Hypoxia

1. DR. CHINTAN
Hypoxia

2. 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.

3. 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;

4. 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

5. 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.

6. 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

7. Picture in Hypoxic hypoxiaPicture in Hypoxic hypoxia
Normal Art Ven
Po2 95 40
%Hb sat 97 75
o2 content 19 14
O2 used 19-14 = 5ml
A-V Po2 diff = 95-40 = 55
H H Art Ven
Po2 40 25
% Hb sat 75 45
O2 content 14 9
O2 used 14-9 = 5ml
A-V Po2 diff = 40-25 = 15

8. 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

9. 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

10. 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

11. Anemic HypoxiaAnemic Hypoxia
Arterial Po2 is normal but amount of Hb
available to carry o2 is reduced.
Causes
1) Anemia
2) Hemorrhage
3) Abnormal Hb– MetHb where iron is in
ferric form instead of ferrous form, HbS,
COHb etc

12. FeaturesFeatures
Anemic Hypoxia Arterial Venous
Po2 95 40
% sat of Hb less less
O2 content less less
A-V Po2 difference 95-40 = 55ml normal

13. 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.

14. 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.

15. Stagnant HypoxiaStagnant Hypoxia
Decreased blood flow or sluggish flow
to the tissues so inadequate o2 supply.
Causes :
1) CCF
2) Circulatory failure
3) Hemorrhage
4) Shock
5) Venous obstruction

16. FeaturesFeatures
Stagnant Hy Arterial Venous
Po2 95 25
% Hb sat 97 45
O2 content 19 9
O2 utilized 19-9 = 10ml
A-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

17. 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.

18. FeaturesFeatures
Histotoxic Hy Arterial Venous
Po2 95 90
% sat of Hb 97 96
O2 content 19 18.5
O2 used 19-18.5 = 0.5 ml
A-V diff 95-90 = 5mmHg
So tissues cannot use o2 so values at
venous end are similar to arterial end.

19. Effect on bodyEffect on body
1) On respiration-
All except anemic hypoxia stimulate peripheral
chemoreceptors and thus increase respiration
2) On CVS-
Increase in HR and BP
3) Anorexia, nausea, vomiting
4) 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.

20. 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.

21. 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.

22. 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.)

23. 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.

24. 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.

25. 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

26. 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

27. 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.

28. 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.

29. HypercapniaHypercapnia
In 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.

30. 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.

31. 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

32. CyanosisCyanosis
The 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.

33. 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

34. 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.

35. 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 and
O2 consumption of tissues reduces markedly as
there is reduced metabolism.
amount of reduced Hb is less and so no cyanosis.

36. Sites for cyanosis- areas of thin Sites for cyanosis- areas of thin
skinskin
1) Mucus membrane of undersurface
of tongue.
2) Lips
3) Ear lobes
4) Nail beds
5) Tip of nose

37. Types of cyanosisTypes of cyanosis
Central cyanosis
It 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 cyanosis
It 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

38. ASPHYXIAASPHYXIA
This is produced by occlusion of airways.
CAUSES:-
•Suffocation,
•Strangulation,
•Drowning,
•Obliteration of blood vessels.

39. ASPHYXIAASPHYXIA
This 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.

40. 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

41. 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

42. 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

43. 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

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