Page 78 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Ventilation, Perfusion
To reach the alveoli, inspired air must pass Massive hypoventilation lowers the O 2 partial
through those respiratory pathways in which pressure in the alveoli and blood, so that oxy-
no gaseous exchange takes place (dead space), gen is at the steep part of the O 2 binding curve
i.e., normally the mouth, pharynx and larynx, of hemoglobin and O 2 uptake is therefore im-
trachea, bronchi and bronchioles. On its way paired much more than CO 2 release is. Hyper-
the air will be warmed, saturated with water ventilation increases the O 2 partial pressure in
vapor, and cleansed. the alveoli and blood, but cannot significantly
The tidal volume (VT) contains, in addition raise the level of O 2 uptake into the blood be-
Acid–Base Balance (VA), the volume of air that remains in the However, hyperventilation boosts CO 2 release.
to the volume of air that reaches the alveoli
cause the hemoglobin is already saturated.
Lung perfusion is increased, for example,
dead space (VD). If tidal volume is less than V D
(normally ca. 150 ml), the alveoli are not venti-
during physical work. It can be reduced by
heart or circulatory failure (→ p. 224), or by
lated with fresh air (→ A, right). When tidal
volume is greater than VD, the proportion of al-
constriction or occlusion of pulmonary vessels
(→ p. 80).
veolar ventilation rises with increasing VT. Al-
A moderate increase in lung perfusion while
Respiration, veolar ventilation may even be reduced during ventilation remains unchanged increases O 2
hyperpnea, if the depth of each breath, i.e., VT,
uptake virtually in proportion to the amount
is low and mainly fills the dead space.
of blood flow (→ C, right). Even though the al-
Increased ventilation can occur as a result of
of the increased O 2 uptake from the alveoli into
pathophysiologically (e.g., in metabolic acido-
4 either physiologically (e.g., during work) or veolar O 2 partial pressure falls slightly because
sis; → p. 88) increased demand, or due to an the blood, this has little influence on O 2 satura-
inappropriate hyperactivity of the respiratory tion in the blood (see above). It is only when
neurons (→ p. 82). the alveolar partial pressure of O 2 falls into
Decreased ventilation can occur not only the steep part of the O 2 dissociation curve that
when the demand is reduced, but also when a decrease of alveolar O 2 partial pressure sig-
the respiratory cells are damaged, or when nificantly affects O 2 uptake into blood. At those
neural or neuromuscular transmission is ab- O 2 partial pressures a further increase in lung
normal. Further causes include diseases of the perfusion only slightly increases O 2 uptake.
respiratory muscles, decreased thoracic mobi- Furthermore, at very high lung perfusion flow,
lity (e.g., deformity, inflammation of the the contact time in the alveoli is not sufficient
joints), enlargement of the pleural space by to guarantee that partial O 2 pressure in blood
pleural effusion or pneumothorax (→ p. 74) as approaches that in the alveoli (→ p. 70). If
well as restrictive or obstructive lung disease lung perfusion is reduced, O 2 uptake is propor-
(→ p. 74ff.). tionally decreased.
Changes in alveolar ventilation do not have CO 2 removal from blood is dependent on
the same effect on O 2 uptake into the blood lung perfusion (→ C, left) to a lesser extent
and CO 2 release into the alveoli. Because of than O 2 uptake. In case of reduced lung perfu-
the sigmoid shape of the O 2 dissociation curve, sion (but constant ventilation and venous CO 2
O 2 uptake in the lungs is largely independent concentration) the CO 2 partial pressure in the
of alveolar partial pressure (PA O 2 ). If there is alveoli falls and thus favors the removal of
only minor hypoventilation, the partial pres- CO 2 from the blood. This, in turn, attenuates
sure of O 2 in the alveoli and thus in blood is re- the effect of the reduction in perfusion. At
duced, but the O 2 dissociation is at the flat part raised lung perfusion an increase of alveolar
of the curve, so that the degree of hemoglobin CO 2 concentration prevents a proportional
saturation and thus O 2 uptake in blood is prac- rise in CO 2 release.
tically unchanged (→ B, right). On the other
hand, the simultaneous increase in CO 2 partial
68 pressure in the alveoli and blood leads to a no-
ticeable impairment of CO 2 release (→ B, left).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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