Events involved in a normal tidal breath
– Inspiration –
1) Brain initiates inspiratory effort
2) Nerves carry the inspiratory command to the inspiratory muscles
3) Diaphragm and/or external intercostal muscles contract
4) Thoracic volume increases as the chest wall expands
5) Intrapleural pressure becomes more negative
6) Alveolar transmural pressure difference increases
7) Alveoli expand in response to the increased transmural pressure difference. This increases alveolar elastic recoil
8) Alveolar pressure falls below atmospheric pressure as the alveolar volume increases, thus establishing a pressure difference for airflow
9) Air flows into the alveoli until alveolar pressure difference equilibrates with atmospheric pressure
– Expiration (passive) –
1) Brain ceases inspiratory command
2) Inspiratory muscles relax
3) Thoracic volume decreases, causing intrapleural pressure to become less negative and decreasing the alveolar transmural pressure difference
4) Decreased alveolar transmural pressure difference allows the increased alveolar elastic recoil to return the alveoli to their preinspiratory volumes
5) Decreased alveolar volume increases alveolar pressure above atmospheric pressure, thus establishing a pressure difference for airflow
6) Air flow out of the alveoli until alveolar pressure equilibrates with atmospheric pressure
Basic Concepts and Ideas
Several factors besides the elastic recoil of the lungs and the chest wall must be overcome to move air into or out of the lungs. These factors include the inertia of the respiratory system, the frictional resistance of the lung and chest wall tissue, and the frictional resistance of the airways to the flow of air. The inertia of the system is negligible. Pulmonary tissue resistance is caused by the friction encountered as the lung tissues move against each other or the chest wall as the lung expands. The airway resistance plus the pulmonary tissue resistance is often referred to as the pulmonary resistance.
Pulmonary tissue resistance normally conributes about 20% of the pulmonary resistance, with airways resistance responsible for the other 80%. Pulmonary tissue resistnace can be increased in such conditions as pulmonary sarcoidosis, silicosis, asbestosis, and fibrosis. Because the airway resistance is the major component of the total resistance and because it can increase tremendously both in healthy people and in those suffering from various diseases, the remainder of this chapter will concentrate on airways resistance.
Generally, the relationship among pressure, flow, and resistance is stated as
Resistance = Pressure Difference (cm H2O) / Flow (L/s)
This means that the resistance is a meaningful term only during flow. When airflow is considered, the units of resistance are usually cm H2O/L/s. Similarly to blood flow, the resistances in series and parallel are as follows, respectively.
Rtot = R1 + R2 + … (in series)
1/Rtot = 1/R1 + 1/R2 + … (in parallel)
And again similarly to blood flow, the resistance (Poiseuille's law) is directly proportional to the viscosity of the fluid (air) and the length of the tube and is inversely proportional to the fourth power of the radius of the tube:
R = 8 x n x L / (Pi x r4)
In a normal adult about 35% to 50% of the total resistance to airflow is located in the upper airways: the nose, nasal turbinates, oropharynx, nasopharynx, and larynx. Resistance is higher when one breathes through the nose than when one breaths through the mouth. As for the tracheobronchial tree, the component with the highest individual resistance is the smallest airway, which has the smallest radius. Nevertheless, because the smallest airways are arranged in parallel, their resistances add as reciprocals, so that the total resistance to airflow offered by the numerous small airways is extremely low during normal, quiet breathing. Therefore, under normal circumstances the greatest resistance to airflow resides in the large to medium-sized bronchi.
Forced Vital Capacity
The main concept underlying these pulmonary function tests is that elevated airways reistance takes time to overcome.
One way of assessing expiratory airways resistance is to look at the results of a forced expiration into a spirometer, as shown in Figure 2-21. This measurement is called a forced vital capacity (FVC). The VC is the volume of air a subject is able to expire after a maximal inspiration to the total lung capacity (TLC). An FVC means that a maximal expiratory effort was made during this maneuver.
In an FVC test, a person makes a maximal inspiration to the TLC. After a moment, he or she makes a maximal forced expiratory effort, blowing as much air as possible out of the lungs. At this point, only a residual volume (RV) of air is left in the lungs. This procedure takes only a few seconds, as can be seen on the time scale.
The part of the curve most sensitive to changes in expiratory airways resistance is the first second of expiration. The volume of air expired in the first second of expiration (the FEV1, or forced expiratory volume in 1 second), especially when expressed as a ratio with the total amount of air expired during the FVC, is a good index of expiratory airways resistance. In normal young subjects, the FEV1/FVC is greater than 0.80; that is, at least 80% of the FVC is expired in the first second. An FEV1/FVC of 75% would be more likely in an older person. A patient with airway obstruction caused by an episode of asthma, for example, would be expected to have an FEV1/FVC far below 0.80, as shown in the middle and bottom panels in Figure 2-21.
The bottom panel of Figure 2-21 shows similar FVC curves that would be obtained from a commonly used rolling seal spirometer. The curves are reversed right to left and upside down if they are compared with those in top and middle panels. The TLC is at the bottom left, and the RVs are at the top right. The time scale is left to right. Note the calculations of FEV1 to FVC ratios.
Another way of expressing the same information is the FEF25%-75%, or forced (mid) expiratory flow rate (formerly called the MMFR, or maximal midexpiratory flow rate). This variable is simply the slope of a line drawn between the points on the expiratory curve at 25% and 75% of the FVC. In cases of airway obstruction, this line is not nearly as steep as it is on a curve obtained from someone with normal airway resistance. The FEV1/FVC is usually considered to represent larger airways, the FEF25%-75%, smaller to medium-sized airways.
Physiologic Quantitive Relationships and Phenomenon
Lung Volume and Airways Resistance
Airways resistance decreases with increasing lung volume, as shown in the figure on the left. This relationship is still present in an emphysematous lung, although in emphysema the resistance is higher than that in a healthy lung, especially at low lung volumes.
Transmural Pressure and Traction on Airway by elastic recoil of alveolar septa
There are 2 reasons for this relationship; both mainly involve the small airways, which have little or no cartilaginous support. The small airways are therefore rather distensible and also compressible. Thus, the transmural pressure difference across the wall of the small airways is an important determinant of the radius of the small airways: Since resistance is inversely proportional to the radius to the fourth power, changes in the radii of small airways can cause dramatic changes in airways resistance, even with so many parallel pathways. To increase lung volume, a person breathing normally takes a "deep breath", that is, makes a strong inspiratory effort. This effort causes intrapleural pressure to become much more negative than the -7 or -10 cm H2O seen in a normal, quiet breath. The transmural pressure difference across the wall becomes much more positive, and small airways are distended.
Transmural pressure = inside pressure – outside pressure
PS: Transumral presssure = Pin – Pout = Ptrans; Pin = Palve, Pout = Ppleu; at static, Ptrans = Preco; so, Preco = Ptrans = Pin – Pout = Palve – Ppleu; finally we ge this conclusion, Palve = Ppleu + Preco.
A second reason for the decreased airways resistance seen at higher lung volume is that the so-called traction on the small airways increases. As shown in the schematic drawing in the Figure 2-18, the small airways traveling through the lung from attachments to the walls of alveoli. As the alveoli expand during the course of a deep inspiration, the elastic recoil in their walls increases; this elastic recoil is transmitted to the attachments at the airway, pulling it open.
Dynamic Compression of Airways
Airways resistance is extremely high at low lung volumes, as can be see in the airways resistance versus lung volume curve above. To achieve low lung volumes, a person must make a forced expiratory effort by contracting the muscles of expiration, mainly the abdominal and internal intercostal muscles. This effort generates positive intrapleural pressure, which can be as high as 120 cm H2O during a maximal forced expiratory effort. (Maximal inspiratory intrapleural pressures can be as low as -80 cm H2O.)
The effect of this high positive intrapleural pressure on the transmural pressure gradient during a forced expiration can be seen at right in Figure 2-19, a schematic drawing of a single alveolus and airway.
Alveolar Pressure = Intrapleural Pressure + Alveolar Elastic Recoil Pressure
At this instant, during the course of a forced expiration, the muscles of expiration are generating a positive intrapleurual pressure of +25 cm H2O. Pressure in the alveolus is greater than intrapleural pressure because of the alveolar elastic recoil pressure of +10 cm H2O, which together with intrapleural pressure, given an alveolar pressure of +35 cm H2O. The alveolar elastic recoil pressure decreases at lower lung volumes because the alveolus is not as distended. In the figure, a gradient has been established from the alveolar pressure of +35 cm H2O to the atmospheric pressure of 0 cm H2O. If the airways were rigid and incompressible, the large expiratory pressure gradient would generate very high rates of airflow. However, the airways are not uniformly rigid and the smallest airways, which have no cartilaginous support and rely on the traction of alveolar septa to help keep them open, may be compressed or may even collapse. Whether or not they actually collapse depends on the transmural pressure gradient across the walls of the smallest airways. Small airway collapse is the main reason that airways resistance appears to be approaching infinity at low lung volumes.
The situation during a normal passive expiration at the same lung volume (note the same alveolar elastic recoil pressure) is shown in the left part of Figure 2-19. The transmural pressure gradient across the smallest airways is
+1 cm H2O – (-8) cm H2O = +9 cm H2O
tending to hold the airway open. During the forced expiration at right, the transmural pressure gradient is 30 cm H2O – 25 cm H2O, or only 5 cm H2O holding the airway open. The airway may then be slightly compressed, and its resistance to airflow will be even greater than during the passive expiration. This increased resistance during a forced expiration is called dynamic compression of airways.
Consider what must occur during a maximal forced expiration. As the expiratory effort is increased to attain a lower and lower lung volume, intrapleural pressure is getting more and more positive, and more and more dynamic compression will occur. Furthermore, as lung volume decreases, there will be less alveolar elastic recoil pressure and the difference between alveolar pressure and inrapleural pressure will decrease.
One attention must be paid when dynamic compression of airways occur. During a passive expiration the presure gradient for airflow is simply alevolar pressure minus atmospheric pressure. But if dynamic compression occurs, the effective pressure gradient is alveolar pressure minus intrapleural pressure (which equals the alveolar elastic recoil pressure) because intrapleural pressure is greater than atmospheric pressure and because intrapleural pressure can exert its effects on the compressible portion of the airways.