Important Measurements of Lung Functions
The tidal volume (VT) is the volume of air entering or leaving the nose or mouth per breath. It is determined by the activity of the respiratory control centers in the brain as they affect the respiratory muscles and by the mechanics of the lung and the chest wall. During normal, quiet breathing the VT of a 70-kg adult is about 500 mL per breath, but this volume can increase dramatically, for example, during exercise.
The residual volume (RV) is the volume of gas left in the lungs after a maximal forced expiration. It is determined by the force generated by the muscles of expiration and the inward elastic recoil of the lungs as they oppose the outward elastic recoil of the chest wall. Dynamic compression of the airways during the forced expiratory effort may also be an important determinant of the RV as airway collapse occurs, thus trapping gas in the alveoli. The RV of a healthy 70-kg adult is about 1.5 L, but it can be much greater in a disease state such as emphysema, in which inward alveolar elastic recoil is diminished and much airway collapse and gas trapping occur. The RV is important to a healthy person because it prevents the lungs from collapsing at very low lung volumes. The collapsed alveoli would require very great inspiratory efforts to reinflate.
The expiratory reserve volume (ERV) is the volume of gas that is expelled from the lungs during a maximal forced expriation that starts at the end of a normal tidal expiration. It is therefore determined by the difference between the functional residual capacity (FRC) and the RV. The ERV is about 1.5 L in a heathy 70-kg adult.
The inspiratory reserve volume (IRV) is the volume of gas that is inhaled into the lungs during a maximal forced inspiration starting the end of a normal tidal inspiration. It is determined by the strength of contraction of the inspiratory myscles, the inward elastic recoil of the lung and the chest wall, and the starting point, which is the FRC plus the VT. The IRV of a normal 70-kg adult is about 2.5 L.
The functional residual capacity (FRC) is the volume of gas remaining in the lungs at the end of a normal tidal expiration. The FRC consists of the RV plus the ERV. It is therefore about 3 L in a healthy 70-kg adult. FRC=RV+ERV
The inspiratory capacity (IC) is the volume of air that is inhaled into the lungs during a maximal inspiratory effort that begins at the end of a normal tidal expiration. It is therefore equal to the VT plus the IRV. The IC of a normal 70-kg adult is about 3 L. IC=VT+IRV
The total lung capacity (TLC) is the volume of air in the lungs after a maximal inspiratory effort. It is determined by the strength of contraction of the inspiratory muscles and the inward elastic recoil of the lungs and the chest wall. The TLC consists of all 4 lung volumes: the RV, the VT, the IRV, the ERV. The TLC is about 6 L in a healthy 70-kg adult. TLC=RV+ERV+VT+IRV
The vital capacity (VC) is the volume of air expelled from the lungs during maximal forced expiration starting after a maximal forced inspiration. The VC is therefore equal to the TLC minus the RV, or about 4.5 L in a healthy 70-kg adult. The VC is also equal to the sum of the VT and IRV and ERV. It is determined by the factors that determine the TLC and RV. VC=TLC-RV=VT+IRV+ERV
Physiologic Dead Space
The volume of air entering and leaving the nose or mouth per minute, the minute volume, is not equal to the volume of air entering and leaving the alveoli per minute. Alveolar ventilation is less than the minute volume because the last part of each inspiration remians in the conducting airways and is not expelled from the body. No gas exchange occurs in the conducting airways for anatomic reasons: The walls of the conducting airways are too thick for mucn diffusion to take place; mixed venous blood does not come into contact with the air. The conducting airways are therefore referred to as the anatomic dead space. A reasonable estimate of anatomic dead space is 1 mL of dead space per pound of ideal body weight.
Besides the anatomic dead space, there is another form of wasted ventilation, where the alveoli are ventilated but not perfused with venous blood. No gas exchange occurs in these alveoli for physiologic, rather than anatomic, reasons. A healthy young person has little or no alveolar dead space, but a person with a low cardiac output might have a great deal of alveolar dead space. The anatomic dead space plus the alveolar dead space is known as the physiologic dead space.
Physiologic dead space = anatomic dead space + alveolar dead space [Bohr equation]
The Bohr equation makes use of a simple concept: Any meaurable volume of carbon dioxide found in the mixed expired gas must come from alveoli that are both ventilated and perfused because there are negligible amounts of carbon dioxide in inspired air. Inspired air remaining in the anatomic dead space or entering unperfused alveoli will leave the body as it entered (except for having been heated to body temperature and humidified), contributing little or no carbon dioxide to the mixed expired air:
FEco2 X VT = FIco2 X VDco2 + FAco2 X VA,
FEco2 X VT is volume of CO2 in mixed expired air
FIco2 X VDco2 is volume of CO2 coming from dead space
FAco2 X VA is volume of CO2 coming from alveoli
F means fractional concentration
E means mixed expired
I means inspired
A means alveolar
VDco2 is dead space for CO2 (physiologic dead space)
FAco2 is fractional concentration of CO2 in alveoli that are both ventilate and perfused
Since FIco2 is approximately equal to zero, the FIco2 X VDco2 term drops out. Substituting (VT – VDco2) for VA:
FEco2 X VT = FAco2 X (VT – VDco2)
VDco2 X FAco2 = VT X (FAco2 – FEco2)
After these mathematic processes, we can calcuate the dead space for CO2/physiologic dead space by the following equation:
VDco2 = VT x (PAco2 – PEco2)/PAco2
The Pco2 of the collected mixed expired gas can be determined with a CO2 meter. The CO2 meter is often also used to estimate the alveolar Pco2 by analyzing the gas expelled at the end of a normal tidal expiration, the "end-tidal CO2". But in a person with significant alveolar dead space, the estimated alveolar Pco2 obtained in this fashion may not reflect the Pco2 of alevoli that are ventilated and perfused because some of this mixed end-tidal gas comes from unperfused alveoli. This gas dilutes the CO2 coming from alveoli that are both ventilated and perfused.
Because there is an equilibrium between the Pco2 of perfused alveoli and their end-capillary Pco2, so that in patients without significant venous-to-arterial shunts, the arterial Pco2 represents the mean Pco2 of the perfused alveoli. Therefore, the equation above could be rewritten as:
VDco2 = VT x (Paco2 – PEco2)/Paco2
If the Paco2 is greater than the mixed alveolar Pco2 determined by sampling the end-tidal CO2, then the physiologic dead space is probably greater than the anatomic dead space; that is, a significant arterial-alveolar CO2 difference means that there is siginifcant alveolar dead space. Situations in which alveoli are ventilated but not perfused include those in which portions of the pulmonary vasculature have been occluded by blood clots from the venous blood (pulmonary emboli), situations in which there is low venous return leading to low right ventricular output, and situations in which alveolar pressure is high (positive-pressure ventilation with positive end-expiratory pressure).
Alveolar Ventilation and Alveolar Oxygen and Carbon Dioxide Levels
The levels of oxygen and carbon dioxide in the alveolar gas are determined by the alveolar ventilation, the pulmonary capillary perfusion, the oxygen consumption of the body, and the carbon dioxide production of the body. Alveolar gas is composed of the 2.5 to 3 L of gas already in the lungs at FRC and the approximately 350 mL per breath entering and leaving the alveoli. About 300 mL of oxygen is continuosusly diffusing from the alveoli into the pulmonary capillary blood per minute at rest and is being replaced by alveolar ventilation. Simiarly, about 250 mL of carbon dioxide is diffusing from the mixed venous blood in the pulmonary capillaries into the alveoli per minute and is then removed by alveolar ventilation.
PS: normal PAO2 is 104 mm Hg and normal PACO2 is 40 mm Hg.
The alveolar PO2 increases by 2 to 4 mm Hg with each normal tidal inspiration and falls slowly until the next inspiration. Similarly, the alveolar PCO2 falls 2 to 4 mm Hg with each inspiration and increases slowly until the next inspiration.
The concentraton of carbon dioxide in the alveolar gas is dependent on the alveolar ventilation and on the rate of carbon dioxide production by the body (and its delivery to the lung in the mixed venous blood). The volume of carbon dioxide expired per unit of time (VECO2) is equal to the alveolar ventilation VA times the alveolar fractional concentration of CO2 (FACO2). No carbon dioxide comes from the dead space: VECO2 = VA X FACO2. Simarily, the fractional concnetration of carbon dioxide in the alveoli is directly proportional to the carbon dioxide production by the body (VCO2) and inversely proportional to the alveolar ventilation: FACO2 is directly proportional to VCO2/VA.
Since FACO2 X (PB – PH2O) = PACO2, then PACO2 is directly proportional to VCO2/VA.
After these mathematic proving, we got the following formula to estimate the PACO2:
PACO2 is in directly proportional to VCO2/VA
where PACO2 is the alveolar CO2 pressure, VCO2 is the carbon dioxide production by the body, and the VA is the alveolar ventilation. In healthy people, alveolar PCO2 is in equilibrium with PaCO2. Thus, if alveolar ventilation is doubled, then the alveolar and arterial PCO2 are reduced by one-half. If alveolar ventilation is cut in half, near 40 mm Hg, then alveolar and arterial PCO2 will double.
For O2, it is evident that as alveolar ventilation increases, the alveolar PO2 will also increase. Doubling alveolar ventilation, however, cannot double PAO2 in a person whose alveolar PO2 is already approximately 104 mm Hg because the highest PAO2 one could possibly achieve (breathing air at sea level) is the inspired PO2 of about 149 mm Hg.
After some mathematic calculation, we got the following formula to estimate the PAO2:
PAO2 = PiO2 – PACO2/R + F
where, R= respiratory exchange ratio, VCO2/VO2, which represents the whole body carbon dioxide produced per time divided by the whole body oxygen consumption per time. It is primarily dependent on the foodstuffs metabolized by the cells of the body. In a person with a typical mixed diet, it is approximately 0.8; a person consuming a diet consisting of mainly carbohydrates or proteins would have an R of approximately 1.0; a person consuming a diet consisting of mainly fat would have an R of approximately 0.7.
As alveolar ventilation increases, the alveolar PCO2 decreases, bringing the alveolar PO2 closer to the inspired PO2.
Regional Distribution of Alveolar Ventilation
As previously discussed, a 70-kg person has about 2.5 to 3 L of gas in the lungs at the FRC. Each eupneic breath brings about 350 mL of fresh gas into the alveoli and removes about 350 mL of alveolar air from the lung. Although it is reasonable to assume that the alveolar ventilation is distributed fairly evenly to alveoli throughout the lungs, this is not the case. Studies performed on normal subjects seated upright have shown that alveoli in the lower regions of the lungs receive more ventilation per unit volume than do those in the upper regions of the lung.
Precise measurements made of the intrapleural surface pressures of intact chests in the upright position have shown that intrapleural surface pressure is not uniform throughout the thorax: The intrapleural surface pressure is less negative in the lower, gravity-dependent regions of the thorax than it is in the upper, nondependent regions. There is a gradient of the intrapleural surface pressure such that for every centimeter of vertical displacement down the lung (from nondependent to dependent regions) the intrapleural surface pressure increses by about +0.2 to +0.5 cm H2O. This gradient is apparently caused by gravity and by mechanical intereactions between the lung and the cehst wall.
Because the difference in intrapleural surace pressure throughout the lung, the transmural pressure of the alveoli between nondependent and dependent lung areas at FRC are not the same. The left side of Figure 3-12 shows that alveolar pressure is zero (equals to atmophere) in both regions of the lung at the FRC. Since the intrapleural pressure is more negative in upper regions of the lung than it is in lower regions of the lung, the transpulmonary pressure (alveolar minus intrapleural) is greater in upper regions of the lung than it is in lower regions of the lung. Because the alveoli in upper regions of the lung are subjected to greater distending pressures than those in more dependent regions of the lung, they have greater volumes than the alveoli in more dependent regions.
It is this difference in volume that leads to the difference in ventilation between alveoli located in dependent and nondependent regions of the lung. This can be seen on the hypothetical pressure-volume curve shown on the right side of Figure 3-12. This curve is similar to the pressure-volume curve for a whole lung, except that this curve is drawn with the pressure-volume characteristics of single alveoli in mind. The abscissa is the transpulmonary pressure. The ordinate is the volume of the alveolus expressed as a percent of its maximum.
The alveolus in the upper, nondependent region of the lung has a larger transpulmonary pressure than does the alveolus in a more dependent region because the intrapleural pressure in the upper, nondependent regions of the lung is more negative than it is in more dependent regions. Because of this greater transpulmonary pressure, the alveolus in the upper region of the lung has a greater volume than the alveolus in a more gravity-dependent region of the lung. At the FRC, the alveolus in the upper part of the lung is on a less steep portion of the alveolar pressure-volume curve in Figure 3-12 than is the more compliant alveolus in the lower region of the lung. Therefore, any change in the transpulmonary pressure during a normal respiratory cycle will cause a greater change in volume in the alveolus in the lower, gravity-dependent region of the lung than it will in the alveolus in the nondependent region of the lung, as shown by the arrows in the figure. Because the alveoli in the lower parts of the lung have a greater change in volume per inspiration and per expiration, they are better ventilated than those alveoli in nondependent regions (during eupneic breathing from the FRC).
A second effect of the intrapleural pressure gradient in a person seated upright is on regional static lung volume, as is evident from the above discussion. At the FRC, most of the alveolar air is in upper regions of the lung because those alveoli have larger volumes. Most of the ERV is also in upper protions of the lung On the other hand, most of the IRV and IC are in lower regions of the lung.
Alterations of Distribution at Different Lung Volumes (low volumes/RV, high volumes/)
Most of the air inspired during a tidal breath begun at the FRC enters the dependent alveoli. If a slow inspiration is begun at the RV, however, the initial part of the breath (inspiratory volume less than the ERV) enters the nondependent upper alveoli, and dependent alveoli begin to fill later in the breath. The intrapleural pressure gradient from the upper parts of the lung to the lower parts of the lung is also the cause of this preferential ventilation of nondependent alveoli at low lung volumes.
Positive intrapleural pressures are generated by the expiratory muscles during a forced expiration to the RV. This results in dynamic compression of small airways. At the highest intrapleural pressures these airways close, and gas is trapped in their alveoli. Because of the graident of intrapleural pressure found in the upright lung, at low low lung volumes the pleural surface pressure is more positive in lower regions of the lung than it is in upper regions. Also, alveoli in lower lung regions have less alveolar elastic recoil to help hold small airways open because they have smaller volumes than do the alveoli in upper regions. This means that airway closure will occur first in airways in lower regions of the lung. The expiratory effort has ended and the inspiratory effort has just begun. Airways in the lowest regions of the lung are still closed, and the local pleural surface pressure is still slightly positive. No air enters these alveoli during the first part of the inspiratory efforts until sufficient negative pressure is generated to open these closed airways.
In contrast to the situation at the FRC, at the RV the alveoli in the upper regions of the lungs are now on a much steeper portion of the pressure-volume curve. They now have a much greater change in volume per change in transpulmonary pressure – they are more compliant at this lower lung volume. Therefore, they receive more of the air initially inspired from the RV.
It has already been noted that even at low lung volumes the upper alveoli are larger in volume than are the lower gravity-dependent alveoli. They therefore constitute most of the RV.
Patients with emphysema have greatly decreased alveolar elastic recoil, leading to high FRCs, extremely high RVs, and airway closure in dependent parts of the lung even at high lung volumes. They therefore have relatively more ventilation of nondependent alveoli.
Reference Range of Critical Parameters
Dry Atmospheric Gas at Standard Barometric Pressure
PO2 = FiO2 X Ptot = 0.2093 X 760 mm Hg = 159 mm Hg
PCO2 = FiCO2 X Ptot = 0.0004 X 760 mm Hg = 0.3 mm Hg
Inspired Gas at Standard Barometric Pressure
PO2 = FiO2 X (PB – PH2O) = 0.2093 X (760 – 47) mm Hg = 149 mm Hg
PCO2 = FiCO2 X (PB – PH2O) = 0.0004 X (760 -47) mm Hg = 0.29 mm Hg
Alveolar Gas at Standard Barometric Pressure
PAO2 = 104 mm Hg, PACO2 = 40 mm Hg, PAN2 = 569 mm Hg, PAH2O = 47 mm Hg
Mixed Expired Air at Standard Barometric Pressure
PEO2 = 120 mm Hg, PECO2 = 27 mm Hg, PEN2 = 566 mm Hg, PEH2O = 47 mm Hg