Mechanics of Breathing

Introduction

Breathing is a dynamic mechanical process driven primarily by diaphragmatic contraction and changes in thoracic volume. Inspiration occurs through expansion of the lungs, whereas quiet expiration depends largely on elastic recoil. Pulmonary surfactant maintains alveolar stability, and pulmonary function tests help identify airway obstruction.

General Concepts

• Mechanics of breathing deals with the physical properties of the lungs, airways, and thoracic cage that enable pulmonary ventilation.
• Mechanical behavior of the respiratory system is studied under two conditions: static properties, when airflow is absent, and dynamic properties, when air moves into or out of the lungs.
• During normal quiet breathing, inspiration is an active process requiring contraction of inspiratory muscles.
• In contrast, quiet expiration is usually a passive process that occurs because of the elastic recoil of the lungs and chest wall.
• Contraction of inspiratory muscles enlarges the thoracic cavity and lowers intrapleural pressure.
• The fall in intrapleural pressure expands the lungs because the visceral pleura remains adherent to the parietal pleura through the pleural fluid.
• Lung expansion increases alveolar volume and reduces intrapulmonary (alveolar) pressure below atmospheric pressure.
• This pressure gradient drives air from the atmosphere into the lungs.
• At the end of inspiration, inspiratory muscles relax.
• Relaxation permits elastic recoil of the lungs and thoracic structures, which decreases lung volume.
• As lung volume decreases, intrapulmonary pressure rises slightly above atmospheric pressure, causing air to flow out of the lungs.
• Therefore, quiet expiration normally requires minimal muscular effort.
• During increased ventilatory demand, such as exercise or respiratory disease, forced expiration occurs with active contraction of expiratory muscles.

Muscles of Respiration

• The lungs lie within the thoracic cavity and are separated from the abdominal cavity by the diaphragm, a dome-shaped skeletal muscle that is the principal muscle of inspiration.
• Contraction of the diaphragm causes it to descend, thereby increasing the vertical dimension of the thoracic cavity.
• The thoracic wall consists of the sternum anteriorly, the vertebral column posteriorly, and twelve pairs of ribs connected by intercostal muscles.
• External intercostal muscles elevate the ribs during inspiration, increasing the anteroposterior and transverse diameters of the thorax.
• Internal intercostal muscles participate mainly in forced expiration.
• The rib cage moves upward and outward during inspiration and downward during expiration.
• Coordinated movements of the diaphragm and rib cage generate the pressure changes necessary for airflow and ensure effective pulmonary ventilation.

Muscles of Inspiration

• Inspiratory muscles expand the thoracic cavity, thereby increasing lung volume during inspiration.
• Contraction of these muscles makes intrapleural pressure more negative, facilitating lung expansion and airflow into the alveoli.
• Air enters the lungs because alveolar pressure falls below atmospheric pressure.
• Inspiratory muscles are classified into primary muscles, which function during quiet breathing, and accessory muscles, which are recruited during deep or labored breathing.

Primary Muscles of Inspiration

• The diaphragm and external intercostal muscles are the primary muscles responsible for quiet inspiration.
• The diaphragm is the most important inspiratory muscle and contributes the majority of tidal ventilation during normal breathing.

Diaphragm

• The diaphragm is a dome-shaped skeletal muscle that separates the thoracic and abdominal cavities.
• It is attached to the lower ribs, sternum, and lumbar vertebrae.
• During contraction, the diaphragm flattens and descends toward the abdominal cavity.
• This downward movement increases the vertical or craniocaudal diameter of the thoracic cavity, thereby expanding the lungs.
• Contraction of the diaphragm also elevates and displaces the lower ribs outward, increasing the transverse and anteroposterior diameters of the thorax.
• Enlargement of the thoracic cavity decreases intrapleural pressure, allowing air to enter the lungs.
• During quiet breathing, the diaphragm descends by approximately 1–2 centimeters.
• During deep or forced inspiration, diaphragmatic excursion may increase to approximately 10 centimeters or more, producing a marked rise in thoracic volume.

Clinical Significance

• Conditions such as moderate or severe obesity, advanced pregnancy, and tight abdominal or thoracic garments restrict diaphragmatic descent and reduce lung expansion.
• Consequently, inspiratory efficiency and ventilation may be impaired in these situations.
• The diaphragm receives motor innervation from the phrenic nerves, which arise from cervical spinal segments C3, C4, and C5.
• Each phrenic nerve supplies the corresponding half of the diaphragm.
• Injury to a phrenic nerve causes paralysis of the ipsilateral hemidiaphragm.
• During inspiration, the paralyzed hemidiaphragm exhibits paradoxical upward movement instead of descending, significantly compromising ventilation, particularly during exertion.

External Intercostals

• The external intercostal muscles are primary inspiratory muscles located between adjacent ribs.
• Their fibers run obliquely downward and forward from the upper rib to the lower rib.
• Contraction of these muscles elevates the ribs and expands the thoracic cavity during inspiration.
• Elevation of the ribs increases both the transverse and anteroposterior dimensions of the thorax through two characteristic movements.
• The second to tenth ribs move upward and outward in a bucket-handle movement, which predominantly increases the transverse diameter of the thoracic cavity.
• The upper ribs and sternum move upward and forward in a pump-handle movement, mainly increasing the anteroposterior diameter of the thorax.
• These coordinated rib movements enlarge thoracic volume, lower intrapleural pressure, and facilitate entry of air into the lungs.
• Contraction of the external intercostal muscles also stabilizes and stiffens the rib cage and intercostal spaces.
• This increased rigidity prevents inward collapse of the chest wall during inspiration when intrapleural pressure becomes increasingly negative.
• Effective action of the external intercostal muscles is therefore essential for maintaining normal ventilatory mechanics, particularly during deep inspiration and increased respiratory effort.

Accessory Muscles of Inspiration

• Accessory muscles of inspiration are recruited during deep, labored, or forced breathing when ventilatory demand increases.
• These muscles augment thoracic expansion and improve airflow into the lungs.
• The scalene muscles arise from the cervical vertebrae and insert into the first and second ribs.
• During forceful inspiration, they elevate the upper ribs, thereby increasing thoracic volume.
• The sternocleidomastoid muscles elevate the sternum and upper rib cage during vigorous inspiration.
• Their action enhances the pump-handle movement, increasing the anteroposterior diameter of the thorax.
• Several muscles of the neck and upper back also participate in forced inspiration.
• Contraction of these muscles elevates the pectoral girdle, which enlarges the transverse diameter of the thoracic cavity.
• Extension of the vertebral column by back muscles further increases the vertical dimension of the thorax.
• Important accessory muscles include the posterior cervical muscles, suprahyoid muscles such as the digastric and mylohyoid muscles, and muscles of the upper back.
• Muscles of the upper airway, including the alae nasi, palatal muscles, and cheek muscles, also assist inspiration.
• Their contraction widens the upper airway and decreases airway resistance, thereby facilitating airflow during increased respiratory effort.
• Prominent use of accessory inspiratory muscles at rest is an important clinical sign of respiratory distress or increased work of breathing.

Muscles of Expiration

Expiration is a simpler process than inspiration. During inspiration, lungs and airways store enough energy in their elastic recoil, which is used for expelling air during expiration. When inspiration ends, the inspiratory muscles relax, the rib cage drops, and the thoracic volume decreases. The elastic recoil of the lungs is now unopposed, which helps lungs deflate. This results in expiration during normal breathing. Thus, quiet expiration is purely a passive process. Therefore, there are no primary muscles of expiration. However, expiratory muscles come into play during forced expiration. These muscles are called accessory muscles of expiration that include abdominal muscles, internal intercostals, and neck and back muscles.

1. Abdominal muscles: Muscles of abdominal wall that take part in expiration are internal oblique, external oblique, and transverse abdominis. Contraction of these muscles increases intra-abdominal pressure and pushes diaphragm upward into the chest cavity. This decreases rostro-caudal diameter of thorax and increases intrapleural pressure.
2. The internal intercostals: Internal intercostal muscles pull the rib cage downward and decrease thoracic volume both in anteroposterior and transverse diameter (opposite actions of external intercostal muscles). These muscles are especially helpful for forced expiration during coughing, vomiting, and strenuous defecation.
3. Neck and back muscles: Muscles of neck and back that lower the pectoral girdle decrease cross-sectional area of the thorax, and muscles that flex the trunk decrease rostrocaudal diameter of the chest cavity.

Physiological Significance

Following three important points should be noted for muscles of expiration.

1. During forced inspiration, accessory muscles are used to increase lung volume rather than to overcome the resistance to airflow, whereas during forced expiration accessory muscles are used mainly to overcome the resistance to airflow.
2. Quiet expiration is purely passive. However, exception to this is the individuals suffering from lung diseases like bronchial asthma in which airway resistance is high. They require active participation of expiratory muscles even in normal expiration.
3. The strength of expiratory muscles is important in endurance trainings like running, etc. Therefore, for long-distance runners, physical exercises are advocated to strengthen their abdominal and chest muscles as part of their training programmes.

Pressure Changes During Breathing

Pressures in the Thoracic Cavity

Various pressures exist in different structures in the thorax. The pressures are generated and modified in different phases of respiration. Changes in different pressures in the thoracic cavity that result in breathing are:

1. Intrapleural pressure
2. Transmural pressure
3. Alveolar pressure

Intrapleural Pressure

The pressure in the pleural space is the intrapleural pressure

1. The pleural space is the space between the lungs and chest wall, i.e. the virtual space between the visceral and parietal pleura (refer Fig. 103.4; Chapter 103).
2. The intrapleural pressure also reflects the pressure in other regions of the thoracic cavity like the interstitial space surrounding the airways in the lungs, the space around the heart and great vessels, pressure inside and outside the esophagus when esophagus is not in peristalsis.
3. Thus, intrapleural pressure is the pressure everywhere in the thorax except the pressure in the airways, and in the lumen of the thoracic blood vessels and lymphatics.

How is the Intrapleural Pressure created and Why is It Negative?

The pleural space is a relative vacuum. The lungs have the tendency to collapse and the chest wall has the tendency to expand (Fig. 104.3). Therefore, the elastic recoil effects of lungs and chest wall are exerted equally but in opposite directions.

1. Lungs recoil inwardly and chest wall recoil outwardly. These equal and opposing forces cause the intrapleural pressure to be negative (less than atmospheric pressure).
2. Pleural pressure is negative during quiet breathing and more negative during deep inspiration.
3. During forced expiration only, intrapleural pressure may become positive.

Normal Value

In quiet breathing, intrapleural pressure (relative to atmospheric pressure) during expiration is about –2.5 to –4 mm Hg (approximately, –5 cm of H2O) and during inspiration is about – 6 mm Hg (approximately, –8 cm of H2O) (Fig. 104.4).

However, during forced expiration, intrapleural pressure becomes positive and, during forced inspiration, it becomes further negative, may be up to –30 mm Hg.

Measurement of Intrapleural Pressure

The intrapleural pressure can be measured by inserting a needle into the intrapleural space. But, it is not safe to introduce a needle into the intrapleural space as it may result in pneumothorax. As intrapleural pressure reflects esophageal pressure, in practice it is measured by recording intraesophageal pressure by introducing a balloon catheter through mouth into the esophagus.

Effects of Posture and Gravity

Upright Posture

In upright posture, intrapleural pressure is about –2.5 cm H2O at the base of the lung and –10 cm H2O at the apex of the lung.

1. This apex to base increasing negative gradient of intrapleural pressure is due to the effect of gravity.
2. In standing position, the vacuum in intrapleural space is greater in the apex and less in the base of the lung, because gravity pulls the lungs downward (away from the apex of the thoracic cage).
3. This creates the intrapleural pressure gradient in vertical direction.

Supine Posture

In supine posture, this difference does not exist.

1. However, lying on one’s side creates the intrapleural pressure gradient in transverse direction.
2. As there is no gravitational force in the outer space, intrapleural pressure gradient is absent.

Significance of Intrapleural Pressure

Physiological Significance

It has two physiological significances.

1. The thoracic cavity is an airtight chamber. Therefore, expansion of the thoracic cage as occurs during inspiration causes the intrapleural pressure (the pressure between the lung and chest wall) to fall (to become more negative). A decrease in intrapleural pressure helps the lungs to expand, which in turn results in inflow of air into the lungs. Thus, fall in intrapleural pressure facilitates inspiration.
2. Intrapleural pressure maintains normal shape of chest wall and lungs as it resists the recoiling of these structures. Loss of normal intrapleural pressure results in lung collapse and barrel shaped chest.

Clinical Significance

The clinical significance of intrapleural pressure is observed when the chest wall is perforated and air enters the pleural space.

1. The normal pleural pressure is subatmospheric. Thus, when a connection is made between the atmosphere and the pleural space, air moves into the pleural space (air moves from regions of high to low pressure) and intrapleural pressure becomes atmospheric. This condition, in which air accumulates in the pleural space, is known as pneumothorax.
2. Due to loss of normal intrapleural pressure in this condition, the lungs collapse immediately due to inward recoiling, and the rib cage expands outward due to its outward recoiling (Fig. 104.5). In such a situation, the transpulmonary pressure is zero because the pressure difference across the lung is eliminated.

Causes of Pneumothorax

1. A gunshot wound that perforates the chest wall.
2. Injury with a knife in which the chest wall is punctured.
3. In diseases in which the lung ruptures into the pleural cavity, e.g. rupture of a lung abscess or rupture of a parenchymal bullae by severe coughing.
4. During aspiration of pleural fluid for analysis, air enters into the pleural cavity due to faulty technique.
5. As part of therapy for some lung diseases, e.g. for treatment of tuberculosis, pneumothorax is purposefully created by inserting a sterile needle into the pleural cavity. For such purposes, nitrogen is injected into the pleural space to provide rest to the diseased lung.

Transmural Pressure

Transmural pressure is the pressure difference across an airway or across the lung wall. There are two major transmural pressures involved in breathing: transpulmonary pressure, and trans-airway pressure.

Transpulmonary Pressure

Transpulmonary pressure is the pressure difference across the lung wall (Fig. 104.6). This is measured by subtracting pleural pressure from alveolar pressure. Transpulmonary pressure is the pressure that keeps the lungs inflated and prevents the lungs from collapsing. An increase in transpulmonary pressure causes the inflation of lungs above the resting volume.

Transairway Pressure

Transairway pressure is the pressure difference across the airway, which is the difference between the pressure inside and outside the airway (Fig. 104.6). Transairway pressure is important in keeping the airways open during forced expiration.

Alveolar Pressure

The alveolar pressure is the pressure inside the alveoli.

1. Change in alveolar pressure moves air in and out of the lungs.
2. During inspiration, alveolar pressure decreases (becomes subatmospheric) that sucks air into the lungs, and, during expiration, the alveolar pressure increases that removes air from the lungs (Fig. 104.4).

Normal Value

During inspiration, it is approximately −1 mm Hg, and during expiration 1 mm Hg.

Physiological Significance of Transmural and Alveolar Pressures

At the end of expiration, when there is no flow of air into airways, the alveolar pressure is zero, i.e. equal to atmospheric pressure. Transpulmonary pressure, which is the difference in alveolar pressure and pleural pressure, is therefore +5 cm H2O [0 – (–5) = +5] at the end of expiration.

1. Transpulmonary pressure is always positive in normal breathing.
2. Transpulmonary pressure is also referred to as distending pressure as it helps in inflation of lungs.
3. When transpulmonary pressure becomes more positive, the lungs are more inflated.

Summary of Mechanics of Inspiration and Expiration

Sequence of Events Leading to Inspiration

1. Diaphragm and other inspiratory muscles contract that cause expansion of thoracic cage which in turn makes intrapleural pressure more negative.
2. This increases transpulmonary pressure as a result of which inflation of lungs occurs.
3. Alveolar pressure decreases (becomes subatmospheric) and therefore, air flows into airways and lungs.
4. Inflow of air stops when alveolar pressure equalizes with atmospheric pressure (Flowchart 104.1).
5. The cessation of contraction of inspiratory muscles ends inspiration.

Sequence of Events Leading to Expiration

1. Due to relaxation of inspiratory muscles, rib cage drops.
2. Therefore, intrapleural pressure becomes less negative which decreases the transpulmonary pressure.
3. Lungs that were stretched in inspiration start deflating, due to which alveolar diameter decreases.
4. The alveolar pressure becomes greater than the atmospheric pressure that pushes air out of the lungs (Flowchart 104.2).
5. Airflow out of lungs continues till alveolar pressure equalizes atmospheric pressure.

Types of Breathing

Physiologically, breathing is of two types: Abdominothoracic and thoracoabdominal.

Abdominothoracic Breathing

Abdominothoracic breathing is usually seen in males.

1. During inspiration, diaphragm descends that pushes abdominal viscera down and, therefore, abdominal wall is raised.
2. Thus, abdominal movement becomes prominent. Contraction of abdominal muscles facilitates breathing.

Thoracoabdominal Breathing

This is predominant in females and children, as in them the movement of the chest wall is prominent during respiration.

1. In females, descent of diaphragm is resisted by the abdominal viscera; the exact cause of which is not known. Therefore, there is increased movement of the rib cage that increases thoracic cage volume. Hence, thoracic movement becomes prominent during breathing.
2. One contributing factor may be the free mobility of the ribs at sternocostal and costovertebral joints in females compared to males.
3. Also, diaphragm is more powerful in males that contributes to abdominothoracic breathing in males.

Lung Volumes and Capacities

Classification

There are four lung volumes and four lung capacities (Fig. 104.7) as follows:

Lung Volumes

Tidal Volume

Tidal volume (TV) is the volume of gas inspired or expired during quiet breathing. This is about 500 ml in adults. About 150 ml of this volume fills the airways from the nose and mouth down to the respiratory bronchioles and this volume does not take part in gas exchange. This is called anatomical dead space. The remaining volume, i.e. 350 ml is available for alveolar ventilation.

Inspiratory Reserve Volume

The amount of air inspired with a maximal inspiratory effort in excess of the normal tidal inspiratory volume is called inspiratory reserve volume (IRV). The normal IRV is 3.3 liters in men and 1.9 liters in women.

Expiratory Reserve Volume

The volume of air that can be expired with a maximum expiratory effort after the normal tidal expiration is called expiratory reserve volume (ERV). The normal ERV is 1.2 liter in men and 0.7 liter in women.

Residual Volume

The volume of air left in the lungs at the end of maximal expiratory effort is the residual volume (RV). The normal value of RV in men is 1.2 liter and in women is 1.1 liter.

Lung Capacities

Vital Capacity

The maximum volume of air that can be expired after a maximal inspiratory effort is called the vital capacity (VC). The normal value of VC in men is about 4 liters and, in women, about 3 liters.

Forced Vital Capacity (FVC)

The total volume of air that can be expired with greatest force and speed after a maximal inspiration is the FVC. FVC differs very little from VC in the normal subject, but it is proportionately more reduced when there is airway obstruction with air trapping. Physiological importance of FVC: The maximum volume of air that can be exhaled after a maximum inspiration is the VC. When expiration is performed as rapidly and as forcibly as possible, the volume is the FVC.

1. Normally, VC and FVC have same values.
2. To measure FVC, the individual inspires maximally and then exhales into the spirometer as forcefully, rapidly, and completely as possible.
3. From FVC, two other important lung functions are obtained: the forced expiratory volume of air exhaled in 1 second (FEV1), and the forced expiratory flow (FEF25–75) that represents the expiratory flow rate over the middle half of the forced vital capacity, i.e. between 25 and 75%. Details of FEV1 and FEF25–75 are discussed below.

Inspiratory Capacity

This is the maximum volume of air that can be inspired after tidal expiration. This is the sum of tidal volume and inspiratory reserve volume (TV and IRV). Normally, it is about 3.5 liter.

Functional Residual Capacity

This is the volume of air remaining in the lungs at the end of each tidal expiration. This is the sum of expiratory reserve volume and residual volume (ERV and RV). Normally, it is about 2.2−2.5 liters.

Physiological Importance of FRC

FRC is important for maintaining stable gas tension in the lung, so that at all times, enough air is available for gas exchange along the alveolocapillary membrane. It prevents sudden alteration in gas tension due to any brief interruption of respiration. Reduction in FRC may result in hypoxia. FRC increases when there is air trapping in lungs as seen in asthma or emphysema.

Total Lung Capacity

The volume of the air present in the lungs at the end of maximal inspiration is the total lung capacity (TLC). The normal value in men is about 6 liters and in women is about 4.2 liters.

Measurement

The lung volume and capacities are measured directly by simple spirometry. However, as lungs cannot be emptied completely following forced expiration, RV and FRC cannot be measured directly by simple spirometry. RV and FRC are measured indirectly using a dilution technique involving helium (helium dilution technique). In this procedure, the subject is connected to a spirometer filled with 10% helium in oxygen (helium-oxygen mixture) and subject breathes from the spirometer. After the subject rebreathes, helium-oxygen mixture and equilibrates with the spirometer, the helium concentration in the lungs becomes same as in spirometer.

Applying the conservation of mass principle, we derive that:

C1 × V1 = C2 × (V1 + V2); where C1 is the initial concentration of helium in the spirometer, V1 is the initial volume of helium-oxygen mixture in the spirometer, C2 is helium concentration after equilibrium, and V2 is unknown volume in the lungs.

Thus,  

1. If the test begins at the end of a normal tidal volume (end of expiration), the volume of air remaining in the lungs represents functional residual capacity.
2. If the test begins at the end of a forced vital capacity, then the test will measure residual volume.
3. Similarly, if the test starts after a maximal inspiration, then V2 would equal total lung capacity.

FRC can also be measured by body plethysmography. Dynamic lung volumes and capacities are FEV1, PEFR, MMEFR, MVV, MEFVC, etc. (discussed below).

Factors Affecting

Lung volumes and capacities are influenced by various factors, such as age, gender, built, height, level of physical training, etc. (for details, refer chapter 114 “Pulmonary Function Tests”).

Mechanical Properties of Lungs and Chest Wall

The lung parenchyma, airways and pulmonary vasculature are embedded in elastic tissue. The inflation and deflation of lungs depend on their elastic properties. The physical principles that govern the process of breathing act mainly by affecting the mechanical properties of lungs and chest wall.

Elastic Properties of the Lungs and Chest Wall

The elastic properties of lungs and chest wall determine the lung volume and capacities. In an intact thoracic cage, the lungs have the tendency to collapse and the chest wall has the tendency to distend outward. These two forces acting in opposite direction precisely balance each other.

Elastic Properties of Lungs

Lungs are elastic tissues. An elastic tissue once stretched recoils back to its un-stretched position like a spring. Similarly, lungs recoil when stretched.

1. The ability of the lungs to be inflated is called its stretchability or distensibility. Distensibility and elastic recoil are opposite to each other. Overstretching of the lungs causes loss of elastic recoil.
2. Lung elasticity depends on the presence of the amount of elastin and collagen fibers enmeshed in its parenchyma.
3. Elastin fibers are highly distensible and can be stretched easily, but collagen fibers resist stretch and limit lung expansion.
4. The arrangement of elastin fiber networks in the lung parenchyma is similar to the arrangement of fibers of a nylon stocking. When the stocking is stretched to fit into the leg, the length of individual fibers does not change much.
5. However, the arrangement of the nylon mesh in the stocking is such that it allows the stocking to be easily stretched and fit into the leg. If the nylon stocking is overstretched, it loses its elasticity and becomes loose (baggy). Similarly, an overstretched lung (baggy lung) as seen in emphysema, can not be deflated easily due to the loss of its ability to recoil.

Lung Compliance

Compliance means the ability to stretch (stretchability) or the ability to recoil. Lung compliance (distensibility and elastic recoil of the lung) can be assessed from the pressure-volume curve of the lung. This is similar to the inflation of a balloon in which for each unit of change in pressure, balloon is distended to a new volume. Lung compliance is a measure of its distensibility. Compliance is represented by the volume change per unit pressure change, i. e.

Compliance = ΔV/ΔP, where ΔV is the change in volume and ΔP is the change in pressure.

Measurement of Lung Compliance

Two types of lung compliances are measured: static lung compliance and dynamic lung compliance.

Static Lung Compliance Measurement

A pressure-volume relationship is obtained for human lungs by simultaneously measuring changes in lung volume (with the help of a spirometer) and changes in pleural pressure (by measuring pressure changes in the esophagus with the help of a balloon catheter).

1. For recording pressure-volume curve, an individual inspires maximally to total long capacity (TLC) and then expires slowly.
2. During the process of slow expiration, airflow is periodically interrupted (so that alveolar pressure is zero), and lung volume and pleural pressure are measured (Fig. 104.8).
3. Lung volume is recorded as percentage of TLC. The compliance (volume change per unit pressure change) recorded in these conditions is called static lung compliance, as airflow does not occur during the recording.
4. As lung is deflated from TLC, the deflation pressure-volume curve is obtained by this procedure.
5. To obtain the inflation pressure-volume curve, lung is inflated from functional residual capacity (FRC) to the TLC.

There are four stages in the inflation pressure-volume curve:

1. Stage 1 (stage of stable lung volume): The initial change in intrapleural pressure has no effect on lung volume. This is because a decrease in intrapleural pressure increases transpulmonary pressure and unless transpulmonary pressure is large enough to overcome the collapsing effect of surface tension created by the air-water interface in the airways, the decrease in intrapleural pressure has no effect on lung volume.
2. Stage 2 (stage of opening of airways): When intrapleural pressure decreases above –8 cm H2O, lung volume increases first due to opening of proximal airways and then by opening of distal airways.
3. Stage 3 (stage of linear increase in lung volume): When intrapleural pressure decreases further (becomes more negative) opening and expansion of all airways occur. This results in steep but linear increase in lung volume.
4. Stage 4 (stage of cessation of inflation): As increase in lung volume approaches TLC, further increase in the volume becomes less, and finally ceases. This occurs due to decrease in airway and chest wall compliance and limitation of muscle strength.

Hysteresis Loop: The difference between the inflation and deflation pressure-volume curves (Fig. 104.9) is known as hysteresis.

1. The hysteresis loop occurs because a greater pressure difference is needed to open an already closed airway than to keep airway open that has already been opened (to maintain airway opening, i.e. to prevent open-airway from closing).
2. For example, to keep open a previously opened airway at FRC requires a pressure of only about –5 cm H2O (as noted in the deflation limb of pressure-volume curve), whereas to inflate a collapsed lung at FRC requires a pressure of about –15 cm H2O (as noted in the inflation limb of pressure-volume curve). However, the hysteresis loop is much smaller during normal breathing and is located close to the deflation limb of the pressure-volume curve.
3. The slope of pressure-volume curve is the compliance and is the measure of distensibility of lungs.

Dynamic Lung Compliance Measurement

Dynamic lung mechanics are the mechanics in play when the lungs are in motion.

1. Dynamic lung compliance is measured by continuously recording the change in intrapleural pressure and lung volume.
2. In pressure-volume loop of dynamic record, the rise in volume in inspiration is in the form of a curve and returning to the starting point during inspiration is another curve.
3. The difference in inflation and deflation limbs of the curve produces a hysteresis, which is much similar to the pattern obtained in pressure-volume curve of static lungs, but the difference is that dynamic compliance of lung is less than its static compliance.
4. Dynamic lung compliance increases during exercise. However, dynamic compliance of chest wall does not differ significantly from its static compliance in normal conditions (Application Box 104.1).

Regional Variation of Lung Compliance

In upright posture, the lung compliance is less at the top portion of the lungs than at the base. This regional difference in compliance is due to the effect of gravity. As discussed above, due to the gravitational effect, the pleural pressure is less (more negative) at the apex than at the base of the lungs.

1. At the apex, transpulmonary pressure is therefore more, which causes the alveoli in the apical region to be more distended. This decreases compliance of lung at the apex. Thus, the apex of the lung is less distensible (Application Box 104.2).
2. Thus, at the base of the lung, there is a larger change in volume for the same pressure change, which ensures greater expansibility.

Factors Affecting Lung Compliance

1. Distensibility and elastic recoil: More the lung is distensible and elastic more is the compliance. A stiff lung has less compliance.
2. Lung volume: The pressure-volume curve of the lung is nonlinear, which indicates that the compliance is not equal at all lung volumes. The compliance is high at low lung volumes and low at high lung volumes.
3. Lung size: In general, compliance is proportionate to the size of the lung. Thus, the lung of rat has less compliance than the lung of elephant. Children lung is less compliant than the adult lung. However, compliance expressed per unit tissue may be less in advancing age due to increased stiffness of the lung tissue.
4. Surface tension inside the alveoli: Surface tension mainly affects lung compliance (discussed below). Surface tension at the air-water interface of airways accounts for more than half of the lung compliance.

Clinical Significance of Lung Compliance

Diseases of lung alter the lung compliance.

Low Compliance

The low lung compliance indicates less distensibility. This means more work is required in a lung with low compliance to inflate the lungs to achieve the normal tidal volume.

1. In restrictive lung diseases, the compliance of the lungs is significantly low. For example, in pulmonary fibrosis, fibrous tissue is deposited in the lungs, which makes lungs stiff and difficult to inflate.
2. In a normal lung, tidal volume of 500 ml is achieved at about 2.5 cm H2O of transpulmonary pressure.
3. In lung fibrosis, the same change in pressure produces a much less increase in lung volume (Fig. 104.10). This indicates that the static lung compliance in this condition is much less.

High Compliance

High compliance is also equally bad as low compliance. High compliance is seen in obstructive lung diseases like emphysema.

1. In emphysema, which occurs in chronic habitual smokers, the lung tissue (extracellular matrix including elastin) is destroyed by elastase released from macrophages. In this disease, it is much easy to inflate lung, since a higher lung volume is obtained at any particular pressure (Fig. 104.10). The static lung compliance is higher.
2. However, the elastic recoil of lungs is much less, due to which getting air out of lung is severely impaired.

Therefore, emphysematous lungs have abnormally high residual volume.

Elastic Properties of Chest Wall

Like lungs, chest wall has elastic properties, but the elastic recoil of the chest wall is in outward direction. Thus, chest wall has the intrinsic tendency to expand.

1. The outward recoil of chest wall balances the inward recoil of lungs. Therefore, if the elastic recoil of the chest wall is unopposed, as occurs in lung collapse, chest wall expands to about 70% of total lung capacity (TLC).
2. That means, when the volume is less than 70% of TLC, the chest wall starts recoiling outward.
3. It should be noted that, the outward elastic recoil of the chest wall is maximum at residual volume (and the inward elastic recoil of the lung is maximum at TLC).

At functional residual capacity (FRC), the elastic recoil of lung and chest wall balance each other. That means for the lung volumes at FRC, chest wall and lung have equal elastic recoil forces in opposite directions. Alterations in these elastic forces significantly affect FRC.

Measurement of Thoracic Wall Compliance

To measure thoracic wall compliance, first the compliance of thoracic cage and lungs are measured combinedly. Intrapulmonary pressure (which is the total pressure of lungs and thoracic wall) is measured for each lung volume inhaled. Then, lung compliance is measured separately (as described above). Thoracic wall compliance is then determined from the following formula:

$$\mathrm{\frac{1}{Thoracic\ wall\ compliance} = Total\ compliance\ -\ \frac{1}{Lung\ compliance}}$$

So, thoracic wall compliance

$$\mathrm=\ \mathrm{\frac{Lung\ compliance}{Total\ compliance\ \times\ Lung\ compliance\ -\ 1}}$$

Lung-Chest Wall Interaction

During respiration, lung and chest wall move simultaneously in opposite direction. The change in volume of lungs and thoracic wall is equal as they move together. The pressure changes across the lung and chest wall during the respiratory movements are called transmural pressures (see above). These pressures are:

1. Transpulmonary pressure: This is the transmural pressure for lung. This is the pressure difference between the alveolar pressure and the intrapleural pressure. To increase its volume, lung requires positive transpulmonary pressure. When transpulmonary pressure is zero, the size of the lung is minimum. At zero transpulmonary pressure, though the lung is smallest in size, alveoli are not fully collapsed due to surface tension lowering property of surfactant.
2. Transmural pressure across the chest wall: This is the difference between intrapleural pressure and the pressure surrounding the chest wall (the body surface pressure or the barometric pressure). Transmural pressure across chest wall is usually negative as the intrapleural pressure is negative relative to the atmospheric pressure.
3. Pressure across the respiratory system: This is the sum of the pressure across the lung and across the chest wall. This is calculated as the difference between alveolar pressure and the barometric pressure.

Relaxation Pressure-Volume Curves

Interaction between these transmural pressures determines the lung-volumes and capacities, which can be studied by analyzing the relaxation pressure-volume curves of lung, chest wall and respiratory system (Fig. 104.9).

1. At functional residual capacity (FRC), transmural pressure across the respiratory system is zero, and at total lung capacity (TLC), both lung and chest wall pressures are positive.
2. This indicates that both lung and chest need positive transmural distending pressures.
3. The resting volume for chest wall is the 60% of TLC. This (the resting volume for chest wall) is the volume at which the transmural pressure for the chest wall is zero.
4. This means that at volumes less than 60% of TLC, chest wall tends to recoil outward and at volumes more than 60% of TLC, chest wall recoils inward.
5. It should be noted that at transpulmonary pressure of 20 cm of H2O, lung reaches its elastic limit; therefore, the pressure curve flattens beyond this pressure.
6. The increase in transpulmonary pressure above 20 cm of H2O does not increase lung volume much, as the distension of lung is limited by the connective tissues of the lung.
7. Further increase in pressure results in rupture of alveoli near the lung surface that can lead to pneumothorax (escape of air into the pleural space).

Role of Surface Tension

The force that pulls the surface molecules together of a liquid at an air-liquid interface is called surface tension. There is a thin layer of surfactant (a liquid film) lining the inner surface of the alveoli and the alveoli is filled with air; this forms the air-liquid interface.

1. The surface tension at the air-liquid interface in the lung alveoli is a major factor that influences lung compliance. In fact, surface tension at the air-liquid interface of lung airways accounts for more than half of the elastic recoil of lungs.
2. At the air-liquid interface of alveoli, surface tension is created because water molecules are strongly attracted to one another than to air molecules.
3. The surface tension in the alveoli produces a force, which is directed inward, and therefore, tends to decrease the alveolar size. Thus, surface tension favors collapse of alveoli.

The importance of surface tension in lung functions is best studied by analyzing the pressure-volume curves of lungs filled with air and liquid (Fig. 104.11). In this experiment, lungs are removed from chest and inflated or deflated at various pressures separately, first filled with air and then with saline. Surface tension is generated in the lung filled with air as air-liquid interface is created, whereas, surface tension is absent in the lung filled with saline as air-liquid interface is eliminated.

Two important points are noted in these pressure-volume curves:

1. Hysteresis (difference between inflation and deflation limbs of pressure-volume curve) is very less in saline-lung than air-lung. This indicates that in saline-lung, pressure needed to inflate the lung is almost same as to deflate the lung.
2. The slope of inflation limb of saline-lung is much steeper than the inflation limb of air-lung. This is because the static compliance is very high in saline-lung as lung was inflated with much less pressure (lung was more compliant due to elimination of surface tension). Thus, above evidences clearly signify that surface tension significantly affects compliance and work of breathing.

Application of Laplace Law

Surface tension also maintains alveolar stability. The Laplace law explains the relationship of surface tension with pressure inside a sphere like alveolus. The Laplace law states that the pressure in a spherical structure is equal to twice the wall tension divided by the radius,

i.e.

, where, P is the pressure, T is surface tension and r is radius.

In lungs, all alveoli do not have same diameter, alveoli size also changes during inspiration and expiration, and alveoli are interconnected with each other.

1. If the surface tension was the same in all alveoli, according to the Law of LaPlace, pressure would be greater in smaller alveoli than in bigger alveoli. The smaller alveoli would empty into the larger alveoli if they are interconnected and larger distending pressure would be needed to keep the smaller alveoli inflated (Fig. 104.12).
2. Thus, one can presume that larger alveoli tend to distend more and smaller alveoli tend to collapse, especially at low lung volumes. But this does not happen. Surface tension is constant per unit surface area (i.e. 50 dyne/cm2). So, the surface tension of the alveoli decreases with the decrease in surface area.
3. Therefore, as the alveoli become smaller, the surface tension also reduces and as the alveoli distends (becomes larger), surface tension increases.
4. Thus, the smaller alveoli do not collapse as pressure (2T/r) within the alveoli remains same and, therefore, volume of interconnected alveoli remains almost same.

Role of Surfactant in Pulmonary Mechanics

The inner lining of alveoli is coated by surfactant. The surfactant means a surface-active agent that decreases surface tension. The pulmonary surfactant is a thin liquid film of alveolar lining that decreases surface tension at the gas-liquid interface of alveoli and alters surface tension with change in alveolar diameter.

Pulmonary Surfactant

Structure and Composition

Pulmonary surfactant is a mixture of lipoprotein rich in phospholipid. The principal surface tension-lowering agent in surfactant is dipalmitoylphosphatidyl-choline (DPPC), which is also called dipalmitoyllecithin (DPL).

1. Phospholipids of surfactant have a hydrophilic head and a hydrophobic tail. The hydrophobic tail consists of fatty acids. The tail of phospholipids faces toward the alveolar lumen (Fig. 104.13).
2. The alveolar surface tension is inversely proportional to the concentration of phospholipids in the surfactant.

Surfactant consists of:

1. Lipids: 90%
   • Dipalmitoylphosphatidylcholine (62%)
   • Phosphatidylglycerol (5%)
   • Other phospholipids (10%)
   • Neutral lipids (13%)
2. Proteins: 8%
   • Albumin
   • Immunoglobulin A (IgA)
   • Apoproteins (SP-A, -B, -C, – D)
3. Carbohydrates: 2%

Source

Surfactant is synthesized in Type II pneumocytes. There are two types of cells in alveolar epithelium: type I and type II alveolar epithelial cells.

1. Alveolar type II cells are called type II pneumocytes. Though, the ratio of type I to type II epithelial cells is about 1:1, type I cells form about two-third of the surface area due to their flat surface.
2. However, type II cells are metabolically more active and contain more number of mitochondria. The special histological feature of type II cells is the presence of electron-dense lamellar inclusion bodies (Fig. 104.13).
3. In fact, the lamellar inclusion bodies store surfactant in type II cell.

Synthesis and Secretion

Palmitate, choline and glucose are substrate molecules for surfactant synthesis. The substrate molecules are taken up by alveolar type II cells from the circulating blood.

1. In mitochondria, they are synthesized into DPPC.
2. The surfactant is then stored in the lamellar inclusion bodies.
3. Lamellar inclusion bodies are continuously discharged onto the alveolar surface by constitutive exocytosis (exocytosis which is continuous and unregulated).
4. The released lamellar body-materials are converted into tubular myelin that forms the film of surfactant on the alveolar surface (steps of surfactant synthesis are summarized in Flowchart 104.3).
5. The active synthesis of lipid in the lung accounts for high rate of replacement of surfactant. Thus, an integrated layer of surfactant is continuously formed on the alveolar epithelium.
6. Some amount of surfactant is recycled (reuptake by type II cells) back.

Time of Surfactant Synthesis in Fetal Life

Lungs are among the last organs to develop during intrauterine life. Therefore, synthesis of surfactant occurs toward later part of pregnancy.

1. Surfactant synthesis starts at about 34 weeks of pregnancy, which is completed by about 90% at term (38−40 weeks). That means, maturation of surfactant production continues to the perinatal period.
2. Therefore, inadequate surfactant synthesis resulting in lung collapse is among the major causes of death in premature deliveries.
3. In premature newborns, adequate amounts of surfactant are not available to reduce surface tension and stabilize surface forces during breathing.

Regulation of Synthesis and Secretion

Surfactant synthesis is regulated by hormones, concentration of protein in the surfactant, stretching of lung and various pharmacological agents.

A. Hormonal factors

1. Glucocorticoid hormones: Cortisol stimulates surfactant synthesis. Secretion of glucocorticoids increases toward term. Number of glucocorticoid receptors in lungs also increases in third trimester of pregnancy.
2. Thyroxine: Thyroxine promotes surfactant synthesis. Maternal thyroid deficiency and cretinism decrease surfactant secretion.
3. Insulin: Insulin facilitates surfactant synthesis. Therefore, diabetes during pregnancy decreases surfactant secretion.

B. Quantity and quality of proteins in surfactant

Formation of phospholipid film of surfactant is greatly facilitated by proteins present in the surfactant. Surfactant proteins are albumin, immunoglobulin (IgA) and apoproteins (surfactant proteins).

1. There are 4 types of surfactant proteins (SP): SP-A, SP-B, SP-C, and SP-D. SP-B and SP-C control synthesis of monomolecular film of phospholipid.
2. SP-A controls reuptake of surfactant by type II cells.
3. The protein content of surfactant depends on concentration of protein in the plasma.

C. Stretching of lungs

Hyperinflation of lungs like yawning enhances surfactant synthesis. Yawning and sighing during infancy are effective stimuli for surfactant synthesis.

D. Pharmacological agents

• β adrenergic agonists enhance surfactant secretion
• Calcium stimulates surfactant secretion.

E. Exercise

Practice of regular physical exercise stimulates surfactant synthesis in both children and adults.

Functions of Surfactant

1. Prevents lung collapse: Surfactant decreases surface tension at the air-liquid interface of alveoli. By decreasing surface tension, surfactant prevents lung collapse. During lung deflation, compression of surfactant molecules decreases surface tension. Especially at low lung volumes, the molecules are tightly compressed. During lung inflation, new surfactant is extruded onto the alveolar surface that forms a new film on the alveolar epithelial lining.
2. Promotes alveolar stability: In lungs, alveoli of different diameters are connected in parallel to each other. By law of Laplace, smaller alveoli could drain into larger alveoli and collapse. However, that does not happen and alveoli coexist. This alveolar stability is maintained by surfactant. Surfactant achieves this by lowering surface tension proportionately more in the smaller alveoli.
3. Helps to prevent edema in the lung: The inward force of surface tension that tends to collapse alveoli also tends to decrease interstitial pressure in the lungs. Decreased interstitial pressure pulls fluid out of capillaries and facilitates pulmonary edema formation. Surfactant reduces surface forces and thus prevents pulmonary edema formation. This is an important function of surfactant.
4. On work of breathing: Surfactant decreases the work of breathing, so that breathing becomes easier.
5. On immunity: IgA and apoproteins (SP-A and SP-D) in surfactant provide innate immunity by acting as opsonins. They promote phagocytosis of bacteria and viruses by alveolar macrophages.

Clinical Importance

1. Infant respiratory distress syndrome: After birth, the newborn makes strong inspiratory effort so that the lungs expand. Surfactant helps in lung inflation and prevents collapse of expanded lung. Thus, respiration continues throughout life after the first breath. Lung maturation is incomplete in premature infants. Also, hormonal disturbances like diabetes during pregnancy interfere with lung maturation. In such conditions, due to lack of surfactant synthesis, lung expansion becomes difficult after birth. Breathing becomes extremely labored due to high surface tension. It becomes difficult to inflate lungs. This is called infant respiratory distress syndrome (IRDS) or hyaline membrane disease. Pulmonary edema and atelectasis develop due to high surface tension.

Treatment of IRDS:

1. Administration of phospholipid by inhalation
2. Inhalation of synthetic surfactant (or a surfactant preparation derived from bovine lungs)
3. Glucocorticoid therapy (glucocorticoid promotes surfactant synthesis)

2. Atelectasis following surgery: During deep breathing, the lungs inflate to a larger volume and new surfactant molecules spread thoroughly on the alveolar surface, whereas, during shallow breathing, the spreading of surfactant is impaired. Therefore, patients recovering from anesthesia after surgery are often encouraged to breathe deeply to enhance the proper spreading of surfactant on the alveolar surface (Clinical Box 104.1).

Alveolar Stability

Alveolar stability is maintained by two factors:

1. Pulmonary surfactant (discussed above)
2. Principle of interdependence

Interdependence is the mutual support among adjacent alveoli. Normally, alveoli are interconnected with surrounding alveoli. They support each other because of their structural arrangement (with many interconnecting links).

• When one alveolus collapses, it prevents the collapse of adjacent alveoli. This is because, when alveoli tend to collapse, surrounding alveoli develop greater expanding forces. Thus, interdependence not only prevents atelectasis but also opens up alveoli that have already collapsed.
• Alveolar interdependence is the major factor in adult lungs that maintain alveolar stability.
• This is not important in newborns, as newborn lungs have fewer interconnecting links.
• Surfactant is the major factor for maintaining alveolar stability in newborns and infants.

Properties of the Dynamic Lung

Properties of dynamic lung are studied when the lungs are in motion, associated with flow of air in and out of the respiratory tract. Under dynamic conditions (during air-flow), force is not only required to maintain the lung and chest wall at certain volume but also to overcome the inertia and resistance of tissues and air molecules.

Airflow in Airways

Flow occurs through a tube when the pressure difference exists at both ends of the tube. During inspiration, intrapleural pressure becomes negative that causes lung expansion due to which pressure decreases in the airways. This allows air to be sucked into the airway from outside. Two types of airflow occur in the lung: laminar flow and turbulent flow.

1. Laminar flow: When airflow is slow, laminar flow occurs. This is characterized by a streamlined flow. The flow is silent because layers of air molecules slide over each other. Normally, this type of flow occurs in small peripheral airways.
2. Turbulent flow: Turbulent flow occurs at high flow rates. This is normally observed in large airways, especially in the trachea and large bronchi. It consists of a disorganized pattern of airflow that produces sound. Therefore, in fast and deep breathing, the sound is heard both in inspiration and expiration.

Details of dynamics of inspiratory and expiratory flows and their importance are discussed above (in lung volumes and capacities).

Airway Resistance

The air flow causes resistance to air moving in the airways. It is defined as the ratio of driving pressure (ΔP) to airflow (V). Airway resistance (Raw) is expressed in cm H2O/L per second. For total airway resistance (Raw), the driving pressure is the pressure difference between the mouth (Pmouth) and the alveoli (PA).

Normal Value

In healthy individuals, the airway resistance is about 1−3 cm H2O/L per second (with lungs at FRC). Airway resistance is more in children due to their smaller airways.

Site of Resistance

The primary site of airway resistance is the medium bronchi (lobar and segmental) and bronchi down to about the seventh generation (Fig. 104.14). As per Poiseuille’s law, the airway resistance increases with the fourth power of airway radius. Thus, one would expect that the small airways would offer more resistance to airflow. However, contribution of by small airways to the total airway resistance is only about 10 to 15%. This is because most of the small airways are aligned in parallel and the total surface area of small airways (like capillaries in vascular system) is more.

Clinical Importance

In the early stage, airway diseases mainly affect small airways. However, diagnosing diseases in the initial stage becomes difficult because small airways contribute less to the total airway resistance. Airway diseases are diagnosed usually in their advanced stage.

Factors affecting Airway Resistance

1. Diameter of airways: Caliber of the airway is the most important factor affecting airway resistance. Bronchodilation decreases and bronchoconstriction increases resistance.
2. Lung volume: Lung volume is among the major factors affecting airway resistance because caliber of airways is directly proportionate to the lung volumes. Bronchi and small airways are embedded in lung tissue. Therefore, airway diameter increases with lung expansion. Thus, airway resistance decreases during inspiration and increases during expiration. It should be noted that airway resistance rises sharply at low lung volumes (Fig. 104.15).
3. Bronchial smooth muscle tone: Bronchial smooth muscle tone also affects airway resistance as it controls airway diameter. The smooth muscle tone of the airway is influenced by following factors:
4. Autonomic control:
5. Parasympathetic: Parasympathetic (vagal cholinergic fibers) stimulation causes bronchial constriction and increases mucus secretion. These effects are mediated by muscarinic receptors.
6. Sympathetic: Sympathetic Stimulation (adrenergic fibers) causes bronchodilation and inhibits glandular secretion. Activation of β2 receptors causes bronchodilation increases bronchial secretion, whereas activation of α2 receptors inhibits secretion.
7. Noncholinergic-nonadrenergic innervation: Also, there is noncholinergic-nonadrenergic innervation of bronchiole that causes bronchodilation, most likely mediated by VIP.
8. Humoral factors: Epinephrine, norepinephrine and other hormones that stimulate β2-adrenergic receptors cause dilation of airways. Histamine causes constriction of alveolar duct and increases airway resistance.
9. Drugs: Drugs, such as isoproterenol (β2-adrenergic receptor agonists), produce bronchodilation. These drugs are usually used in the treatment of asthmatic attacks as they alleviate bronchial constriction.
10. Environmental factors: Breathing chemical irritants, dusts and smoke particles cause reflex constriction of airways. Vagus nerve is the efferent pathway in the reflex arc that mediates bronchoconstriction in response to such irritants like cigarette smoke.
11. PCO2 in breathing air: Increased PCO2 in the conducting airways causes local bronchodilation. However, bronchoconstriction caused by the decreased PCO2 is of more importance.
12. Viscosity and density of inspired gas: Increase in gas density as occurs in deep-sea diving increases airway viscosity. The air density increases because of increased barometric pressure. Gas mixture containing oxygen-helium has low density. Therefore, a helium-oxygen mixture is often used during dive to make breathing easier. Oxygen-helium mixture is also used in the treatment of status asthmaticus.
13. Phases of respiration: Airway resistance is not significantly altered during quiet breathing. However, during forced expiration as seen in severe exercise, resistance is significantly increased. A high resistance is associated with decreased expiratory flow. The marked increase in resistance during forced expiration occurs due to compression of airways. This effect is well demonstrated by a flow-volume curve that depicts the relationship between airflow and lung volume during a forced inspiratory and expiratory effort (Fig. 104.16).

Flow-Volume Curve

A small loop of flow-volume curve is seen during tidal breathing, whereas, a large loop is observed during forced breathing.

1. During forced inspiration, inspiratory flow is limited only by effort; that means the force with which the individual inspires.
2. During forced expiration (forced vital capacity), flow rises sharply to a peak (peak expiratory flow) and then decreases linearly over most part of expiration as lung volume decreases.
3. The first phase of expiratory flow-volume curve is dependent on effort, but after the peak expiratory flow is reached, flow becomes independent of effort.
4. Thus, during forced expiration, flow is mostly independent of effort. This indicates the importance of dynamic airway compression during expiration.
5. Dynamic airway compression increases airways resistance, which effectively limits the forced expiratory flow (Clinical Box 104.2).

Dynamic Lung Volumes and Capacities

Timed Vital Capacity (FEV1)

This is also called forced expiratory volume in 1 second (FEV1). This is defined as the percentage of FVC expired in the specified time, e.g. FEV1, the percentage of air expired in 1^st second; FEV2, in 2nd second and so on.

1. This measures the FVC in relation to time and gives the percentage of FVC expired in the stipulated time. This is an index of air-flow rate.
2. In normal conditions, 72 to 85% of the forced vital capacity is expired in the first second, 95% in two seconds and 97% in three seconds (Fig. 104.17).
3. It is one of the most useful tests to detect generalized airway obstruction.
4. The ratio of FEV1 to FVC is more important clinically than their individual measurements, which is normally about 0.8 as calculated from clinical spirogram (Fig. 104.18).

Clinical Importance of FEV1

FEV1 is the single most useful test to detect generalized airway obstruction.

1. FEV1 less than 72% indicates difficulty in exhaling air from the lungs due to obstruction. This is a hallmark of obstructive lung disease like bronchial asthma.
2. In restrictive lung disease like emphysema though FVC is decreased, FEV1 as percentage of FVC remains normal (Fig. 104.19).
3. Thus, FEV1 curve differentiates obstructive from restrictive lung diseases.

Maximum Mid-expiratory Flow Rate (MMEFR)

This is the maximum flow achieved during the middle third of the total expired volume.

1. This is expressed as forced expiratory flow at 25% to 75% of the lung volume (FEF25–75%). FEF25–75% indicates the patency of small airways.
2. The measurement of flow rate between 200 and 1200 mL (FEF200–1200 mL) in liters per second indicates the patency of larger airways.

Maximum Voluntary Ventilation

This is also called as maximum breathing capacity (MBC).

1. Maximum voluntary ventilation (MVV) indicates the maximum volume of gas that can be breathed per minute by maximal voluntary effort.
2. The normal value of MVV in adult male is 150 liters per minute and for adult female is 125 liters per minute.

Peak Expiratory Flow Rate

Peak expiratory flow rate (PEFR) is the maximum velocity of flow in liters per minute with which air is forced out of the lungs. PEFR is recorded by using peak-flow meter.

1. The normal value of PEFR is 400 to 600 L/min or 6 to 10 L/s.
2. PEFR is an index of patency of airways.
3. However, MMEFR is a more sensitive indicator than PEFR.

Maximum Expiratory Flow Volume Curve

Because of the limitation of FEV1, certain other tests are performed to detect airways obstruction in its early phase.

1. These include Vmax 75%, 50% and 25% responses of maximum expiratory flow, which are studied by plotting maximum expiratory flow volume curve (MEFVC) by inhalation of helium. In MEFVC, flow is plotted against volume exhaled.
2. Vmax 75% is the flow rate at which 75% of the total FVC has been exhaled, Vmax 50% is the flow rate at which 50% of FVC remains to be exhaled and Vmax 25% is the flow rate at which 25% of the FVC has been exhaled. The maximum flow occurs early (in the first 20%) and decreases progressively thereafter (Fig. 104.20).
3. When the individual performs at three different efforts (maximum, moderate and minimum), the MEFVC curves indicate that PEFR increases with effort.
4. However, at lower lung volumes (toward residual volume) the effort has no impact on flow-rate as all the three curves merge in the later part (Fig. 104.21).
5. This indicates that in expiratory maneuver, the early part is effort dependent and the later part is effort independent.

Work of Breathing

During breathing, work is done to expand the lungs and overcome the airway resistance. Work is involved during inspiration to expand the thoracic cavity, inflate the lungs, and to overcome airway resistance. The work done is expressed as a change in lung volume multiplied by the change in trans-pulmonary pressure. Thus, work (W) is equal to the product of pressure (P) and volume (V).

W = P × ΔV, where P is transpulmonary pressure and ΔV is change in lung volume.

Energy is spent with muscular contraction to create a force (transpulmonary pressure) to increase lung volume (inflate the lungs). Therefore, more muscular work is done to create greater trans-pulmonary pressure, which is required to bring more air into the lungs. The pressure-volume curve depicts the work required for breathing in normal lung that spends about 5% of the body’s total energy expenditure (Fig. 104.22A). During exercise, total energy expenditure for breathing is increased.

Restrictive Lung Disease

In restrictive lung disease, work of breathing is increased, as greater inspiratory effort is required due to marked decrease in lung compliance (Fig. 104.22B). Therefore, patients with a restrictive disorder economize their ventilation by taking rapid and shallow breaths.

Obstructive Lung Disease

In obstructive lung disease, work of breathing increases due to more expenditure of energy to overcome increased airway resistance (Fig. 104.22C). Patients with obstructive disorders economize their ventilation by taking slow and deep breaths.