Page 94 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Hypoxia and Hyperoxia
Hypoxia occurs when O 2 transport from ambi- function, but ultimately leads to irreversible
ent air to the cell is impaired. There may be cell damage.
several causes: (→ A): Hypoventilation, abnormal pulmonary dif-
! Hypoventilation reduces the diffusion gra- fusion, and circulatory failure cause cyanosis
dient to venous blood and thus impairs O 2 up- (blue discoloration of the skin and mucous
take. However, ventilation has to be markedly membranes) if the average concentration of
reduced before O 2 uptake is noticeably de- deoxygenated hemoglobin in the capillaries is
creased (→ p. 68). lower than ca. 0.7 mmol/L (5 g/100 mL) (→ A).
Acid–Base Balance vents equilibration of gas concentrations in al- diffusion the arterialized blood is hypoxic
! Reduced diffusing capacity (→ p. 70) pre-
In hypoventilation and disorders of pulmonary
veoli and capillary blood.
(central cyanosis). It must be stressed that cya-
nosis is not always due to O 2 deficiency. If the
! Reduced O 2 uptake capacity of the blood
hemoglobin concentration in blood is in-
occurs in anemia (→ p. 30ff.) or can be caused
creased, cyanosis may occur even though there
by the inability of hemoglobin to bind or re-
lease O 2 . Carbon monoxide (CO), for example,
is no lack of O 2 (pseudocyanosis). Conversely,
Respiration, binds to hemoglobin with an affinity that ex- an O 2 deficiency may occur in hemoglobin de-
ficiency (anemia), without the concentration
ceeds that of O 2 by a factor of 200. CO bound
of deoxygenated hemoglobin reaching the
to one heme group raises the affinity of the
level required for cyanosis.
other three heme groups of the affected hemo-
The organism can be damaged not only in
O 2 but is also less ready to release the oxygen
4 globin molecule so that it not only binds less hypoxia but also in hyperoxia, the latter as a
bound to it. Increased O 2 affinity with reduced result of the reactibility of O 2 (→ B). Hyperoxia,
peripheral O 2 release also occurs in a deficien- for example, produced by hyperbaric ventila-
cy of 2,3-bisphosphoglycerate (2,3-BPG) or al- tion with a breathing apparatus during diving
kalosis. or by inhalation of pure O 2 over many days,
! Circulatory failure (→ p. 224) impairs O 2 can inhibit the cellular oxidation of glucose.
transport in the cardiovascular system. High O 2 partial pressure lowers cardiac output
! Tissue diffusion is impaired if the distance and blood flow through the kidneys and brain,
between a cell and its nearest capillary is in- the latter resulting in dizziness and cramps. In
creased, as in tissue hypertrophy without ac- the lung, irritation of the airway can cause
companying increased capillary formation, or coughing and pain, while oxidative damage to
edema. The diffusion distance is also increased the alveolar epithelium and endothelium lead
when the precapillary sphincter of the nearest to increased permeability, and to the develop-
capillary contracts, because the O 2 supply ment of pulmonary edemas (→ p. 80). Oxida-
must then come from the second nearest tion can inactivate surfactant, the fluid that
capillary. normally reduces surface tension in the alveoli
! Several poisons of the respiratory chain can and ensures they unfold evenly. The lack of
inhibit O 2 utilization. surfactant may lead to different sizes of alveoli
The most important effect of all the above- with subsequent abnormal distribution of
mentioned causes is the impairment of the ventilation (→ p. 72). Artificial ventilation
cells’ aerobic energy supply. with O 2 also facilitates the collapse of alveoli
If the O 2 supply is deficient, some cells are (atelectasis; → p. 72). In neonates mixtures
able to meet their energy needs by breaking containing over 40% O 2 lead to the develop-
down glucose into lactic acid. However, the en- ment of hyaline membranes in the lung and
ergy gain from this is small (2 molecules of ATP thus impair gaseous exchange. In the vitreous
per molecule of glucose compared with 36 body and cornea, vascular and connective tis-
ATPs in oxidative metabolism), and the disso- sue proliferates, possibly leading to blindness
ciation of lactic acid results in metabolic (not (retrolental fibroplasia).
84 respiratory) acidosis (→ p. 88). The lack of en-
ergy at first causes a reversible impairment of
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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