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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

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

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).

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.veinsleft side of heartarterial 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

FACTORS AFFECTING O2 CASCADE AT EACH LEVEL • Atmosphere to alveolus • High altitude. At high

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 &

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

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

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

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

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

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% •

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

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

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

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

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

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

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

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

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

• Treatment • Administration of o2 with 5%co2 • METHAEMOGLOBINEMIA &SULPHAEMOGLOBINAEMIA •

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 P CO2 and rise in mixed venous P O2 .

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

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

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

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

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 ,

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

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

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

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

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 chemoreceptoractivation of sympathetic systemincrease 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

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

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

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

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

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

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

At 10000ft

At 20000ft

At 50000ft

A normal person loses consciousness when arterial oxygen saturation fall about 50% or below.

159mmHg (21.2kpa)

110mmHg (14.7kpa)

73mmHg(9.7kpp)

18mmHg(2.4kpa)

• On ascent to high altitude acute hypoxia causes hyperventilation by stimulating peripheral chemoreceptors .

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

few days renal excretion of bicarbonates induces a compensate metabolic acidosis and in addition CSF bicarbonate concentration fall

the increase in ventilation the next

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

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

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, 5 th edition, Wylie and Churchill Davidson

Clinical Anesthesiology, 5th Edition, G. Edward Morgan, Jr., Maged S. Mikhail, Michael J. Murray

Textbook of medical physiology, 11 th edition, Guyton and Hall

Clinical anaesthesia, 7 th edition, Paul G Barash

THANK YOU

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