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Ventilation college
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Exercise physiology college
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Ventilation = gas exchange uitbreiding guytonThe Po2 and the Pco2 in the alveoli are determined by:
1. The rate of alveolar ventilation.
2. The rate of transfer of oxygen and carbon dioxide through the respiratory membrane.
Some areas of the lungs are well ventilated but have almost no blood flow, whereas other areas may
have excellent blood flow but little or no ventilation.
The ventilation-perfusion ratio is expressed as Va/Q.
When Va (alveolar ventilation) is normal for a given alveolus and Q (blood flow) is also normal for the
same alveolus, the ventilation-perfusion ratio is also said to be normal.
When the ventilation is zero, yet there is still perfusion of the alveolus, the Va/Q is zero.
Or, at the other extreme, when there is adequate ventilation but zero perfusion, the ratio Va/Q is
infinity. At a ratio of either
zero or infinity, there is no exchange of gases through the respiratory membrane of the affected
alveoli.
Alveolar Oxygen and Carbon Dioxide Partial Pressures When VA/Q Equals Zero.
When Va/Q is equal to zero—that is, without any alveolar ventilation—the air in the alveolus comes
to equilibrium with the blood oxygen and carbon dioxide because these gases diffuse between the
blood and the alveolar air. Because the blood that perfuses the capillaries is venous blood returning
to the lungs from the systemic circulation, it is the gases in this blood with which the alveolar gases
equilibrate. Normal venous blood has a Po2 of 40 mm Hg and a Pco2 of 45 mm Hg. Therefore, these
are also the normal partial pressures of these two gases in alveoli that have blood flow but no
ventilation.
Alveolar Oxygen and Carbon Dioxide Partial Pressures When VA/Q Equals Infinity.
The effect on the alveolar gas partial pressures when Va/Q equals infinity is entirely different from
the effect when Va/Q equals zero because now there is no capillary blood flow to carry oxygen away
or to bring carbon dioxide to the alveoli.Therefore, instead of the alveolar gases coming to
equilibrium with the venous blood, the alveolar air becomes equal to the humidified inspired air. That
is, the air that is inspired loses no oxygen to the blood and gains no carbon dioxide from the blood.
And because normal inspired and humidified air has a Po2 of 149 mm Hg and a Pco2 of 0 mm Hg,
these will be the partial pressures of these two gases in the alveoli.
Gas Exchange and Alveolar Partial Pressures When VA/Q Is
Normal.
When there is both normal alveolar ventilation and normal
alveolar perfusion, exchange of oxygen and carbon dioxide
through the respiratory membrane is nearly optimal, and
alveolar Po2 is normally at a level of 104 mm Hg, which lies
between that of the inspired air (149 mm Hg) and that of
venous blood (40 mm Hg). Likewise, alveolar Pco2 lies between
two extremes; it is normally 40 mm Hg, in contrast to 45 mm
Hg in venous blood and 0 mm Hg in inspired air.Thus, under
normal conditions, the alveolar air Po2 averages 104 mm Hg
and the Pco2 averages 40 mm Hg.
PO2-PCO2, VA/Q Diagram
The concepts presented in the preceding sections can be
shown in graphical form, as demonstrated in Figure 39–11,
called the Po2-Pco2, Va/Q diagram. The curve in the diagram
represents all possible Po2 and Pco2 combinations
, between the limits of Va/Q equals zero and Va/Q equals infinity when the gas pressures in the
venous blood are normal and the person is breathing air at sea-level pressure.
Abnormal VA/Q in the Upper and Lower Normal Lung.
In a normal person in the upright position, both pulmonary capillary blood flow and alveolar
ventilation are considerably less in the upper part of the lung than in the lower part; however, blood
flow is decreased considerably
more than ventilation is. Therefore, at the top of the lung, Va/Q is as much as 2.5 times as great as
the ideal value, which causes a moderate degree of physiologic dead space in this area of the lung.
At the other extreme, in the bottom of the lung, there is slightly too little ventilation in relation to
blood flow, with Va/Q as low as 0.6 times the ideal value. In this area, a small fraction of the blood
fails to become normally oxygenated, and this represents a physiologic shunt.
In both extremes, inequalities of ventilation and perfusion decrease slightly the lung’s effectiveness
for exchanging oxygen and carbon dioxide. However, during exercise, blood flow to the upper part of
the lung increases markedly, so that far less physiologic dead space occurs, and the effectiveness of
gas exchange now approaches optimum.
Regulation of Respiration During Exercise
In strenuous exercise, oxygen consumption and carbon dioxide
formation can increase as much as 20-fold.The arterial Po2,
Pco2, and pH remain almost exactlynormal therefore, they
can’t have so much effect on the increased ventilation.
The brain, on transmitting motor impulses to the exercising
muscles, is believed to transmit at the same time collateral
impulses into the brain stem to excite the respiratory center.
This is analogous to the stimulation of the vasomotor center of
the brain stem during exercise that causes a simultaneous
increase in arterial pressure.
Actually, when a person begins to exercise, a large share of the
total increase in ventilation begins immediately
on initiation of the exercise, before any blood chemicals have
had time to change.
Interrelation Between Chemical Factors and Nervous: Factors in the Control of Respiration During
Exercise.
When a person exercises, direct nervous signals presumably stimulate the respiratory center almost
the proper amount to supply the extra oxygen required for exercise and to blow off extra carbon
dioxide. Occasionally, however, the nervous respiratory control signals are either too strong or too
weak. Then chemical factors play a significant role in bringing about the final adjustment of
respiration required to keep the oxygen, carbon dioxide, and hydrogen ion concentrations of the body
fluids as nearly normal as possible.
This is demonstrated in Figure 41–9, which shows in the lower curve changes in alveolar ventilation
during a 1-minute period of exercise and in the upper curve changes in arterial Pco2. Note that at the
onset of exercise, the alveolar ventilation increases instantaneously, without an initial increase in
arterial Pco2. In fact, this increase in ventilation is usually great enough so that at first it actually
decreases arterial Pco2 below normal, as shown in the figure. The presumed reason that the
ventilation forges ahead of the buildup of blood carbon dioxide is that the brain provides an
“anticipatory” stimulation of respiration at the onset of exercise, causing extra alveolar ventilation
even before it is needed. However, after about 30 to 40 seconds, the amount of carbon dioxide
released into the blood from the active muscles approximately matches the increased rate of
ventilation, and the arterial Pco2 returns essentially to normal even as the exercise continues,
as shown toward the end of the 1-minute period of exercise in the figure.
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