Hypoxia

DR. CHINTAN

Hypoxia

DefinitionDefinition

Hypoxia is O2 deficiency at the tissue level.

It is a more correct term than anoxia - no O2 at all left in the tissues.

It is classified into four types.

Hypoxic hypoxia, anemic hypoxia, stagnant hypoxia and histotoxic hypoxia.

ClassificationClassification

(1) hypoxic hypoxia, the PO2 of the arterial blood is reduced;

(2) anemic hypoxia, the arterial PO2 is normal but the amount

of hemoglobin available to carry O2 is reduced;

ClassificationClassification

(3) stagnant or ischemic hypoxia, the blood flow to a tissue is so low that

adequate O2 is not delivered to it despite a normal PO2 and hemoglobin concentration;

(4) histotoxic hypoxia, the amount of O2 delivered to a tissue is

adequate but, the tissue cells cannot make use of the O2 supplied to them

Hypoxic hypoxiaHypoxic hypoxia

In this the arterial Po2 is reduced. O2 content and O2 saturation is decreased.

Causes are:1) There is less o2 in inspired air as in high

altitudes or closed room.

2) Decreased pulmonary ventilation as in asthma, paralysis of respiratory muscles, emphysema, airway obstruction, resp. center depression, etc.

Hypoxic hypoxiaHypoxic hypoxia

3) Defective gas exchange and o2 transfer due to problems in respiratory membrane eg pulmonary edema

4) Defective ventilation-perfusion ratio due to

a) uneven alveolar ventilation as in asthma, emphysema, pulm. fibrosis, pneumothorax, CCF

b) due to non uniform pulmonary blood flow as in Anatomical shunts (Fallot’s Tetralogy), right to left shunts causing venous admixture

Picture in Hypoxic hypoxiaPicture in Hypoxic hypoxia

Normal Art VenPo2 95 40%Hb sat 97 75o2 content 19 14

O2 used 19-14 = 5ml

A-V Po2 diff = 95-40 = 55

H H Art VenPo2 40 25% Hb sat 75 45O2 content 14 9

O2 used 14-9 = 5ml

A-V Po2 diff = 40-25 = 15

Characteristics of hypoxic hypoxiaCharacteristics of hypoxic hypoxia

1) Low arterial Po2

2) Low % saturation of Hb

3) Low content of o2

4) Low Arterio-venous Po2 difference

Pathophysiology of Hypoxic Pathophysiology of Hypoxic HypoxiaHypoxia

Hypoxic hypoxia--- via peripheral chemoreceptors --- stimulates resp to increase Po2--- but washout of co2--- so less Pco2--- shifts the o2-Hb dissociation curve to

left--- so less release of o2 to tissues--- so tissue hypoxia occurs

Compensatory changesCompensatory changes

1) Hypoxic stimulation of respiration

2) Alkaline urine which is due to alkalosis which results from co2 washout by hyperventilation.

3) Rise of BP

4) Polycythemia with increased Hb

5) increased 2,3 DPG in RBC

Anemic HypoxiaAnemic Hypoxia

Arterial Po2 is normal but amount of Hb available to carry o2 is reduced.

Causes1) Anemia2) Hemorrhage3) Abnormal Hb– MetHb where iron is in

ferric form instead of ferrous form, HbS, COHb etc

FeaturesFeatures

Anemic Hypoxia Arterial VenousPo2 95 40% sat of Hb less lessO2 content less less

A-V Po2 difference 95-40 = 55ml normal

PathophysiologyPathophysiology

Here at rest hypoxia is not severe as, in anemia there is more 2,3 DPG which releases o2 from Hb

During exercise more o2 demand by tissues as more o2 is consumed so severe hypoxia develops.

Compensatory changesCompensatory changes

1) Hyper dynamic circulation, increased CO and HR

2) Increased speed of blood flow so that same Hb can be used repeatedly to transport o2.

3) Rise of 2,3 DPG

4) More erythropoiesis due to more EP in an attempt to correct anemia.

Stagnant HypoxiaStagnant Hypoxia

Decreased blood flow or sluggish flow to the tissues so inadequate o2 supply.

Causes :1) CCF2) Circulatory failure3) Hemorrhage4) Shock5) Venous obstruction

FeaturesFeatures

Stagnant Hy Arterial VenousPo2 95 25% Hb sat 97 45O2 content 19 9

O2 utilized 19-9 = 10mlA-V Po2 diff 95-25 = 70mm Hg

Due to slow speed of blood flow or stagnation blood stays for long in tissues,

venous Po2 is less and accumulation of co2 in tissues shifts the curve to right so more o2 is released to tissue

Histotoxic HypoxiaHistotoxic Hypoxia

O2 delivered to the tissues is normal but the tissues cannot utilize o2.

Causes:1) Cyanide Poisoning- cyanide blocks

action of cytochrome oxidase enzyme completely so tissues cannot utilize o2.

2) Vitamin B def or Beri Beri where also several important steps of o2 utilization are blocked.

FeaturesFeatures

Histotoxic Hy Arterial VenousPo2 95 90% sat of Hb 97 96O2 content 19 18.5

O2 used 19-18.5 = 0.5 mlA-V diff 95-90 = 5mmHg

So tissues cannot use o2 so values at venous end are similar to arterial end.

Effect on bodyEffect on body1) On respiration-All except anemic hypoxia stimulate peripheral

chemoreceptors and thus increase respiration2) On CVS-Increase in HR and BP3) Anorexia, nausea, vomiting4) On CNS-brain is affected in all the types.Depressed mental activity, impaired judgment,

drowsiness, disorientation, headache and coma.5) Reduced work capacity of the muscles.

Oxygen therapy in different types Oxygen therapy in different types of hypoxiaof hypoxia

Oxygen can be administered by

(1) placing the patient’s head in a “tent” that contains air fortified with oxygen,

(2) allowing the patient to breathe either pure oxygen or high concentrations of oxygen from a mask, or

(3) administering oxygen through an intranasal tube.

In atmospheric hypoxiaIn atmospheric hypoxia

Here oxygen therapy can completely correct the depressed oxygen level in the inspired gases and, therefore, provide 100 per cent effective therapy.

Hypoventilation hypoxiaHypoventilation hypoxia

In hypoventilation hypoxia, a person breathing 100 per cent oxygen can move five times as much oxygen into the alveoli with each breath

Therefore, oxygen therapy can be extremely beneficial.

(this provides no benefit for the excess blood carbon dioxide also caused by the hypoventilation.)

Oxygen therapyOxygen therapy

In hypoxia caused by impaired alveolar membrane diffusion,

oxygen therapy can increase the Po2 in the lung alveoli from the normal value of about 100 mm Hg to as high as 600 mm Hg.

In histotoxic hypoxia o2 therapy not useful.

Oxygen therapyOxygen therapy

In hypoxia caused by anemia, abnormal hemoglobin transport of oxygen, circulatory deficiency or physiologic shunt,

oxygen therapy is of much less value because normal oxygen is already available in the alveoli.

The problem instead is that one or more of the mechanisms for transporting oxygen from the lungs to the tissues is deficient.

Oxygen toxicityOxygen toxicity

100% O2 has been demonstrated to exert toxic effects not only in animals but also in bacteria, fungi, cultured animal cells and plants.

The toxicity seems to be due to the production of

the superoxide anion (O2-), which is a free radical, and H2O2.

When 80-100% O2 is administered to humans for periods of 8 hours or more, the respiratory passages become irritated, causing sub sternal distress, nasal congestion, sore throat and coughing

O2 therapy problems in infantsO2 therapy problems in infants

Some infants treated with O2 for RDS develop a chronic condition characterized by

lung cysts and densities (bronchopulmonary dysplasia)

Another complication in these infants is retinopathy of prematurity (retrolental fibroplasia),

the formation of opaque vascular tissue in the eyes, which can lead to serious visual defects

HypercapniaHypercapnia

Hypercapnia means excess carbon dioxide in the body fluids.

Hypercapnia usually occurs in association with hypoxia only when the hypoxia is caused by hypoventilation or circulatory deficiency.

HypercapniaHypercapnia

circulatory deficiency, diminished flow of blood decreases carbon dioxide removal from the tissues, resulting in tissue Hypercapnia in addition to tissue hypoxia.

the transport capacity of the blood for carbon dioxide is more than that for oxygen, so that the resulting tissue Hypercapnia is much less than the tissue hypoxia.

HypercapniaHypercapniaIn hypoxia resulting from poor diffusion through

the pulmonary membrane or through the tissues,

serious Hypercapnia usually does not occur at the same time because carbon dioxide diffuses 20 times as rapidly as oxygen.

If Hypercapnia does begin to occur, this immediately stimulates pulmonary ventilation, which corrects the Hypercapnia but not necessarily the hypoxia.

HypercapniaHypercapnia

When the alveolar Pco2 rises above 60 to 75 mm Hg – breathing becomes rapid and deep - “air hunger” - dyspnea becomes severe.

If the Pco2 rises to 80 to 100 mm Hg, the person becomes sluggish and sometimes even semi comatose

Anesthesia and death can result when the Pco2 rises to 120 to 150 mm Hg.

Cause of deathCause of death

At higher levels of Pco2, the excess carbon dioxide begins to depress respiration rather than stimulate it, thus causing a vicious circle:

(1) more carbon dioxide, (2) further decrease in respiration, (3) then more carbon dioxide, and so forth

ending rapidly in a respiratory death

CyanosisCyanosisThe term cyanosis means blueness of the

skin, and its cause is excessive amounts of deoxygenated hemoglobin in the skin blood vessels, especially in the capillaries.

This deoxygenated hemoglobin has an intense dark blue-purple color that is transmitted through the skin.

In general, definite cyanosis appears whenever the arterial blood contains more than 5 gm of deoxygenated hemoglobin in each 100 milliliters of blood.

Cyanosis seen in polycythemia not Cyanosis seen in polycythemia not in anemiain anemia

person with anemia almost never becomes cyanotic because there is not enough hemoglobin for 5 grams to be deoxygenated in 100 milliliters of arterial blood.

in a person with excess RBCs, as occurs in polycythemia vera, the great excess of available hemoglobin that can become deoxygenated leads frequently to cyanosis

CyanosisCyanosis

In Hypoxic Hypoxia, less arterial Po2, so more reduced Hb and when it exceeds more than 5gm% cyanosis develops.

In stagnant hypoxia due to slow blood flow more o2 extracted from blood so more reduced Hb so chances of cyanosis.

In histotoxic hypoxia no o2 used no reduced Hb produced so no cyanosis.

CyanosisCyanosis

Local factors - like exposure to mild cold (20 degrees) causes cyanosis.

This is due to cutaneous Vasoconstriction of both arteries and veins so less blood flow and stagnant hypoxic like condition.

Exposure to severe cold no cyanosis because, O2-Hb curve shifts to left and prevents release of o2

from Hb andO2 consumption of tissues reduces markedly as

there is reduced metabolism.amount of reduced Hb is less and so no cyanosis.

Sites for cyanosis- areas of thin Sites for cyanosis- areas of thin skinskin

1) Mucus membrane of undersurface of tongue.

2) Lips3) Ear lobes4) Nail beds5) Tip of nose

Types of cyanosisTypes of cyanosis

Central cyanosisIt is due to hypoxic

hypoxia and all its causes.

Features 1) extremities are warm and blue due to hyper dynamic circulation and HT.

2) Cyanosis on tip of nose, lips, under tongue.

Peripheral cyanosisIt is due to stagnant

hypoxia and all its causes.

Features 1) extremities are cold and blue due to less blood flow and vasoconstriction of vessels.

2) Cyanosis on Nail beds

ASPHYXIAASPHYXIAThis is produced by occlusion of airways.

CAUSES:-• Suffocation,• Strangulation,• Drowning, • Obliteration of blood vessels.

ASPHYXIAASPHYXIAThis results in hypoxia [lack of oxygen] and

Hypercapnia [increased Pco2]

TYPES:-• General asphyxia• Local asphyxia

STAGES:- Stage of exaggerated breathing. Stage of convulsions. Stage of exhaustion and collapse.

Stage of exaggerated breathingStage of exaggerated breathing• Lasts for about 1-2 mins• It is due to powerful stimulation

of respiratory center by co2• Increased depth of respiration• Increased ventilation• Increased respiratory rate• Dyspnea & cyanosis occurs

Stage of convulsionsStage of convulsions• Lasts for about one minute• It is due to spread of impulse from

respiratory centers to other parts of CNS• During this period convulsions occurs• Increased HR-tachycardia• Increased cardiac output• Increased sympathetic activity• Increased vasoconstriction• Increased BP

Stage of exhaustion and collapseStage of exhaustion and collapse• Lasts for about 5 min • Due to lack of o2• Depression of respiratory center &

respiration becomes gasping• deep respiration with wide mouth • Pupils widely dilated• Pulse becomes feeble• Reflexes are abolished• Semi consciousness• Unconsciousness, Coma, Death

TREATMENTTREATMENT• By artificial respiration subject may be

able to survive, but care has to be taken for

• Hypoxic damage of myocardium &

• Increased epinephrine & nor-epinephrine secretion may cause ventricular fibrillation due to multiple ectopic foci

Thank U…Thank U…