Ventilation



Ventilation


Robert L. Chatburn and Ehab G. Daoud




The primary functions of the lungs are to supply the body with oxygen (O2) and to remove carbon dioxide (CO2). To perform these functions, the lungs must be adequately ventilated. Ventilation is the process of moving gas (usually air) in and out of the lungs. Ventilation is to be distinguished from respiration, which involves complex physiologic processes at the blood and cellular levels.


In health, ventilation is regulated to meet the body’s needs under a wide range of conditions. In disease, this process can be markedly disrupted. Inadequate ventilation or increased work of breathing often results. Respiratory care is often directed toward restoring adequate and efficient ventilation. Respiratory care modalities try to reduce the work of breathing and provide artificial ventilation if necessary. Providing effective respiratory care requires an understanding of normal ventilatory processes and of how various diseases may affect ventilation.



Mechanics of Ventilation


Normal ventilation is a cyclic activity that has two phases: inspiration and expiration. During each cycle, a volume of gas moves in and out of the respiratory tract. This volume, measured during either inspiration or expiration, is called the tidal volume (VT). The normal VT refreshes the gas present in the lung removing CO2 and supplying O2 to meet metabolic needs. The VT must be able to meet changing metabolic demands, such as during exercise or sleep. The vital capacity and its subdivisions provide the necessary reserves for increasing ventilation (see Chapter 19).


Ventilation can be related to a simplified version of the equation of motion for the respiratory system:


Pressure=VolumeCompliance+(Resistance×Flow)


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where:



In this equation, the terms (elastance × volume) and (resistance × flow) have units of pressure and represent the elastic and resistive loads against which the respiratory muscles or ventilator must work to ventilate the lungs. In healthy lungs, this work is minimal and performed during the inspiratory phase. Expiration is normally passive (i.e., no muscle force involved).



Pressure Differences During Breathing


The equation of motion is a mathematical model describing the behavior of a graphic model of the lungs. The graphic model is shown in Figure 10-1.1 The model lumps all the resistive properties of the many airways into a single flow-conducting tube and lumps all the elastic properties of the alveoli and airways into a single elastic compartment. Surrounding the “lungs” is another elastic compartment representing the chest wall. This graphic representation of the respiratory system allows us to define points in space where pressures may be measured (or inferred) as defined in Table 10-1. Mathematical models relating pressure, volume, and flow corresponding to this graphic model are constructed using pressure differences between the points. The various components of the graphic model are defined as everything that exists between these points in space. The respiratory system is everything that exists between the pressure measured at the airway opening (PAO) and the pressure measured at the body surface (PBS). The associated pressure difference is transrespiratory pressure (PTR):




PTR=PAOPBS


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The term PAO comes before the term PBS in the equation. This order is dictated by the direction of flow. For inspiration, PAO is higher than PBS, and PTR is calculated by subtracting PBS from PAO. The same general principle applies to all the other pressure differences described subsequently.


The components of transrespiratory pressure correspond to the components of the graphic model (i.e., airways, lungs, and chest wall). The airways are whatever exists between pressure measured at the airway opening and pressure measured in the alveoli of the lungs (PA). The graphic model makes the lungs look like one giant alveolus, which means that alveolar pressure represents an average pressure over all alveoli in real lungs. The associated pressure difference is transairway pressure (PTAW):


PTAW=PAOPA


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The alveolar region is whatever exists between pressure measured in the model alveolus and pressure measured in the pleural space (Ppl). The associated pressure difference is transalveolar pressure (PTA):


PTA=PAPpl


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The chest wall exists between pressure measured in the pleural space and the pressure on the body surface. The associated pressure difference is trans–chest wall pressure (PTCW):


PTCW=PplPBS


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Some of these components can be combined to get respiratory subsystems. Most commonly, the pulmonary system (airways and alveolar region) is defined in terms of the transpulmonary pressure difference (PTP):


PTP=PAOPpl


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The literature is very confused regarding the definition of transpulmonary pressure. Authors often define PTP as PA − Ppl. The confusion arises from the fact that PTA = PA − Ppl but only under static conditions. Static conditions can be imposed during mechanical ventilation by using an inspiratory hold maneuver. This situation should be considered a special case of PTP, however; the general case is PTP = PAO − Ppl, which shows what pressures must be measured to derive the mechanical properties of the pulmonary system under either static or dynamic (breathing) conditions. If we want to evaluate the elastance and resistance of the pulmonary system, we substitute PTP for P in the equation of motion. Alternatively, if we want to evaluate total respiratory system elastance and resistance, we substitute PTR for P.


Sometimes it is useful to define transthoracic pressure difference (PTT) as:


PTT=PAPBS


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Table 10-2 summarizes these equations.



The transrespiratory pressure gradient causes gas to flow into and out of the alveoli during breathing. For a spontaneously breathing subject, PA is subatmospheric in the beginning of inspiration compared with PAO causing air to flow into the alveoli. The opposite happens in the beginning of exhalation; PA is higher than PAO causing air to flow out of the airway opening.


During a normal breathing cycle, the glottis remains open. PBS and PAO remain at zero (i.e., atmospheric) throughout the cycle; only changes in PA and Ppl are of interest. Before inspiration, pleural pressure is approximately −5 cm H2O (i.e., 5 cm H2O below atmospheric pressure), and alveolar pressure is 0 cm H2O. The transpulmonary pressure gradient is also approximately 5 cm H2O in the resting state, that is, PTP = PAO − Ppl = 0 − (−5) = 5. This positive end expiratory PTP maintains the lung at its resting volume (i.e., functional residual capacity [FRC]). Airway opening and alveolar pressures are both zero, so the transairway pressure gradient also is zero. No gas moves into or out of the respiratory tract.


Inspiration begins when muscular effort expands the thorax. Thoracic expansion causes a decrease in pleural pressure. This decrease in pleural pressure causes a positive change on expiratory PTP and PTA, which induces flow into the lungs. The inspiratory flow is proportional to the positive change in transairway pressure difference; the higher the change in PTA, the higher the flow.


Pleural pressure continues to decrease until the end of inspiration. Alveolar filling slows when alveolar pressure approaches equilibrium with the atmosphere, and inspiratory flow decreases to zero (Figure 10-2). At this point, called end-inspiration, alveolar pressure has returned to zero, and the intrapleural pressure—and hence transpulmonary pressure gradient—reaches the maximal value (for a normal breath) of approximately 10 cm H2O.



As expiration begins, the thorax recoils, and Ppl starts to increase, and the transpulmonary pressure difference starts to decrease. Because transpulmonary pressure difference is decreasing (e.g., from 10 cm H2O to 5 cm H2O), the opposite of inspiration, flow is in the opposite (negative) direction. The equation of motion shows this, setting the driving pressure, Pmus, to zero:


Pmus=0=(Elastance×Volume)+(Resistance×Flow)


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Rearranging, we get:


(Elastance×Volume)=(Resistance×Flow)=Resistance×(Flow)


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This equation says two important things: (1) Flow is negative, indicating expiration, and (2) the driving force (transthoracic pressure, equal to elastance × volume) for expiratory flow is the energy stored in the combined elastances of lungs and chest wall (the total elastance is the sum of the chest wall and lung elastances).


These events occur during normal VT excursions. Similar pressure changes accompany deeper inspiration and expiration. The magnitude of the pressure changes is greater with deeper breathing. Pleural pressures are always negative (subatmospheric) during normal inspiration and exhalation. During forced inspiration with a big down movement of the diaphragm, the pleural pressure can decrease to −50 cm H2O, whereas during a forced expiration, pleural pressure may increase above atmospheric pressure to 50 to 100 cm H2O.



Forces Opposing Inflation of the Lung


The lungs have a tendency to recoil inward, whereas the chest wall tends to move outward; these opposing forces keep the lung at its resting volumes (FRC). To generate the above-described pressure gradients, the lungs must be distended. This distention requires several opposing forces to be overcome for inspiration to occur. Normal expiration is passive, using the energy stored during inspiration. As indicated in the equation of motion, the forces opposing lung inflation may be grouped into two categories: elastic forces and frictional forces. Elastic forces involve the tissues of the lungs, thorax, and abdomen, along with surface tension in the alveoli. Frictional forces include resistance caused by gas flow through the airways (natural and artificial) and tissue movement during breathing.



Elastic Opposition to Ventilation


Elastin and collagen fibers are found in the lung parenchyma. These tissues give the lung the property of elasticity. Elasticity is the physical tendency of an object to return to an initial state after deformation. When stretched, an elastic body tends to return to its original shape. The tension developed when an elastic structure is stretched is proportional to the degree of deformation produced (Hooke’s law). An example is a simple spring (Figure 10-3). When tension on a spring is increased, the spring lengthens. However, the ability of the spring to stretch is limited. When the point of maximal stretch is reached, further tension produces little or no increase in length. Additional tension may break the spring.



In the respiratory system, inflation stretches tissue. The elastic properties of the lungs and chest wall oppose inflation. To increase lung volume, pressure must be applied. This property may be shown by subjecting an excised lung to changes in transpulmonary pressure and measuring the associated changes in volume (Figure 10-4). To simulate the pressures during breathing, the lung is placed in an airtight jar. The force to inflate the lung is provided by a pump that varies the pressure around the lung inside the jar, simulating Ppl. This action mimics the pleural pressure changes associated with thoracic expansion and contraction. The changes in transpulmonary pressure are made in discrete steps, allowing the lungs to come to rest in between so that all of the applied pressure opposes elastic forces and none of it opposes resistive forces (i.e., flow is zero when the measurements are made). The amount of stretch (inflation) is measured as volume by a spirometer. Changes in volume resulting from changes in transpulmonary pressure are plotted on a graph.



During inspiration in this model, increasingly greater negative pleural pressures are required to stretch the lung to a larger volume. As the lung is stretched to its maximum (total lung capacity [TLC]), the inflation “curve” becomes flat. This flattening indicates increasing opposition to expansion (i.e., for the same change in transpulmonary pressure, there is less change in volume).2


As with a spring when tension is removed, deflation occurs passively as pressure in the jar is allowed to return toward atmospheric. Deflation of the lung does not follow the inflation curve exactly. During deflation, lung volume at any given pressure is slightly greater than it is during inflation. This difference between the inflation and deflation curves is called hysteresis.2 Hysteresis indicates that factors other than simple elastic tissue forces are present. The major factor, particularly in sick lungs, is the opening of collapsed alveoli during inspiration that tend to stay open during expiration until very low lung volumes are reached.


Chest wall and lung elastances are connected in series, meaning that they both experience the same flow and change in volume, but they do not have the same pressure differences. Series elastances are simply additive. The elastance of the respiratory system is the sum of lung (pulmonary) elastance (EL) and chest wall elastance (ECW):


ERS=EL+ECW


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Expressed in terms of compliance:


CRS=CL×CCWCL+CCW


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The resistance of the natural and artificial airways (e.g., endotracheal tube) is also in series so that the total system resistance is simply the sum of resistance of the components.



Surface Tension Forces


Part of the hysteresis exhibited by the lung is a result of surface tension forces in the alveoli. If a lung is filled with fluid such as saline, the pressure-volume curves look much different than the pressure-volume curves of an air-filled lung (Figure 10-5). Less pressure is needed to inflate a fluid-filled lung to a given volume. This phenomenon indicates that a gas-fluid interface in the air-filled lung changes its inflation-deflation characteristics.



The recoil of the lung is a combination of tissue elasticity and these surface tension forces in the alveoli. During inflation, additional pressure is needed to overcome surface tension forces. During deflation, surface tension forces are reduced, resulting in altered pressure-volume characteristics (i.e., the leftward shift seen in Figure 10-4). In the intact lung (i.e., within the chest), the volume history also affects the degree of hysteresis that occurs. Factors such as the initial volume, the tidal excursion, and whether the lungs have been previously inflated or deflated help determine the volume history and the shape of the pressure-volume curves of the lung.



Mini Clini


Surfactant Replacement Therapy and Lung Mechanics




Discussion


The liquid molecules that line each alveolus attract one another. This attraction creates a force called surface tension, which tends to shrink the alveolus. Pulmonary surfactant molecules have weak intramolecular attractive forces. When surfactant molecules are mixed with other liquid molecules that have higher intramolecular attraction, the surfactant molecules are pushed to the surface of the liquid, where they form the air-liquid interface. Because of the weak intramolecular attraction between these surfactant molecules at the surface, the liquid lining of the alveoli exhibits much less surface tension than it would in the absence of pulmonary surfactant. A premature infant with inadequate surfactant has abnormally high intraalveolar surface tension; this produces a collapsing force that increases lung recoil and reduces lung compliance. Greater muscular effort is required to overcome increased recoil during inspiration, and the work of breathing is increased. The infant may eventually become fatigued and develop ventilatory failure. Instillation of artificial surfactant into the lungs reduces surface tension to its normal level. Lung compliance is increased, elastic recoil is reduced, and the muscular work required to inflate the lung is reduced.


A phospholipid called pulmonary surfactant reduces surface tension in the lung. Alveolar type II cells probably produce pulmonary surfactant (see Chapter 8). In contrast to typical surface-active agents, pulmonary surfactant changes surface tension according to its area.3 The ability of pulmonary surfactant to reduce surface tension decreases as surface area (i.e., lung volume) increases. Conversely, when surface area decreases, the ability of pulmonary surfactant to reduce surface tension increases. This property of changing surface tension to match lung volume helps stabilize the alveoli. Any disorder that alters or destroys pulmonary surfactant can cause significant changes in the work of distending the lung.



Lung Compliance


Tissue elastic forces and surface tension oppose lung inflation. Compliance is the reciprocal of elastance:


Compliance=1Elastance=ΔVΔP


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Compliance is defined as volume change per unit of change in the pressure difference across the structure. It is usually measured in milliliters per centimeter of water.


A graph of change in lung volume versus change in transpulmonary pressure (Figure 10-6, A) is the compliance curve of the lungs. Figure 10-6, B compares a normal lung compliance curve with curves that might be observed in patients who have emphysema (obstructive lung disease) or pulmonary fibrosis (restrictive lung disease). The curve from a patient with emphysema is steeper and displaced to the left. The shape and position of this curve represent large changes in volume for small pressure changes (increased compliance). Increased compliance results primarily from loss of elastic fibers, which occurs in emphysema. The lungs become more distensible so that the normal transpulmonary pressure results in a larger lung volume. The term hyperinflation is used to describe an abnormally increased lung volume. A distinctly opposite pattern is seen in pulmonary fibrosis. Interstitial fibrosis is characterized by an increase in connective tissue. The compliance curve of a patient with pulmonary fibrosis is flatter than the normal curve, shifted down and to the right. As a result, there is a smaller volume change for any given pressure change (decreased compliance). Consequently, the lungs become stiffer, usually with a reduced volume.




Chest Wall Compliance


Inflation and deflation of the lung occur with changes in the dimensions of the chest wall (see Chapter 8). The relationship between the lungs and the chest wall can be illustrated by plotting their relaxation pressure curves separately and combined (Figure 10-7). In the intact thorax, the lungs and chest wall recoil against each other. The point at which these opposing forces balance determines the resting volume of the lungs, or functional residual capacity. This is also the point at which alveolar pressure equals atmospheric pressure. The normal FRC is approximately 40% of the TLC. If the normal lung–chest wall relationship is disrupted, the lung tends to collapse to a volume less than the FRC, and the thorax expands to a volume larger than the FRC.




The lung–chest wall system may be compared with two springs that are pulling against each other. The chest wall spring tends to expand, whereas the lung spring tends to contract. At the resting level, the forces of the chest wall and lungs balance. The tendency of the chest wall to expand is offset by the contractile force of the lungs. This balance of forces determines the resting lung volume, or FRC. The opposing forces between the chest wall and lungs are partially responsible for the subatmospheric pressure in the intrapleural space. Diseases that alter the compliance of either the chest wall or the lung often disrupt the balance point, usually with a change in lung volume.


Inhalation occurs when the balance between the lungs and chest wall shifts. Energy from the respiratory muscles (primarily the diaphragm) overcomes the contractile force of the lungs. At the beginning of the breath, the tendency of the chest wall to expand facilitates lung expansion. When lung volume nears 70% of the vital capacity, the chest wall reaches its natural resting level. To inspire to a lung volume greater than about 70% of TLC, the inspiratory muscles must overcome the recoil of both the lungs and the chest wall (see Figure 10-7).


For exhalation, potential energy “stored” in the stretched lung (and chest wall at high volumes) during the preceding inspiration causes passive deflation. To exhale below the resting level (FRC), muscular effort is required to overcome the tendency of the chest wall to expand. The expiratory muscles (see Chapter 8) provide this energy.


Compliance of the chest wall, similar to lung compliance, is a measure of distensibility. The compliance of the normal chest wall is similar to that of the lungs (0.2 L/cm H2O). Obesity, kyphoscoliosis, ankylosing spondylitis, and many other abnormalities can reduce chest wall compliance and lung volumes.





Airway Resistance


Gas flow through the airways also causes frictional resistance. Impedance to ventilation by the movement of gas through the airways is called airway resistance. Airway resistance accounts for approximately 80% of the frictional resistance to ventilation.


Airway resistance is the ratio of driving pressure responsible for gas movement to the flow of the gas, calculated as follows:


Raw=ΔPTAΔV˙=PAOPAΔV˙


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where Raw is resistance, PTA is transairway pressure difference, image is flow, PAO is pressure at the airway opening, and PA is alveolar pressure.


Driving pressure is measured in centimeters of water (cm H2O), and flow is measured in liters per second (L/sec). Airway resistance (Raw) is recorded in cm H2O/L/sec or, more accurately, cm H2O • sec • L−1. Airway resistance in healthy adults ranges from approximately 0.5 to 2.5 cm H2O/L/sec. To cause gas to flow into or out of the lungs at 1 L/sec, a healthy subject needs to lower his or her alveolar pressure only 0.5 to 2.5 cm H2O below atmospheric pressure.


Raw in nonventilated patients is usually measured in a pulmonary function laboratory (see Chapter 19). Flow (image) is measured with a pneumotachometer. Alveolar pressures are determined in a body plethysmograph, an airtight box in which the patient sits. By momentarily occluding the patient’s airway and measuring the pressure at the mouth, alveolar pressure can be estimated (i.e., mouth pressure equals alveolar pressure under conditions of no flow). By relating flow and alveolar pressure to changes in plethysmograph pressure, airway resistance can be calculated.



Mini Clini


HeO2 Therapy for Large Airway Obstruction




Discussion


Because most (approximately 80%) of the resistance to breathing occurs in the upper and large airways, disease processes that increase resistance in these airways cause tremendous increases in the work of breathing. Traumatic injuries to the vocal cords or trachea, along with tumors or foreign bodies in the trachea or main stem bronchi, are examples of the types of clinical conditions that can markedly increase the work of breathing. Patients who must breathe against high levels of resistance are prone to respiratory muscle fatigue and failure. Gas flow in the upper and large airways is predominantly turbulent. Turbulent flow is highly influenced by gas density. Patients with large airway obstruction can often be treated with a mixture of helium and oxygen (heliox or HeO2). HeO2, usually an 80/20 or 70/30 mixture, can be administered to reduce the work of breathing until the obstructive process can be treated. HeO2 mixture does little for patients with small airway obstruction, as occurs in emphysema or asthma. Flow in the small airways is mainly laminar and largely independent of the density of the gas breathed. However, heliox therapy can be used for patients with small airway obstruction to allow them to exercise longer and more strenuously with less dyspnea and dynamic hyperinflation.


Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Ventilation
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