Airflow into and out of the lungs requires pressure gradients between the mouth and the alveolus, which are created by mechanical changes in lung volume. Breathing becomes difficult if the lung or the chest wall is stiff (there is low compliance) or if the resistance to gas flow along the airway is high. Resistance is a dynamic property determined during gas flow. Compliance is referred to as an elastic property and is measured without gas flow.
A spirometer is an instrument that is used during pulmonary function testing to measure lung volumes and gas flow rates. A patient breathes normally for a given period, and then inspires maximally before forcefully expiring as much air as possible. Figure 5-3 illustrates primary lung volumes and capacities and lists essential terminology necessary for describing and understanding respiratory function.
Normal spirogram showing four primary lung volumes and four capacities.
Tidal volume (Vt) is the amount breathed in and out during normal breathing.
Vital capacity (VC) is the maximum possible volume that can be expired following the largest breath inspired.
Residual volume (RV) is the volume of gas remaining in the lung at the end of forceful expiration and cannot be expelled without collapsing the lung.
Functional residual capacity (FRC) is the resting lung volume at the end of quiet expiration.
Normal FRC is approximately 40% of total lung capacity (TLC). Many variables are optimized at normal FRC, including work of breathing, vascular resistance, and ventilation/perfusion (/) matching. Mechanical ventilation of patients is often used to correct an abnormal FRC to help restore normal respiratory function.
Certain pulmonary conditions can be divided into restrictive versus obstructive lung disease. Restrictive lung diseases (e.g., pulmonary fibrosis and acute respiratory distress syndrome) are characterized by reduced lung volumes. In contrast, obstructive lung diseases (e.g., asthma, emphysema, and chronic bronchitis) are characterized by obstruction to airflow.
The diaphragm is the most important muscle of inspiration. Its contraction increases the vertical height of the thoracic cavity due to flattening of the domes of the diaphragm. The external intercostal muscles slope downward and forward between the adjacent ribs, which produces a “bucket-handle” movement of the ribs and increases the lateral and anteroposterior diameter of the chest. Expiration is passive during quiet breathing but becomes active during exercise. The most important muscles of expiration are those of the abdominal wall. The internal intercostal muscles are arranged at right angles to the external oblique muscles and assist expiration by pulling the ribs downward and inward.
Neuromuscular diseases such as Guillain-Barré syndrome can affect respiratory function by causing respiratory muscle weakness. If there is severe muscle weakness, patients may require mechanical ventilation.
As air is drawn into the lungs, it is distributed through a highly branched airway. The first 16–17 generations of airway division comprise the conducting zone (i.e., from the trachea through the various bronchi and bronchioles to the terminal bronchioles). Gas exchange occurs in the respiratory zone of the airway and begins distal to the terminal bronchioles (Figure 5-4). A lung acinus is a functional unit formed by the division of a terminal bronchiole into the respiratory bronchioles, the alveolar ducts, and the terminal alveoli. Gas moves by diffusion within lung acini because the cross-sectional area of the respiratory zone is so large that bulk gas flow approaches zero.
Airway divisions. The first 16–17 generations are conducting airways only. Gas exchange only occurs in the respiratory zone from generations 17–23. A lung acinus is formed from the divisions of a terminal bronchiole. A lung unit includes a lung acinus and associated blood vessels.
When describing certain lung pathologies, it is helpful to visualize the concept of a lung acinus. Alveolar damage in patients with emphysema is either centriacinar (most common) or panacinar. In centriacinar emphysema, the primary site of damage is the respiratory bronchioles, with sparing of the distal alveoli. This type of emphysema is associated with smoking, and most damage is seen in the apical regions of the upper lobes. In panacinar emphysema, the entire acinus is damaged. Panacinar emphysema is associated with α1-antitrypsin disease. α1-Antitrypsin is a serum protein produced by the liver and combats damaging protease activity, particularly in the lung. α1-Antitrypsin disease is a genetic condition in which α1-antitrypsin accumulates in the liver (resulting in cirrhosis), causing the protein to be systemically unavailable. The panacinar emphysema that develops typically involves the entire lung, with the lung bases being most diseased.
Lung and Chest Wall Recoil
The presence of subatmospheric pressure within the chest accounts for a person's ability to draw air into the airway during inspiration. Subatmospheric pressure in the intrapleural space is created by the opposing recoil of the lungs and chest wall. When all the respiratory muscles are relaxed, the lung is at its resting lung volume (FRC), and there is equilibrium between the recoil of the lung and the chest wall. At this point, the lung tends to collapse and the chest wall tends to expand, with the two being held together by a thin layer of pleural fluid. By acting to pull the lung and chest wall apart, the opposing recoil forces create negative pressure in the intrapleural space. If the chest wall is punctured, air will flow into the pleural space (pneumothorax) until intrapleural pressure (Pip) equals atmospheric pressure; the lung will then collapse and the chest wall will spring outward (Figure 5-5).
Effect of pneumothorax on lung volume and thoracic volume.
Pneumothorax can be spontaneous or traumatic in origin. In either case, the intrapleural air must be evacuated and is usually achieved by connecting a chest tube to suction, which restores negative intrapleural pressures and reexpands the collapsed lung.
The force acting across the wall of the lung to expand it is a transmural pressure called the transpulmonary pressure (Ptp). Ptp is calculated as the difference in pressure between the alveoli (Pa) and the intrapleural space (Pip):
When the respiratory muscles are relaxed, the alveolar pressure is the same as the atmospheric pressure (given a relative value of 0 cm H2O) and the intrapleural pressure (PIP) is about −5 cm H2O:
The force between the lung and the chest wall increases when the inspiratory muscles contract, causing PIP to become more negative; for example, Pip is −10 cm H2O during normal quiet inspiration. The lung expands because Ptp is increased:
It is a general convention in physiology to calculate transmural pressures as the inside pressure minus the outside pressure. In the case of transpulmonary pressure, a positive value indicates a distending force for lung expansion (inspiration). A negative Ptp is a compression force on the airway as would be observed, for example, during forced expiration.
Air flows into or out of the lung when there is a difference in pressure along the airway between the mouth and alveoli. Airflow is driven by changes in alveolar pressure, which in turn result from changes in intrapleural pressure. Contraction of the inspiratory muscles reduces Pip and increases Ptp, providing a force for lung expansion. Increased lung volume decreases alveolar pressure, which drives inspiration. Note in Figure 5-6 that airflow is in phase with alveolar pressure changes. As air flows into the lung to occupy the increased volume, alveolar pressure returns to atmospheric pressure, ending inspiration. Passive recoil of the lung and chest wall during quiet expiration causes the lung volume to decrease. As a result, the alveolar pressure increases and gas flows out of the lung.
Ventilation cycle. Lung volume changes due to airflow into or out of the lung. Gas flow depends on a gradient of pressure from the mouth to the alveolus; alveolar pressure change occurs in response to altered intrapleural pressure.
Pressure-Volume Relation of the Lung
During the cycle of ventilation, several factors contribute to the work of breathing, including lung and chest wall compliance and resistance to gas flow. Compliance is a pressure volume relation, and is defined as the transpulmonary pressure change that is required to produce a unit change in lung volume. If measurements are recorded at the start and end of a tidal breath when gas flow has stopped, static compliance is determined as:
Patients with pulmonary fibrosis or lung edema have reduced lung compliance and, therefore, have increased the work of breathing, which is sensed as dyspnea or shortness of breath. These patients tend to take small tidal breaths to minimize the change in Ptp needed to inspire. On the other hand, patients with pulmonary emphysema have increased lung compliance. They do not have difficulty breathing in but experience airway obstruction on expiration (see Dynamic Airway Compression).
Figure 5-7 shows a pressure-volume relationship of a healthy person inspiring and expiring from RV to TLC, revealing several important features of lung mechanics:
Lung compliance is low at both high and low lung volumes.
At high volume, lung tissue is already stretched and further distension requires more force.
At low volume, many lung acini are collapsed and more force is needed to initiate inspiration.
The steepest part of the pressure-volume relation, where compliance is largest, is at the point of FRC. This explains why it is easier for a person to breathe around FRC and uncomfortable to breathe at high or low lung volume.
Pressure-volume (compliance) curve for a maximal breath. Compliance is low at both high and low lung volumes. Hysteresis is the phenomenon of the different path of the expiration curve compared to inspiration. TLC, total lung capacity; FRC, functional residual capacity; RV, residual volume.
Figure 5-7 shows that the pressure-volume relation for expiration is positioned to the left of that of inspiration. This phenomenon is called hysteresis and exists because of the action of lung surfactants. Surfactants are phospholipids, mainly dipalmitoyl phosphatidylcholine, secreted by type 2 pneumocytes in the alveolar walls. The surfactant molecules line up on the inner surface of the alveoli. As the lung volume decreases during expiration, adjacent surfactant molecules are forced closer together. Surfactant molecules repel each other and resist the tendency of alveoli to become smaller. The left shift of the pressure-volume relation on expiration, compared to inspiration (hysteresis), is explained by the action of surfactant to maintain alveoli open during expiration. An advantage of this phenomenon is that there is more time for gases to diffuse across the alveolar membranes.
Surface tension acts at the air-liquid interface of alveoli and tends to reduce the area of the alveolus and to generate pressure within it. Surfactants are required to counteract surface tension, which is the main reason that the lung tends to collapse. The presence of the detergent-like surfactant molecules at the air-liquid interface of the alveoli reduces surface tension, thereby maintaining normal lung compliance and preventing alveolar atelectasis (collapse).
Atelectasis is an area of collapsed lung, and is often considered the culprit that causes the mild fever that can occur within the first 24–48 hours after surgery. Atelectasis predisposes the patient to pneumonia, but can be reversed or prevented by having the patient cough or perform breathing exercises.
The law of Laplace (Equation 5-3) predicts another problem caused by surface tension (as well as the collapse of alveoli)—alveoli with small radii (r) will have higher internal pressure (P) for a given surface tension (T) than will larger alveoli. As a consequence, small alveoli will empty into larger alveoli unless lung surfactants maintain a low surface tension.
Respiratory distress syndrome of the newborn (hyaline membrane disease) is caused by a deficiency of surfactant and is associated with prematurity and with infants of diabetic mothers. Without surfactant, the infant's lungs undergo widespread alveolar collapse, producing low lung compliance. A collection of debris consisting of damaged cells, exudative necrosis, and proteins lines the alveoli and is referred to as the hyaline membrane. Treating the mother with corticosteroids 48 hours prior to the delivery of the premature infant has been shown to increase surfactant production and decrease the incidence of respiratory distress syndrome of the newborn.
Elastic Properties of the Lung and Chest Wall
Examination of the pressure-volume relation of the lung shows that compliance is optimal (largest) around FRC. A normal FRC is therefore associated with the smallest work of breathing. FRC is controlled by the relative strength of the lung and the chest wall recoil forces. Normally, there is opposition of the elastic forces of the lung and chest wall, and the lung tends to collapse and the chest wall tends to expand, as illustrated in Figure 5-8. The figure shows relaxation pressures in the airway if a patient is asked to take several breaths of different volume, and after each inspiration to then completely relax the respiratory muscles. When airway pressure is zero and all muscles are relaxed, equilibrium occurs between the lung and chest wall recoil and lung volume is at FRC. If the lung volume is increased or decreased away from this equilibrium position, effort must be applied by the respiratory muscles but the lung will return passively to FRC. In normal, quiet breathing, therefore, inspiration is active and expiration is passive.
Control of functional residual capacity (FRC). Equilibrium between opposing lung and chest wall recoil forces determines FRC. In general, lungs tend to collapse and the chest wall tends to expand. TLC, total lung capacity; RV, residual volume.
Figure 5-8 shows how the individual elastic properties of the lung and chest wall compare to properties of the combined lung and chest wall unit (note: individual lung and chest wall properties cannot be directly measured in a living person). Lungs tend to collapse at all lung volumes from RV to TLC, shown by positive recoil pressures in the airway after the lung is inflated. The tendency of the lung to collapse is due to surface tension and also to the elastic nature of lung tissue. In contrast, the equilibrium position of the chest wall, where recoil pressure is zero, is at approximately 75% of TLC. At all volumes below 75% of TLC, recoil pressures are negative and the chest wall expands passively. At thoracic volumes above 75% of TLC, both the lung and the chest wall passively decrease their volumes. When overall compliance of the lung and chest wall unit is reduced, greater force is needed for inspiration. Low compliance has many causes, some of which are summarized in Table 5-3.
Table 5-3Causes and Effects of Low Thoracic Compliance ||Download (.pdf) Table 5-3Causes and Effects of Low Thoracic Compliance
|Cause ||Effect |
|Pulmonary fibrosis ||Lung tissue is difficult to distend; lung compliance is low. |
|Pulmonary edema ||Lung is difficult to distend; lung compliance is low. |
|Pleural effusion ||Increased fluid in pleural space resists lung expansion. |
|Thoracic musculoskeletal pain ||Patient avoids deep inspiration due to pain. |
|Rib fracture ||Example of musculoskeletal pain but with reflex spasm of intercostal muscles to produce rigid chest wall. |
|Morbid obesity ||Especially in supine position, weight of tissue on the chest wall and abdomen resists thoracic expansion. |
|Increased abdominal pressure (e.g., ascites, bowel distension) ||The diaphragm is normally the most compliant part of the chest wall; pressure from below resists descent of the diaphragm during inspiration. |
Interstitial lung disease is a general term used for many diseases that involve the lung parenchyma and cause the lung to be stiff and fibrotic with low compliance. Regardless of the cause, patients with interstitial lung disease typically present with similar manifestations of progressive exertional dyspnea, nonproductive cough, fatigue, and weight loss.
Mechanical work required for gas flow into and out of the lung requires overcoming airway resistance and the elastic properties of the lung and the chest wall. Airway resistance is referred to as a dynamic property because it is only apparent during gas flow. Airway resistance (R) determines the rate of gas flow () for a given pressure gradient from the alveolus to the mouth (ΔP). According to Ohm's law,
There are three major factors that affect resistance to air flow:
Airway radius is the main component of airway resistance. Figure 5-9 illustrates the resistance changes along the airway. The upper airway offers significant fixed resistance, which then declines rapidly from the fifth through the tenth generation of airway division. Because the collective cross-sectional area of lung acini is enormous, the respiratory zone of the lung has very low resistance. Bronchi and bronchioles contain smooth muscle and, therefore, are sites of variable resistance. Parasympathetic nerves release acetylcholine and cause bronchoconstriction. Catecholamines relax bronchial smooth muscle through β2 receptors. Selective β2-receptor agonists are used to induce bronchodilation and reduce airway resistance in patients with asthma.
Location of airway resistance. The upper airway offers high fixed resistance. Bronchiolar resistance is variable and depends on smooth muscle tone. Resistance is very low in the respiratory zone due to the large total cross-sectional area of the airway at this location.
Asthma is a classic, obstructive lung disease whose key differentiating feature demonstrated on spirometry is reversible bronchoconstriction following treatment with a β2 agonist such as albuterol. Asthma is characterized by inflammatory hyperreactive airways, and triggers can include allergens (most common), infections (often viral), exercise, cold air, and drugs such as aspirin. When attempting to diagnose airway hyperreactivity, methacholine (a parasympathomimetic agent) can be given during pulmonary function testing to provoke bronchospasm.
Lung volume is an important determinant of airway resistance because the overall cross-sectional area of airways varies with lung volume, causing global changes in airway radius (Figure 5-10). At low lung volume, the cross-sectional area is reduced and airway resistance increases. For example, patients with pulmonary fibrosis have low lung compliance and low resting lung volume; high airway resistance contributes to their increased work of breathing.
Turbulent gas flow increases airway resistance. Turbulent flow occurs in the larger central airways, where flow velocity is high, and at branch points along the conducting airways. Disorganization of the gas stream requires more pressure to drive flow and effectively increases resistance. Bronchoconstriction reduces the airway diameter and increases the velocity of flow. High velocity causes turbulent flow, which generates a wheezing sound (e.g., in asthma). Table 5-4 describes different breath sounds (including wheezing) and the common causes of these sounds.
Effect of lung volume on airway resistance. Low lung volume increases airway resistance due to reduced airway diameter. RV, residual volume; TLC, total lung capacity.
Idiopathic pulmonary fibrosis is a specific type of interstitial lung disease. It is the most common cause of idiopathic interstitial pneumonia and has a poor prognosis. The histologic hallmark of idiopathic pulmonary fibrosis is alternating areas of a normal lung with areas of inflammation and fibrosis with architectural changes known as honeycombing. These patients have a restrictive pattern of lung disease (see Clinical Spirometry).
Table 5-4Breath Sounds ||Download (.pdf) Table 5-4Breath Sounds
|Breath Sound ||Description ||Occurrence |
|Wheezing ||Prominent “musical” or whistling sound, typically during expiration, created by high velocity airflow from restricted airways ||Commonly occurs during bronchospasm (asthma), airway edema (allergic reaction/anaphylaxis), or airway partial obstruction (neoplasm, secretions, foreign object) |
|Rales (crackles, crepitus) ||Typically inspiratory; described as fine (sounds similar to rubbing a strand of hair between the fingers) or coarse (sounds like Velcro), created by forceful opening of alveoli ||Commonly occurs in pulmonary edema, atelectasis, and interstitial lung disease |
|Rhonchi ||Low-pitched vibration (snoring), often rattling, occurring during inspiration and/or expiration; created by mucus-air interface ||Commonly occurs in bronchitis or chronic obstructive pulmonary disease (COPD) |
|Stridor ||Harsh high-pitched wheeze during inspiration created by severe upper-airway obstruction; often indicates a medical emergency ||Commonly occurs in infants with croup (laryngotracheobronchitis), foreign body obstruction at the level of the larynx, epiglottitis, or laryngeal tumor or edema |
Dynamic Airway Compression
Airway resistance increases during forced expiration because intrapleural pressure becomes positive and the airways are compressed. Figure 5-11A shows the normal state at the end of inspiration, in which there is a positive Ptp that tends to maintain airways open. Figure 5-11B shows transmural pressures acting to compress airways during forced expiration. Forceful contraction of the expiratory muscles increases both intrapleural pressure and alveolar pressure to positive values. A positive pressure gradient between the alveolus and the mouth drives the expiratory gas flow. Notice that there is a roughly linear decline in airway pressure from the alveolus to the mouth. Because the same positive intrapleural pressure now surrounds all the airways, the transmural pressure gradient compressing the airways increases with more distance from the alveolus. The largest compression forces are applied to larger airways, which have cartilaginous support to resist collapse. The distal bronchioles do not have cartilaginous support to resist dynamic compression and, therefore, are at risk of collapsing.
Dynamic airway compression. At the end of deep inspiration (A), A positive transmural pressure maintains open airways. In the example of forced expiration, shown in (B), 35 cm H2O is added to both alveolar pressure and intrapleural pressure (Pip = −10 + 35 = +25; Pa = 0 + 35 = + 35). Airways are compressed by high intrapleural pressure. The transmural pressure compressing the airways increases with distance from the alveolus because pressure inside the airway decreases from the alveolus to the mouth. Small airways only have radial traction forces to prevent airway collapse.
The distal lung units normally resist collapse because each unit is connected to several neighboring units; therefore, if one unit collapses, other units are distorted. This mutual support is called radial traction force. Nevertheless, normal airways are compressed in forced expiration and airway resistance rises. Dynamic airway compression is a particular problem in patients with emphysema, where destruction of the lung architecture weakens the radial traction forces. Airway collapse occurs upon forced expiration, dramatically increasing airway resistance and trapping gas in the alveoli.
Air trapping is a chronic problem for patients with emphysema. The effects of air trapping can be detected through observation of the patient's respiratory pattern and by physical examination.
Observation of the respiratory pattern. Patients with emphysema usually take large, slow tidal breaths starting from a high lung volume. They often expire through pursed lips as well. Each of these behaviors reduces dynamic airway collapse. Slow expiration requires less force so that intrapleural pressure is smaller, reducing the compression force on airways. High resting lung volume has the advantage of increasing airway diameter and reducing airway resistance. Blowing out through pursed lips creates a positive pressure in the mouth, which increases pressure inside the airways. As a result, the transmural pressure that compresses the airways is reduced.
Clinical examination findings associated with air trapping include:
Physical examination. Increased anterior to posterior diameter, known as barrel chest.
Auscultation. Decreased breath sounds.
Chest radiography. Large, hyperlucent lung fields, flattened diaphragm, and increased retrosternal airspace.
Expiratory Flow Limitation
Maximal expiratory flow rate is achieved with relatively little expiratory effort due to the existence of dynamic airway compression. Figure 5-12A shows plots of expiratory flow rate as a function of lung volume when a patient uses different degrees of effort to breathe out from TLC to RV. In forced expiration from TLC, there is a rapid initial increase in flow rate to a peak, and then a steady decline in flow rate as RV is approached. The remarkable feature shown in Figure 5-12A is that, regardless of effort, the descending limb of the flow-volume loop follows the same curve.
Expiratory flow limitation. A series of expirations from total lung capacity are measured with varying degrees of effort. Curves converge at mid and low lung volumes (A), showing that expiratory rate is independent of effort in this region. If alveolar pressure is measured as an index of effort (B), expiratory flow rate plateaus, demonstrating expiratory flow limitation. TLC, total lung capacity; RV, residual volume.
Figure 5-12B shows that expiratory flow becomes independent of effort (measured as the size of alveolar pressure). At medium to low lung volumes, maximal expiratory flow rate is established with modest effort. Increases in voluntary force do not increase expiratory flow. Although alveolar pressure increases with effort, it cannot drive more gas flow because intrapleural pressure also becomes progressively larger. Thus, the force driving expiratory gas flow (alveolar pressure) and the force compressing the airway (intrapleural pressure) increase in parallel, and the net effect is that there is no change in expiratory flow rate. Patients with emphysema may experience expiratory flow limitation during normal quiet breathing; they attempt to breathe at even higher lung volumes, which usually lead to dyspnea, coughing, and discomfort.
Static and Dynamic Compliance
When patients are mechanically ventilated, positive pressure is used to push gas into the lung. If airway pressure is too high, there is a risk that the lung will rupture. The peak airway pressure reached when a Vt is delivered includes the pressure required to overcome both elastic forces (static compliance) and airway resistance. When static compliance is calculated, using Equation 5-2, pressure measurements are recorded at the beginning and end of inspiration, after gas flow has stopped. If measurements are recorded during gas flow, an additional component of airway pressure is present due to air flowing through a resistance (Equation 5-4). Dynamic compliance includes the pressure component due to airway resistance.
Figure 5-13A shows a protocol to determine if development of high airway pressure in a mechanically ventilated patient is due to low static compliance (e.g., the patient has developed pulmonary edema) or to increased airway resistance (e.g., bronchoconstriction). The respirator applies a positive end-expiratory pressure (PEEP) between breaths to help maintain open airways, which will reduce atelectasis in the mechanically ventilated patient. A known Vt is pushed into the lung and airway pressure is recorded. The highest pressure recorded is called peak inspiratory pressure (PIP) (note: PIP is distinct from intrapleural pressure, which is notated by PIP). The respirator then pauses for a short period but does not allow expiration. During this pause, airway pressure decreases to a stable plateau pressure (PPLAT). Pressure decreases because gas flow has stopped and the component of airway pressure caused by gas flow through resistance is no longer present. PPLAT only reflects the force needed to overcome elastic (static) properties of the lung and chest wall. Static compliance can be calculated as:
Measurement of static and dynamic compliance during mechanical ventilation. A tidal volume is delivered, causing a peak in airway pressure; dynamic compliance is calculated at the peak inspiratory pressure (PIP). A short pause is applied before expiration to eliminate airway pressure caused by gas flow, and airway pressure decreases to a plateau (PPLAT). Static compliance is calculated during the plateau. A. Normal response. B. Low lung compliance causes a global increase in airway pressure and a decrease in both static and dynamic compliance. C. High airway resistance increases peak airway pressure but does not change the plateau pressure; dynamic compliance is decreased but static compliance is unchanged.
Effective dynamic compliance (CDYN) is then calculated, taking into account all components of airway pressure:
A patient receiving positive pressure mechanical ventilatory support has been stable for 24 hours. The following variables have been set by the ventilator:
Breathing frequency = 12 breaths/min
Tidal volume (Vt) = 1000 mL
End-expiratory pressure (PEEP) = 5 cm H2O
Peak inspiratory airway pressure (PIP) = 25 cm H2O
End-inspiratory plateau pressure (Pplat) = 20 cm H2O (determined periodically)
Calculations of static and dynamic compliance are helpful to reveal the cause of high airway pressure in a mechanically ventilated patient. Compliance is inversely proportional to pressure; thus increased airway pressures are associated with reduced compliance.
The patient in Example 1 has abruptly developed an increase in airway pressure due to bronchospasm. The results of his pulmonary function tests are:
Breathing frequency = 12 breaths/min (set by respirator)
Tidal volume (VT) = 1000 mL (set by respirator)
End-expiratory pressure (PEEP) = 5 cm H2O (set by respirator)
Peak inspiratory airway pressure (PIP) = 45 cm H2O
End-inspiratory plateau pressure (Pplat) = 20 cm H2O
Figures 5-13B and 5-13C compare the two general causes of increased airway pressure in a mechanically ventilated patient. Figure 5-13B is an example of reduced static lung compliance in which both PIP and Pplat are increased (both static and dynamic compliance are reduced). Figure 5-13C is an example of high airway resistance in which PIP increases but PPLAT does not change (dynamic compliance is reduced but static compliance is unchanged). In Example 2, the patient developed bronchospasms, the pattern shown in Figure 5-13C, and would benefit from treatment with a bronchodilator to reduce peak airway pressure when the respirator delivers a tidal breath.
Figure 5-14A shows the results of a forced expiration test using a spirometer, in which the patient inspires and expires maximally.
The volume expired in the first second is called the forced expiratory volume (FEV) in 1 sec (FEV1.0).
The total volume expired under maximum effort is the forced vital capacity (FVC).
FEV1.0 is normally about 80% of FVC (FEV1.0:FVC ratio = 0.8). FEV1.0 represents forced expiration from high lung volume and is effort-dependent.
Expiratory flow through the middle 50% of the expired breath (FEF25–75) is also determined. FEF25–75 is useful in patients who do not use maximal effort, recalling that expiratory flow becomes effort-independent at lower lung volumes (see Figure 5-12).
Spirograms showing a normal lung (A) and obstructive (B) and restrictive (C) lung diseases. Obstructive and restrictive lung diseases are associated with smaller forced vital capacity (FVC) and forced expired volume in the first second (FEV1.0). In obstructive lung disease, the FEV1.0 : FVC ratio is significantly decreased, whereas in restrictive lung disease, the FEV1.0 : FVC ratio is normal or increased.
Two general patterns of disease can be distinguished using spirometry: obstructive and restrictive disease. Obstructive lung diseases (e.g., emphysema, chronic bronchitis, and asthma) are characterized by difficulty in moving gas out of the lung due to high airway resistance (Figure 5-14B). The FEV1.0 and the FEV1.0 : FVC ratios are both reduced. In restrictive lung diseases (e.g., pulmonary fibrosis), it is difficult to move gas into the lung due to low lung compliance (Figure 5-14C). Virtually all lung volumes, particularly TLC and FVC, are decreased. Expiration is not impeded because lung recoil forces are increased. The absolute value of FEV1.0 is low because inspired volume is initially low, but the FEV1.0:FVC ratio is either normal or increased.
Figure 5-15 illustrates the appearance of obstructive and restrictive lung disorders using maximal expiratory flow-volume curves. Emphysema is used as an example of an obstructive disease. The flow-volume loop is displaced to the left because weak lung recoil force causes hyperinflation of the lung. Although TLC is larger, peak expiratory flow is small due to dynamic airway collapse. In Figure 5-15, the loop is displaced to the right in restrictive disorders because patients have reduced TLC and RV. Peak expiratory flow is lower than normal because the patient is not able to reach high inspiratory volumes, where flow rate is effort-dependent. The slope of the descending part of the curve may be steeper, reflecting higher lung recoil forces.
Flow-volume curves in obstructive and restrictive lung disease. TLC, total lung capacity; RV, residual volume.
Chronic obstructive pulmonary disease (COPD) is a term that applies to patients with either emphysema or chronic bronchitis. Patients with emphysema are known as “pink puffers” because they are able to maintain adequate O2 saturation by hyperventilating. The classic profile of a “pink puffer” is a thin person sitting in tripod position, breathing with pursed lips. Patients with chronic bronchitis are known as “blue bloaters” because they have a blunted respiratory response to high blood CO2 (hypercarbia), which produces an inappropriately low respiratory drive that results in hypoxemia and cyanosis. Blue bloaters are typically overweight and have red faces due to polycythemia secondary to chronic hypoxemia. They suffer from cor pulmonale (structural and functional changes in the right ventricle caused by chronic pulmonary hypertension).
Work of breathing has two major components: “elastic work” to overcome static compliance, and “resistive work” to overcome airway and tissue resistance. Patients usually adopt a pattern of breathing that minimizes work. In restrictive disease, small tidal breaths are taken more rapidly because a large amount of elastic work is needed to inflate the lungs. Patients with obstructive lung disease often expire slowly, which reduces dynamic airway collapse and resistive work of breathing.