Ventilation, Perfusion

To reach the alveoli, inspired air must pass through those respiratory pathways in which no
gaseous exchange takes place (dead space), i.e., normally the mouth, pharynx and larynx,
trachea, bronchi and bronchioles. On its way the air will be warmed, saturated with water vapor,
and cleansed.

The tidal volume (VT) contains, in addition to the volume of air that reaches the alveoli (VA), the
volume of air that remains in the dead space (VD). If tidal volume is less than V D (normally ca.
150 ml), the alveoli are not venti- lated with fresh air (→ A, right). When tidal volume is greater
than VD, the proportion of al- veolar ventilation rises with increasing VT. Al- veolar ventilation
may even be reduced during hyperpnea, if the depth of each breath, i.e., VT, is low and mainly
fills the dead space.

Increased ventilation can occur as a result of either physiologically (e.g., during work) or
pathophysiologically (e.g., in metabolic acido- sis; → p. 88) increased demand, or due to an
inappropriate hyperactivity of the respiratory neurons (→ p. 82).

Decreased ventilation can occur not only when the demand is reduced, but also when the
respiratory cells are damaged, or when neural or neuromuscular transmission is ab- normal.
Further causes include diseases of the respiratory muscles, decreased thoracic mobi- lity (e.g.,
deformity, inflammation of the joints), enlargement of the pleural space by pleural effusion or
pneumothorax (→ p. 74) as well as restrictive or obstructive lung disease (→p.74ff.).

Changes in alveolar ventilation do not have the same effect on O2 uptake into the blood and CO2
release into the alveoli. Because of the sigmoid shape of the O2 dissociation curve, O2 uptake in
the lungs is largely independent of alveolar partial pressure (PAO2). If there is only minor
hypoventilation, the partial pres- sure of O2 in the alveoli and thus in blood is re- duced, but the
O2 dissociation is at the flat part of the curve, so that the degree of hemoglobin saturation and
thus O2 uptake in blood is prac- tically unchanged (→B, right). On the other hand, the
simultaneous increase in CO2 partial pressure in the alveoli and blood leads to a no- ticeable
impairment of CO2 release (→ B, left).

Massive hypoventilation lowers the O2 partial pressure in the alveoli and blood, so that oxy- gen
is at the steep part of the O2 binding curve of hemoglobin and O2 uptake is therefore im- paired
much more than CO2 release is. Hyper- ventilation increases the O2 partial pressure in the alveoli
and blood, but cannot significantly raise the level of O2 uptake into the blood be- cause the
hemoglobin is already saturated. However, hyperventilation boosts CO2 release.

Lung perfusion is increased, for example, during physical work. It can be reduced by heart or
circulatory failure (→ p. 224), or by constriction or occlusion of pulmonary vessels (→ p. 80).

A moderate increase in lung perfusion while ventilation remains unchanged increases O2 uptake
virtually in proportion to the amount of blood flow (→ C, right). Even though the al- veolar O2
partial pressure falls slightly because of the increased O2 uptake from the alveoli into the blood,
this has little influence on O2 satura- tion in the blood (see above). It is only when the alveolar
partial pressure of O2 falls into the steep part of the O2 dissociation curve that a decrease of
alveolar O2 partial pressure sig- nificantly affects O2 uptake into blood. At those O2 partial
pressures a further increase in lung perfusion only slightly increases O2 uptake. Furthermore, at
very high lung perfusion flow, the contact time in the alveoli is not sufficient to guarantee that
partial O2 pressure in blood approaches that in the alveoli (→ p. 70). If lung perfusion is reduced,
O2 uptake is propor- tionally decreased.

CO2 removal from blood is dependent on lung perfusion (→C, left) to a lesser extent than O2
uptake. In case of reduced lung perfu- sion (but constant ventilation and venous CO2
concentration) the CO2 partial pressure in the alveoli falls and thus favors the removal of CO2
from the blood. This, in turn, attenuates the effect of the reduction in perfusion. At raised lung
perfusion an increase of alveolar CO2 concentration prevents a proportional rise in CO2 release.