Anoxia: Classification and Therapy | Respiration | Humans | Biology

In this article we will discuss about the classification and therapy of anoxia.

Anoxia is a condition characterised by inadequate or decreased supply of oxygen to the lungs because of extrinsic reasons. The term ‘hypoxia’ is more appropriate and is used synonymously with anoxia.

Classification of Anoxia:

1. Anoxic Type of Anoxia or Arterial Hypoxia:

This type is characterised by low oxygen tension in the arterial blood.

2. Anaemic Type of Anoxia:

This type is characterised by low oxygen content of the blood due to diminished quantity of haemoglobin or non-functionating haemoglobin.

3. Stagnant Anoxia or Hypokinetic Hypoxia:

This type is characterised by decreased rate of blood flow through the tissue. The oxygen content and tension of the arterial blood is normal but that of the venous blood is abnormally low due to sluggish circulation.

4. Histotoxic Anoxia:

This means inability of the tissues to utilise oxygen and occurs in cynide poisoning. Anoxaemia is a term which means diminished oxygen in the blood.

1. Anoxic Anoxia or Arterial Hypoxia:

The main cause is diminished Po₂ of the arterial blood which, of course, results in diminished saturation of hae­moglobin with oxygen. The total oxygen content of the arterial blood, therefore, is lower than normal, since the O₂ tension in the tissues is normally low (40 mm Hg) it may be that in spite of diminished Po₂ the arterial blood may unload its normal quota of oxygen to the tissues resulting in lower Po₂ and low oxygen saturation of haemoglobin in the venous blood than would occur normally.

O₂ content of the mixed venous blood is reduced from 15 volume % to 12 volume %. The final value of O₂ in the mixed venous blood, of course, depends on degree of anoxia.

Causes of Arterial Hypoxia:

i. Diminished O₂ tension in the inspired air may occur due to:

a. Admixture with foreign gases like CO or CH₄ etc. at the bottom of the mines.

b. High altitude due to low barometric pressure-the partial pressure of O₂ in the alveoli is diminished.

ii. Diseased conditions in which the ventilation/perfusion ratio (normal 0.8) is disturbed. This may be due to ineffective ventilation (dead space effect), e.g. in advanced pulmonary emphysema, asthma, obstruction of air passages, or due to venous-admixture effect as may occur in pneumonia or septal defect of the heart.

iii. Diseased conditions in which there occurs defective diffusion across the alveolo-capillary membrane, e.g. pulmonary oedema or alveolo-capillary block syndrome.

2. Anaemic Hypoxia:

The characteristic feature of this type of hypoxia is diminished quantity of functioning haemoglobin in blood. The oxygen content of blood, therefore, is diminished proportionately to the reduction of haemoglobin but the oxygen tension of blood and percentage saturation of haemoglobin with oxygen is normal.

Causes:

i. Anaemia:

Anaemia from any causes.

ii. Co Poisoning:

Here a large amount of haemoglobin remains combined with CO and as such is not available for oxygen carriage.

iii. Altered Haemoglobin:

E.g. methaemoglobin found after poisoning with chlorates, nitrites, ferriaynides and acetanilide etc.

Anaemic hypoxia, is of moderately severe intensity, is attended with increased cardiac output, that is increased blood flow through the tissues so as to compensate to some extent for the diminished O₂ content of blood.

3. Stagnant Anoxia or Hypokinetic Anoxia:

The characteristic feature of this condition is diminished blood flow through the tissues due to sluggish circula­tion. The cardiac output is low but the O₂ content and tension of the arterial blood is normal. Due to sluggish cir­culation after the tissues abstract normal amount of O₂ they need – the venous blood is considerably reduced, with its Po₂ much less than normal. Consequently, the Po₂ of the tissue fluid and tissues in general is reduced which has got a damaging influence on the tissues.

Myocardial infaraction is an example of localised hypoxia resulting in loss of function which leads to generalised hypoxia and worsening of the ischaemia of the heart.

Causes of Stagnant or Hypokinetic Anoxia:

i. Congestive cardiac failure.

ii. Haemorrhage.

iii. Shock.

iv. Obstruction to venous return.

4. Histotoxic Anoxia:

This type of anoxia is due to poisoning with cynides or sulphide in which the respiratory enzymes are inhibited and so the tissues cannot utilise O₂ of the blood which contains adequate amount of O₂ at normal tension.

Altitude Anoxia:

Anoxia at high altitude is due to low barometric pressure. The percentage composition of atmospheric air in so far as O₂ and N₂ concentration is concerned is same at all altitude but due to fall in barometric pressure at high altitude there occurs a disproportionate fall in Po₂ of the alveolar air and consequent percentage saturation of haemoglobin with oxygen.

Respiratory changes in Hypoxia Acute and Chronic at High Altitude:

Anoxia of gradual onset occurs in mountaineering and the respiratory responses of a subject to such type of anoxia differs to some extent depending on whether the subject is conditioned for high altitude atmosphere (acclimatised subject) or ascending to high altitude for the first time and is un-acclimatised for the high altitude environment.

Respiration in Altitude Anoxia in Un-Acclimatised Subjects:

Breathing 14% O₂ in N₂ (simulated altitude 3 km or 10,000 feet) produces practically no change in respiration. When the oxygen in the inspired air is brought down to 10% (simulated altitude about 5.5 km or 18,000 feet) there occurs 8% increase in ventilation over the resting value. Respiration is doubled when the respired air contains 8% oxygen in nitrogen. Anoxia, therefore, is not so effective a stimulant to respiration as is excess of CO₂.

Anoxic stimulation occurs reflexly through the chemoreceptors of the Sino-aortic area. The anoxic hyperventi­lation, however, is associated with fall in alveolar and arterial Pco₂ and with (H⁺) in blood, and also in the c.s.f. and interstitial fluid of the brain which bath the CO₂ sensitive chemoreceptor cells which form part of the respiratory centre complex of the brain stem. This causes depression of respiration.

However, if the anoxic stimulus is sufficiently intense the chemoreceptor reflexes from the Sino-aortic area assumes a prepotent role in maintaining hyperventilation in spite of the fall in Pco₂ and (H⁺) resulting from anoxic hyperventilation.

Further, it has been proved that the chemoreceptor cells of the respiratory centre become hypersensitive to CO₂ and (H⁺) in presence of oxygen deficiency. This is shown in Fig. 8.41 which indicates that the respiratory stimulant effect of CO₂ is significantly greater when the alveolar Po₂ is maintained at a steady value of 40 mm Hg than when it is kept at its normal value of 100 mm Hg. The slope of V/Pco₂ line increase as the alveolar PCo₂ is lowered. Anoxia, therefore, increases the sensitivity of respiratory chemoreceptors to CO₂ and (H⁺).

Respiration in Subjects Exposed to Anoxia of Long Duration (Acclimatised Subjects):

The above discussion applies to person exposed to anoxia for the first time (acute anoxia). The respiratory pattern of subjects exposed to anoxia for a long time or who are permanent residents of high altitudes (acclimatised subjects) is shown by the lower curve in the same diagram.

As can be seen from the diagram the alveolar PCO₂ value of an acclimatised subject begins to fall from an altitude of 1.5 km or 5000 feet upwards and is always lower than that of an un-acclimatised subject. Thus at an altitude of 5.4 km or 18,000 feet the alveolar Pco₂ value of an acclimatised subject is only 22mm Hg as compared to 30mm Hg of an un-acclimatised subject.

This of course, is due to the fact that the acclimatised subjects can and do hyperventilate more than his un-acclimatised friend in spite of the consequent fall in alveolar Pco₂. The alveolar Po₂ rises consequently with obvious advantage for better oxygenation of venous blood.

It has been pointed out in  that the (H⁺) of the blood and c. s. f. depends on the ratio of PCO₂/(HCO₃^–) and that CO₂ being highly soluble and diffusible the changes in Pco₂ of the blood is more or less the same as that in the c. s. f. But the [HCO₃^–] in the c. s. f. is controlled independently and that active transport of HCO₃^– occurs from the c. s. f. to blood in anoxia so that the fall in [HCO₃^–] is always more marked in the c. s. f. than in the blood in cases of low arterial and c. s. f. Pco₂.

Thus (TP) of the c. s. f. and interstitial fluid of the brain is quickly brought back to normal level so that the chemoreceptors of the brain stem influencing the respiratory centre can function properly in spite of the fall in Pco₂ of alveolar air and arterial blood. Thus 4 subjects were studied at an altitude of about 3.8 km or 12 500 feet. In 24 hours the Pco₂ of the arterial blood fell on an average from 40 to 30 mm Hg and the pH increased from 7.43 to 7.48.

The Pco₂ of the c. s. f. fell to the same extent, i.e., by 10 mm Hg but there was no increase in pH of the c. s. f. This was due to remarkable fall in [HCO₃^–] of the c. s. f. to the extent of 5 mEq/litre compared to about 2 mEq/litre in blood. The stabilisation of (H⁺) in the c. s. f. and tissue fluid of the brain was thus achieved by active transport of (HCO₃^–) from the c. s. f. to the cerebral capillaries. The sensitivity of the bulbar chemoreceptors acting on the respiratory centre was thus unaffected in spite of fall in Pco₂ of the c. s. f. and brain.

It may be summarised, therefore, that during acclimatisation the low Pco₂ of the c. s. f. and interstitial fluid of the brain resulting from anoxic hyperventilation is counteracted by active secretion (HCO₃^–) from the c. s. f. and tissue fluid of the brain to the blood so that the (H⁺) of the c. s. f. and brain remains unaltered and that the activity of the respiratory chemoreceptors are not depressed.

After some time, however, kidneys also play an important role in adjustment of pH of the blood and c. s. f. by excreting urine with high pH value. The advantage of this hyperventilation is obvious because it enables to maintain high alveolar Po₂ and ensures more effective oxygenation of venous blood.

In residents of high altitude-the lung volume is increased so that the lungs can hold more air. Further the alveolar wall is stretched out facilitation gaseous interchange. More pulmonary capillaries open up increasing the surface area for diffusion.

Oxygen Therapy in Anoxia or Hypoxia:

Three methods are commonly employed in administration of oxygen.

These are:

1. Nasal Catheter:

It is possible to raise the alveolar Po₂ from its normal value 100 mm Hg to 600 mm Hg by this method.

2. Oxygen Tent:

The patient is put in an atmosphere enriched with oxygen. The alveolar PO₂ usually goes upto about 300 mm Hg.

3. Oxygen Mask:

Either pure oxygen on high concentration of oxygen is breathed through a mask. Sometimes a specially designed mask (B L B mask) is used in which part of the oxygen in the expired air is utilised for rebreathing.

In altitude anoxia or hypoxia due to presence of foreign gases in the atmosphere at high concentration administration of pure O₂ is of great value and offers absolute protection except when the altitude is very high and O₂ must be delivered through a pressure mask.

In hypoxia due to alveolar hypoventilation breathing 100 percent O₂ can increase the alveolar concentration of oxygen 5 times the normal value and thus is extremely beneficial.

In alveolo-capillary block syndrome oxygen therapy is extremely beneficial because the rise in concentration of oxygen in the alveoli raises the diffusion gradient and thereby facilitates diffusion of oxygen across the diffusing membrane.

In anaemic anoxia the functionating haemoglobin is low but the oxygen saturation of functionating haemoglobin is normal and Po₂ of plasma is normal. Oxygen therapy, therefore, is of limited benefit because only the O₂ in solution can be increased by O₂ therapy, the O₂ content is but little affected.

In hypokinetic hypoxia, the O₂ content and tension of arterial blood leaving the lung is normal and so O₂ inhalation is of limited value. However, the normal amount of O₂ in solution in arterial blood is 0.3 ml per 100 ml. This can be increased to 1.8 volume of O₂ per ml of blood when the alveolar Po₂ is raised to 600 mmHg by O₂ inhalation. This means only an increase of about 10% of O₂ content at high pressure and may mean the difference between life and death.

In histotoxic anoxia, the enzymes are paralysed so that the tissues fail to pick up oxygen from blood therapy, therefore, are of no avail.

Danger of Oxygen Therapy in Anoxia or Hypoxia:

In patients suffering from chronic hypoxia, the respiration is maintained by reflex stimulation of the Sino- aortic bodies and the sensitivity of the chemoreceptors to CO₂ is diminished. Sudden relief of hypoxia by oxygen therapy may produce hypoventilation with hypercapnia or hypercarbia and unconsciousness which may lead to death.