Mechanics of Ventilation

The balance between the outward elastic recoil of the chest wall and the inward elastic recoil of the lungs generates a subatmospheric intrapleural pressure

The interaction between the lungs and the thoracic cage determines V _L . The lungs have a tendency to collapse because of their elastic recoil, a static property represented by the inwardly directed arrows in Figure 27-1 A . The chest wall also has an elastic recoil. However, this elastic recoil tends to pull the thoracic cage outward (see Fig. 27-1 B ). The stage is thus set for an interaction between the lungs and the chest wall: at equilibrium, the inward elastic recoil of the lungs exactly balances the outward elastic recoil of the chest wall (see Fig. 27-1 C ). This interaction between lungs and chest wall does not occur by direct attachment but via the intrapleural space between the visceral and parietal pleurae (see p. 597 ). This space is filled with a small amount of pleural fluid and is extremely thin (5 to 35 µm). Because the lungs and chest wall pull away from each other on opposite sides of the intrapleural space, the intrapleural pressure (P _IP ) is less than barometric pressure (P b ); that is, the intrapleural space is a relative vacuum. Although the designation P _IP implies that we are referring exclusively to the intrapleural space, this description is not entirely accurate. Indeed, P _IP is probably similar to the pressure in several other regions of the chest cavity in addition to the intrapleural space:

• 1

  The virtual space between the chest wall or diaphragm and the parietal pleura

• 2

  The virtual space between the lung and the visceral pleura

• 3

  The interstitial space that surrounds all pulmonary airways

• 4

  Around the heart and vessels

• 5

  Around and—to the extent that smooth-muscle tone can be neglected—inside the esophagus

It is helpful to think of P _IP as the intrathoracic pressure—the pressure everywhere in the thorax except in the lumens of blood vessels, lymphatics, or airways. N27-1

The vacuum is not uniform throughout the intrapleural space. When the subject is upright, the vacuum is greatest (i.e., P _IP is least) near the apex of the lungs and progressively falls along the longitudinal axis to its lowest value near the bases of the lungs ( Fig. 27-2 ). If a subject whose lungs are ~30 cm tall has finished a quiet expiration, and if P b is 760 mm Hg, P _IP is ~753 mm Hg near the apices of the lungs and ~758 mm Hg near the bases. The P _IP gradient is about what one would expect, given the density of the lungs. Note that P _IP is subatmospheric throughout the chest cavity. Because respiratory physiologists historically measured these small pressures with water manometers rather than with less sensitive mercury manometers, it has become customary to express P _IP in centimeters of H ₂ O relative to a P b of 0 cm H ₂ O. Thus, P _IP is about −10 cm H ₂ O at the apex and −2.5 cm H ₂ O at the base of the lungs.

The reasons for the apex-to-base P _IP gradient are gravity and posture. When an individual stands vertically on the surface of the earth, gravity pulls the lungs downward and away from the apex of the thoracic cage. This force creates a greater vacuum (i.e., a lower P _IP ) at the apex. Gravity also pushes the bases of the lungs into the thoracic cavity, reducing the vacuum there. Standing on one's head would invert these relationships. Lying on one's side would create a P _IP gradient along a frontal-horizontal axis (i.e., from side to side), although the P _IP gradient would be much smaller because the side-to-side dimension of the thorax (and therefore the gradient created by the weight of the lungs) is less than the longitudinal dimension. In outer space, the P _IP gradient would vanish. Thus, the local P _IP depends on the position within the gravitational field.

For most of the remainder of this book, we ignore the P _IP gradient and refer to an average P _IP of about −5 cm H ₂ O after a quiet expiration (see Fig. 27-2 ).

Contraction of the diaphragm and selected intercostal muscles increases the volume of the thorax, producing an inspiration

We have seen that the opposing elastic recoils of the lungs and chest wall create a negative P _IP that keeps the lungs expanded. Any change in the balance between these elastic recoils will cause V _L to change as well. For example, imagine a healthy person with a functional residual capacity (FRC) of 3 L and a P _IP of −5 cm H ₂ O. If that person now develops pulmonary fibrosis, which increases the elastic recoil of the lungs, FRC would decrease because a P _IP of −5 cm H ₂ O would no longer be adequate to keep the resting V _L at 3 L. Moreover, as the lungs shrink, P _IP would become more negative, causing chest volume to decrease as well. Under normal circumstances, the key elastic recoil is the one we control: the elastic recoil of the chest wall, which we change moment to moment by modulating the tension of the muscles of respiration.

The muscles of inspiration expand the chest, increasing the elastic recoil of the chest wall and making P _IP more negative. Despite the P _IP gradient from the apex to the base of the lungs when no air is flowing at FRC (see Fig. 27-2 ), the ΔP _IP during inspiration is similar throughout the thoracic cavity. Responding to this enhanced intrathoracic vacuum, the lungs expand passively. The increase in V _L is virtually the same as the increase in thoracic volume. The muscles that produce a quiet inspiration are called the primary muscles of inspiration and include the diaphragm and many intercostal muscles.

The most important component of the increase in chest volume is the rise in the chest cavity's rostral-caudal diameter, a result of the action of the diaphragm. Stimulated by the phrenic nerves (derived from cervical roots C3 to C5), the diaphragm contracts and moves downward into the abdomen ~1 cm during quiet ventilation.

The external and internal intercostal muscles, innervated by segmental spinal nerves, span the space between adjacent ribs. The action of each such muscle depends partly on its orientation but especially—because of the shape of the rib cage—on its position along the rostral-caudal axis and around the dorsal-ventral circumference of the rib cage. Thus, not all external intercostals are inspiratory, and not all internal intercostals are expiratory. Inspiratory neurons preferentially stimulate the most rostral and dorsal external intercostals and the parasternal internal intercostals, both of which have inspiratory mechanical advantages. N27-2 The contraction of these muscles has two consequences ( Fig. 27-3 A ). First, the rib cage and the tissues between the ribs stiffen and are therefore better able to withstand the increasingly negative P _IP . Second, thoracic volume increases as (a) ribs 2 through 10 rotate upward and outward, increasing the transverse diameter (bucket-handle effect; see Fig. 27-3 B ) and (b) the upper ribs rotate the sternum upward and outward, increasing the anterior-posterior diameter (water pump–handle effect).

During a forced inspiration, the accessory (or secondary ) muscles of inspiration also come into play:

• 1

  Scalenes. These muscles lift the first two ribs.

• 2

  Sternocleidomastoids. These muscles lift the sternum outward, contributing to the water pump–handle effect.

• 3

  Neck and back muscles. These elevate the pectoral girdle (increasing the cross-sectional area of the thorax) and extend the back (increasing the rostral-caudal length).

• 4

  Upper respiratory tract muscles. The actions of these muscles decrease airway resistance.

Relaxation of the muscles of inspiration produces a quiet expiration

During a quiet inspiration, normal lungs store enough energy in their elastic recoil to fuel a quiet expiration, just as stretching of a rubber band stores enough energy to fuel the return to initial length. Thus, a quiet expiration is normally passive, accomplished simply by relaxation of the muscles of inspiration. Thus, there are no primary muscles of expiration.

Expiration is not always entirely passive. One example is a forced expiration in an individual with normal airway resistance. Another is even a quiet expiration of a person with a disease that increases airway resistance (e.g., asthma, chronic bronchitis, emphysema). In either case, the accessory muscles of expiration help make P _IP more positive:

• 1

  Abdominal muscles (internal and external oblique, rectoabdominal, and transverse abdominal muscles). Contraction of these muscles (see Fig. 27-3 C ) increases intra-abdominal pressure and forces the diaphragm upward into the chest cavity, decreasing the rostral-caudal diameter of the thorax and increasing P _IP .

• 2

  Intercostals. The most ventral and caudal external intercostals, the most dorsal and lateral of the caudal internal intercostals, and an intercostal-like muscle called the triangularis sterni all have an expiratory mechanical advantage. Expiratory neurons selectively stimulate these muscles so as to reduce both the anterior-posterior and the transverse diameters of the thorax. These actions are particularly important for coughing.

• 3

  Neck and back muscles. Lowering of the pectoral girdle reduces the cross-sectional area of the thorax, whereas flexion of the trunk reduces the rostral-caudal diameter.

During a forced inspiration, the accessory muscles of inspiration use their energy mainly to increase V _L (rather than to overcome resistance to airflow); the lungs store this extra energy in their elastic recoil. During a forced expiration, the accessory muscles of expiration use their energy mainly to overcome the resistance to airflow, as discussed below.

An increase of the static compliance makes it easier to inflate the lungs

Imagine that a person experiences a puncture wound to the chest cavity, so that air enters the thorax from the atmosphere, raising P _IP to the same level as P b . This condition is called a pneumothorax (from the Greek pneuma [air]). With no vacuum to counter their elastic recoil, alveoli will collapse—a condition known as atelectasis. The upper part of Figure 27-4 A illustrates an extreme hypothetical case in which pressure is atmospheric throughout the thorax. Even though the lungs are collapsed, V _L is not zero because prox­imal airways collapse before smaller ones farther downstream, trapping air. The resulting minimal air volume is ~10% of total lung capacity (TLC), typically ~500 mL.

We now wish to re-expand the collapsed lungs to their original volume (i.e., FRC). What are the forces at work during such a re-expansion? The force responsible for distending an airway is the transmural pressure (P _TM ) —the radial pressure difference across an airway wall at any point along the tracheobronchial tree:

P _AW is the pressure inside the airway, and P _IP is the pressure in the interstitial space surrounding the airway. A special case of P _TM is the transmural pressure across the alveolar wall— trans pulmonary pressure (P _TP ):

P a is alveolar pressure. When the glottis is open and no air is flowing, the lungs are under static conditions, and P a must be 0 cm H ₂ O:

Thus, with the glottis open under static conditions, the pressure that inflates the alveoli (i.e., P _TP ) is simply the negative of P _IP . We can re-expand the lungs to FRC by any combination of an increase in P a and a decrease in P _IP , as long as P _TP ends up at 5 cm H ₂ O (see Fig. 27-4 A , lower panels). Thus, it makes no difference whether we increase P a from 0 to +5 cm H ₂ O with P _IP fixed at zero (the principle behind positive-pressure ventilation in an intensive care unit) or whether we decrease P _IP from 0 to –5 cm H ₂ O with P a fixed at zero (the principle behind physiological ventilation). In both cases, V _L increases by the same amount.

A clinician would treat the pneumothorax by inserting a chest tube through the wound into the thoracic cavity and gradually pumping out the intrathoracic air. The clinician might also insert a tube through the mouth and into the upper trachea (to ensure a patent airway), use a mechanical ventilator (to ensure gas exchange), and sedate the patient (to prevent the patient from fighting the ventilator). Between the inspiratory cycles of the ventilator, the lungs are under static conditions and V _L depends only on P _TP —that is, the difference between P a (which is set by the ventilator) and P _IP . As we remove air from the thorax, P _IP becomes more negative and the alveoli re-expand. We can characterize the elastic (or static) properties of the lungs by plotting V _L versus P _TP as V _L increases (see Fig. 27-4 B , purple curve). How do we obtain the necessary data? In principle, we could determine V _L by using Equation 26-4 . We could read off P a (needed to compute P _TP ) directly from the ventilator. Finally, we could in principle measure P _IP by using a pressure transducer at the tip of the chest tube. Most important, we must take our readings between inspiratory cycles of the ventilator—under static conditions.

During the reinflation, measured under static conditions, we can divide the effect on V _L into four stages, starting at the left end of the purple curve in Figure 27-4 B :

• Step 1: Stable V _L . In the lowest range of P _IP values, making P _IP more negative has little or no effect on V _L . For example, decreasing P _IP from 0 to –1 cm H ₂ O (i.e., increasing P _TP from 0 to +1 cm H ₂ O), we record no change in V _L . Why? As discussed below, it is very difficult—because of the surface tension created by the air-water interface—to pop open an airway that is completely collapsed. Until P _TP is large enough to overcome the collapsing effects of surface tension, a decrease in P _IP has no effect on V _L .

• Step 2: Opening of airways. Decreasing P _IP beyond about –8 cm H ₂ O produces V _L increases that are at first small, reflecting the popping open of proximal airways with the greatest compliance. Further decreasing P _IP produces larger increases in V _L , reflecting the expansion of already-open airways as well as recruitment of others.

• Step 3: Linear expansion of open airways. After all the airways are already open, making P _IP increasingly more negative inflates all airways further, causing V _L to increase in a roughly linear fashion.

• Step 4: Limit of airway inflation. As V _L approaches TLC, decreases in P _IP produce ever smaller increases in V _L , which reflects decreased airway and chest-wall compliance and the limits of muscle strength.

What would happen if, having inflated the lungs to TLC, we allowed P _IP to increase to 0 cm H ₂ O once again? Obviously, the V _L would decrease. However, the lungs follow a different path during deflation (see Fig. 27-4 B , red curve), creating a P _IP -V _L loop. The difference between the inflation and the deflation paths— hysteresis —exists because a greater P _TP is required to open a previously closed airway, owing to a deficit of surfactant at the air-water interface, than to keep an open airway from closing, due to the abundance of surfactant. We will discuss surfactant in the next section. The horizontal dashed line in Figure 27-4 B shows that inflating previously collapsed lungs to FRC requires a P _IP of –12 cm H ₂ O (purple point), whereas maintaining previously inflated lungs at FRC requires a P _IP slightly less negative than –5 cm H ₂ O (red point). During normal ventilation, the lungs exhibit much less hysteresis, and the green P _IP -V _L loop in Figure 27-4 B lies close to the red deflation limb of our original loop. The changes in V _L in Figure 27-4 B reflect mainly changes in the volume of alveoli, with a small contribution from conducting airways.

We will now focus on just the red curve in Figure 27-4 B , a portion of which is the middle curve in Figure 27-5 . Here, P _TP is +5 cm H ₂ O when V _L is at FRC. As the subject makes a normal inspiration with a tidal volume (V _T ) of 500 mL, P _TP increases (i.e., P _IP decreases) by 2.5 cm H ₂ O. The ratio of ΔV _L to ΔP _TP (i.e., the slope of the P _TP -V _L curve) is the compliance, a measure of the distensibility of the lungs. In our example,

Because we made this measurement under conditions of zero airflow, C is the static compliance. Static compliance, like V _L , is mainly a property of the alveoli. The elastance of the lungs, which is a measure of their elastic recoil, is the reciprocal of the compliance ( E = 1 /C ). Lungs with a high compliance have a low elastic recoil, and vice versa.

Figure 27-5 also shows representative P _TP -V _L relationships for lungs of patients with pulmonary fibrosis (bottom curve) and emphysema (top curve). In pulmonary fibrosis, the disease process causes deposition of fibrous tissue, so that the lung is stiff and difficult to inflate. Patients with restrictive lung disease, by definition, have a decreased C (i.e., a decreased slope of the V _L -P _TP relationship in Fig. 27-5 ) at a given V _L . The same ΔP _TP that produces a 500-mL V _L increase in normal lungs produces a substantially smaller V _L increase in fibrotic lungs. In other words, static compliance (ΔV _L /ΔP _TP ) is much less, or elastic recoil is much greater.

In emphysema, the situation is reversed. The disease process, a common consequence of cigarette smoking, destroys pulmonary tissue and makes the lungs floppy. An important part of the disease process is the destruction of the extracellular matrix, including elastin, by elastase released from macrophages. Normal mice that are exposed to cigarette smoke develop emphysema rapidly, whereas the disease does not develop in “smoker” mice lacking the macrophage elastase gene. The same increase in P _TP that produces a 500-mL V _L increase in normal lungs produces a substantially larger V _L increase in lungs with emphysema. In other words, static compliance is much greater (i.e., much less elastic recoil).

Because it requires work to inflate the lungs against their elastic recoil, one might think that a little emphysema might be a good thing. Although it is true that patients with emphysema exert less effort to inflate their lungs, the cigarette smoker pays a terrible price for this small advantage. The destruction of pulmonary architecture also makes emphysematous airways more prone to collapse during expiration, which drastically increases airway resistance.

Two additional points are worth noting. First, compliance (i.e., slope of the P _TP -V _L curve) decreases as V _L increases from FRC to TLC (see Fig. 27-5 ). Second, the P _TP -V _L curve is the amalgam of pressure-volume relationships of all alveoli. Different alveoli have different P _TP -V _L curves and may experience different intrapleural pressures, depending on their position within a gravitational field (see Fig. 27-2 ). This inhomogeneity of static parameters contributes to regional differences in ventilation (see pp. 687–689 ; Box 27-1 ).