 3- Lung collapse
3- Temperature (T)
4- Diffusion coefficient: i.e., - solubility in water
- CO2 is 24 times more soluble in water than O2
[B] Diffusion rate is inversely proportional to:
1)- The square root of the molecular weight
2)- Thickness of the respiratory membrane
→ Normally: It is 0.2 μ
➔ It increases with: 1- Pulmonary edema 2- Lung fibrosis
Diffusion rate of CO2 is 20 times faster than O2

Alveolar ventilation (VA) / pulmonary perfusion (Q) ratio

❖ Normally:
 Alveolar ventilation is 4L / min.
 Pulmonary perfusion is 5L / min
So, the V/Q ratio is 0.8 [An ideal V/Q = 0.8 – 1.2 (matched V/Q)]
NB: Both ventilation & perfusion are not equal all through the lung:
38 
At lung apex: The perfusion is less (so the V/Q ratio is high "3")
At lung base: The perfusion is more (so the V/Q is low "0.6")
❖ Causes of regional difference in lung ventilation:
➔ Normally: The intrapleural pressure at the apex of the lung is more (-ve)
than at the base
• So trans pulmonary pressure is higher at the apex.
• So apical alveoli are more expanded.
So, the ventilation at the apex is high & at the base is low
❖ Causes of regional difference in perfusion:
➔ (Due to the effects of gravity on pulmonary arterial pressure)
➔ At the lung apex: the pulmonary arterial pressure ↓↓ (< the alveolar
pressure) → the capillaries nearly close At the lung base: the pulmonary
arterial pressure ↑↑ → ↑↑ blood flow.
➔ At the lung base: the pulmonary arterial pressure ↑↑ → ↑↑ the blood flow
❖ Assessment of Regional ventilation & Perfusion:
1- To test for ventilation: Xenon gas is inhaled & its distribution in lung is
measured
2- To test for alveolar perfusion: Tc99 is injected IV & its distribution in lung
is measured
❖ V/Q mismatch :
➢ ↑ V/Q (when Perfusion ↓) eg by a Pulmonary Embolism "PE"
➢ ↓ V/Q (when ventilation ↓) eg by a emphysema.

Gas transport by the blood

A)- Oxygen (O2) transport (carriage) by blood

Diffusion of oxygen from a peripheral tissue capillary to the cells.

[(PO2 in interstitial fluid = 40 mm Hg, and in tissue cells = 23 mm Hg]

-Forms of O2 transported: O2 is transported (carried) in blood in two forms:

1- Oxygen in physical form:
39 
 ❖ Nature: Free O2 molecules dissolved in blood
❖ Volume: Normally:
➔ 0.3 ml/100 cc arterial blood ie:
• 3 ml in one liter
• As normal blood volume is 5 liter, so O2 in physical form is 15 ml
➔ 0.13 ml/100 cc venous blood ie: Tissue take 0.17 ml/ 100 cc
❖ Importance: It determines:
➢ The O2 tension (PO2)
➢ O2 tension; in turn determines the rate & direction of O 2 diffusion

O2 tension (PO2) - PO2 in arterial blood = 100 mmHg

- PO2 in venous blood = 40 mmHg
2-Oxygen in chemical form:
❖ Nature: O2 combines with the iron of hemoglobin, while still in the ferrous
state, this reaction is called oxygenation
❖ Volume: Normally:
➔ 19.5 ml/ 100 cc arterial blood
• 65 times as physical
• It depends on O2 tension
• 98% of O2 is transported in chemical combination with Hb to supply tissues.
➔ 14.5 ml/100 cc venous bloods.
- The amount of O2 taken by tissues during rest = 19.5-14.5 = 5 ml
❖ Importance: It constitutes the main supply of O2 to the tissues
Definitions:
Oxygen content: It is the volume of O2 in ml present in chemical
combination in l00cc blood.
Oxygen capacity: It is the volume of O2 in ml present in chemical
combination in 100 cc blood when Hb is fully saturated with O2
- It does not depend on O2 tension but on amount of Hb:
- The adult: Contains 15 g Hb/100ml of blood
Each gm combines with 1.34 ml O2

So O2 capacity = 15 × 1.34 = 20 ml O2/100 ml blood

40 
 % Saturation of Hb With O2 = O2 content  100
O2 capacity

In anemia: Reduction in Hb→ Decreases both O2 content & O2 capacity. Thus

the % saturation is not affected
Coefficient of O2 utilization: It is % of O2 in arterial blood which is taken
by tissues
Arterial O2 content - Venous O2 content  100
= Arterial O2 content
= 19.5 – 14.5  100 25%
during rest
19.5 = 25% 75%
during exercise

It is: →Directly proportional with: Activity of tissues

→Inversely proportional with: Rate of blood flow
The oxygen dissociation curve
 The oxygen dissociation curve of hemoglobin (oxyhemoglobin dissociation
curve)
 This curve shows the relationship between:
- O2 tension (PO2)
- Percentage (%) saturation of hemoglobin with O2 (not O2 content)

Why? Because O2 content varies from person to person according to hemoglobin

content which decreases in anemia, so it will not be a universal curve.

Oxygen-hemoglobin dissociation curve Effect of blood PO2 on the quantity of oxygen bound with
hemoglobin in each 100 milliliters of blood
➢ It is S shaped (not linear) because: hemoglobin is made of 4- subunits that
load and unload O2 with different affinities

41 
 ❖ Physiological significance of oxyhemoglobin dissociation curve:
➔ At lungs (Alveoli) (Flat or plateau part of the curve)
➢ While PO2 drops from 100 to 60 mmHg, the % of saturation drops only
from 97 to 90%.
➢ This allows easy and nearly complete Saturation even if the O2 tension is
low (as in high altitude → allowing persons to get enough O2 from their
blood) because at high tensions of O2, there is high affinity of Hb to O2
➔ At tissue (Venous) (Steep part of the curve)
➢ While O2 tension drops from 60 to 40 mmHg (resting venous blood), the
% saturation drops from 90 to 70%
➢ With exercise, O2 tension drops to 20 mmHg (due to increase O2
consumption) & % of saturation drops to 30 %, ie an extra 40% of O2 is
given to tissues.
➢ So, O2 dissociation curve for Hemoglobin at tissues allows easy and rapid
Dissociation even if the O2 tension is not markedly lowered (as in muscular
exercise) allowing tissues to take more O2. This is because at low tensions
of O2, there is low affinity of Hb to O2
❖ Factors affecting oxyHb “Oxygen-hemoglobin” dissociation curve:
[A] Shift of the curve to the right:
➢ Decrease affinity of Hb to O2 ie unloading of Hb
1. Increase CO2
2. Increase H+ (low pH)
3. Increase temperature
+
- Effect of CO2 & H on oxyHb dissociation curve is called Bohr
Effect 1 & 2 & 3 occurs during muscular exercise to supply the
active muscles with oxygen.
+
- Mechanism: CO2 & H combine with sites on Hb changing its
configuration & facilitating off-loading of O2
4. Increase 2, 3-DPG: (2, 3 diphosphoglycerate):
- It is an end product of RBC metabolism. It occurs in cases of hypoxia
& exercise
[B] Shift of the curve to the left:
➢ Means: Increase affinity of Hb to O2 ie loading of Hb.
➢ Causes: 1- Decrease CO2 2- Decrease H+ (high pH)
3- Decrease temperature 4- Decrease 2, 3 DPG
5- Carbon monoxide: It form carboxy Hb and causes shift of the
remaining oxyhemoglobin to the left
42 
 Shift of the oxygen-hemoglobin dissociation curve to the right caused by an increase in
hydrogen ion concentration (decrease in pH). BPG, 2.3-biphosphoglycerate

➢ The position of O2 dissociation curve can be expressed by stating Po2 at

which Hb is 50% saturated (P50)
➢ The P50 is an inverse function of the Hb Affinity for O2: SO
• Hb With ↑O2 affinity will have a dissociation curve with ↓ P50 that lies
to the left (shift to left)
• Hb With ↓O2 affinity will have a dissociation curve with ↑P50 that lies
to the right (shift to right)
• The normal P50 for arterial blood is 27 mmHg.
B)- Carbon dioxide (CO2) transport (carriage) by blood

Uptake of carbon dioxide by the blood in the tissue capillaries

[(PCO2) in tissue cells = 46 mm Hg, & in interstitial fluid = 45 mm Hg)]

➔ CO2 moves down its pressure gradient from tissue → blood plasma →
RBCs → lungs.
Forms of CO2 transported: CO2 is transported in blood in two forms:
Carbon dioxide in physical form
➢ Nature: Soluble CO2 [CO2 is a more soluble gas than O2]
➢ Volume: Normally: - 3 ml/100 cc arterial blood
- 3.4 ml/100 cc venous blood

43 
 CO2 tension (PCO2)
- PCO2 in arterial
blood = 40 mmHg
- PCO2 in venous blood= 46 mmHg

CO2 + H2O  H2CO3  H+ + HCO3

➢ This reversible reaction in RBCs is 13000 times faster than in plasma

because of the presence of carbonic anhydrase enzyme in RBCs & not
in plasma
- At tissues: The reaction goes to the right (due to addition of CO 2)
- At the lungs: The reaction goes to the left (due to removal of CO2 into air)

➢ Definitions:
➔ Venous CO2:
- Is the venous CO2/100 cc blood.
- Venous CO2 = Tidal CO2 + Total CO2
- It equals = 52 ml which are distributed as follows
• 3.4 ml in physical form
• 4 ml in form of carbamino compound
• 44.6 ml in form of bicarbonate
➔ Tidal CO2
- Is the CO2 given by tissues to each 100 ml blood
- It equals = 4 ml/100cc which are distributed as follows:
• 0.4 (10%) in physical form
• 1 ml (25%) in form of carbamino compound
• 2.6 (65%) in form of bicarbonate
➔ Total CO2
- Is the arterial CO2/100cc blood.
- It equals= 48 ml/100cc which are distributed as follows:
• 3 ml in physical form
• 3 ml in form of carbamino compound

44 
 • 42 ml in form of bicarbonate
➔ Buffering of the tidal CO2:
- The 4 ml added by the tissues should
be buffered; otherwise they will
decrease the pH of the blood to a
dangerous level

Transport of carbon dioxide in the blood

- They are carried as follows:

• 0.4 ml in physical solution, so the pH of the blood will decrease from 7.4
to 7.35
• 1 ml as carbamino compound. The reduction of oxy-Hb to reduced Hb
at the tissues allows the formation of more carbamino compound.
• 2.6 ml are buffered by Hb with resultant production of HCO3. This is done
through Cl- shift phenomenon

Chloride shift phenomenon (=Hamburger's) phenomenon

or Gas exchange at tissues
➢ Definition: Exchange of anions between RBCs & plasma to maintain
pH constant & keep electrical equilibrium.
➢ It is responsible for carrying most of CO2 in form of HCO3.
➢ The membrane of RBCs Is:
• Permeable to anions (eg Cl- & HCO3-).
• But impermeable to cations (K+& Na+) EXCEPT H+
• However, any Na+ enters the RBCs is immediately pumped
➢ When blood is exposed to high CO2 tension (at tissues), the
following occurs:
1- CO2 enters the blood from the tissues:
- It passes through the plasma to RBCs #
- RBCs contain carbonic anhydrase (CA) enzyme:
➢ It is a protein having MW 30,000 & contain zinc
➢ This enzyme accelerates the reaction: CO2 + H2O → H2CO3-
→This reaction occurs very slowly in plasma in absence of CA
2- The H2CO3 dissociates to H+ & H2CO3-.
3- At the same time, oxygen is given by the red cells to tissues.
45 
 4- Reduced hemoglobin is weaker acid than oxyHb → so, K+ is released
& combines with H2CO3- to form KHCO3.
5- H+ of carbonic acid is buffered primarily by reduced Hb (reduced Hb
binds more H+ than oxy Hb)
6- At the same time, the reduced Hb can form more carbamino compound
with CO2.
7- According to concentration gradient, both K+ & H2CO3-try to pass to
plasma, but only anions (H2CO3-) pass. About 70% of H2CO3-formed in
the red cells enters the plasma.
8- According to electrostatic gradient, Cl- passes from plasma toRBCs.
This process continues until: Cl- in plasma H2CO3-in RBCs
(Donnan'
=
Cl- in RBCs H2CO3-in plasma Equilibrium)

9- Due to increase osmotic pressure of RBCs (by Cl-), H2O shifts from
plasma to red cells leading to increase red cell size. Thus, the
haematocrit value of venous blood is normally 3% greater than that of
arterial blood

The net results are:

RBCs Plasma
HCO3 Increase Increase
Cl Increase Decrease
Cations (Na+& K+) Constant Constant
Osmotic pressure Increase due to HCO3 & Cl Constant
H2O Diffuse from plasma to RBCs →
46 
 increase hematocrit
pH Constant Constant
Carbon dioxide in chemical form
➢ Nature: CO2 is in form of bicarbonate & carbamino compounds.
➢ Volume: Normally: 45 ml/100 cc arterial blood:
- - 42 ml in form of bicarbonate
- - 3 ml in form of carbamino
1- Bicarbonate:
• Is the most important form of CO2
• In RBCs: CO2 is carried as KHCO3
• In plasma: CO2 is carried as NaHCO3 (which is alkali reserve).

2- Carbamino compounds: ie combined with protein

• In RBCs: CO2 is carried as carbamino-hemoglobin [combined CO2
with amine group of hemoglobin (Hb-NH-COOH)]
NB: The more the hemoglobin is deoxygenated (reduced) the more
it can combine with carbon dioxide to form carbamino compounds
• In plasma: CO2 is carried as carbamino protein (combined CO2 with
terminal amine group of plasma protein).

Control of Respiration
A. Involuntary control:
➢ Respiratory centres: Are composed of respiratory neurons
❖ Two types:
1- I neurons:
- Discharge during inspiration
- Actively inhibited during expiration
2- E neurons:
- Discharge during expiration
- Actively inhibited during inspiration
- Located in brain stem (pons & medulla)
- Send to respiratory motor neurons via reticulospinal tract
This pathway allows spontaneous rhythmic breathing unconsciously
(During day, sleep, anaesthesia)

47 
 ➢ Medullary centres: are
1- Dorsal Respiratory Group (DRG)
➢ Position: Dorsomedial in medulla bilaterally
➢ Site: Located in: Nucleus of tractus solitaries, it is the sensory termination
of 9th & 10th cranial nerves which are the afferent from: Chemoreceptors,
Baroreceptors and Mechanoreceptors
➢ Contains: Inspiratory neurons only.
➢ Function:
➔ They are responsible for inspiratory activity during normal quiet breathing
➔ Pacemaker activity (Discharge spontaneous)
➢ Rhythmicity:
➔ Rhythmic inspiratory discharge.
➔ Inherent rhythmicity (Discharge spontaneous)
➔ Have inspiratory ramp signals ie:
• Their activity increases gradually for 2 sec
• Then stop for 3 sec to allow passive expiration
➢ Receives from:
1- Apneustic center (excitatory impulses)
2- Lung stretch receptors (inhibitory impulses along vagus
➢ Sends to:
1- Ventral respiratory group (VRG)
2- Inspiratory muscles: Diaphragm & External intercostal muscle
2-Ventral Respiratory Group (VRG)
➢ Position: Ventrolateral in medulla bilaterally
➢ Site: Located in: Nucleus Ambiguous (NA) & Nucleus Retro-ambiguous
(NRA)
➢ Contains: Inspiratory (I)& Expiratory (E) neurons
➢ Function: Contributes to forced inspiration & expiration
➢ Rhythmicity: NO rhythmic inspiratory discharge
➢ Receives from: DRG
➢ Sends to: 1- Muscle of expiration (E neurons)
2-Inspiratory muscles: (I neurones)→ Diaphragm, External intercostal
muscle& Accessory inspiratory muscles

48 
 NB
Medullary centers can maintain rhythmic respiration but it will be irregular & slow.
➢ Pontine centers
A)- Apneustic Center (APC)
➢ Site: Located in: Lower third of pons
➢ Function:
➔ Stimulates the dorsal respiratory group (DRG) ie it represents the
inspiratory on-switch
➔ Increases the duration of inspiration
➢ Receives from:
a)- Inhibitory impulses from:
1- Lung stretch receptors: Along vagus (Herring Bruer reflex)
2- Pneumotaxic center (PNC): Slower than vagus
➢ Sends to: 1- Stimulates DRG
2-APC Stimulates Pneumotaxic center → Inhibits APC →
stops inspiration
- APC & PNC act as modulating feedback control center. [APC stimulates PNC
which when activated inhibit APC]
B)- Pneumotaxic Center (PNC)
➢ It is called nucleus parabrachialis medialis (NPBM)
➢ Site: Located in: Upper pons
➢ Function: 1- Terminates inspiration at fixed regular points by inhibiting
APC ie it represents the inspiratory off-switch (IOS)
2-Limits the duration of inspiration

Organization of the respiratory centre

49 
 B. Voluntary control:
➢ Cerebral cortex send to respiratory motor neurons via:
1. Corticospinal tract
2. Corticobulbar tracts.
This pathway allows voluntary control of breathing during activities such
as: Talking, Singing& Breath holding
➢ Genesis of normal rhythmic breathing (Eupnea)
1. Apneustic centre stimulates the medullary inspiratory neurones of DRG.
2. Inspiratory neurones of the DRG send impulses to the diaphragm &
external intercostal muscles resulting in its contraction.
3. This leads to expansion of the chest and inflation of the lungs
(inspiration).
4. Inhibition of Apneustic centre ie switch off by:
• Signals from: Pneumotaxic center: Apneustic center stimulates
Pneumotaxic center. Pneumotaxic center in turn inhibits Apneustic center.
• Vagus: Herring-Breuer reflex:
➔ Vagus carries impulses from lung stretch receptors → inhibits apneustic
center.
➔ It is active in animals & newly born.
• Muscle spindles of intercostal muscles.
5. Expiration:
- Expiration follows passively
- Lung stretch receptors stop to discharge their inhibitory impulses,
thus APC recovers from Inhibition & sends its impulses to DRG &
the cycle repeat itself

Regulation of Respiration
1- Under normal resting conditions, the adult person consumes 250 ml O2 &
excretes 200 ml CO2/min. The pulmonary ventilation Is about 6 liters/min. ·
2- Respiration is regulated to ensure proper pulmonary ventilation, protect
airways and lungs & maintain O2, CO2, H+ tensions in arterial blood & alveolar
air constant eg muscle exercise (increase metabolism) which leads to increased
CO2, and acid production and increased O2 consumption will, in turn, stimulates
respiration.
3-Regulation of respiration Involves 4 main elements which are:
50 
 A. Sensors to detect physiologic variables in body
B. Central controller (respiratory center)
C. Effectors (respiratory muscles)
D. Negative feedback (the response affects the original stimulus)

➢ There are 2 modes of Regulation of respiration:

A- Chemical regulation
➔ It is the basic mechanism
➔ Chemical factors (PCO2, H+, PO2)
➔ Chemoreceptors are of two types:
a)- Action chemoreceptors b)- Slight inhibitory chemoreceptors
➔ Respiration is stimulated by:
a. Increased CO2 tension (PCO2) of arterial blood
b. Increased H+ ion concentration of arterial blood
c. Decreased O2 tension (PO2) of arterial blood
➔ However, changes in opposite direction have an inhibitory effect
➔ Respiratory rate is adjusted according to metabolic rate
➔ These chemical factors exert their effects on respiration by acting on:
Central chemoreceptor& Peripheral chemoreceptors
1- Central Chemoreceptors:

Stimulation of the brain stem inspiratory area by signals from: the chemosensitive area located
bilaterally in the medulla

➔ Lying only a fraction of a millimeter beneath the ventral medullary surface.

➔ Hydrogen ions stimulate the chemosensitive area,
➔ NB: carbon dioxide in the fluid gives rise to most of the hydrogen ion
➢ Site: They are in bilateral, just beneath the ventral surface of the
medulla (they are separate from neurons of respiratory centre). They
are protected by the blood brain barrier (BBB)
NB: BBB separates blood from CSF
51 
 ➢ Stimulus: 1- H+ in CSF is the only direct stimulus
NB: H+ in blood do not cross BBB
2- CO2 have very potent indirect effect
CO2 in blood cross BBB to reach the CSF
3- In CSF (cerebrospinal fluid):
CO2+ H2O CA H2CO3 Dissociate to HCO3 + H+
4- H+ stimulates the central chemoreceptors (ie responding to local H+)
5- Thus, a small change in arterial PCO2 (3%) will double ventilation
2-Peripheral chemoreceptors
➢ Site: They are nerve endings present
1- In Carotid bodies
- At the bifurcation of the common carotid arteries
- Send impulses along branch of glossopharyngeal nerve (Herring's
nerve)
2- Aortic bodies:
- Two or more bodies in the aortic arch send impulses along vagus nerve
➢ Stimulus: They are stimulated:
1- Mainly by decreased O2 tension of arterial blood
• The receptors depend only on dissolved O2 (physical form)
• This is because the blood flow to the aortic and carotid bodies is high i. e
20 ml/min/gm (20 times the weight of bodies themselves)
• Therefore, the receptors are not stimulated on conditions of anemia in
which the amount of dissolved O2 and accordingly O2 tension be normal
• They are stimulated when blood flow decreases markedly as in hemorrhage
& hypotension
2- By increased H+ ion concentration & CO2 tension (to a slight extent)
❖ Mechanism of stimulation of peripheral chemoreceptors:
1- Oxygen tension:
 Hypoxia is the most potent stimulus for peripheral chemoreceptors
 Drop of PO2 from 100 to 60mmHg (plateau part of O2 dissociation curve)
→ increased is charge from peripheral chemoreceptors but not affect
ventilation.
 At PO2 = 60 mmHg → ventilation is doubled

52 
  At PO2 from 60 to 30 mmHg (steep part of curve) → ventilation increases
6 times
 At PO2 20 mmHg or less → inhibition of respiratory center.
2- CO2 tension:
 Peripheral chemoreceptors are less sensitive to PCO2 than central
chemoreceptors
 Denervation of carotid bodies reduce ventilatory effect of hypercapnia by
20%.
Ventilatory Response to CO2:
-CO2 excess is more effective stimulus for respiration than O2 lack
-CO2 affects both central (more Important) and peripheral chemoreceptors
(discuss).
-Increase CO2 to 3% → in Inspired air will double the ventilation.
-Increase CO2 to 6% → in Inspired air will Increase ventilation 6 times
-Increase CO2 to 10% →in Inspired air will Increase the ventilation 10 times
- Increase CO2 to 20% or 50 mmHg will depress the respiratory center
-Pathways: Through central & peripheral chemoreceptors......discuss
3- H+ concentration:
- Change in H+ concentration as in metabolic acidosis &alkalosis affect
respiration eg: Metabolic acidosis→ Caused by lactic acid
- Stimulates ventilation through peripheral chemoreceptors. This lowers
PCO2 & therefore H+ content returning pH to normal.
B-Non-chemical regulation
➢ The respiratory center is influenced by various impulses reaching it
from:
- Higher centers
- Large number of sensors located in the:
1. Lungs
2. Cardiovascular system
3. Muscles Along afferent nerves
4. Tendons
5. Skin & viscera
[1] Afferent from higher centers:
(A)Cerebral cortex:
➢ Controlled - Expiration -Talking -Singing - Playing instruments

53 
 ➔ excitatory and inhibitory impulses pass from cortex to respiratory centers
or bypass centers and pass directly to spinal motor neurons of respiratory
muscles
➢ Voluntary hyperventilation: Its duration is limited by CO2 level in blood.
Hyperventilation is followed by a period of apnea due to increased PO2 &
decreased CO2. This is followed by few shallow breaths due to decreased
PO2 i.e periodic breathing occurs
➢ Voluntary apnea: Is voluntary breath holding. The point at which the
person is obliged to breathe again (45-60 sec) is called the breaking point
➔ It is due to increased PCO2 & decreased PO2 & increased H+.
➔ It is mainly due to Increased PCO2 which stimulate central chemoreceptors
➔ It can be prolonged by:
1- Hyperventilation before breath holding (prolong by 15-20 sec) to wash
CO2 →decreased arterial CO2 tension
2- Breathing 100% O2 for one minute before experiment
3- Holding the breath in full inspiration This discharges inhibitory
impulses to respiratory center
4- Swallowing (Deglutition) which inhibits respiration
B)- Hypothalamus:
➢ It is higher center for integration of visceral & somatic functions. It
contains many centers which are related to respiration.
➢ Parasympathetic center: If it is stimulated (eg pain) → inhibit respiration
➢ Sympathetic center: If it is stimulated (eg emotions) stimulate respiration
➢ Temperature center: If it is stimulated (eg fever) stimulates respiration
[2] Afferent from Respiratory centers
A)- Afferents from upper respiratory passages:
➢ These reflexes (Protection reflex) protect alveoli from invasion by
harmful irritants
Sneezing reflex Cough reflex Swallowing
Stimulus Irritation of nasal Irritation of larynx, trachea & Stimulation of
mucosa bronchi pharyngeal mucosa
Afferent Trigeminal nerve Vagus nerve Glossopharyngeal
Response Deep inspiration Deep inspiration followed by Swallowing apnea
followed by - forced expiration against a i.e. stoppage of
-forced expiration closed glottis which opens respiration and
against an opened suddenly. closure of glottis
glottis

54 
 - Contraction of abdominal
muscles & rise of intra-
abdominal pressure
(100 mmHg)
Results Rush of air to Rush of air to outside getting To prevent
outside getting rid rid of foreign body or sputum aspiration of food
of irritants from air passages
B)- Afferents from lungs:
1. Lung stretch receptors:
➢ Stimulus: Lung inflation and airway distension
➢ Receptors: Stretch receptors in airway smooth muscles-slowly adapting
Receptors
➢ Afferent: Vagus nerve
➢ Response :
1. Initiates Herring Breuer reflex which switch off Inspiration by inhibiting
APC & DRG.
2. Not powerful in human but functions in newborns & animals
3. It is protective as it prevent lung over inflation.
4. Control rate & depth of breathing
1. Lung irritant receptors
➢ Stimulus: Mechanical eg dust particles-chemical: Exogenous eg noxious
gases, cigarette or endogenous eg histamine
➢ Receptors: In mucosa of bronchi & bronchioles
➢ Afferent: Vagus nerve
➢ Response:
1. Cough to expel irritant substances
2. Bronchospasm & apnea to limit penetration of dangerous substance
2. J receptors (juxta pulmonary capillary receptors)
➢ Stimulus: Pulmonary congestion (increase pulmonary interstitial fluid
pressure or capillary pressure) as in left sided heart failure
➢ Receptors: In alveolar wall close to pulmonary capillaries
➢ Afferent: Vagus nerve
➢ Response: Tachypnea (shallow rapid breathing)-dyspnea (difficult resp)
3)- Afferent from Cardiovascular system
(A) Arterial baroreceptors (High pressure receptors)
➢ Site: Aortic arch & carotid sinus
55 
 ➢ Stimulus: Arterial blood pressure (60-180 mmHg) & pulse pressure
➢ Afferent: Vagus & glossopharyngeal nerves
➢ Response:
• Increased ABP inhibits respiration and decrease tone of abdominal
muscles→ this decreases venous return, cardiac output and so, ABP return
to normal.
• Proof: Injection of nor adrenaline or large dose of adrenaline leads to
vasoconstriction and rise ABP which inhibits respiration (Adrenaline
apnea)
(B) Atrial receptors (Low pressure receptors)
➢ Site: Right atrium & big veins opening into it
➢ Stimulus: Increased venous return & increases central venous pressure
(CVP)
➢ Afferent : Vagus nerve
➢ Response:
1. Increased venous return will stimulate stretch receptors in the wall of the
right atrium.
2. They send afferent Impulses along the vagus to stimulate the respiratory
center.
3. This helps to increase ventilation to oxygenate the increased venous return
(Harrison's reflex). This helps to increase ventilation during muscular
exercise.
4)- Afferent from chest wall receptors:
➢ Site: Chest wall muscles & tendons
➢ Stimulus: Chest wall expansion & also tidal volume
➢ Response:
1. Inhibition of inspiration to determine tidal volume
2. In case of increase airway resistance or decrease compliance, the receptors
stimulation gives rise to→ dyspnea
5)- Afferent from proprioceptors:
➢ Site: Skeletal muscles, tendons, joints, ligaments
➢ Stimulus: Active & passive movements during exercise
➢ Response: Increase ventilation during exercise
6)- Visceral reflexes:
(A) Swallowing &Vomiting :
56 
 ➢ Stimulus: Food in pharynx
➢ Receptors: In mucosa of pharynx
➢ Afferent: Glossopharyngeal nerve
➢ Response:
1. Temporary apnea to prevent food from entering respiratory passages
2. Similar apnea occurs during straining & defecation
(B)Hiccup:
➔ It is a spasmodic contraction of the diaphragm which produces a sudden
inspiration during which the glottis suddenly closes producing
characteristic sound. It is due to abnormal stimulation of afferent endings
in diaphragm.
➔ The afferent is the phrenic nerve. Most attacks are of short duration. It can
be stopped by breath holding or inhalation of 6-7% CO2
(C)Yawning:
➔ It is a peculiar respiratory act, which leads to deep inspiration:
- To prevent collapse of under ventilated alveoli
- To increase venous return to heart
- Its physiological basis & significance are uncertain

Hypoxia
❖ Definition: Oxygen deficiency at tissue level
❖ It may be due to:
- Decrease O2 supply or.
- Decrease O2 utilization ability
❖ Anoxia: Complete absence of oxygen
❖ Types: Hypoxia is divided into four types:
1)- Hypoxic hypoxia (arterial hypoxia)
➔ In which PO2 of arterial blood is reduced
➔ This is the most common form of hypoxia seen clinically
➔ Causes:
1. Low oxygen tension in inspired air e.g. in: High altitudes & Mines
2. Pulmonary disorders:
A. Impaired ventilation: (hypoventilation)
• Depression of respiratory centres e.g. Morphine, Barbiturate&
Anaesthesia
• Obstructive lung diseases: Bronchial asthma (acute), Emphysema
(chronic) & Airway obstruction by foreign body
57 
 • Restrictive lung diseases:
i. Collapse (tumor), Compression (pneumothorax), Consolidation
(pneumonia)& Fibrosis (TB)
ii. Chest cage causes: Paralysis of respiratory muscles (poliomyelitis),
Skeletal deformities (kyphoscoliosis)& Myopathy
B. Impaired diffusion:
➢ Normal rate of diffusion is 25 ml O2/min/mmHg.
➢ It decreases in:
1. Pulmonary diseases which decrease surface area eg lobectomy
2. Pulmonary diseases with increase thickness of pulmonary membrane e.g.:
a. Pneumonia (alveoli filled with pus)
b. Edema (filled with lymph)-fibrosis
C. Impaired ventilation perfusion:
➢ Area with low V/Q ratio (Ventilation Perfusion ratio) result in hypoxic
hypoxia eg obstructive lung diseases (emphysema) has low ventilation
and normal perfusion
➢ So, the blood remains venous (physiological shunt)
D. Shunting of venous blood into arterial blood:
➢ Congenital heart diseases like atrial septal defect (ASD) in which there
is right to left shunt & arterial po2 = venous po2
❖ Symptoms of hypoxic hypoxia:
1) Sudden severe hypoxia:
i. PO2 < 20 mmHg
ii. Loss of consciousness within 15 sec
iii. Death within 5 minutes
2) Acute hypoxia: (PO2=25-40 mmHg)
➔ symptoms like alcohol intoxication
- Drowsiness - Poor mental judgment - Euphoria - Headache
- Nausea - Vomiting
3) Chronic hypoxia:(40-60 mmHg: On top of mountain)
➔ symptoms like fatigue:
- Drowsiness - Headache - Nausea - Anorexia
- Dyspnea
❖ Sign of hypoxic hypoxia: Generalized cyanosis
2)- Anemic hypoxia (deficiency of Hb)
➔ In which PO2 of the arterial blood is normal but the amount of Hb
available to carry O2 is reduced
➔ Causes:
58 
 1. Quantitative (insufficient Hb):
• In all types of anemia
• At rest hypoxia is not severe because 2, 3 DPG of RBCs is increases and
causes shift to right of O2 dissociation curve decreasing affinity of Hb to
O2
• At exercise, hypoxia is severing because increased O2 needs of tissues
2. Qualitative (abnormal forms):
1- Carbon monoxide (CO) poisoning:
• CO is a gas formed by incomplete combustion of carbon or gasoline
• It is toxic because:
1. CO combines with Hb to form carboxy hemoglobin at same site as O2
2. The affinity of Hb to CO is 210 times that for O2
3. Amount of carboxy Hb depends on duration of exposure and amount of
CO in inspired air. CO in inspired air (0.1%) results in transformation of
50% Hb to carboxy HB. Death occurs when 70-80% of Hb is converted to
COHb
4. Carobxy Hb shifts the O2 dissociation curve of the rest of oxy Hb to the
left
5. Carobxy Hb breaks down very slowly
➔ Signs:
1. Cherry red color of carobxy-Hb in skin & mucous membrane
2. Increased cardiac output
3. NO increase in ventilation because peripheral chemoreceptors are not
stimulated (arterial PO2 is normal)
4. Headache, nausea, loss of concentration
➔ Treatment:
1. Termination of exposure by removal from CO atmosphere
2. Artificial respiration
- Oxygen therapy: Pure O2
• 95% O2- + 5% CO2 because: CO2 stimulates
respiration Decrease affinity of Hb to O2
• Hyperbaric O2: O2 under pressure (1-3 atmosphere)
3. Blood transfusion
4. Complete rest for several hours
2- Met hemoglobin: (Oxidation of heme ferrous to ferric incapable to
carry O2)
❖ Cause: Oxidizing agents eg Drugs like nitrates or chlorates
❖ Signs: Dull grayish blue color in skin & mm resembling cyanosis
3- Sulf hemoglobin:(reduction of Hb to be incapable to carry O2)
59 
 ❖ Cause: Powerful reducing agents eg Sulfur containing drugs
❖ Signs: Leaden color of sulf-Hb in skin & mm resembling cyanosisuse:
Oxidizing agents eg Drugs like nitrates or chlorate
3)- Stagnant (ischemic) hypoxia (Inadequate blood flow through tissue or slow
circulation)
➔ In which PO2 in arterial blood is normal & Hb is normal but blood flow
to tissues is low
➔ Causes:
1- Generalized: Decreased cardiac output as in Heart failure & Shock.
➢ It affects mostly the brain, heart, liver & kidneys
2- Localized: Due to vascular obstruction of veins or arteries to a specific
organ (eg atherosclerosis, thrombosis & embolism)
➔ Signs: Generalized or localized cyanosis
4)- Histotoxic hypoxia (Inhibition of tissue oxidative or cytochrome system)
➔ In which PO2 in arterial blood is normal, Hb is normal & blood flow is
normal but due to toxic agents, tissue cells cannot utilize O2
➔ Causes:
1- Cyanide poisoning: Cyanide inhibits the cytochrome oxidase →
cytochrome remains in the reduced form → cells cannot use (utilize)
oxygen
2- Alcohol (methylalcohol)+ narcotics: Block dehydrogenase enzyme, so
tissues cannot use oxygen
➔ Treatment:
❖ Methylene blue or nitrits are used to treat cyanide poisoning.
❖ They act by forming methemoglobin, which then react with cyanide to
form nontoxic compound (cyanmethemoglobin).
❖ Oxygen therapy in different types of hypoxia:
1)- O2 therapy is highly beneficial in: Hypoxic hypoxia due to decrease:
a. Atmospheric O2 b. Hypoventilation c. Impaired diffusion
→ It increases the amount of O2 bound to Hb as well as the dissolved O2.
Also highly beneficial in CO poisoning
2)- O2 therapy is less beneficial in:
[Link] hypoxia due to: AV shunt anaemic hypoxia [Link] hypoxia
→ It increases only the dissolved O2 in physical solution

60 
3)- O2 therapy is not beneficial in Histotoxic hypoxia

Cyanosis
❖ Definition: It is bluish coloration of skin & mucous membranes due to
presence of excess reduced hemoglobin in blood capillary
❖ Threshold: - For cyanosis: 5 gm reduced HB/100 ml capillary blood
- Reduced Hb has blue colour seen in:
A. Lips B. MM (Mucus membranes) C. Nail beds D. Lobule of the
ear
❖ Types:
A. Generalized (or central) cyanosis
B. Localized (or peripheral) cyanosis
❖ Causes of cyanosis & its relation with hypoxia:
1) Hypoxic hypoxia due to decrease % saturation of Hb with O2 in arterial
& venous blood
2) Stagnant hypoxia: due to low blood flow & extra O2 is removed from
Hb.
3) Asphyxia eg airway obstruction, drowning
❖ Cyanosis does not appear with:
a. Anaemic hypoxia (because total amount of Hb is reduced & hence
reduced Hb is reduced)
b. Histotoxic hypoxia (because there is failure of reduction of Hb)
c. CO poisoning (because of cherry red colour of carboxy Hb)

61 
 Effects of increased barometric pressure

Effect of sea depth on pressure

➢ At sea level, the person is exposed to pressure of one atmosphere. At this

pressure, 1000 ml of Nitrogen gas are dissolved in tissues mainly in fatty
tissues, nervous tissue as N2 is five times more soluble in fat.
➢ Every 10 meters of depth in sea water (10.4 meter in fresh water), the
pressure increases by one atmosphere.
➢ So, at depth of 30 meter: The diver is exposed to pressure of atmosphere
& the amount of dissolved N2 is 4000 cc. ie an extra 3000 cc N 2 are
dissolved in tissues.
➢ Those who dig under water tunnel are also exposed to the same pressure
in the chambers (caisson's) in which they work.
➢ The pressure of the gas, the diver breaths must be equal to pressure on his
chest, otherwise he has difficulty in breathing (SCUBA device)

Open-circuit demand type of SCUBA apparatus

Problems associated with increased barometric pressure (under sea diving):

➢ During Descend (compression)
A. CO2 toxicity: Rare & seen only at great depths.
62 
 B.O2 toxicity:
- Prolonged exposure >12 hrs → oxygen toxicity develop rapidly.
- It can be avoided by using gas mixture of O2 & Inert gas (helium)
[Link] narcosis: Increased amount of dissolved N2 as a result of
increased atmospheric pressure → lead to increase N2 in nervous tissue
decreasing their excitability & anesthetic effects
- At 30 meter- euphoria
- At greater depth-- depression of CNS
- This is can be avoided by breathing gas mixture of oxygen & helium.
NB: Helium Is less soluble In body fluids than nitrogen
➢ During Ascend (Decompression)
❖ Decompression sickness:
1. If the person is decompressed slowly, the excess N2 is liberated, through
lung & expired
2. If the person is decompressed rapidly, the excess N2 escapes from
solution to form bubbles in tissues and blood.
• Bubbles in the tissues cause severe pain especially at joints
• Bubbles in the blood stream, which occur in more severe cases, obstruct
arteries of the brain (cerebral) causing major paralysis, convulsions and
respiratory failure
• Bubbles in coronary arteries may cause myocardial damage
• Bubbles in pulmonary vessels may cause dyspnea.

❖ Treatment:
1. Recompression in pressure chamber followed by slow decompression.
2. Decompression sickness may occur during rapid ascend in unpressurised
airplanes
Only Nitrogen:
✓ Which can cause decompression sickness, Not CO2 because it can unite
with buffers of tissues & blood
✓ Nor O2 because it is taken with hydrogen & utilized by time.

63 