Physiologic Features

The primary functions of the respiratory system are to

remove the appropriate amount of CO2 from blood
entering the pulmonary circulation and to provide
adequate O2 to blood leaving the pulmonary
circulation.
For these functions to be carried out properly :
There must be adequate provision of fresh air to the
alveoli for delivery of O2 and removal of CO2 (ventilation),
Adequate circulation of blood through the pulmonary
vasculature (perfusion), adequate movement of gas
between alveoli and pulmonary capillaries (diffusion),
Appropriate contact between alveolar gas and pulmonary
capillary blood (ventilation-perfusion matching).
 A normal individual at rest inspires 1216
times per minute, each breath having a tidal
volume of ~500 mL.
A portion (30%) of the fresh air inspired with
each breath does not reach the alveoli but
remains in the conducting airways of the lung.
This component of each breath, which is not
generally available for gas exchange, is called
the anatomic dead space component.
The remaining 70% reaches the alveolar zone,
mixes rapidly with the gas already there, and
can participate in gas exchange.
 Ex : total ventilation/min 7 L (14000 ml)
Composed of 2 L/min dead space ventilation
5 L/min alveolar ventilaation

Certain disease some alveoli are ventilated but

not perfused, so that some ventilation in
addition to the anatomic dead space
component is wasted.
If total dead space ventilation is increased but
total minute ventilation is unchanged, then
alveolar ventilation must fall correspondingly.
 Gas exchange is dependent on alveolar
ventilation rather than total minute
ventilation.
The partial pressure of CO2 in arterial blood
(PaCO2) is directly proportional to the amount
of CO2 produced per minute (CO2) and
inversely proportional to alveolar ventilation
(A), according to the relationship :
PaCO2 = 0.863 x VCO2/VA
VCO2is expressed in mL/min
VA in L/min
PaCO2 in mmHg.
 Both O2 and CO2 diffuse readily down their respective
concentration gradients through the alveolar wall and
pulmonary capillary endothelium.
Under normal circumstances :
This process is rapid.
Equilibration of both gases is complete within one-third of the transit time
of erythrocytes through the pulmonary capillary bed.
Even in disease states in which diffusion of gases is impaired,
the impairment is unlikely to be severe enough to prevent
equilibration of CO2 and O2.
Consequently, a diffusion abnormality rarely results in arterial
hypoxemia (subnormal oxygenation of general blood, short of
anorexia) at rest.
 If erythrocyte transit time in the pulmonary
circulation is shortened, as occurs with exercise, and
diffusion is impaired, then diffusion limitation may
contribute to hypoxemia.
Exercise testing can often demonstrate such
physiologically significant abnormalities due to
impaired diffusion.
Even though diffusion limitation rarely makes a
clinically significant contribution to resting
hypoxemia, clinical measurements of what is known
as diffusing capacity can be a useful measure of the
integrity of the alveolar-capillary membrane.
 Absolute levels of alveolar ventilation and perfusion, gas exchange depends
critically on the proper matching of ventilation and perfusion.
The spectrum of possible ventilation-perfusion (V/Q) ratios in an alveolar-capillary
unit ranges from zero, in which ventilation is totally absent and the unit behaves as
a shunt, to infinity, in which perfusion is totally absent and the unit behaves as
dead space.
The PO2 and PCO2 of blood leaving each alveolar-capillary unit depend on the gas
tension (of blood and air) entering that unit and on the particular V/Q ratio of the
unit.
At one extreme, when an alveolar-capillary unit has a high V/Q ratio of 0 and
behaves as a shunt, blood leaving the unit has the composition of mixed venous
blood entering the pulmonary capillaries, i.e., PO2 40 mmHg and PCO2 46 mmHg.
At the other extreme, when an alveolar-capillary unit has a high V/Q ratio, it
behaves almost like dead space, and the small amount of blood leaving the unit
has partial pressures of O2 and CO2 (PO2 150 mmHg, PCO2 0 mmHg while
breathing room air) approaching the composition of inspired gas.
 In the ideal situation, all alveolar-capillary
units have equal matching of ventilation and
perfusion, i.e., a ratio of ~1 when each is
expressed in L/min. However, even in the
normal individual, some V/Q mismatching is
present, since there is normally an increasing
gradient of blood flow from the apices to the
bases of the lungs.
There is a similar gradient of ventilation from
the apices to the bases, but it is less marked
than the perfusion gradient.
 As a result, ventilation-perfusion ratios are higher at the lung
apices than at the lung bases.
Therefore, blood coming from the apices has a higher PO2 and
lower PCO2 than blood coming from the bases.
The net PO2 and PCO2 of the blood mixture coming from all
areas of the lung is a flow-weighted average of the individual
components, which reflects both the relative amount of blood
from each unit and the O2 and CO2 content of the blood
coming from each unit. Because of the sigmoid shape of the
oxyhemoglobin dissociation curve, it is important to
distinguish between the partial pressure and the content of
O2 in blood. Hemoglobin is almost fully (~90%) saturated at a
PO2 of 60 mmHg, and little additional O2 is carried by
hemoglobin even with a substantial elevation of PO2 >60
mmHg.
 On the other hand, significant O2 desaturation of
hemoglobin occurs once PO2 falls to <60 mmHg and
onto the steep descending limb of the curve.
As a result, blood coming from regions of the lung
with a high V/Q ratio and a high PO2 has only a small
elevation in O2 content and cannot compensate for
blood coming from regions with a low / ratio and a
low PO2, which has a significantly decreased O2
content.
Although / mismatching can influence PCO2, this
effect is less marked and is often overcome by an
increase in overall minute ventilation.