PUA respiration

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

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

Mechanics of respirationThe lungs are enclosed in an air tight compartment & the only

connection with atmosphere is through the mouth & noseThe 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

Figure 22.12

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

The ribs are connected with two layers of muscles:

• External intercostal: pass downwards & forwards

• Internal intercostal: pass downwards & backwards

• 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

descent of diaphragm

elevation of rib cage

V1V2

VaVb

V1 < V2

Va < Vb

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.

Normal Breathing Cycle

The Intrapleural Pressure Def: It is the pressure inside the pleural sacsValue: 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 pressure1-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 pressureCauses of the tendency of the lung to recoil1)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

Intrapleural pressure

Pneumothorax

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 & antero-posterior 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)

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

Alveolar Pressure Changes

Inspiration

Figure 22.13.1

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 intra-alveolar pressure… air is forced out

• It is a passive process (relaxation of muscles & recoil of elastic fibers)

Expiration

Figure 22.13.2

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

Ventilation

• It is the movement of air between lungs & atmosphere

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

Spirometer and Lung Volumes/Capacities

Lung volumes

Vital capacity (sum total of all except RV)

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.

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

Work of BreathingWork 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)

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)

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

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

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

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.

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

decreases, surfactant’s ability to lower surface tension increases.

3) Prevent pulmonary oedema

Surfactant Deficiency:

RDS of the newborn. The lung is rigid and oedematous and the alveoli collapse

air air air

What is surface tension?

How do we deal with surface tension??

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.

Measurement of the dead space

• Bohr`s equation:• Anatomical dead space=

tidal volume x (alveolar CO2- expired CO2) Alveolar CO2

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.

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

Comparison between the respiratory gases

atmospheric atmospheric airair

Alveolar airAlveolar airExpired airExpired air

O2O2159mmHg159mmHg104mmHg104mmHg120mmHg120mmHg

CO2CO20.3mmHg0.3mmHg40mmHg40mmHg27mmHg27mmHg

H2OH2Ovariablevariable47mmHg47mmHg47mmHg47mmHg

N2N2597mmHg597mmHg569mmHg569mmHg566mmHg566mmHg

Total Total pressurepressure

760mmHg760mmHg760mmHg760mmHg760mmHg760mmHg

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.

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

Total AREA available for diffusion of gases is large

in human 70 m2

Diffusion PATH LENGTH is very small, =2µm Pulmonary

Epithelium

The respiratory membraneThe respiratory membrane::

• 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

• 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

• 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

Exchange of gases

Atmospheric airAtmospheric airAlveolar airAlveolar air

%%pressurepressure%%pressurepressure

COCO220.04%0.04%0.3mmHg0.3mmHg5.6%5.6%40mmHg40mmHg

OO2220.95%20.95%159mmHg159mmHg14.8%14.8%105mmHg105mmHg

NN2279.00%79.00%600mmHg600mmHg79.6%79.6%568mmHg568mmHg

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.

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

HemoglobinEach 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

• 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

• 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.

Hemoglobin-O2 Binding Curve

0 20 40 60 80 1000

20

40

60

80

100

0

5

10

15

20

26

50

75

9097.5

PaO2 (mm Hg)

% S

atu

rati

on

of

Hem

og

lob

inH

b-O

2 con

tent

(ml O

2 /100 ml b

loo

d)

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

ml

O2/

100

ml

blo

od

0

5

10

15

20

High affinity onlyCan’t release much O2 to tissues

Low affinity onlyDoesn’t hold on to But can’t pick up much O2 at tissues much O2 at lungs

S-shaped hemoglobin curveReleases much Becomes saturated

O2 at tissues with O2 at lungs

Advantages of “S-shaped” curve for Hb-O2 association

Active cell

Bohr Shift Hb-02 Curve

0 20 40 60 80 1000

20

40

60

80

100

Normal Hb

Bohr Shift H+], CO2, Temp or DPG

H+], CO2

Temp

PaO2 (mm Hg)

% S

atu

rati

on

of

Hem

og

lob

in

• 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

• 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)

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

• 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

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:

CO2

Tissues

C.A.CO2 + H2O H2CO3 H+ + HCO3

-

HCO3-

slow

HbO2 Hb.H + O2+

O2

How is CO2 carried by the blood??

Plasma: dissolved

HCO3-

carbamino proteins

RBCs: dissolved

HCO3-

Carbamino Hb

Hb + CO2 Hb.CO2 (carbamino cmpd.)

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

• 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)

• 4-Pneumotaxic centre: in the upper pons• It sends inhibitory impulses to apneustic

center & to inspiratory areas to switch off respiration

• Both inspiratory & expiratory areas are influenced by impulses from pneumotaxic & apneustic center & higher centers

• DRG are the integrating site for different inputs

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)

• 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

• 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 over-inflation. 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

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

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

BBB CSFPlasma

CO2

HCO3

+

H+

CO2 HCO3 + H+

RespiratoryAlkalosis

high pHCSF limits Hyperventilation

When pHCNS

returns to norm (HCO3 pumped out)VE is less restrained

Chemoreceptors

• Monitor changes in blood PC02, P02, and pH.

• Central:– Medulla.

• Peripheral:– Carotid and aortic bodies.

• Control breathing indirectly.

Insert fig. 16.27

Figure 16.27

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

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

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 veno-

arterial shunts & congenital heart disease • Low PO2, low % saturation of Hb, low O2 content in the

arterial &venous blood

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

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

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

Types of Types of hypoxiahypoxia

Arterial bloodArterial bloodVenous bloodVenous blood

PO2PO2%sat%sat%O2%O2PO2PO2%sat%sat%O2%O2

HypoxicHypoxiclowlowlowlowlowlowlowlowlowlowlowlow

AnaemicAnaemicnormalnormalnormalnormallowlowlowlowlowlowlowlow

Stagnant Stagnant normalnormalnormalnormalnormalnormallowlowlowlowlowlow

histotoxichistotoxicnormalnormalnormalnormalnormalnormalhighhighhighhighhighhigh

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)