The neck is the part between the face and the trunk. The front part is of gristle and through it speech and respiration take place; it is known as the windpipe.

Aristotle, Historia animolium. 4th century bc

It is unlikely that any of our readers have escaped the unpleasant obstruction to breathing associated with the common cold. The major discomfort of this condition is the result of an inflammation of the nose (rhinitis) and, if more severe, the paranasal sinuses. In about 50% of cases this rhinosinusitis is initially caused by rhinoviruses, 25% by corona viruses and the remainder by other viruses. A transient vasoconstriction of the mucous membrane (see below) is followed by vasodilatation, oedema and mucus production. With secondary bacterial infection the secretions become viscid, contain pus cells and bacteria, and contribute to the obstruction of breathing.

Rhinosinusitis may also be allergic in aetiology or idiopathic (i.e. intrinsic, of no external cause). Idiopathic rhinitis is thought to be a result of an imbalance of the activity of the sympathetic and parasympathetic nerves serving the mucosal blood vessels, and in this type of rhinitis anticholinergic medication often relieves symptoms.

Allergic rhinitis may be seasonal in response to allergens such as pollen, or perennial, where a major cause is the allergen Der pl in the faeces of the house-dust mite Dermatophagoides pteronyssinus.

The mite is just invisible to the unaided eye and lives on shed skin scales, particularly in human bedding. The allergen from this creature is also responsible for much asthma, but the rhinitis it provokes demonstrates the filtering action of the upper airways in trapping it in the nose.

Much more sinister and life-threatening than rhinitis is obstructive sleep apnoea (OSA; apnoea = absence of breathing). This should not be confused with central sleep apnoea, where the patient ceases to make respiratory efforts while they are sleeping. In OSA the patient’s attempts to breathe are physically obstructed by anatomical and physiological peculiarities of the upper airways.

In Figure 2.1 the subject is breathing through his nose because the lips are closed and the tongue lies against the palate. When you breathe through the mouth – for example when you blow out a candle or suck through a straw – the soft palate is arched upward to form a seal against Passavant’s ridge at the top of the pharynx. This form of airways obstruction is a normal function. Similarly, under normal circumstances, the genioglossus muscle of the tongue has a high resting tone in conscious subjects, and this holds the tongue forward, preventing it from obstructing the airway. During sleep, and particularly in those suffering from the dangerous condition of obstructive sleep apnoea, the tongue falls against the back wall of the pharynx and obstructs breathing. The muscle tone of the pharynx itself becomes reduced, particularly during REM (rapid eye movement) sleep and in OSA the pharynx collapses under the negative pressure of inspiration. Blocking of the airways by the tongue also and almost inevitably occurs during general anaesthesia and requires immediate attention from the anaesthetist.

Most, but not all, healthy persons breathe through the nose unless exercising. The resistance to breathing of the nose is about twice that of the mouth and nearly half the total resistance of the airways. The disadvantage of this is offset by the advantage obtained by the air-conditioning and filtering activities of the nose, which warm, moisten and filter the air before it comes in contact with the delicate respiratory regions of the lungs. Newborn babies have great difficulty breathing through their mouths: they are almost obligate nose breathers and become very distressed when their nose is blocked. Their predominantly nose breathing may be associated with their ability to suckle and breathe at the same time. On the other hand, many animal species, such as rabbits, manage to eat and breathe at the same time by having lateral food channels on either side of the larynx (see below) that bypass the airway. Marine mammals such as whales have completely separate air and food channels, with the airway ending at the back of the head.

In humans the nose extends from the nostrils (external nares) to the choanae (internal nares), which empty into the nasal part of the pharynx. Each nostril narrows to form its nasal valve, and at this level the total cross-sectional area of the airways is narrower (3 mm²) than anywhere else in the system. This narrowing imposes the majority of the high resistance to airflow found in the nose (see Chapter 5) and, combined with the sharp turn the inspiratory air must make as it enters the wide (140 mm²) lumen of the cavum of the nose, causes turbulence. The walls of the nasal cavum are rigid bone projecting out into the airway from the lateral walls as the turbinates. These have a large surface area (150 cm²) covered by vascular mucosal erectile tissue important in the ‘air-conditioning’ activities of the nose. This mucosal tissue can swell considerably in conditions such as rhinitis (described above), and it is here that nasal decongestants such as oxymetazoline, an agonist of α adrenergic receptors on vascular smooth muscle, act to clear a blocked nose by causing the vascular smooth muscle to contract.

Normal physiological swelling of the mucosa and consequent restriction of airflow takes place asymmetrically over a period of time, so that one nasal passage is more constricted than the other. Thus both nasal passages are not uniformly constricted, with the major constriction, and therefore airflow, alternating between nostrils over a period of hours. This oscillation of airflow may help to sustain the nose in its air-conditioning activities by allowing one channel to rest while the other carries out most of the work.

The major function of the upper airway is to air-condition the inspirate. It is not essential to breathe through the nose to do this, and the mouth will make a fairly good job of warming and humidifying inhaled air before it reaches the larynx. However, the mouth has not evolved for that purpose and the unpleasant consequences of using it are well known to anyone who has had to breathe through their mouth because a cold has obstructed their nasal airways.

A common cause of accidental airway obstruction is the inhalation of food into the trachea. Normally, to prevent this during swallowing, the larynx, a box-like structure at the upper end of the trachea, is elevated (moved towards the head) by the muscles attached to it and the epiglottis folds backward, forming a very effective seal, like the ‘trapdoor’ over the entrance to the larynx. Because the ‘trapdoor’ can only open outwards, increased pressure in the pharynx makes the seal of the epiglottis on the larynx tighter and it can withstand considerable inward pressures of up to 100 kPa.

If this system of preventing solids entering the airways fails, powerful cough reflexes can be provoked by nerves in the lining of the larynx and trachea.

The larynx (see Fig. 2.1) is in fact a rather complicated box made up of plates of cartilage. It can be closed off by drawing together the two curtains of muscle which make up the vocal folds across the lumen of the larynx. Effective coughs depend on the closure and rapid opening of these ‘curtains’, which under less extreme circumstances are used to produce and modify the sounds that make up speech. The vocal folds can be drawn together so strongly that they are airtight against the greatest efforts to breathe the subject can make. This is clearly a ‘bad thing’ and can occur accidentally when an anaesthetist is trying to get an endotracheal tube into a patient’s trachea. This dangerous closing of the larynx is called laryngospasm. A picture of what an anaesthetist would see when approaching the larynx is shown in Fig. 2.2.

It is frequently useful to inspect the airways below the larynx. First the trachea (part of which is extrathoracic), and then the intrathoracic airways. The instrument used for this is called a bronchoscope and may be of the rigid ‘open tube’ type through which the airways are inspected, or the flexible fibreoptic variety (Fig. 2.3) which, as well as providing a view of the inside of the airways through its fibreoptic system, contains channels through which a variety of sampling and surgical instruments may be passed. Each type of bronchoscope has its advantages, but 95% of bronchoscopic procedures carried out these days are fibreoptic. Biopsy forceps, brushes and needles, balloon catheters and laser fibres can all now be passed through flexible bronchoscopes to carry out procedures after an initial inspection of even very small intrathoracic airways.

The microscopic structure of the wall of the airways changes as you go deeper into the lungs. Three ‘snapshots’ of airway wall structure are shown in Figure 2.7 but of course the structure changes gradually from generation to generation.

The conducting airways consist of three general layers which vary in proportion depending on airway type:

The arrangement representing bronchial structure illustrated in Figure 2.7 and described above is modified in chronic bronchitis in a way that provides a histopathological quantitative diagnosis of the disease. The Reid Index provides a measure of proportion of bronchial glands to total wall thickness (Fig. 2.8). In normal lungs mucous glands occupy less than 40% of total wall thickness. In chronic bronchitis this proportion is altered by hyperplasia of the glands. A characteristic of chronic bronchitis is an increase in the products of these glands.

The respiratory regions of the lungs show a wonderful degree of adaptation. They carry out the functions of a respiratory surface while withstanding the assaults of a polluted atmosphere and the mechanical trauma of being stretched and then relaxed about 12 times a minute for the whole of your life as a result of the movements of breathing.

One of the characteristics of the respiratory surface of any animal is that it should be thin, offering minimal separation between the outside medium (air or water) and the blood. This is beautifully demonstrated in the lungs, which are the only place in our body where blood capillaries come into direct contact with the outside air, as a result of the fusion of the type I epithelial cells (which make up about 95% of the lining of the respiratory zone; Fig. 2.6) with the pulmonary capillary endothelium. This fusion results in an ultrathin layer ideal for the diffusion of gas but not much good for support. Evolution has resulted in this thinning occurring on only one side of the pulmonary capillaries, whereas the cells on the other side remain separate and more robust, supporting the capillary in its place (Fig. 2.9).

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