Mechanics of Ventilation

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Mechanics of Ventilation

Objectives

After reading this chapter, you will be able to:

• Explain how elastic recoil forces of the lungs and chest wall interact to establish the resting lung volume

• Describe how static lung volumes and capacities are influenced by changes in the elastic recoil forces of the lungs and chest wall

• Explain which pressure gradients maintain alveolar volume and create airflow into and out of the lung

• Describe how spontaneous breathing and positive pressure mechanical ventilation are different and similar in the way they create pressure gradients throughout the respiratory cycle

• Describe how the rib cage, diaphragm, and abdomen components of the thorax move and interact differently in normal and abnormal conditions

• Interpret static and dynamic pressure-volume curves of the lungs, thorax, and lung-thorax system

• Determine whether high inflation pressure during mechanical ventilation is caused by a change in lung compliance or in airway resistance

• List factors that cause lung compliance and airway resistance to change

• Describe how surface tension and pulmonary surfactant influence lung compliance, inflation pressure, alveolar stability, and work of breathing

• Explain what causes the lung’s pressure-volume curve to exhibit hysteresis

• Explain how to use pressure-volume and time-pressure curves to distinguish between elastic and frictional forces that oppose lung inflation

• Describe why greater muscular effort fails to increase expiratory flow rates under certain physical conditions

• Explain how compliance and resistance are related to the emptying and filling rates of the lung during breathing

• Describe what factors predispose to incomplete exhalation and trapping of positive pressure in the alveoli at the end of expiration

• Explain the way in which work of breathing, respiratory muscular strength, and respiratory muscular fatigue are assessed

Resistance to lung inflation is categorized as (1) elastic resistance and (2) frictional resistance. Frictional resistance exists only under dynamic conditions—that is, when gas is moving through the airways. However, elastic resistance exists under both dynamic and static (no air movement) conditions. Normally, the ventilatory muscles easily overcome elastic and frictional resistances, and the work of breathing (WOB) is minimal and endlessly sustainable.

The lungs and chest wall (thorax) have equal but oppositely directed recoil forces that exactly balance each other when the respiratory muscles are relaxed and there is no airflow; the equilibrium between these forces determines the resting lung volume when ventilatory muscles are relaxed. The static and dynamic characteristics of the lung and chest wall system influence the WOB and distribution of inspired gas in the lung. Understanding normal lung-thorax mechanics is essential in treating patients needing respiratory therapy.

Static Lung and Chest Wall Mechanics

Elastic Recoil of the Lungs and Thorax

Elasticity is the tendency of an object to return to its original shape after being deformed. Stretching an object that has high elasticity generates a strong recoil force. The healthy lung has a tendency to recoil inward and pull away from the chest wall. At the same time, the thorax has a tendency to recoil outward, away from the lung. These two oppositely directed recoil forces create a subatmospheric pressure between the lung and chest wall. The lung’s elastic recoil force is generated by (1) elastic and collagen fibers of the lung parenchyma and (2) surface-tension forces of the thin liquid film lining the alveoli. Of these two factors, surface tension contributes the most to the elasticity of the lung.

As the lung and chest wall recoil in opposite directions, the pressure between the pleural membranes decreases (Boyle’s law). No true space exists between the visceral and parietal pleurae. However, if a small tube were placed through the chest wall between these membranes, a space would be created, and the pressure measured through the tube would be subatmospheric. This method of obtaining intrapleural pressure (Ppl) would be too invasive and hazardous for clinical purposes; changes in Ppl can be measured more safely through a balloon-tipped catheter placed in the esophagus with the tip of the catheter well inside the thoracic cavity (Figure 3-1). The thin-walled esophagus has little muscle tone and easily transmits Ppl changes to the balloon on the end of the catheter. Changes in intraesophageal balloon pressure reflect changes in Ppl. Figure 3-1 shows lung and thorax recoil forces and the resulting pressures.

Pressure Gradients during Ventilation

Figure 3-2 illustrates various pressure differences or gradients involved in ventilation. Airway pressures are usually expressed using atmospheric pressure as the zero reference value. A pressure of 0 mm Hg does not refer to an absolute lack of pressure but to atmospheric pressure (760 mm Hg at sea level). In this sense, a subatmospheric pressure of 755 mm Hg is below 0 mm Hg, or “negative.” Likewise, a pressure of 765 mm Hg is above 0 mm Hg, or “positive.” (All pressures are positive and cannot be truly negative. However, in this book, the terms negative and positive with regard to pressure refer to subatmospheric and above atmospheric pressures.)

Pressure at the mouth or the airway opening (Pao) is always equal to atmospheric pressure, or 0 mm Hg during normal spontaneous breathing. Pressure at the body surface (Pbs) is also by definition 0 mm Hg. Alveolar pressure (PA), sometimes called intrapulmonary pressure, is negative during inspiration, 0 mm Hg when airflow is absent, and positive during expiration. Ppl is always negative during normal quiet breathing for reasons discussed previously. The more strongly the lung’s recoil force tries to pull the lung away from the chest wall, the more negative the Ppl. When no air is moving and the lung is stationary, the inward recoil pressure of the lung is exactly balanced by the outward recoil pressure of the chest wall, creating a negative pressure between the two structures (i.e., the Ppl is negative); because there is no air movement, the PA is zero. In other words, PA is equal to the sum of chest wall and lung recoil pressures.

Pressure gradients are simply pressure differences between two points that cause air to move in or out of the lungs and are responsible for keeping the lungs in an inflated state. Air always flows from a point of high pressure to a point of low pressure; a pressure gradient of 0 mm Hg means there is no pressure difference between the two points and thus no airflow. Important pressure gradients in ventilation are the transpulmonary pressure (PL), transthoracic pressure (Pw), and transrespiratory pressure (Prs) (see Figure 3-2). (See Appendix I for a summary of pressure symbols in ventilatory mechanics.)

Prs is the difference between alveolar and body-surface pressures (Prs = PA − Pbs) or the pressure gradient across the entire respiratory system (lungs plus chest wall). Because both Pbs and Pao are atmospheric during normal breathing, Pao can be substituted for Pbs in the previous equation (Prs = PA − Pao, as shown in Figure 3-2). This equation shows that Prs is also equal to the pressure gradient across the airways, between the mouth and alveoli; thus, this pressure gradient is sometimes called the transairway pressure (PTA). PTA is responsible for airflow in and out of the lung. No airflow exists at the end of inspiration or at the end of expiration because PA is equal to Pao under both of these conditions; Prs or PTA is 0 mm Hg at these two points in the breathing cycle. In normal spontaneous breathing, Prs changes only when the PA changes because Pao is atmospheric and remains constant at 0 mm Hg. The magnitude of Prs (i.e., the difference between mouth and alveolar pressures) reflects the airways’ frictional resistance to airflow: the greater the pressure gradient needed to drive gas through the airways, the greater the airway resistance.

The transpulmonary pressure (PL) gradient is the difference between alveolar and intrapleural pressures (PL = PA − Ppl); in other words, PL is the distending pressure across the alveolar walls. PL is equal to the elastic recoil force of the lungs when there is no airflow—that is, the lung’s inward recoil creates a subatmospheric Ppl that exactly counterbalances the lung’s recoil force and prevents it from recoiling further. PA is always greater than Ppl in the intact normal lung-thorax system; thus, PL is a pressure gradient that keeps the alveoli inflated. If PL increases, alveolar volume increases, and vice versa; lung volume can change only if PL changes. Breathing, whether spontaneous or mechanically induced, consists of the increase or decrease of PL

CONCEPT QUESTION 3-2

Refer to Figure 3-4. At the end of a spontaneous 500-mL inspiration, the PA is 0 mm Hg; at the end of a positive pressure lung inflation to 500 mL, PA is 10 mm Hg. Explain how it is possible for the lung to contain the same volume at these two different alveolar pressures.

Transthoracic pressure (Pw) is the difference between Ppl and Pbs, or the pressure difference across the thoracic wall (Pw = Ppl − Pbs). It is equal to the outward recoil force of the thorax when there is no airflow. The stronger this outward recoil force, the greater the Pw. Pw is a reflection of thoracic wall recoil force alone.

Figure 3-3 illustrates changes in pressures during the respiratory cycle (inspiration and expiration). At the end of a resting expiration when all airflow has ceased, PA = 0 cm H2O, and the elastic recoil force of the lungs (Pel) is equal to a pressure of about 5 cm H2O (Figure 3-3, A). This means Ppl must be −5 cm H2O (PA is the sum of alveolar recoil pressure plus Ppl). Therefore, transpulmonary pressure (PL) at this point is about 5 cm H2O. The PL is calculated as follows:

< ?xml:namespace prefix = "mml" />PL=PAPpl

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PL=0(5)

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PL=5cmH2O

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By convention, PL is expressed as a positive number because it is the pressure that distends the lung. Corresponding with a PL of 5 cm H2O is a counterbalancing transthoracic pressure of −5 cm H2O, shown as follows:

Pw=PplPbs

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Pw=(5)0

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Pw=5cmH2O

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When all muscles are relaxed and no air is flowing, the inward and outward recoil forces of the lungs and thorax are in equilibrium with each another (see Figure 3-3, A). The Prs (pressure difference between the alveoli and the body surface) is the sum of PL plus Pw and is 0 mm Hg under the resting conditions just described. This is illustrated as follows:

Prs=PL+Pw

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Prs=5cmH2O+(5cmH2O)

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Prs=0cmH2O

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The act of inspiration (see Figure 3-3, moving from A to B to C) disrupts the equilibrium between lung and thoracic recoil forces. The ventilatory muscles contract and increase the thoracic dimensions as explained in Chapter 2. Consequently, Ppl decreases (Boyle’s law), which increases the PL gradient (PA − Ppl), “pulling” the alveoli to larger volumes. This causes PA to fall below Pao, establishing a pressure gradient for airflow into the lungs (see Figure 3-3, B). Air stops flowing into the lungs when PA equalizes with Pao (see Figure 3-3, C). At this point, PL is at its maximum value in the respiratory cycle (i.e., the difference between PA and Ppl is greatest), corresponding with an inhaled volume of 500 mL in this example.

Expiration begins when ventilatory muscles relax, allowing lung recoil forces to shrink the thoracic cavity passively (see Figure 3-3, moving from C to D). As the thoracic volume decreases, Ppl increases (becomes less negative), narrowing the gap between Ppl and PA. This decreases PL, reducing the lung’s dimensions, which compresses the lung’s air, increasing PA above Pao. Gas flows out of the lungs, reestablishing the initial preinspiratory conditions (see Figure 3-3, from D to A).

Rib Cage and Diaphragm-Abdomen Components of the Thorax

To this point, the thorax has been considered as if it were a single unit. It is more accurate to think of the thorax as having two components: the rib cage and the diaphragm-abdomen complex.1 The rib cage and diaphragm are coupled but can act independently during ventilation. Rib cage movements change the anterior-posterior and lateral dimensions of the thorax, and diaphragm movements displace the abdominal organs and change vertical thoracic dimensions. Normally, abdominal displacement predominates during quiet breathing, whereas rib cage displacement predominates when one breathes large volumes near maximum lung capacity.1 If abdominal displacement by the diaphragm is hampered by obesity, pregnancy, or an otherwise distended abdomen, breathing becomes more dependent on rib cage displacement. The work of breathing increases because it is more difficult to inflate the lung when the diaphragm resists movement.

Static Lung Volumes and Capacities

The total lung capacity (TLC) is the amount of gas the lung contains after a maximal inspiratory effort. All other lung volumes are natural subdivisions of the TLC. The term “capacity” refers to the combination of two or more volumes, which are basic, nonoverlapping entities in the TLC.

Measurement of Lung Volumes—Spirometry

Spirometry is the process of measuring volumes of air moving in and out of the lungs. A spirometer is the device used to measure these volumes. The spirogram is a graphical volume versus time representation of the lung volumes made by the spirometer. A classic water-seal spirometer is shown in Figure 3-5. Knowledge of the function of the water-seal spirometer helps a

Clinical Focus 3-1   Pressure Gradients in Positive Pressure Ventilation and Spontaneous Breathing

During mechanical positive pressure ventilation (PPV), Pao is increased above atmospheric pressure during inspiration, forcing gas into the alveoli. This is the opposite of spontaneous breathing (SB), in which PA first decreases below Pao. During PPV, the alveoli transmit some of their positive pressure into the intrapleural space. This causes Ppl to increase toward zero (become less negative), which is again the opposite of spontaneous inspiration, in which Ppl decreases and becomes even more negative. Two important points to remember are (1) both SB and PPV accomplish inspiration by increasing PL, the pressure distending the lungs, and (2) because PPV raises the Ppl, it tends to compress the veins that bring blood back to the heart, ultimately impeding cardiac output. SB has the opposite effect because inspiration lowers Ppl further, augmenting venous blood return to the heart.

Figure 3-4 compares PPV and SB. The lung diagrams illustrate conditions at the end of an inspiration. Although the transpulmonary pressures were achieved by different means in SB and PPV, PL is 10 cm H2O in both instances. This means elastic lung fibers are stretched to the same extent in both instances. The PPV inspiration places no more stress on the lung than the SB inspiration, although PA is 10 cm H2O greater in PPV than in SB. This fact has relevance to therapeutic lung-expansion techniques used in respiratory care. Given normal inspiratory muscle function, a mechanical positive pressure inspiration is not superior to a spontaneous inspiration in expanding the lung, and a 500-mL positive pressure breath is not any more likely than a 500-mL spontaneous breath to injure the lungs. PPV may generate a greater PL and volume than SB only in a person with weakened inspiratory muscles.

Clinical Focus 3-2   Misguided Therapy: Why High Alveolar Pressure Does Not Always Expand the Lung

In years past, respiratory therapists and nurses taught patients to use blow bottles, thinking this technique would help expand the lungs. Blow bottles consisted of two large capped jars half full of water connected by a single long tube penetrating through each bottle cap. Each end of the connecting tube was submerged below the water surface near the bottom of each jar. Each jar had an additional short tube fitted through its cap that did not reach the water’s surface. By blowing forcefully through this short tube, the patient could force water up through the long connecting tube into the other jar. The high pressure generated in the lungs during the water transfer was believed to reexpand collapsed alveoli. However, a rational examination of pulmonary mechanics reveals that the high PA created in a blow bottle exercise cannot expand the lungs.

Discussion

The PL (i.e., the pressure difference between the alveoli and the intrapleural space) determines the lung’s volume. This gradient increases during inspiration (enlarging the lung’s volume) and decreases during expiration (reducing the lung’s volume). Exhaling against resistance through the blow bottles’ tubes increases PA, but it increases Ppl even more, decreasing the transpulmonary pressure gradient. Consequently, lung volume decreases during this expiratory maneuver, even though PA is high—the opposite of the intended therapeutic outcome. Coughing maneuvers (because they are bursts of forced expiration) also do not increase the transpulmonary pressure gradient for the same reasons. The deep breath individuals must take before a cough or before they can blow water from one bottle to the other is the only part of the procedure that can produce lung expansion. It is more rational simply to coach the patient to take deep breaths, which focuses attention on inspiration and lung expansion rather than on expiration and lung deflation—which is precisely what modern incentive spirometry techniques accomplish.

person understand the interrelationships between volumes and capacities. (Modern spirometers are electronic, microprocessor-controlled devices.)

While wearing nose clips to occlude the nostrils, the patient inhales and exhales through a large tube inserted snugly into the mouth (see Figure 3-5). Exhaled air enters the inverted cylinder (bell) suspended by a chain and pulley. This bell fits loosely over a smaller cylinder and floats in a water-filled sleeve. The other end of the chain is attached to a recording pen and counterweight, which exactly balance the weight of the floating bell. The water provides a seal from atmospheric air and allows nearly frictionless movement of the bell. Bell movements cause the pen to move up and down, inscribing reciprocal tracings on recording paper wrapped around a drum rotating at a constant speed, creating a graphic representation of volume (vertical axis) versus time (horizontal axis) (Figure 3-6).

Figure 3-6 reveals that not all of the TLC is accessible to the spirometer. The residual volume (RV) cannot be exhaled, even with the greatest expiratory effort, because the rigid rib cage prevents total lung deflation. RV must be measured indirectly through other techniques (see Chapter 5).

Figure 3-6 illustrates the four lung volumes and four lung capacities. The measurements for each are approximate and vary according to an individual’s height, gender, and age. The descriptions and symbols for the static lung volumes and capacities are shown in Table 3-1. (See also Appendix I.)

TABLE 3-1

Static Lung Volumes and Capacities

Volume and Capacity Symbol Definition
Residual volume RV Volume of air remaining in the lung after a maximal-effort expiration
Expiratory reserve volume ERV Volume of air that can be exhaled with maximal effort from a resting (tidal) end-expiratory level
Tidal volume TV or VT Volume of air normally inhaled or exhaled with each breath during resting, quiet breathing
Inspiratory reserve volume IRV Volume of air that can be inhaled with maximal effort from the tidal end-inspiratory level
Total lung capacity TLC Volume of air in the lung after a maximal-effort inspiration; the sum of all volumes
Inspiratory capacity IC Volume of air that can be inhaled with maximal effort from a resting (tidal) end-expiratory level; sum of TV and IRV
Vital capacity VC Maximum volume of air that can be exhaled after a maximal-effort inspiration; sum of IRV, TV, and ERV
Functional residual capacity FRC Volume of gas remaining in the lung at the end of a normal tidal exhalation (relaxed ventilatory muscles); sum of ERV and RV

The tidal volume (VT) is the volume of air inhaled or exhaled with each breath. The vital capacity (VC) defines the maximum limits of a single breath—that is, from a maximum-effort inspiration to a maximum-effort expiration. Theoretically, the VT can increase until it equals the VC, but this never occurs, even with the most strenuous exercise. The functional residual capacity (FRC) is the amount of air in the lungs at the point of ventilatory muscle relaxation, also known as the resting level, or end-tidal exhalation level. Normally, about 40% of the TLC is contained in the lung at this resting FRC level. Expiratory (abdominal) muscle contraction is required to exhale any portion of the FRC, which involves the exhalation of expiratory reserve volume (ERV). The balance point between inward lung recoil and outward chest wall recoil determines the FRC level. Any factor that decreases lung recoil force increases the FRC and decreases the inspiratory capacity (IC). Any factor that increases lung recoil force decreases the FRC and decreases the TLC and VC. (Chapter 5 reviews these interrelationships in more detail.)

CONCEPT QUESTION 3-3

Referring to Figure 3-6 and Table 3-1, what effect does an increased RV have on other volumes or capacities, assuming TLC stays the same?

During resting VT breathing, only inspiration requires muscular (diaphragmatic) contraction. The end-tidal level is the point of total relaxation for all ventilatory muscles. Tidal exhalation is passive, a result of passive lung recoil. Tidal exhalation ends when lung and chest wall recoil forces reestablish their equilibrium point.

Maximum Static Inspiratory and Expiratory Pressures

Maximum inspiratory pressure (MIP) and maximum expiratory pressure (MEP) depend on ventilatory muscle strength. (Alternative symbols are PImax and PEmax.) These pressures are measured under static conditions while a person inhales or exhales with maximal effort against an occluded tube attached to a pressure gauge. During this measurement, the nose is blocked and the lips are sealed tightly around the tube to prevent air leaks.

The maximum pressures generated depend on the lung volumes at which they are measured. The MIP generating capacity is greatest at RV because diaphragmatic muscle fibers are maximally lengthened. The same principle is true for MEPs. At TLC, expiratory muscles are fully stretched, and a maximal expiratory effort may generate 230 cm H2O. At RV, expiratory muscle fibers are maximally contracted, and no expiratory pressure can be generated.

Average MEP and MIP results for adults are shown in Table 3-2.2 These pressures represent high reserve muscle strength, which may become involved during a cough or the birth process. Measurements of MIP and MEP are often used clinically to assess the ability of a patient to maintain spontaneous, unassisted ventilation; MIP is more often used in this regard. Severe compromise of ventilatory muscle strength is evident when no more than −20 cm H2O MIP can be generated.3

TABLE 3-2

Maximum Inspiratory and Expiratory Pressures

Gender MIP—Measured at RV MEP—Measured at TLC
Males −126 cm H2O 229 cm H2O
Females −92 cm H2O 151 cm H2O

MIP, Maximum inspiratory pressure; RV, residual volume; MEP, maximum expiratory pressure; TLC, total lung capacity.

Static Pressure-Volume Relationships

The elastic properties of the lung-thorax system are assessed by measuring the pressure required to inflate the lung under static conditions. Inflation pressures are measured many times at several volumes, and a pressure-volume (P-V) graph is constructed. Static pressures are plotted on the horizontal axis, and volumes are plotted on the vertical axis.

Hooke’s Law and Elastic Recoil

Over the normal physiological range of tidal breathing, the lung’s expansion in response to increasing pressures conforms to Hooke’s law. Hooke’s law states that an elastic structure changes dimensions in direct proportion to the amount of force applied. Each unit of pressure applied to the lung causes an additional unit of volume to be generated. As the lung volume increases, the recoil force increases. This linear relationship is maintained up to the elastic limit. If the elastic limit is exceeded, lung rupture is imminent.

Hooke’s law oversimplifies the response of the lungs to increasing pressures. Although the P-V curve is relatively linear in the VT range, a curve that plots the VC against the lung’s distending pressure (PL) is more S-shaped. The deflation curve follows a different path than the inflation curve, which is explained in the next section.

Static Pressure-Volume Curve

The lung’s PL (i.e., PA − Ppl) must be measured to create a static P-V curve for the lung alone (not taking the chest wall into account). The Ppl can be measured with an esophageal balloon, as described previously. PA is measured at the mouth under static conditions (i.e., when air flow is absent, mouth and alveolar pressures are equal).

An inspiratory P-V curve can be constructed (Figure 3-7) by applying pressure to the trachea, inflating the lung in volume increments in a stepwise fashion from RV to TLC. Each volume increment is held in the lung until all airflow ceases and PL is recorded. If the lung is deflated in an identical stepwise fashion back to RV, an expiratory P-V curve is constructed. The inflation-deflation curves are traced in a counterclockwise fashion when the lung is inflated by positive pressure applied to the trachea. The curves are nonlinear, partly because the collagen and elastic fibers composing the lung parenchyma are not uniform springs. Elastic fibers are easily stretched, whereas collagen fibers are more resistant to deformation. As the lung volume approaches TLC during inspiration, collagen fibers resist stretching more, causing the slope of the P-V curve to flatten at its upper end, creating an upper inflection point (see Figure 3-7).

Hysteresis and Mechanism of Lung Volume Change

The inflation and deflation limbs of the P-V curve in Figure 3-7 trace different paths, showing that for the same distending pressure, lung volume is greater during deflation than inflation. This phenomenon is called hysteresis, which occurs because the lungs dissipate energy during inflation.4 In other words, part of the energy used to inflate the lungs is not recovered during deflation; this means it takes less force to keep the lungs inflated during deflation than it does during inflation. This phenomenon has been experimentally shown: at the same pressure, the lung volume fixed in inflation is lower than the volume fixed in deflation.4

The phenomenon of hysteresis is related to the mechanism whereby lung volume changes. The idea that lung inflation and deflation are the result of collective balloon-like changes in 300 million alveolar diameters is overly simplistic. It is now widely understood that the major mechanism of lung expansion and retraction involves the sequential opening and closing (recruitment and derecruitment) of peripheral alveoli.4,5 At the end of a maximally forceful expiration (at RV), numerous alveoli are closed; lung volume increases during the subsequent inspiration mainly because an increasingly greater number of alveoli open up, not because individual alveolar diameters increase. The lungs dissipate energy in the alveolar recruitment process, mostly in overcoming the molecular adhesive forces of surface tension—forces not present during expiration when alveoli are already open.4

The lung’s recruitment expansion mechanism has been confirmed by in vivo microscopy of subpleural alveoli in animal models; inflation of the lung from 20% to 80% of TLC increased the number of recruited alveoli but did not increase individual alveolar diameters.5 A different investigation yielded similar results; when lung inflation pressure was increased from 10 cm H2O to 20 cm H2O and then again from 20 cm H2O to 30 cm H2O, alveolar size did not change, but the number of recruited alveoli changed in direct proportion to applied pressure.4

The alveolar recruitment-derecruitment mechanism is illustrated in Figure 3-8. At the beginning of inspiration (Figure 3-8, A), numerous alveoli are closed, their walls stuck together. As inspiration continues, these alveoli are forced open and recruited by the increasing PL (Figure 3-8, B). Recruitment occurs in two phases: in the first phase, from deflation to about 50% of the TLC, lung volume increases secondary to a linear increase in the number of alveoli recruited (i.e., the number recruited is directly proportional to PL). From 50% to 100% of TLC, the rate of recruitment accelerates, and the number of recruited alveoli increases exponentially. This accelerated recruitment rate is reflected by a steeper slope on the P-V curve, marked by a lower inflection point (LIP) on the inspiratory limb (see Figure 3-7).4

It was previously thought that the LIP marked the point at which alveolar recruitment was complete and that if expiratory pressure were not allowed to fall below this point in mechanically ventilated critically ill patients, alveolar closure on expiration would be prevented. It is now known that alveolar recruitment continues beyond the LIP to TLC; the entire P-V curve can be thought of as a recruitment curve.4,6 (See Clinical Focus 3-3 for a discussion of the clinically obtained P-V curve and significance of LIP.)

When the lung deflates, all alveoli are already open; the molecular adhesive forces opposing the recruitment process during inspiration are not present during expiration. During expiration, the lungs contain a greater volume for a given distending force than they contain during inspiration, which explains hysteresis, or the separation of the P-V curve’s inspiratory and expiratory limbs.

Clinical Focus 3-3   What Static and Dynamic Pressure-Volume Curves Tell Us in the Clinical Setting

Static P-V curves (no airflow conditions) are sometimes constructed in mechanically ventilated patients with acute lung injuries with the belief that these curves might be helpful in ventilator management. Beginning at the FRC level, the respiratory therapist progressively inflates the lungs in measured increments, pausing after each inflation to record its corresponding pressure. In healthy lungs, the P-V curve over the VT range is linear, but in severe lung injury (e.g., acute respiratory distress syndrome [ARDS]), the tidal P-V curve often has a sigmoid shape with a distinct lower inflection point (LIP) and possibly an upper inflection point (UIP), as shown in the figure. Traditionally, the LIP was thought to be the critical pressure at which collapsed alveoli reopened, and the UIP was believed to mark the volume at which alveolar overstretching occurred. The conventional wisdom was to ventilate patients with airway pressures between the two inflection points; the ventilator could be set to maintain positive end-expiratory pressure (PEEP) to keep pressures above the LIP on expiration, and VT could be limited to keep inspiratory pressure below the UIP. This strategy, sometimes called the “open-lung” approach to mechanical ventilation, was used to protect against ventilator-induced lung injury.

However, pressures measured at the endotracheal tube reflect the summation of many simultaneously occurring events in a highly complex lung composed of 300 million alveoli; alveolar P-V relationships inferred from measurements made at the endotracheal tube introduce uncertainty, limiting the helpfulness of P-V curves in ventilator management. It is now widely accepted that alveolar reopening in acute lung injury continues along the linear middle part of the static P-V curve even above the UIP and that the UIP probably indicates the end of alveolar recruitment, not necessarily the beginning of overdistention.6 It is possible that overdistention of some alveoli occurring simultaneously with the recruitment of others might delay the appearance of the UIP, which means overdistention and alveolar injury could occur even at pressures below the UIP.6 Regarding the use of the LIP to set PEEP at a level that prevents expiratory alveolar closure, one must keep in mind that PEEP is applied on expiration. The LIP is a feature of the inspiratory P-V curve, more related to alveolar reopening during inspiration than it is to alveolar closure, which occurs during expiration. The LIP appears to be of limited relevance to expiratory alveolar closure and optimal PEEP levels.6

What causes the LIP, and what does it mean? The LIP is probably due to the instantaneous reopening of many alveoli with the same threshold opening pressures, as occurs in evenly distributed (homogeneous) lung disease. In unevenly distributed (heterogeneous) lung disease, alveoli with different threshold opening pressures coexist, and the LIP may be absent because alveoli tend to reopen in a more sequential fashion rather than in large numbers all at once.6 PEEP tends to be more beneficial in homogeneous lung disease in which there is a widespread presence of nonventilated zones, where large numbers of alveoli can be recruited simultaneously. PEEP is not as effective when lung disease is heterogeneous (characterized by interspersed ventilated and nonventilated zones), where an increase in inspiratory pressure is more likely to overdistend already open alveoli rather than recruit large numbers of alveoli en masse. The P-V curve contour may simply indicate the presence of homogeneous or heterogeneous lung disease and the potential for recruitment, not the optimal level of PEEP needed to prevent alveolar closure.6

The VT P-V curve can be displayed in a breath-to-breath real-time fashion on the monitoring screens of modern mechanical ventilators. However, this dynamically traced P-V curve is affected by airflow resistance and the P-V relationships in the ventilator tubing, humidifier, and endotracheal tube; it cannot provide accurate information about the P-V relationships in the alveoli.28 The ventilator pressure sensor measures pressure at the patient connection part of the ventilator tubing. During inflation, tubing pressure increases rapidly (depending on the ventilator’s flow setting) with little initial volume change as endotracheal tube and airway resistances are overcome. Volume increases more rapidly relative to pressure as elastic resistance is overcome. This transition from frictional to elastic resistance creates an “inflection point” on the lower part of the inspiratory P-V loop, but it does not have the same meaning as the inflection point on the static P-V curve.28

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Lung Distensibility: Static Compliance

Compliance is a measure of the lung’s opposition to inflation. The P-V curve (see Figure 3-7) is a compliance curve. Lung compliance (CL) is defined as the change in lung volume produced by a unit of pressure change and is measured in liters per centimeter of water pressure (L/cm H2O), shown as follows:

CL=ΔV(liters)ΔP(cmH2O)

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Compliance can be conceptualized as distensibility; if the lung is easily distended, it has high compliance. A lung with low compliance is stiff and difficult to inflate. Static CL can be obtained from the P-V curve in Figure 3-9 by measuring the volume change (vertical axis) produced by a pressure change (horizontal axis). Normal compliance of the lung alone (CL) is 0.2 L/cm H2O or 200 mL/cm H2O.

The opposite of compliance is elastance, defined as the change in pressure required to produce a unit of volume change (cm H2O/L). Elastance is the mathematical reciprocal of compliance (elastance = 1/compliance). The more elastic the lung, the less its compliance. Elastance can be conceptualized as recoil force; highly elastic lungs are stiff and difficult to inflate and exhibit a high recoil force. By convention, in pulmonary medicine, the elastic characteristics of the lung are quantified in terms of compliance rather than elastance.

Compliance and Lung Volume

The value of CL depends on the volume at which it is measured. The compliance curve is not linear, as shown in Figure 3-9. Near TLC, lung fibers are stretched and close to their elastic limits; a 500-mL inspiration taken at a point near TLC requires more muscular effort than a 500-mL inspiration beginning at FRC. The slope of the compliance curve is steepest and CL is greatest at FRC; this is beneficial because an individual normally inhales the VT from the FRC level where volume changes require little effort. Even during strenuous exercise, people breathe over the lower 70% of the P-V curve, keeping the elastic WOB relatively low. The larger inspired volumes during exercise produce higher lung recoil, which helps provide the force needed to produce high expiratory flow rates during rapid breathing rates.

Compliance (L/cm H2O) is greater in an adult than an infant because adult lungs are larger and accept more volume for a given pressure. Although the inherent elastic properties of lung tissues may be identical in adult and infant lungs, the infant’s measured CL is lower. To correct for lung size, compliance should be calculated per unit of lung volume (CL/vol). This measurement is called specific compliance and is generally referenced to the individual’s FRC (specific compliance = CL/FRC). Adults and infants have about the same specific CL.

Figure 3-10 illustrates the effects of different disease types on CL. Emphysema is characterized by a loss of elastic lung tissue, which means the lungs can be easily distended and have an abnormally low recoil force. Small pressure changes produce large volume changes. Weakened elastic lung recoil changes

Clinical Focus 3-4   Effect of Airway Obstruction on Functional Residual Capacity and Breathing Position on the Compliance Curve

Emphysema is a disease characterized by the destruction of elastic lung tissue. Consequently, the lung’s elastic recoil force decreases (i.e., the lungs become highly compliant). The lungs do not empty completely to their normal resting volume at the end of an exhalation, which increases the FRC. Because of the increased FRC, a patient with emphysema begins each inspiration at a level closer to the TLC (see Figure 3-20, A). Patients with emphysema appear to be in a continuous inspiratory position, even when they are at the end of a normal expiration. However, breathing at this higher lung volume is actually advantageous for the highly compliant emphysematous lung because it increases lung recoil force and assists expiration (i.e., even the highly compliant lung recoils with greater force if it is stretched). In other words, the lung with emphysema has such little recoil force that it must be stretched to near its TLC to generate enough recoil to drive passive expiration. Even then, recoil force is lower than normal. This low recoil force drives expiratory flow out of the lung slowly, unduly prolonging expiratory time. For this reason, patients with emphysema often contract their abdominal expiratory muscles during normal ventilation (always an abnormal sign) to aid exhalation.

the equilibrium point between lung and thoracic recoil forces, which increases the FRC. Pulmonary fibrosis is characterized by high lung recoil forces. The FRC equilibrium point is displaced, this time to a lower point in the TLC than normal.

Surface Tension and Pulmonary Surfactant

The molecules of a water surface are attracted by other water molecules below and adjacent to them. As a result, the water surface has a tendency to contract, creating a force known as surface tension (Figure 3-11, A). Surface tension causes a water droplet to take on the shape of a rounded bead because of the tight intermolecular attraction forces surrounding the droplet.

In 1929, von Neergaard conducted the now classic experiment in which he demonstrated the presence of surface tension in the alveoli. He inflated the lungs of anesthetized cats, first with air and then with a liquid saline solution. He constructed P-V curves for both air and saline inflations. Figure 3-12 illustrates that saline inflation requires much less pressure than air inflation to achieve a given volume. von Neergaard correctly concluded that alveolar air-liquid surfaces produced forces that opposed lung inflation. Saline inflations abolished the air-liquid surfaces and eliminated their opposition to lung inflation. The recoil pressure of the saline-filled lungs reflected only elastic tissue retractile forces, whereas the recoil pressure of the air-filled lung reflected retractile forces of the elastic tissues plus surface tension. von Neergaard found that surface-tension forces are responsible for more than half of the lung’s elastic recoil force.7

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Figure 3-12

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