Hypoxia

MODERATOR : DR MEERA
BALASUBRAMANYAM
Professor Dept of
Anaesthesiology MMCRI
SPEAKER: DR
NANDHINI.K.S.KARAT
Hypoxia
HYPOXIA:is defined as lack of oxygen at the tissue level
HYPOXEMIA: is defined as low arterial oxygen tension below the
normal level
Classified into ;
• Hypoxic hypoxia
• Stagnant hypoxia
• Anaemic hypoxia
• Histotoxic hypoxia
• Low p50
DALTONS LAW OF PARTIAL PRESSURE

• Total pressure exerted by a gaseous mixture is equal to the sum of

the partial pressures of individual component in a gas mixture
• Individual partial pressure exerted by a component gas in a mixture
α volume fraction of that gas component in that gas mixture
• Composition of Dry Air
• 20.98% O2
• 78.06% N2
• 0.04% CO2
• 0.92% Other inert gases
• Barometric Pressure at sea level = 1Atm = 760 mmHg
• P O2 = 0.21X760 = 160 mmHg
• P CO2 = 0.004X760 = 0.3mmHg
OXYGEN CASCADE
It describes the process of decreasing oxygen tension from
atmosphere to mitochondria.
Atmospheric air
↓
Alveoli
↓
Arterial blood
↓
Tissue capillaries
↓
Mitochondria
• Water vapour pressure at body temp = 47mmHg
Thus, Pressure exerted by gas in saturated
moist air = 760-47 = 713mmHg
=> Partial pressure of O2 in saturated moist air = 713 x 0.21 =
149 mmHg
This is the starting point of O2 cascade.
Down the respiratory tree, O2 tension is further diluted by the
alveolar CO2.
• The partial pressure of alveolar oxygen(PAO2 ) is calculated by
alveolar gas equation
• PAO2= PiO2-PACO2/R
• PaCO₂ = PACO₂ ( 40mmHg ) as CO₂ is freely diffusible.
• R is RESPIRATORY QUOTIENT(RQ) , the ratio of rate of CO₂
produced to the rate of oxygen uptake.
• RQ=VCO₂/VO₂
• 200/250=0.8
• RQ depends on the metabolic substrate
• ie,carbohydrate only diet =1. Protein &fat=0.8
• So PAO2 =149-(40/0.8)~100mmHg
• Alveolar PAO2 is 100mmHg. Blood returning from tissues to
heart has low PO2 (40mmHg). So oxygen diffuses from alveoli
to pulmonary capillaries.
After oxygenation,blood moves to pulm.veins→left side of
heart→ arterial system → systemic tissues.

• In a perfect lung pO₂ of pulm. Venous blood would be equal

to pO₂ in the alveolus.
FACTORS AFFECTING O2 CASCADE AT
EACH
LEVEL
• Atmosphere to alveolus
• High altitude.
At high altitude, the barometric pressure is less than that at
sea level, and thus, even though the FiO2 is 21%,the piO2 is
decreased.
• Water vapour
Higher the water vapour lesser will be the
PiO2 . Upper resp. tract, humidifies inspired air , depends upon
temp.
• In the alveolus
Amount of CO2 in the alveolus depends on
the metabolism & degree of hypoventilation.
Fever,sepsis,malignant hyperthermia increases CO2 production.

• Alveous to capillaries
• Ventilation/perfusion mismatch
• Shunt
• Slow diffusion.
VENTILATION PERFUSION MISMATCH

• In normal lung upper zones are over ventilated while lower

zones are relatively over perfused and under ventilated
• V/Q ratio refers to amount of ventilation in relation to
perfusion
• Normal alveolar ventilation is 4l/mt and perfusion is 5l/mt
hence V/Q ratio is 4/5 =0.8
• V/Q ratio upper zone is 3.3,ie blood in this region is hyperoxic
and hypocapnic
• V/Q ratio of lower zone is 0.6 ,blood in this region is hypoxic
and hypercapnic
• Pulmonary venous blood is a mixture of pulmonary capillary
blood from all alveoli ,hence PO2lower than PAO2
• SHUNT
• Occur when deoxygenated blood passes through unventilated
alveoli , without getting oxygenated ,to enter the systemic
arterial system .
As an effect of shunt arterial PaO2 decreases
• These effects are overcome by a compensatory mechanism
termed HYPOXIC PULMONARY VASOCONSTRICTION ( HPV ).
 TYPES OF SHUNT
• Anatomical /Absolute shunt
Called as true shunt
• Cannot be corrected with increase in FiO2
• Extra pulmonary shunt ;thebesian vein in the heart
• Intra pulmonary shunt ; bronchial veins
• It refers the units of lungs where v/Q is 0
• Physiological shunt

• Areas of lung with low but finite V/Q

• Base of lung where alveoli are collapsed V/Q ˂1
• Pathologic shunt
• Extra pulmonary shunt ;cyanotic congenital heart diseases
• Intrapulmonary shunt ;fibrosis ,atlectasis ,ARDS

• Anaesthetic implications
• Only way to correct or treat shunt and related hypoxia is by
increasing Fi02
• Compensation of increase in shunt occurs by HPV.
• Under anaesthesia hypoxic pulmonary vasoconstriction is
suppressed by volatile anaesthetics when used˃1MAC
SLOW DIFFUSION
• Normally diffusion is very rapid and is completed by the time
the blood has passed about 1/3 of the way along the pulm
capillary.
• Diffusion is affected in pulmonary diseases. Fibrosis
,ARDS,PULMONARY OEDEMA
Arterial blood to tissue
• Serum Hb level.
• Percentage of Hb saturated with O2.
• Cardiac output.
• Amount of dissolved oxygen.
• O2 is carried by blood in 2 way
• Dissolved in plasma 5%
• Combination with Hb 95%
• At arterial po2 of 100mmhg Hb is 98%saturated thus 15g of
Hb in 100ml blood carry 20ml of o2
• 1.34ml x 15gm x 98/100=20
• Venous blood have po2 40mmhg and Hb 75%saturated thus it
contain 15ml 0f 02/100ml
• Thus every 100ml blood passing through lung will take up 5ml
02
• Dissolved o2 in arterial blood is 0.3ml/dl ie gas solubility
coefficient x partial pressure (0.003ml/dl x100mmHg)
• Dissolved o2 in venous blood is 0.13ml/dl
• TOTAL OXYGEN CONTENT OF BLOOD
• Is sum of o2 in the solution and that carried by Hb
• .003mlO2/dl x PaO2+1.34 x Hb x % saturation of Hb
HYPOXIC HYPOXIA
• This implies reduction in Pa O2
• Causes
• Reduced PiO2- high altitude
• Hypoventilation-airway obstruction ,paralysis of respiratory
muscle ,depression of respiratory centre,muscle
fatigue,electrolyte imbalance,
• Fink effect or Diffusion hypoxia
• During recovery from N2O/O2 anaesthesia a relatively large
volume of more soluble N2O (31 times more soluble than
N2)diffuses from the tissue into the venous blood and then to
the alveoli and is replaced by relatively small volume of N2
which is less soluble. The alveolar gas therefor loses less N2
than it gain N2O which dilute O2 in the alveoli causing
hypoxia ,this is more common during first 5-10 mts of
recovery
• Reduced alveolar ventilation VA↓
• The pAo2-VA relationship is hyperbolic
• In middle curve 21percent o2 a reduction in ventilation of 2l /mt from 6
to 4 has little effect on pAO2 where as a reduction in from 4to 2l/mt has
very marked effect on PA02
• Raising the inspired po2 by 64mmHg achieved by increasing the Fio2
from .21 0.3 result in rise in PAO2 of same amt

• Raising the 02 consumption shift the relationship downward and right so

what was previously adequate ventilation may be grossly inadequate if
o2 consumption increase halothane shakes are common cause of
increased o2 consumption in early post operative period
Reduced diffusing capacity;
alveolar capillary block,alveolar capillary
membrane thickened ,rare cause of hypoxia
,significant effect during exercise when alveolar
capillary transit time is reduced
• Reduced mixed venous partial pressure of O2:
Pvo2 maybe reduced below 40mmHg as a result of increased
O2 consumption or reduction in O2 flux. In the absence of any
increase in alveolar ventilation or PiO2 ,a fall in PaO2 will occur

Oxygen flux is the amount of o2 leaving the left ventricle per mt

in the arterial blood
=CO x SaO2xHb x 1.34
5000ml/mt x 98/100 x 15/100g/ml x1.34 =1000ml/mt
Normally 250ml of this o2 is used up rest return to lung in mixed
venous blood ie 75% saturated with o2

• Venous admixture ; mixing of shunted ,non oxygenated

blood with re oxygenated blood distal to alveoli result in
decrease pa02 ,sao2,
• normal shunt 5% ,above 15% cause significant hypoxia
CHARACTERISTICS OF HYPOXIC HYPOXIA
• LOW ARTERIAL PO2
• LOW SATURATION OF Hb
• LOW CONTENT OF O2
• LOW ARTERIO – VENOUS PO2 DIFFERENCE
Anaemic hypoxia
• Oxygen content in arterial blood is reduced although arterial
partial pressure of o2 is normal
• Total amount of Hb is less or part of Hb is unavailable for o2
transport
• Anemia;
• at rest hypoxia not severe more 23DPG ↑ release o2 from Hb
• During exercise o2 demand ↑ more o2 consumed by tissue
severe hypoxia occur
• Carbon monoxide poisoning ;
• CO combine with Hb to form carboxy haemoglobin so this
fraction of Hb is not available for 02 transport
• Affinity of CO is about 250 times affinity for o2
• Produce shift to left of dissociation curve of remaining
oxyhaemoglobin in order to off load same amt of o2
• Tissue venous po2 is reduced much ,although shift of oxyHb
DOC has little effect on arterial o2 content ,the effect on
venous Po2 significant at cerebral venous p02 14mmHg the
subject will be unconscious
• In sickel cell anemia
• The red blood cell become rigid sticky and shaped like sickles
,get stucked in blood vessels which can slow or block blood
flow and o2 to part of the body
• The venous points of three curve
• Normal curve Hb 14.4g/dl -40mmHg
• Anaemia curve Hb 7.2g/dl-27mmhg
• 50% HbCOcurve(Total Hb 14.4g/dl)14mmhg
• The venous point for three curves shown
• Treatment
• Administration of o2 with 5%co2
• METHAEMOGLOBINEMIA &SULPHAEMOGLOBINAEMIA
• Methhaemoglobinemia-inherited /acquired
• Acquired caused by drugs such as nitrites and nitrates
• Phenacetin ,acetanilide ,sulphanilamide ,prilocaine
• Iron is in ferric form instead of ferrous form
• Meth Hb give chocolate brown appearance
• Sulph methHb give cyanotic tinge
• Treatment
• inherited form –large dose vit C ,500mg per day or methylene blue
• Acquired form require removal of causative agent and
administration of 1%aqueous methylene blue 1-2mg/kg bodywt
over a period of 5mt
Stagnant hypoxia
• Result of reduced tissue perfusion
Causes
• Generalised tissue hypoperfusion ;low cardiac out put

• Local hypoperfusion ;arterial or venous occlusion

• Due to slow speed of blood flow or stagnation blood stays
long in tissues
• Venous po2 is less and accumulation of co2 in tissue shift the
curve to right so more o2 is released to tissue
Histotoxic hypoxia
• Eg;Cyanide poisoning , beriberi
• When tissue cannot utilise o2 inspite of normal o2supply
• in mitochondria, the food substrates are oxidized by nicotinamide
adenine dinucleotide ( NAD), which removes hydrogen ion.
• The hydrogen is passed down an enzyme chain containing several
cytochromes and finally combines with oxygen to form water.
• Poisoning of this enzyme system means that the cells are not able
to utilize the oxygen and hence aerobic metabolism stops.
Anaerobic metabolism takes over.
• A small amount of ATPs can still be formed as a result of anaerobic
metabolism.
• This results in reduced production of carbon dioxide and
stimulation of ventilation., which produces fall in arterial PCO2 and
rise in mixed venous PO2.
• Sodium nitroprusside contain a cyanide radical overdose can cause
hystotoxic hypoxia
Low p50

• Included under anemic hypoxia

• Its is the partial pressure of oxygen at which Hb is 50%

saturated and has value of 27 mmHg

• If p50 is reduced ,Hb dissociation curve shifted to left ,so that

to off load a given amount of oxygen the po2 has to drop
further . In this way ↓P50 can produce tissue hypoxia

• Cause of shift to left is alkalosis ,reduced 2,3DPG ,

hypothermia, HbCO,FetalHb,hypocarbia
Anchor point in ODC
curve
the arterial pt
;po2=100mmHg
,SO2=97.5%
the mixed venous pt
;po2=40mmHg,SO2=75
%
p50;
po2=27mmHg,SO2=50
%
Cyanosis
• Refers to bluish discoloration of skin and mucous membrane
when absolute level of reduced Hb in capillary exceed 5g/dl

• Central cyanosis
• Caused by reduced arterial oxygen saturation
• Involve highly vascularised tissues such as lips tongues
mucous membranes gum palate cheeks
• Cardiac out put is normal ,patient have warm extremities
• It is evident when o2 saturation fall below 80 -85%
• Peripheral cyanosis
• Normal systemic arterial o2saturation and increased o2
extraction resulting in wide systemic arteriovenous o2
difference
• occur because of central cyanosis or occur alone due to poor
peripheral blood flow best detected looking nail bed ,
circumoral or periorbital areas
• Cyanosis may not be apparent in presence of anemia or
peripheral vasoconstriction
CAUSES OF HYPOXIA IN
THEATRE
Airway: obstructed airway prevent oxygen reaching the lung
• Tracheal tube can be misplaced in oesophagus ,Endobronchial intubation ,kinking of
tube,accidental extubation
• Aspirated vomit can block the air way
Breathing
• High spinal anaesthesia
• hypoventilation
• Pneumothorax
• Pulmonary oedema
• Pulmonary embolism
• Severe bronchospasm
Circulation
• Circulatory failure prevents o2 being transported to tissue
• Hypovolemia ,arrythmia,heart failure
Drugs
Equipment
Disconnection or obstruction of breathing circuit
Problems with o2 supply ,anoxic gaseous mixture
Empty cylinder

Problems with monitoring equipments

Battery failure in oxymeter or faulty probe
• In children
• NEONATES AND CHILDREN ARE MORE PRONE FOR RAPID
DESATURATION
• Smaller diameter of airways
• Chest wall & airway are highly compliant
• Increased oxygen consumption
• Premature infants have deficient surfactant
• Difference in airway anatomy – difficult intubation, mask
ventilation
• Early fatigue & apnoea due to lack of type 1 muscle fibres
Pregnancy
• • FRC reduced by 20% , oxygen reserve decreased
• • Oxygen consumption increased by 20%
• • More prone for precipitous fall in PaO2 even after brief
period of apnoea
• • Difficult intubation , difficult ventilation , aspiration worsen
the situation
• • Preoxygention is must , rapid sequence induction is prefered
using sellick’s maneuver
Elderly
• More prone hemoglobin desaturation
• Compromised respiratory system ( loss of elastin , reduced
chest wall compliance ,increased residual volume , ↓ vital
capacity , impaired efficiency of gas exchange, increased work
of breathing )
• Compromised cardio vascular system
• Prolonged drug effect seen after sedatives , narcotics&
muscle relaxants
In obese patients,
• Difficult mask ventilation, difficult laryngoscopy, difficult intubation
Decreased chest wall and lung compliance
• Decreased lung volumes & capacities FRC,VC,TLC
• 50% ↓in FRC compared to 20%↓in non obese
• Reduction in frc is primarily as a result of decreased ERV
• Obesity increases o2 consumption and increased co2 production at
rest
•rapidly desaturate with minimal period of apnea after induction
inspite of preoxygenation
• FRC is further reduced in supine position
• Airway closure begins during tidal breathing only V/Q mismatch
–intrapulmonary shunting -hypoxemia
• More sensitive to depressant effects of hypnotics & opioids
Hypoxia Prevention Devices
:-
• 1)Mandatory Min O2 Flow (MMOF):-
A MMOF – 50-250 ml/min – must as soon as the master switch
is turned on. O2 flow – cant be reduced below that. Some
machines – Alarms when O2 flow falls below MMOF.

• 2) Min O2 Ratio :-
ASTM Stds require that; A Min O2 ratio/ Min O2 conc of 21% in
the FGF at CGO. 2 types of linkages to achieve this.
• a) Mechanical Linkage – Link 25 Proportionating System :- •
Mechanical Linking of O2 & N2O. O2 – 14 tooth sprocket, &
N2O – 29 tooth sprocket Connected by metal chain. • Both
knobs turn together – to maintain min 25% O2 conc. •
Disadvantage – if 3rd gas is administered (eg He) – hypoxic
mixture may be delivered.
• b) Electronic Linkage :- • An electronic proportionating valve
maintains min 25% O2 conc in FGF.
• A computer continuously calculates the N2O flow for the given
O2 flow ,If higher N2O flow & O2 conc <25% , Electronic
proportionating valve automatically reduces N2O flow
• 3) Alarms :- set off when O2:N2O falls below a preset value.
Post operative causes of
hypoxia
• Diffusion hypoxia
• ↑V/Q mismatch
• Anaesthesia produce reduction in FRC consequences to be
more serious in elderly and pt who are fat or smoke . If FRC
decrease below closing capacity there will be zones of lung
perfused but not ventilated at end of expiration nd beginning
of inspiration. Following upper abdominal surgery FRC
reduced by 30%
• Reduced CO
Result in reduced o2 flux which may be insufficient to meet o2
demand if pt is shivering. The fall in mixed venous po2 will then
produce fall in pa02,which further reduce o2flux
• It will worsen if pt is anemic
• Hypoventilation; most anaesthetic drugs depress ventilation
• Incomplete reversal result in residual paralysis
• Obstruction- tongue
fall,laryngospasm,bronchospasm,aspiration
• Pain; prevent deep breathing,
• Intra operative hyperventilation –many pts are hyperventilted
during operation .when spontaneous ventilation restored
there is considerable total body deficit of CO2. reductio n of
C02excretion by hypoventilation during early post operative
period allow this deficit to build up
• Long operation ,thoracic or upper abdominal incision ,old age
,preexisting lung disease ,heart disease ,sickle cell disease
place pts at special risk
Indicators of tissue hypoxia
• Unstable vital signs
• Tachycardia
• Hypotension
• Tachypnea or dyspnea
• Laboratory and invasive monitor indices
• Mixed venous O2 saturation (SVmO2) <50%
• Central venous O2 saturation (SVcO2) <60%
• Increased O2 extraction ratio (O2ER) >50%
• Lactic acidosis (metabolic acidemia with lactate >2 mmol/L
• Signs of end-organ dysfunction
• Electrocardiographic (ST changes, onset of arrhythmias) or
echocardiographic indications of myocardial ischemia
• Electroencephalographic indications of cerebral hypoperfusion
• New onset oliguria (less than 0.5 mL/kg/h for >6 h)
Effects of hypoxia
• Degree of hypoxia
• Duration of hypoxia
• Idiosyncrasy of the individual
• Other factors like – disease, drugs, temperature
Cardiovascular system

• systemic vasodilatation – direct effect

• Fall in blood pressure.
• Stimulation of peripheral chemoreceptor→ activation of
sympathetic system→ increase in cardiac output
• If the hypoxic insult very severe, cardiac output cannot
compensate for reduced systemic vascular resistance →The
heart will fail and blood pressure falls → hypoxic cardiac
arrest.
• ↑blood flow to most organs, especially brain → ↓ in
extracellular fluid pH →direct vasodilator effect on the
cerebral vessels.
Respiratory system
• Pulmonary arterioles constrict in response to hypoxia –
hypoxic pulmonary vasoconstriction.

• This is beneficial if part of the lung is more hypoxic that the

rest, as it causes diversion of blood to better oxygenated
areas

• In patients with intra cardiac shunt such as VSD hypoxia may

cause ↑ in right side pressure with reversal of shunt
,consequently arterial desaturation

• Chronic hypoxia can lead to irreversible increase in

pulmonary vascular resistance with pulmonary HTN and cor
pulmonale
Metabolism
• When there is insufficient oxygen, metabolism changes from
aerobic to anaerobic. Pastuer point Pao2 1-2 mmhg
• Some amount of ATPs can still be formed with anaerobic
metabolism.
• The lactic acid produced accumulates and lead to severe
metabolic acidosis
Organ failure:
• The brain and retina are very sensitive to hypoxia
• Cerebral function is a sensitive indicator of hypoxia; changes
in mood, deterioration of performance, confusion and
sometimes loss of consciousness
• ‘Survival time’ – time taken for the brain to stop functioning
to the extent of loss of consciousness. Survival time for
cerebral cortex is 0.5 min.
• ‘Revival time’ – the time beyond which recovery of function is
not possible. Revival time of cerebral cortex is 5 min.
• Hepatic cells are arranged in lobules with centrilobular and
peripheral distribution. The centrilobular cells are the first to
show changes, being more remote from systemic circulation.
• In acute hypoxia, centrilobular necrosis occurs; while in
chronic hypoxia, fibrosis develops.
• Kidney has a survival time of 10 min.
• Prolonged hypoxia produces acute tubular necrosis and then
cortical necrosis.
• Chronic renal hypoxia increases synthesis of erythropoietin
which stimulates marrow formation of erythrocytes, resulting
in secondary polycythemia.
Oxygen therapy in different
forms of hypoxia
• HYPOXIC HYPOXIA ; due to decreased pao2 ,o2 therapy very
useful especially it is very essential for hypoxia caused by low po2
in inspired air ,hypoventilation ,and impaired diffusion in lung
• Administration of o2 increases the pressure gradient between
alveoli and blood and facilitate o2 entry into the blood
• However o2 therapy is not beneficial in hypoxic hypoxia due to AV
shunt as admixture occur after oxygenation in lung
• ANEMIC HYPOXIA; O2 therapy increase o2 content of blood by
increasing the quantity of dissolved o2,the quantity of o2 supplied
to tissue by dissolved 02 is very small yet this improves tissue
oxygenation to some extent eg
• If Hb is 7.5 g/dl
• O2 content = (1.34 x .98 x 7.5)+0.003 x100 =10.1
• If 100% 02 given pao2 =6 x FiO2=600mmHg
• (1.34x.98x7.5) +.003x600 =9.84+1.8=11.64
• In CO poisoning hyperbaric o2 is used it facilitate dissociation
of CO frm Hb and increases the transport of o2 in dissolved
state
• STAGNANT HYPOXIA;o2 therapy is not much useful as blood
flow to tissue is reduced
• HISTOTOXIC HYPOXIA;tissue unable to utilise o2 hence 02
therapy not beneficial
• HYPERBARIC O2 THERAPY
• Means administration of 100%o2 at increased pressure
• Transport of o2 in dissolved form in plasma increase
• The o2 solubility in plasma is 0.03ml/100ml/mmHg
• Therefore to achieve the 6ml/100ml dissolved o2 which is
adequate to maintain normal metabolic need of tissues of
body in resting state ,arterial p02 should be 2000mmHg

• This is achieved by administering 100%02at pressure of 3atm

• Hyperbaric o2 therapy is useful in CO poisoning
• However 100%02 at high pressure facilitate o2 toxicity
CHRONIC HYPOXIA
• Occurs due to disease or living at high altitude
• As altitude increases, total atmospheric pressure is reduced
and partial pressure of O2 declines proportionately
• Partial pressure of O2 in air
• At sea level 159mmHg (21.2kpa)
• At 10000ft 110mmHg (14.7kpa)
• At 20000ft 73mmHg(9.7kpp)
• At 50000ft 18mmHg(2.4kpa)
• A normal person loses consciousness when arterial oxygen
saturation fall about 50% or below.
• On ascent to high altitude acute hypoxia causes
hyperventilation by stimulating peripheral chemoreceptors .
• As PCO2 fall PH in CSF and central chemoreceptor rises so
opposing to some extent the increase in ventilation the next
few days renal excretion of bicarbonates induces a
compensate metabolic acidosis and in addition CSF
bicarbonate concentration fall
• Reducing the CSF PH almost to normal and allowing peripheral
chemoreceptor to drive ventilation unopposed ;ventilation
reaches its maximum at 4 days .
• If subject remain at high altitude there is very slow reduction
in ventilation extending over years

• If he descends to sea level PAO2 rises peripheral

chemoreceptor drive is reduced PaO2 increases therefore
brain PCO2 increases .

• Because the PH of CSF and brain extracellular fluid is lower

than normal ,ventilation is driven by increased central drive
which decline as CSF bicarbonate re accumulation bringing
brain PH back to normal
• Mountain sickness may occur in un acclimatised subject who
ascend rapidly to 3000m or above
• It can vary in severity from mild weakness nausea shortness
of breath to fatal pulmonary and cerebral oedema
prophylaxis achieved by slow ascent although acetazolamide
has shown worthwhile.
• It is carbonic anhydrase inhibiter act by stimulating breathing
by metabolic acidosis .if more trivial symptom present the
subject must descend
CONCLUSION
• Hypoxia associated with anaesthesia and surgery has an
etiology which ranges from simple though rare accident such
as airway obstruction to the complicated but common
disturbances in the intrapulmoary relation of ventilation to
perfusion .anaesthesia providers strive to avoid hypoxia
because of risk of irreversible damage to the myocardium
brain and other end organs
REFFERENCES
• A practice of anesthesia, 5th edition, Wylie and Churchill
Davidson
• Clinical Anesthesiology, 5th Edition, G. Edward Morgan, Jr.,
Maged S. Mikhail, Michael J. Murray
• Textbook of medical physiology, 11th edition, Guyton and Hall
• Clinical anaesthesia, 7th edition, Paul G Barash
THANK YOU