1. Respiratory System
• Aim:
• Gas exchange: O2 to the cells & CO2 out of the
body.
• Regulation of pH of extracellular fluid
• Respiration: the different processes by which we
finally obtain energy from different food stuffs

2. Respiration processes includes:
• 1- external respiration:
• a) pulmonary ventilation; gas exchange between lung
& atmosphere
• b) pulmonary respiration; gas exchange between
alveoli & blood
• 2- gas transport; O2 & CO2 transport in the blood &
body fluids to & from the cells
• 3- internal respiration:
• a) gas exchange between cells & tissue fluids
• b) chemical reactions that end by release of energy

5. Mechanics of respiration
The lungs are enclosed in an air tight compartment & the only
connection with atmosphere is through the mouth & nose
The lungs are surrounded by minute space called pleural space
that contains a film of fluid to lubricate the movement of the
lungs
The pleural space is lying between 2 layers of pleura; visceral
pleura, attached to the lungs & parietal pleura lining the
inner surface of thoracic cage and diaphragm
The chest wall is formed of muscles, ribs, vertebrae, skin &
subcutaneous tissue

6. Figure 22.12

7. The diaphragm
• The diaphragm is a muscle, separates the
thoracic cavity from the abdomen
• When relaxed……. Dome shape
• When contract…… It descends & become less
convex

9. The ribs are connected with two layers of
muscles:
• External intercostal: pass downwards &
forwards
• Internal intercostal: pass downwards &
backwards

11. • When external intercostal ms contract….. They
raise the upper ribs & sternum…….. Increasing
the antero-posterior diameter of the chest…..
23 – 30% of volume change and slightly the
transverse diameter…1-2%
• When diaphragm contracts…….becomes less
convex, pushes the abdominal viscera
downwards…….. Increases the vertical diameter
of the chest ….70% of the increase in volume

12. V1
descent of
diaphragm
V2
V1 < V 2
Va
elevation of
rib cage
Va < Vb
Vb

14. Intra-alveolar pressure
• These changes in the intra alveolar pressure are
caused by Changes in the Volume of the lungs.
• At the end of expiration with the glottis open, it is
atmospheric
• During inspiration, the chest size increases, the
pressure falls below atmospheric(-1), air will flow
into the lungs
• During expiration, the lung recoils, the intra-alveolar
pressure rises above atmospheric (+1), air flows out
of the lungs.

15. Normal Breathing Cycle

16. The Intrapleural Pressure
Def: It is the pressure inside the pleural sacs
Value: It is always Negative.
at the end of normal expiration: -2
at the end of normal inspiration: -6 to -8
--During forced inspiration: -30 to -70
--During forced expiration with the glottis closed +50 (Valsalva experiment)
*Functions of the intra pleural pressure
1-It helps lung expansion.
2-It helps venous and lymphatic return.
*Causes of negativity of intrapleural pressure:
Tendency of the lung to recoil and tendency of the chest to expand.
At equilibrium, these two opposing forces lead to the negativity of intrapleural pressure
Causes of the tendency of the lung to recoil
1)Elastic tissues in the lungs
2)The surface tension of the fluid lining the alveoli. At the air water interface, the attractive
forces between the water molecules make the water lining like a stretched balloon that
tries to shrink. This force (Surface tension) is strong enough to collapse the alveoli.
* If air is introduced into the pleural space:
1- the lung will collapse
2- the chest will expand
3- the intrapleural pressure increases, becomes atmospheric 4- venous return decreases

19. Intrapleural pressure

20. Pneumothorax

21. Mechanism of air flow between lungs and
atmosphere
• Stimulation of the phrenic nerve, and the intercostal
nerves… contraction of diaphragm & external
intercostals…. Increasing the vertical & anteroposterior diameter of the chest….. Increase in chest
volume …. Decrease intra-pleural pressure.. The
lungs expands… decrease intra-alveolar
pressure….the air flows into the lungs
• It is an active process (involving muscle contraction)

22. Inspiration
• The diaphragm and external intercostal muscles
(inspiratory muscles) contract and the rib cage
rises
• The lungs are stretched and intrapulmonary
volume increases
• Intrapulmonary pressure drops below
atmospheric pressure (−1 mm Hg)
• Air flows into the lungs, down its pressure
gradient, until intrapleural pressure =
atmospheric pressure

23. Alveolar Pressure Changes

24. Inspiration
Figure 22.13.1

25. Expiration
• When inspiration ends, the muscles relax….
Decrease in the diameters of the chest…. The
thoracic wall recoils …. The intra-pleural
pressure rises…the elastic lungs recoil…
compressing the air… rising of the intraalveolar pressure… air is forced out
• It is a passive process (relaxation of muscles &
recoil of elastic fibers)

26. Expiration
Figure 22.13.2

28. Accessory muscles of respiration
• During quiet breathing, only 1/10 of the external
intercostal muscles & diaphragm are active &
expiration is a passive process
• With more powerful respiration, all fibers of intercostal
& diaphragm are active, this increases the pulmonary
ventilation 10 folds
• More forced respiration, there is accessory ms of
inspiration (sternomastoid, serratus anterior, scaleni) &
expiration (internal intercostal, abdominal recti ms),
these make respiration more deep & decrease airway
resistance

29. Ventilation
• It is the movement of air between lungs &
atmosphere

30. Lung volumes
• Lung volumes:
• 1- Tidal volume (TV or Vt): it is the volume of air inspired or
expired each cycle during normal quiet breathing, it is 500
mL
• 2- Inspiratory reserve volume (IRV): it is the maximum
volume of air can be inspired after normal inspiration, it is
3000 mL
• 3- Expiratory reserve volume (ERV) it is the maximum
volume of air can be expired after normal expiration, it is
1100 mL
• 4- Residual volume (RV): it is the volume of air remaining in
the lungs after maximal expiration, it can not be expired, it
prevent lung collapse & aerates the blood between
breaths, it is 1200 mL

32. Spirometer and Lung
Volumes/Capacities

33. Lung volumes
Vital capacity (sum total of all except RV)

34. Lung capacities
• A capacity is two or more volumes added together
• 1- Inspiratory capacity (IC): it is the maximum volume
of air can be inspired after normal expiration.
• IC= TV+ IRV= 3500mL
• 2- Functional residual capacity (FRC): it is the volume
of air remained in the lung after normal expiration
• FRC=ERV+RV= 2300mL.

35. Lung capacities
• 3-Vital capacity: (VC) it is the maximum volume
of air can be expired after maximal inspiration.
• VC=IRV+ERV+TV=4600mL
• Total lung capacity: (TLC) it is the volume of air
contained in the lung after deep inspiration.
• TLC=IRV+ERV+TV+RV= 5800mL
• All lung capacities are 20-25% more in males
than females, more in athletes, less in
recumbent position

36. Work of Breathing
Energy required during normal respiration is 2-3%
of the total energy expenditure, it increases in
heavy exercise, but the ratio to total energy
expenditure remains nearly the same.
Work is done only in inspiration, but normal
expiration is a passive process depending on the
elastic recoil of the lung and chest wall.
*Contraction of expiratory muscles occurs when air
way resistance or tissue resistance increases as in
asthma. (expiration needs work)

37. Work of breathing
• Energy are needed for contraction of respiratory
muscles. Increase when accessory ms contracts in
deep& forced breathing
• 1- overcome the viscosity of the expanding lung (non
elastic tissue resistance)
• 2- stretch the thoracic & lung elastic fibers & overcome
the surface tension in the alveoli. This energy increase
if surfactant is deficient
• 3- overcome airway resistance. This increase in
bronchial asthma or obstructive emphysema

38. Compliance
• It is the ability to expand or stretch
• It is the reciprocal of elasticity (recoil of stretched
elastic fibers)
• It is a useful measurement for diagnosis of
respiratory diseases
• It is the change in length or volume per unit change
in stretching force.
• Normal compliance of lungs & thorax =
0.11L/cmH2O pressure
• Normal compliance of lungs alone = 0.2 L/cmH2O
pressure

39. Compliance
• High compliance means a given change in pressure
moves a larger volume of air in the lungs
• Low compliance in fibrosis, congestion, oedema,
bronchial obstruction or in increased surface tension
• The compliance is small in newborn, increases
gradually with age, decreases in old age
• The main factors affect compliance are: congestion,
size, surface tension

40. Surface Tension
• Force exerted by fluid in alveoli to resist
distension.
• Lungs secrete and absorb fluid, leaving a very thin film of fluid.
– This film of fluid causes surface tension.
• H20 molecules at the surface are attracted to
other H20 molecules by attractive forces.
– Force is directed inward, raising pressure in alveoli.

41. Surfactant
•
Def:
It is the surface active agent
• Composition: Phospholipid
(dipalmitoyl lecithin), protein and
Carbohydrates
• Secretion: produced by alveolar type II
cells.
• Action: Lowers surface tension.
• Functions of surfactant:
1) Facilitates lung expantion
2) Prevent lung collapse As alveoli radius Surfactant Deficiency:
decreases, surfactant’s ability to lower RDS of the newborn. The
surface tension increases.
lung is rigid and
3) Prevent pulmonary oedema
oedematous and the
alveoli collapse

43. What is surface
air
tension?
air
air
How do we deal with surface tension??

44. Alveolar Ventilation
• The inspired air is distributed between:
• 1- The anatomical Dead Space: It is the part of the respiratory
system where no gas exchange takes place. It extends from the
mouth to the terminal bronchioles. Ventilation of dead space is said
to be wasted ventilation.=1/3 of the resting tidal volume
• 2- the rest of air occupies the respiratory bronchioles, the alveolar
ducts, alveoli and alveolar sacs, gas exchange takes place
• Minute Ventilation= VT (ml/breath) x Respiratory rate (breath/min)
=500 x 12
=6000 ml/min.
• Alveolar ventilation= 2/3 x 500 x12
=4000 ml/min.
• Dead space ventilation= 1/3 x 500 x 12
= 2000ml/min.

47. Measurement of the dead space
• Bohr`s equation:
• Anatomical dead space=
tidal volume x (alveolar CO2- expired CO2)
Alveolar CO2

48. Physiological dead space
• The anatomical dead space + unperfused
alveoli
• In Normal person the anatomical dead space=
the physiological dead space
• In certain diseases the physiological dead
space may be 10 times anatomical dead
space or more.

49. Gas exchange
• Alveolar air contains less O2 & more CO2 than
inspired air (mixed with air that was in the
dead space)
• Expired air constitute a mixture of alveolar air
and dead space (which is atmospheric)
• The exchange of oxygen & CO2 between
alveoli & blood is passive by diffusion

50. Comparison between the respiratory
gases
atmospheric Alveolar air Expired air
air
O2
159mmHg
104mmHg
120mmHg
CO2
0.3mmHg
40mmHg
27mmHg
H2O
variable
47mmHg
47mmHg
N2
597mmHg
569mmHg
566mmHg
Total
pressure
760mmHg
760mmHg
760mmHg

51. Gas exchange
• O2 of air is higher in the
lungs than in the blood, O2
diffuses from air to the
blood.
• C02 moves from the blood
to the air by diffusing
down its concentration
gradient.
• Gas exchange occurs
entirely by diffusion.
• Diffusion is rapid because
of the large surface area
and the small diffusion
distance.

54. Diffusion is determined by several factors:
• 1- Alveolar- capillary membrane:
• Semi-permeable: separates alveolar air from
pulmonary capillary blood
• Layers:
• Fluid film lining the alveoli
• Alveolar membrane
• Interstitial fluid
• Capillary wall

55. :The respiratory membrane
Total AREA available for
diffusion of gases is large
in human 70 m2
Diffusion PATH LENGTH
is very small, =2µm
Pulmonary
Epithelium

56. • 2- Partial pressure gradient of gases across the
alveolar capillary membrane:
• The partial pressure of oxygen in mixed venous blood is
40mmHg
• The partial pressure of oxygen in alveolar air is
100mmHg
• O2 diffuses from the alveoli to the capillary blood along
a partial pressure gradient of 60mmHg
• The partial pressure of CO2 in mixed venous blood is
46mmHg
• The partial pressure of CO2 in alveolar air 40 mmHg
• CO2 diffuses along pressure gradient of 6 mmHg

57. • 3- the physical properties of gases:
• Solubility: the more soluble the gas, the faster its diffusion (CO2
is 23 fold more soluble than O2)
• Molecular weight: the higher the molecular weight of the gas,
the slower its diffusion
• The solubility of a gas & its MW determine diffusion coefficient
(the rate of diffusion through a unit area of a given membrane
per unit pressure difference.
• Diffusion coefficient = solubility / √molecular size
• The diffusion coefficient of O2 = 1.0
• The diffusion coefficient of CO2 = 20
• CO2 can diffuse 20 times faster than O2
• Diffusion failure affects O2 before affecting CO2
• 4- surface area of the alveolar capillary membrane: 70square
meter
• When increased, gas exchange increases

58. • 5-Ventilation- blood flow ratio:
• Effective surface area means the functional alveoli in
contact with functioning capillaries, where the alveolar air
comes in contact with capillary blood
• Ventilation / perfusion ratio = alveolar ventilation/
pulmonary blood flow
• In a normal adult male at rest
• Alveolar ventilation is 4L/min
• Pulmonary blood flow is 5L/min
• Ventilation / perfusion ratio=0.8
• Diseases that affects the alveolar capillary membrane will
lower the diffusion capacity of O2
• Fatal levels of O2 diffusion impairment is reached long
before CO2 diffusion is affected

59. Exchange of gases
Atmospheric air
Alveolar air
%
%
CO2 0.04%
pressure
0.3mmHg 5.6%
pressure
40mmHg
O2 20.95%
159mmHg 14.8%
105mmHg
N2 79.00%
600mmHg 79.6%
568mmHg

61. Gas Transport by The Blood
•
•
•
•
Oxygen transport:
O2 is transported in the blood in two forms:
1- Attached in loose combination with Hb
Over 98% of arterial O2 is carried in the form of
oxyhemoglobin. PO2 in systemic arterial blood is usually
below 100mmHg eventhough it may be 100mmHg in the
pulmonary capillary blood, because some venous blood mixes
with arterial blood
• 2- Physically dissolved: less than 2% of O2 in the arterial
blood. At PO2 100mmHg, about 0.3ml O2 dissolve in 100ml
blood. In venous blood, PO2 is 40mmHg, about 0.12ml O2 /
100ml blood is dissolved.

62. Oxyhaemoglobin
• Haemoglobin has great affinity for O2
• It combines loosely & reversibly with O2 by
process called oxygenation (not oxidation)
• The reaction is very fast, less than 10 msec
• The reaction increases with the increase in
PO2
• The relation between oxyHb formation and
PO2 is studied in the Oxyhaemoglobin
dissociation curve

63. Hemoglobin
Each hemoglobin has 4
polypeptide chains and 4
hemes.
• In the center of each
heme group is 1 atom of
iron that can combine
with 1 molecule 02.
• Fe remains in the ferrous
form (Oxygenation and
not oxidation)
• Hb carries 65 times as
much as plasma at PO2 of
100mmHg
Insert fig. 16.32
Figure 16.32

64. • Hemoglobin dissociation curves:
• Def:It is a relationship between PO2 and %HbO2 saturation (and not
content)
• Characteristics:
• 1-It is not linear, it is sigmoid (S shaped) with flat part and steep part.
• Causes of S shaped curve
• Hb is formed of 4 sub units which load or unload with different
affinity.
• Oxygenation of one haem unit leads to configurational change in the
Hb molecule, increasing affinity of the second, and oxygenation of
the 2nd , increasing affinity of the 3rd ,etc..
• The dissociation curve starts slowly, but rapidly gained sigmoid shape
• 2-there is steep rise in the percentage saturation of Hb between PO2
0& 75mmHg
• 3- above 75mmHg, there is slow rise of the curve, becoming more or
less flat at PO2 of 80mmHg

67. • 1gm of Hb binds up to 1.34ml O2
• The partial pressure of O2 in the arterial blood is about
95mmHg,Hb is 97% saturated (Hb concentration is
150gm/L, O2 content is 195ml/l of blood)
• At PO2 40mmHg, Hb saturation is 75% saturated.
• At rest, Arterio-venous difference (O2 uptake by
tissues) is about 40-45ml /L of blood
• During exercise, oxygen uptake by tissues increase,
PO2 drops to 15 mmHg, % saturation 20%, O2
content=40ml
• During exercise, the arterio-venous O2 difference,
150ml/L
• Quantity of O2 carried in a volume of blood is
dependent on PO2 & Hb concentration.

68. Hemoglobin-O2 Binding Curve
75
% Saturation of
Hemoglobin
60
15
50
80
20
10
40
5
20
26
0
0
20
0
40
60
PaO2 (mm Hg)
80
100
Hb-O2 content
(ml O2 /100 ml blood)
97.5
90
100

69. Factors which affect Oxy-Hb
dissociation curve
• Shift to the right: (facilitate the release of O2 at
tissues) →↓ affinity of Hb for O2→ easier giving
O2 to the tissues
• 1- ↑ PCO2: Bohr effect
• 2-↓ pH :due to lactic acid during exercise,
more CO2 production
• 3-↑ temperature: active tissues during
oxidative processes more heat is released,
more O2 supply to the tissues
• 4- ↑ 2,3 DPG: found in RBCs & increases
in cases of hypoxia & high altitudes

70. Advantages of “S-shaped” curve for Hb-O2 association
20
High affinity only
Can’t release much
O2 to tissues
15
S-shaped hemoglobin curve
ml O2/100 ml blood
Releases much
O2 at tissues
Becomes saturated
with O2 at lungs
10
Low affinity only
Doesn’t hold on to
much O2 at tissues
5
0
Active cell
But can’t pick up
much O2 at lungs

71. Bohr Shift Hb-02 Curve
% Saturation of
Hemoglobin
100
↓ +],↓ 2
[H CO
Temp
↓
80
Normal Hb
60
Bohr Shift
↑ +], ↑ 2, ↑
[H
CO Temp or DPG
40
20
0
0
20
40
60
PaO2 (mm Hg)
80
100

72. • Factors shift the curve to the left: (increases
Hb affinity to O2, Easier picking up O2,
Difficult release of O2)
• 1- ↓ PCO2 at lungs
• 2- ↑pH
• 3- ↓ temperature
• 4- foetal Hb: as it binds to 2,3 DPG less
effectively

73. •
•
•
•
•
•
•
Dissolved O2:
↑ PO2….↑ dissolved O2
O2 is poorly soluble
In 100ml blood, 0.003ml O2 dissolve /1mmHg PO2
In arterial blood, 0.3 ml/100ml
In venous blood, 0.12 ml/100ml
The dissolved O2 is at equilibrium with the O2 combined
with Hb
• It is the dissolved O2 gets transferred to tissues & become
replaced from O2 carried by Hb
• Although dissolved O2 is less than 2% of total O2 transport,
it is essential for tissues that do not have blood supply, as
cartilage & cornea which depend on O2 dissolved in tissue
fluids
• ↑ dissolved O2 by breathing pure or hyperbaric O2 (this is
the base of O2 therapy)

74. CO2 transport
• It is transported from tissues that produce
CO2 to the lungs, where it is unloaded,
removed to the atmosphere
• It is transported by plasma & RBCs

75. • Transport of CO2 in the blood:
• 1- dissolves in the plasma & RBCs: 5%, it is important
because it determines the tension (40mmHg in arterial
blood & 46 mmHg in venous blood) & determine the
direction of flow
• 2- chemically combined: 95% of CO2
• a-carbamino compounds: carried by plasma proteins &
hemoglobin
• b- bicarbonates:
• In the form of KHCO3 & NaHCO3
• 43ml/100ml in arterial blood
• 56ml/100ml in venous blood

76. Tidal CO2 transport
• It is the volume of CO2 added to each 100ml of arterial
blood during its flow through the tissues
• CO2 produced by active cells as a result of metabolism
• Normally 4ml/100ml blood during rest (52-48)
• CO2 carried in 3 forms in plasma:
• 1- dissolves in the plasma
• 2- Bicarbonates:
• 3- Carbamino proteins:

77. Tissues
CO 2
C.A.
slow
HCO 3
CO 2 + H 2 O
HCO 3 -
→
H 2 CO 3
HbO 2 → Hb. H + O 2
+
→ H+ +
O2
-
Hb + CO 2
Hb . CO 2
(carbamino cmpd.)
How is CO2 carried by the blood??
Plasma: dissolved
HCO3carbamino proteins
RBCs: dissolved
HCO3Carbamino Hb

78. •
•
•
•
•
•
•
Control of ventilation
Mechanism of regulation involves:
Nervous & chemical
The respiratory centre:
In the medulla & pons.
Can be divided into 4 groups;
1- dorsal respiratory group: (Rhythmicity centre)
In the medulla, they are inspiratory neurons, they
discharge rhythmically during resting & forced inspiration
• 2- ventral respiratory group:( expiratory neurons)
• In the medulla, they are inactive during resting
breathing
• Activated in forced ventilation as in exercise

79. • 3- Apneustic centre:
• In the pons
• It sends excitatory impulses to dorsal respiratory
group, potentiates the inspiratory drive. Section to
remove the apneustic impulses…. Gasping
breathing( shallow inspiration followed by long
expiration)
• Receives inhibitory impulses from vagus nerve during
inflation of the lungs (Hering Breuer reflex)
• Receives inhibitory impulses from Pneumotaxic
centre in the upper pons
• Section of vagus & abolishing the impulses from
pneumotaxic centre, results in apneustic breathing
(prolonged inspiration)

80. • 4-Pneumotaxic centre: in the upper pons
• It sends inhibitory impulses to apneustic
center & to inspiratory areas to switch off
respiration

82. • Both inspiratory & expiratory areas are
influenced by impulses from pneumotaxic &
apneustic center & higher centers
• DRG are the integrating site for different
inputs

83. Nervous control of ventilation
• The rhythmicity centre sends sends excitatory impulses via phrenic &
intercostal nerves to diaphragm, external intercostal muscles
• The rhythmicity center receives impulses from higher brain centers,
brain stem, special receptors
• Higher brain centers:
• 1- impulses from cerebral cortex: voluntary hyperventilation,
voluntary apnea
• 2- impulses from cerebellum: coordinates breathing with other
activities as swallowing, talking, coughing
• 3- Impulses from hypothalamus: centers of emotions & temperature
regulation, breathing modified during emotional stress, changes of
temperature, (panting of dogs)

84. • Centers in the medulla & pons:
• 1- the rhythmicity center interconnected with the
cardiac & vasomotor centers located in the medulla
• 2- apneustic center sends excitatory impulses to
rhythmicity center to produce deep inspiration
• 3- pneumotaxic center to rhythmicity center to
inhibit deep inspiration & to apneustic center

85. • Special receptors:
• 1- sensory vagal fibers: when lung is inflated, stretch
receptors are stimulated, send inhibitory impulses
through vagus to inhibit the apneustic center (Hering
Breuer inflation reflex) protects the lung from overinflation. There is a weaker Hering Breuer deflation
reflex
• 2- active & passive movement of joints & muscles:
propioceptive stimulation stimulate breathing in
exercise
• 3- skin receptors: noxious stimuli stimulate breathing
• 4- baroreceptors in aortic arch & carotid sinus modify
breathing

86. Chemical control of ventilation
•
•
•
•
•
Central & peripheral chemoreceptors:
Peripheral chemoreceptors:
Site: in the carotid & aortic bodies
Stimuli: ↓ in arterial PO2, ↑PCO2, ↓pH
Stimulation: send stimulatory impulses to
rhythmicity center via glossopharyngeal &
vagus nerves

87. Central chemoreceptors
•
•
•
•
Central chemoreceptors:
Site: medulla
Stimuli: H+ ion concentration in the CSF
H+ ion can not cross the blood brain barrier,
but it increases in the CSF secondary to
↑PCO2 in the blood, which pass through BBB
to the CSF
• It sends simulatory impulse to stimulates
ventilation

88. Plasma
CO2
BBB
CSF
CO2 ←→ HCO3 + H+
HCO3
+
H+
Respiratory
Alkalosis
high pHCSF limits
Hyperventilation
When pHCNS
returns to norm
(HCO3 pumped out)
VE is less restrained

89. Chemoreceptors
• Monitor changes in
blood PC0 , P0 , and pH.
• Central:
2
2
– Medulla.
Insert fig. 16.27
• Peripheral:
– Carotid and aortic
bodies.
• Control breathing
indirectly.
Figure 16.27

90. Hypoxia
•
•
•
•
•
It means deficient O2 supply to the tissues
Causes:
1- interference with O2 in the lungs
2- interference with O2 transport in blood
3- interference with O2 delivery to the tissues

91. Hypoxia
• Types:
• 1- hypoxic hypoxia: low PO2 in the arterial blood
• 2- anaemic hypoxia: lowering O2 carrying capacity of the
blood
• 3- stagnant hypoxia: slow circulation
• 4- histotoxic hypoxia: disturbed uptake of O2 by tissues
• Treatment:
• O2 therapy, correcting underlying cause

92. Hypoxic hypoxia
• Causes: Any interference with normal oxygenation of the
arterial blood leading to low PO2 as in:
• 1- low atmospheric PO2 as in high altitude
• 2- ventilation defects: as in paralysis of respiratory ms,
airway obstruction, poisons that inhibits the
• respiratory center as morphine & barbiturates (high CO2)
• 2- interfere with normal O2 diffusion in the lung
• 3- mixing of arterial blood with venous blood as in venoarterial shunts & congenital heart disease
• Low PO2, low % saturation of Hb, low O2 content in the
arterial &venous blood

93. Anaemic hypoxia
• Causes: anaemia, abnormal hemoglobins, CO
poisoning
• PO2 is normal in the arterial &venous blood
• % saturation is normal in the arterial &venous
blood
• (except in CO poisoning)
• Low O2 content in the arterial &venous blood

94. Stagnant hypoxia
•
•
•
•
Types:
1- localized: e.g. disturbed circulation in a limb
2- generalized as in heart failure
normal arterial blood PO2, % saturation,O2 content
• ↓Venous blood PO2, ↓ % saturation, ↓Content of O2

95. Histotoxic hypoxia
• Disturbance of O2 uptake due to poisoning of
cellular enzymes e.g. cyanide poisoning or tissue
oedema
• normal arterial blood PO2, % saturation,O2
content
• ↑Venous blood PO2, ↑% saturation, ↑Content of
O2

96. Types of
hypoxia
Arterial blood
Venous blood
PO2
%sat
%O2
PO2 %sat %O2
low
low
low
low
low
low
Anaemic normal normal low
low
low
low
Stagnant normal normal normal low
low
low
histotoxic normal normal normal high
high
high
Hypoxic

97. Cyanosis
•
•
•
•
•
Def: blue coloration of the skin & mucous membrane
Cause: reduced Hb more than 5gm/100ml
Types:
Localized type: in the tips of fingers in cold
Generalized: in veno-arterial shunts, severe hypoxia
in the newborn, or at very high altitude
• It is more common seen in polycythemia
• it s very rare in anaemia (the person already has low
Hb, so he cannot have 5gm reduced Hb)