11 Respiratory system

ANATOMY

TRACHEA

The trachea is about 11 cm long, commencing at the lower border of the cricoid cartilage at the level of the 6th cervical vertebra, and terminating by dividing into the right and left main bronchi at the level of the 5th thoracic vertebra. The trachea is composed of fibroelastic tissue and is prevented from collapsing by a series of cartilaginous rings numbering 15–20. The rings are U-shaped, open posteriorly, where they are flattened, the posterior free end of the cartilaginous rings being covered by smooth muscle (trachealis). The trachea is lined by columnar ciliated epithelium containing numerous goblet cells.

BRONCHI

The trachea terminates at the level of the sternal angle by dividing into the right and left main bronchi (Fig. 11.1). The right main bronchus is wider, shorter and more vertical than the left. It is approximately 2.5 cm long and passes downwards and laterally behind the ascending aorta and SVC to enter the hilum of the lung. The azygos vein arches over it from behind to enter the SVC, while the pulmonary artery lies first below it and then anterior to it. The right main bronchus gives off an upper lobe bronchus just before it enters the lung. It then proceeds into the lung where it divides into the bronchi to the middle and inferior lobes.

Fig. 11.1 The trachea and bronchi.

Source: Rogers A W Textbook of anatomy; Churchill Livingstone, Edinburgh (1992).

The left main bronchus is approximately 5 cm long and passes downwards and laterally below the arch of the aorta, in front of the oesophagus and descending aorta. The pulmonary artery lies at first anteriorly and then above the bronchus. On the left side the main bronchus terminates by dividing into the bronchi to the upper and lower lobes of the left lung shortly after entering the lung.

The lungs (Fig. 11.2) are conical in shape. They conform to the shape of the pleural cavities. Each lung has a blunt apex which reaches above the sternal end of the first rib, a base related to the diaphragm, a convex parietal surface related to the ribs, and a mediastinal surface which is concave and related to the pericardium.

Fig. 11.2 The lungs and their lobes.

Each lung is subdivided by an oblique fissure into upper and lower lobes, the right lung being further divided by the horizontal fissure to produce a middle lobe. The surface marking of the oblique fissures is best represented by the line of the vertebral border of the scapula with the arm fully elevated. The horizontal fissure of the right lung passes horizontally and medially from the oblique fissure at the level of the fourth costal cartilage. The equivalent of the middle lobe in the left lung is the lingula which lies between the cardiac notch and the oblique fissure.

Bronchopulmonary segments

Each lobar bronchus divides to supply the bronchopulmonary segments of the lung. Each lung has ten segments. These are shown in Fig. 11.3. Each of the bronchopulmonary segments is supplied by a segmental bronchus, artery and vein. There is no communication with adjacent segments. It is thus possible to remove an individual segment without interfering with the function of adjacent segments. Each segment takes its name from that of the supplying segmental bronchus.

Fig. 11.3 Bronchi and bronchopulmonary segments. Right lung: (a) the divisions of the right main bronchus; (b) bronchopulmonary segments: (i) lateral surface, (ii) medial surface. Upper lobe: 1, apical bronchus; 2, posterior bronchus; 3, anterior bronchus. Middle lobe: 4, lateral bronchus; 5, medial bronchus. Lower lobe: 6, apical bronchus; 7, medial basal (cardiac) bronchus; 8, anterior basal bronchus; 9, lateral basal bronchus; 10, posterior basal bronchus. Left lung: (a) the divisions of the left main bronchus; (b) bronchopulmonary segments: (i) lateral surface; (ii) medial surface. Upper lobe: 1, 2, apicoposterior bronchus; 3, anterior bronchus. Lingula: 4, superior bronchus; 5, inferior bronchus. Lower lobe: 6, apical bronchus; 8, anterior basal bronchus; 9, lateral basal bronchus; 10, posterior basal bronchus.

PLEURA

Each pleural cavity is composed of a thin serous membrane invaginated by the lung. The visceral layer of pleura is intimately related to the surface of the lung and is continuous over the root of the lung with a parietal layer which is applied to the inner aspect of the chest wall, the diaphragm and the mediastinum. The two pleural cavities are totally separate from each other. Below the root of the lung the pleura forms a loose fold known as the pulmonary ligament which allows for distension of the pulmonary veins. The lungs conform to the shape of the pleural cavities but do not occupy the full cavity, as they would not be able to expand as in full inspiration.

Surface anatomy

The cervical pleura extends above the sternal end of the first rib. It follows a curved-line drawn from the sternoclavicular joint to the junction of the inner third and outer two-thirds of the clavicle, the apex of the pleura arising about 2.5 cm above the clavicle. The line of the pleura on each side passes from behind the sternoclavicular joint to meet in the midline at the level of the second costal cartilage. The right pleura then passes vertically down to the 6th costal cartilage before crossing the 8th rib in the midclavicular line, the 10th rib in the midaxillary line, and 12th rib at the lateral border of the erector spinae. On the left side the pleural edge reaches the 4th costal cartilage, where it arches out lateral to the border of the sternum, the pleura being separated from the chest wall by the protrusion of the pericardium. The medial ends of the 4th and 5th intercostal spaces are, therefore, notcovered by pleura. Apart from this, its relationshipsare the same as those on the right side. The pleura actually descends below the 12th rib at its medial extremity.

Nerve supply

The pleura receives its nerve supply from the nerves that supply the structures to which it is attached. The visceral pleura receives an autonomic supply from branches of the vagus nerve that supply the lung. It is sensitive only to stretching. The parietal pleura receives a somatic innervation from the adjacent intercostal nerves as they run round the chest wall. The diaphragmatic pleura is supplied by the phrenic nerve. The parietal pleura is, therefore, sensitive to pain, and this may be referred via the intercostal nerves to the abdomen: i.e. diseases of the chest wall and pleura may present as abdominal pain.

THORACIC CAGE

The thoracic cage is formed by the vertebral column behind, the ribs and intercostal spaces on either side, and the sternum and costal cartilages in front.

Ribs

There are 12 pairs of ribs (Fig. 11.4). The first seven pairs are connected anteriorly via their costal cartilages to the sternum. The 8th, 9th and 10th ribs articulate with their costal cartilages, each with the rib above. The 11th and 12th ribs remain free anteriorly and are known as ‘floating ribs’.

Fig. 11.4 Ribs 1, 4 and 12 viewed from the left side. superior view. posterior view.

Source: Rogers op. cit.

A typical rib comprises:

1. a head with two articular facets for articulation with the corresponding vertebra and the vertebra above;

2. a neck giving rise to the costotransverse ligaments;

3. a tubercle with a smooth facet for articulation with the transverse process of the corresponding vertebra; and

4. a shaft which is flattened from side to side and possesses an angle. The shaft possesses a groove on its lower surface, the subcostal groove. The intercostal vessels and nerves lie in this groove.

The first, 2nd, 10th, 11th and 12th ribs are atypical. Only the first and 12th are clinically important. The first rib is the shortest, flattest and most curved of the ribs. It is flattened from above downwards. The features of the first rib are shown in Fig. 11.4. The 12th rib is short, has no tubercle, and has only a single facet. There is no angle and no subcostal groove. Its only importance is in the loin approach to the kidney, where its relationship to the pleura is important. The pleura descends below the 12th rib at its medial extremity.

Clinical points

DIAPHRAGM

The diaphragm (Fig. 11.6) is a dome-shaped septum separating the thorax from the abdomen. It is composed of a peripheral muscular part and a central tendon.

Fig. 11.6 The inferior aspect of the diaphragm.

The muscular fibres arise from several sources: the crura, the arcuate ligaments, the ribs and the sternum. The right crus of the diaphragm arises from the front of the bodies of the first three lumbar vertebrae and the intervening intervertebral discs. The left crus arises from the first and second lumbar vertebrae and the intervening disc. The arcuate ligaments are a series of arches, the lateral being a condensation of the fascia overlying quadratus lumborum and the medial of the fascia overlying psoas major. The medial borders of the medial arcuate ligaments join anteriorly over the aorta as the median arcuate ligaments. The costal part of the diaphragm arises from the inner aspect of the lower six ribs and the sternal portion as two small slips from the posterior surface of the xiphisternum.

The central tendon is trefoil in shape and receives the insertion of the muscular fibres. Above, it fuses with the lower part of the pericardium.

There are three main openings in the diaphragm, although strictly speaking the aortic ‘opening’ is not in the diaphragm but lies behind it. The aortic ‘opening’ transmits the abdominal aorta, the thoracic duct, and often the azygos vein. The oesophageal opening lies in the right crus of the diaphragm and transmits the oesophagus, the vagus nerves, and branches of the left gastric artery and vein. The opening for the inferior vena cava lies in the central tendon of the diaphragm and transmits, in addition to the IVC, the right phrenic nerve.

The greater and lesser splanchnic nerves pierce the crura, and the sympathetic chain passes behind the medial arcuate ligament lying on psoas major.

Nerve supply

The diaphragm is supplied by the phrenic nerves (C3, 4, 5) which have long course in the neck and the thorax. Damage to the nerve leads to paralysis of the diaphragm, which results in elevation of the diaphragm seen on x-ray and paradoxical movement on respiration. The phrenic nerve also gives a sensory supply to the central part of the diaphragm. Irritation of the diaphragm, e.g. in peritonitis or pleurisy, results in referred pain to the cutaneous area of supply, i.e. the shoulder tip via dermatome C4. The peripheral part of the diaphragm receives sensory innervation from the lower six intercostal nerves.

ANATOMY OF RESPIRATION

There are two main mechanisms for increasing the volume of the thorax:

• movements of the rib cage, thoracic breathing; and

• contraction of the diaphragm, abdominal breathing.

Thoracic breathing

During inspiration, the ribs are elevated, and this occurs in two ways, as follows:

1. The anterior ends of the ribs are raised in the so-called pump handle action. Since the anterior ends are normally below the posterior ends, this increases the anteroposterior diameter of the thorax.

2. The most lateral and lowest parts of ribs 4–7 are raised in the so-called bucket handle action. Since the centre of these ribs is normally below the anterior and posterior ends, the transverse diameter of the chest is increased when they move upwards.

Abdominal breathing

This is controlled by the diaphragm. The peripheral muscle fibres of the diaphragm are more or less verticaland take origin from the lower six ribs. When the muscular fibres of the diaphragm contract, the diaphragm descends, increasing the vertical diameter of the thorax. As the central tendon descends, its vertical movement eventually arrests as it reaches the upper surface of the liver. The central tendon then behaves as an origin for the muscle fibres, which now elevate the lower six ribs in the final stages of inspiration. The combination of thoracic and abdominal breathing results in an increase in all diameters of the thorax. This in turn brings about an increase in the negative intrapleural pressure and expansion of the lung tissue occurs. Abdominal and thoracic breathing occur in quiet inspiration. In deep and in forced inspiration, additional muscles are used, i.e. the accessory muscles of respiration. These include sternocleidomastoid, the scalene muscles, pectoralis minor, pectoralis major and serratus anterior.

Expiration

Expiration is normally a passive process produced by the elastic recoil of the lungs and the tissues of the chest wall. However, forced expiration such as in coughing or playing a trumpet requires muscular activity. Such muscles include: rectus abdominus, external oblique, internal oblique, transversus abdominus and latissimus dorsi.

STRUCTURE OF THE RESPIRATORY TREE

The basic structure of the lower respiratory tree is shown in Fig. 11.7. The respiratory tree is designed to transport humidified air into the distal airways and alveoli where exchange between CO₂ and oxygen takes place. The trachea is composed of C-shaped plates of cartilage with the curve of the C anteriorly; the ring is completed posteriorly with smooth muscle. The trachea contains mucous glands and is lined with ciliated epithelium. The trachea divides into bronchi and these contain discontinuous pieces of cartilage in their wall together with smooth muscle. They too are lined by columnar ciliated epithelium and contain mucous glands. The cilia beat rhythmically in a thin liquid layer and effectively transport the surface film of mucus and particles out of the lungs by way of the trachea.

Fig. 11.7 The structure of the respiratory tree.

The bronchi decrease in diameter and length with each successive branching. The cartilaginous support eventually disappears. In airways of about 1 mm the cartilage disappears completely. By convention all subsequent airways are called bronchioles. Bronchioles contain no cartilage or submucosal mucous glands. They contain cuboidal epithelium with ciliated cells as well as some additional cells which are thought to provide a watery secretion. The most distal air passages are the respiratory bronchioles, which are so-called because the first alveoli open directly into them. Respiratory bronchioles end in several alveolarducts, which are short channels which open into alveolar sacs which contain many alveoli. A single respiratory bronchiole, its alveoli and their blood supply are called a primary lobule or acinus. The alveoli are lined by flattened Type I pneumocytes together with some Type II pneumocytes. Type II cells secrete surfactant and replicate rapidly after injury to alveolar walls. These alveolar cells lie on a basement membrane together with an interstitial matrix including some elastin fibres which separate the air spaces from the pulmonary capillary walls. The structure of the alveolar-capillary membrane permits rapid and efficient diffusion of oxygen and carbon dioxide.

MEDIASTINUM

The mediastinum (Fig. 11.8) is the name given to the space between the two pleural cavities. It extends from the sternum in front to the thoracic vertebrae behind and from the thoracic inlet above to the diaphragm below.

Fig. 11.8 The divisions of the mediastinum.

For descriptive purposes it is divided into a superior and an inferior mediastinum, the latter being again subdivided into anterior, middle and posterior.

Superior mediastinum

This is bounded in front by the manubrium sterni and behind by the first four thoracic vertebrae. Above, it continues up to the root of the neck; below, it is continuous with the three divisions of the inferior mediastinum at a level of a line drawn horizontally through the angle of Louis. It contains the lower end of the trachea, the oesophagus, the thoracic duct, the arch of the aorta, the innominate artery, part of the carotid and subclavian arteries, the innominate veins, the upper part of the SVC, the phrenic and vagus nerves, the left recurrent laryngeal nerve, the cardiac nerves, lymphatic glands, and the remnants of the thymus gland.

Anterior mediastinum

This is the space between the two pleural cavities in front of the pericardium and behind the sternum. In children part of the thymus gland may occupy this space, but in the adult it contains only the anterior mediastinal lymph glands.

Middle mediastinum

The middle mediastinum contains the pericardium itself with the heart and great vessels. The phrenic nerve and pericardiacophrenic vessels run down the lateral surface of the pericardium to reach the diaphragm.

Posterior mediastinum

This lies behind the pericardium and the diaphragm below. Anteriorly lie the pericardium and roots of the lungs, with the diaphragm lying anteriorly below. Posteriorly lies the vertebral column from the lower border of the 4th to the 12th thoracic vertebrae. Inferiorly lies the diaphragm and superiorly is a horizontal plane drawn through the angle of Louis. The posterior mediastinum contains the descending thoracic aorta, the oesophagus, the vagus and splanchnic nerves, the azygos and hemiazygos veins, the thoracic duct and the posterior mediastinal lymph glands.

Because of the arrangement of structures in the mediastinum, its appearance is different when viewed from the right and left hand sides. These differences and their relationships to the roots of the lungs are shown in Figs. 11.9 and 11.10.

Fig. 11.9 The mediastinum seen from the right side.

Source: Rogers op. cit.

Fig. 11.10 The mediastinum seen from the left side.

Source: Rogers op. cit.

PHYSIOLOGY

CONTROL OF VENTILATION

The body succeeds in keeping arterial PO₂ and PCO₂ within remarkably narrow limits. This is made possible by highly developed negative feedback systems that consist of sensors, controllers and effectors. These are summarized in Table 11.1.

Table 11.1 Summary of the basic mechanisms controlling respiration

Element	Location	Function
Controllers	Medullary Centre (Medulla) Apneustic Centre (Pons) Pneumotaxic Centre (Pons) Cortex Central Chemoreceptors (Ventral surface of medulla) Peripheral Chemoreceptors (Carotid Bodies at common carotid bifurcation and aortic arch)	Thought to produce the inherent rhythmicity of respiration Divided into inspiratory (dorsal) and expiratory (ventral) Function unclear, possibly initiates inspiration Inhibits inspiration beyond a certain point Voluntary control of respiration can override other mechanisms within limits Most important sensors in ventilatory control. Surrounded by ECF and very sensitive to changes in H⁺ concentration. As H⁺ increases so to does rate and depth of ventilation – and vice-versa. ECF H⁺ concentration is proportional to arterial PCO₂ concentration Respond to a fall in PaO₂ or in pH, or an increase in PaCO₂. All these result in increased ventilation. (Only the carotid bodies are sensitive to pH)
Sensors	Stretch Receptors (lung) Irritant Receptors (airway) J-Receptors (near lung capillaries) Receptors outside the lung (joint and muscle receptors, nasal receptors)	Sense lung distension sending impulses via vagus which result in decreased respiratory effort ‘Herring-Breuer Reflex’ Respond to chemical irritation e.g. smoke with coughing and bronchospasm Respond to chemicals in the pulmonary circulation causing rapid shallow breathing – function unclear Relay information about force of respiratory effort, sense noxious stimuli for sneezing, respectively
Effectors	Aortic and Carotid Sinus baroreceptors Diaphragm Intercostals Abdominal wall Accessory Muscles	Sudden increases in blood pressure produce hypoventilation and sudden falls in blood pressure produce hyperventilation – function unclear Expands the volume of the thorax Expands the volume of the thorax (bucket handle effect) Forced expiration and coughing Maximal inspiratory effort and volume

Effectors

These are the muscles of respiration: the diaphragm, intercostals, abdominal wall muscles and accessory muscles (see anatomy section).

In order for respiration to be effective in extremes of demand these muscles must work in a fully coordinated way, under the auspices of the central control.

Sensors

These are the central chemoreceptors, peripheral chemoreceptors, and several others. In the lung, sensors include primary stretch receptors, irritant receptors and J receptors. In the nose and upper airway there are sensitive irritant receptors, while joints and muscles utilise the gamma stretch receptor and associated reflex.

Central chemoreceptors

The most important receptors involved in respiratory control, they are situated on the ventral surface of the medulla. Here the extracellular fluid (ECF) of the brain surrounds the central chemoreceptors. Changes in hydrogen ion concentration of the ECF cause these receptors to respond. As hydrogen ion concentration increases, so ventilation increases, and the opposite is true. The pH of the ECF is most affected by the cerebrospinal fluid (CSF) hydrogen ion content. CSF is separated from the circulation by the blood-brain barrier. Whilst ions such as hydrogen and bicarbonate do not easily cross the blood-brain barrier, CO₂ can cross readily. Thus as arterial PCO₂ (PaCO₂) rises, CSF PCO₂ goes up, liberating hydrogen ions, which in turn lower the pH of the ECF. This stimulates central chemoreceptors to effect increased ventilation. Increasing ventilation decreases arterial PaCO₂. An increased PaCO₂ also causes cerebral vasodilatation, facilitating more rapid diffusion of CO₂ into the CSF.

A feature of CSF is that it has much lower buffering capacity than blood. Small changes in PCO₂ effect larger changes in CSF pH than in blood pH. However, bicarbonate can only diffuse slowly across the blood-brain barrier, and so changes in pH of CSF are eventually compensated for by a rise or fall in bicarbonate. This process takes about 36 h to complete, so that if PaCO₂ is elevated for a prolonged period the chemoreceptors will ‘reset’, e.g. chronic lung disease, where patients may have an elevated PaCO₂ with a normal CSF pH and normal respiratory rates. (See acid-base section.)

Peripheral chemoreceptors

These bodies contain glomus cells, with a large dopamine content. Because of their location, they have a very high blood flow per unit weight. These receptors increase their firing rate in response to:

• decreased PaO_2;

• decreased pH; and

• increased PaCO₂.

Curiously the response to a fall in PaO₂ begins at about 70 kPa, a state not likely to be encountered naturally. However, the sensitivity of the cells is much greater in the range below 13.5 kPa, when the firing rate increases dramatically.

These receptors are responsible for the decrease in ventilation which occurs in hypoxaemia – a response easily abolished by small doses of morphine or anaesthetic agents. The response to hypoxaemia is the important one. The peripheral chemoreceptors have a much less important response than the central ones to changes in PaCO₂.

The response to a change in arterial pH is mediated only by the carotid bodies – hydrogen ions cannot readily cross the blood-brain barrier. A fall in pH will increase ventilation.

Receptors within the lung

Mechanical

Stretch receptors within the lungs discharge in response to distension of the lungs. Impulses are sent via the vagus nerve and result in a decreased respiratory rate. This is often referred to as the Hering-Breuer reflex. This may be important in newborn babies but is not useful for day to day control of respiration.

Chemical

1. J receptors. ‘J’ stands for juxta capillary, i.e. in juxtaposition to the capillaries, but in the alveolar wall. Injection of chemicals into the pulmonary circulation can produce almost instantaneous rapid shallow breathing, even apnoea. The function of these receptors is unclear.

2. Irritant receptors. These respond to noxious gases, smoke, cold air, etc. They probably lie in airway epithelial cells and their impulses are sent via the vagus nerve, resulting in bronchospasm and hyperpnoea.

How do these mechanisms combine to control ventilation?

Consider the three main chemical factors which affect respiration:

1. arterial CO₂;

2. arterial O₂; and

3. arterial pH.

Arterial CO₂

Under normal conditions the most important determinant of ventilation control is the PaCO₂. The mechanism is sufficiently sensitive to keep the variation in arterial level of CO₂ within about 0.4 kPa. Sedation, alcohol and sleep will all tend to increase PaCO₂.

If subjects are given CO₂ to breathe then their rate and depth of respiration increase so that for each 0.1 kPa increase in PaCO₂ an increase in minute volume of about 1.5 L occurs. If the subject becomes hypoxic the rate of increase in minute volume increases. If the amount of CO₂ inspired is allowed to increase to very high levels (15%) then no further increase in minute volume occurs and the subject may become drowsy and exhibit depressed ventilation. Conversely, if PaCO₂ levels are allowed to fall (e.g. following hyperventilation), then ventilation becomes depressed. This can easily occur when mechanically ventilating patients.

Arterial O₂

Arterial oxygen tensions do not control respiration on a minute to minute basis in the same way as PaCO₂. Indeed lowering PaO₂ by breathing hypoxic mixtures produces no effect until PaO₂ = 6.5 kPa. These are very low levels of arterial O₂ and they are not seen in day to day life. They may occur in illness (e.g. pneumonia) or on ascent to high altitude. However, when PaCO₂ is raised, the effects of a low PaO₂ are seen at levels approaching 13 kPa.

In severe, longstanding, lung disease, patients may exhibit a persistent PaCO₂ elevation with a low PaO₂. These patients may rely on hypoxaemia to provide an adequate respiratory drive. If oxygen is administered to these patients it may well result in depression of ventilation. This is a relatively rare event and should not prevent the prescription of oxygen in adequate amounts to patients who remain tachypnoeic. It can be predicted by taking arterial blood for baseline gas analysis and then administering oxygen in increasing percentages. If the patient has a ventilatory drive dependent on hypoxaemia then the minute volume will decrease as oxygen is administered, and arterial carbon dioxide will increase. (NB: the response to hypoxaemia is mediated by peripheral chemoreceptors – it has no effect on central chemoreceptors except when hypoxia in the brain directly depresses output from the CNS.)

Arterial pH

As might be expected a decrease in arterial pH gives rise to increased ventilation. pH will, of course, fall as PaCO₂ increases, so it is difficult to separate the two phenomena. However, patients who develop a metabolic acidosis exhibit a marked increase in minute volume. This is mediated by peripheral chemoreceptors (the blood-brain barrier is relatively impermeable to hydrogen ions).

Summary

In summary, a rise in PaCO₂ or H⁺ stimulates respiration via the central and peripheral chemoreceptors. Hypoxia stimulates only the peripheral chemoreceptors. Stimulation of either sensor mechanism increases both rate and depth of respiration.

MECHANICS OF BREATHING

The major function of the lungs is the transport of gas in and out of the alveoli and the exchange of respiratory gases. This is achieved not just by the lungs, but by the surrounding tissues, bones and muscles.

Muscles of respiration

See the anatomy section.

Elastic properties of the lung

As the thoracic volume increases during inspiration the lung tissues become stretched; the greater the degree of chest expansion, the greater the degree of stretching of the lungs. However this relationship is not entirely linear. Figure 11.11 shows the relationship between the volume of the lung and the negative pressure surrounding it. As the negative pressure increases, so the lung volume increases, up to a point where further negative pressure does not increase lung volume. When the pressure around the lung decreases, the lung volume also decreases, but it does not follow the same curve. This is called hysteresis. The lung volume at any given pressure during deflation is larger than that during inflation.

Fig. 11.11 Compliance and hysteresis. The graph illustrates the differences in compliance between the lungs inflated with air and the lungs inflated with saline. The saline-filled lungs have greater compliance and less hysteresis. The difference can be explained by the lack of surface tension in saline-filled lungs.

The slope of the volume pressure curve (the volume change per unit pressure) is known as the compliance. The usual compliance of the human lung is about 200 mL/cmH₂O pressure, but from the slope of the line it can be seen that compliance decreases at higher lung volumes as the lungs become stiffer. Lung compliance can also be reduced, for example, in pulmonary venous engorgement or in alveolar oedema. The compliance of the lung falls if the lung remains unventilated for a long period. This may occur, for example, following anaesthesia, resulting in atelectasis. Lung compliance is decreased by fibrosis of the lung and certain diseases. Age and emphysema increase it.

Because the change in lung volume per unit change in pressure will be larger in a large lung and smaller in a small lung, the compliance per unit volume of lung is often quoted. This is known as the specific compliance.

The elastic properties of the lung are in part due to the elastic tissue clearly visible in histological section. The arrangement of the elastin fibres is also important to the compliance of the tissue, and this has been likened to that of the filaments in nylon stocking.

For all its elastic properties the compliance of the lung would be greatly reduced without the presence of surfactant.

The following is a summary of the major factors affecting compliance:

• increasing lung size increases the volume per unit pressure change;

• compliance decreases on adopting a supine position;

• small tidal volumes decrease compliance, probably due to changes in alveolar size;

• a decline in pulmonary blood flow will increase compliance. This will occur, for example, when a patient is put on a ventilator;

• breathing 100% oxygen decreases compliance, probably because of alveolar collapse, as oxygen is rapidly absorbed in the alveoli with no nitrogen to maintain pressure;

• age increases compliance;

• emphysema increases compliance; and

• fibrosis and inflammation, and engorgement decrease compliance.

Surface tension

Surface tension is defined as the force acting along an imaginary line drawn on the surface of a liquid. This force exists because of the strong cohesive forces between molecules along the surface. Its importance in the lung can be demonstrated by comparing the pressure volume behaviour in isolated lungs inflated with either water or air. Lungs inflated with air have a much greater compliance and so are easier to distend than lungs filled with water (Fig. 11.11).

Uninhibited, the surface tension within the alveoli would significantly decrease the compliance of the lungs, perhaps by as much as 50%. However, specialised cells within the alveolar epithelium secrete surfactant, a lecithin-rich, detergent-like substance that significantly decreases surface tension. Although these cells are plentiful in adult life they are not productive until a late stage of fetal maturity. Premature babies are very prone to develop respiratory distress, characterised by stiff lungs, atelectasis and pulmonary oedema.

Surfactant promotes several important properties within the lung, as follows:

• lower surface tension within the alveoli promotes increased stability and lessens atelectasis. It is important to note that alveoli are inherently unstable and smaller alveoli have a tendency to inflate larger alveoli – Laplace’s law states that the pressure in a bubble is equal to twice the wall tension divided by the radius, i.e. smaller bubbles (alveoli) have greater pressures;

• surfactant helps keep the alveoli dry and free from oedema. Surface tension forces within the alveoli tend to force liquid from the capillaries into the alveoli. This tendency is reduced by surfactant;

• compliance of the lung is increased; and

• work of respiration is decreased.

Regional differences in ventilation

Ventilation of the lung does not occur uniformly. Indeed dependent regions of the lung are much better ventilated than non-dependent regions of the lung. There are two main reasons for this:

• the weight of the lung; and

• the shape of the compliance curve (Fig. 11.12). In the dependent regions of the lung, resting intrapleural pressure is lower than in the apical regions. The dependent parts of the lung are on the steeper part of the compliance curve and are more easily distended. Thus ventilation is about 50% greater at the lung bases than at the apex.