1 . The airways act as conduits connecting the atmosphere to the alveoli. Normally the resistance to airflow is very low. Contraction and relaxation of smooth muscle in the bronchi and bronchioles can alter this resistance, with bronchoconstriction and bronchodilatation increasing and decreasing airways resistance, respectively. This is under ANS control, with adrenergic sympathetic nerves leading to bronchodilatation and cholinergic parasympathetic nerves stimulating bronchoconstriction.
2 . Various mechanisms protect the lungs from the entry of foreign matter . The air is partially filtered by the nasal hairs, and bacteria and particles of atmospheric pollutants which escape this are usually trapped in the layer of mucus lining the airways. The motile cilia in the trachea, bronchi and bronchioles transport this mucus back up towards the larynx and out into the pharynx where it is swallowed.
The vocal folds in the larynx, which are responsible for phonation, protect the lungs from inhalation of food by reflexly closing the glottis during swallowing. A cough reflex is triggered by any large particles which make contact with the mucosa of the vocal folds or airways, producing an explosive expulsion of gas which expels the solid matter.
FUNCTIONS OF THE AIRWAYS ( WARMING AND HUMIDIFYING GASES )
3 . As air passes through the airways it is warmed and humidified . Gases are completely saturated with water vapour before they reach the alveoli, producing a water vapour pressure of 47 mmHg at 37°C (body temperature).
The lungs lie within the thoracic cavity. The outer surface of the lung is covered by a membrane known as the visceral or pulmonary pleura , and this is separated from the parietal pleura , which lines the inside of the thoracic cavity, by the thin layer of pleural fluid filling the intrapleural space (10-15 ml).
Liquids cannot be easily expanded or compressed and so the two layers of pleura normally remain tightly adherent to one another.
During quiet breathing, three forces act on the lungs. Two tend to collapse the lung but these are opposed by a third, distending force or pressure.
1. ELASTIC TISSUE. The elastic tissue of the lungs is stretched under normal conditions and the resulting tension acts as a collapsing force pulling inwards on the visceral pleura.
2. SURFACE TENSION. The surface tension of the fluid lining the alveoli also tends to collapse them, pulling inwards, away from the chest wall.
3. NEGATIVE INTRAPLEURAL PRESSURE. The elastic and surface tension effects in the lungs are normally opposed by a distending pressure caused by the negative (subatmospheric) pressure in the intrapleural space (the intrapleural pressure). This is developed as a consequence of the chest wall and diaphragm pulling outwards on the parietal pleura. Since the two layers of pleurae are being pulled in opposite directions, a negative pressure is developed in the intrapleural fluid.
Surfactant is a natural detergent-like substance which is secreted into the alveoli by type II alveolar cells. This reduces the surface tension and allows the lungs to be kept expanded at a much less negative intrapleural pressure than would otherwise be possible.
Then alveolar diameter decreases, the concentration of surfactant in the alveolar fluid increases, reducing surface tension. Thus, alveolar wall tension and radius decrease (or increase) in parallel with each other and alveolar pressure is little affected.
Inspiration is an active process in which the thoracic volume is increased by the action of the relevant muscles. The dome of the diaphragm is pulled down during diaphragmatic contraction, thereby increasing the vertical height of the thoracic cavity.
This is augmented by contraction of the external intercostal muscles between the ribs, which raises them into a more horizontal position, increasing the width of the thorax from front to back.
Accessory muscles in the neck, including sternocleidomastoid and scalenus, may also be used during maximal inspiration to elevate the sternum and first two ribs.
The volume of gas which can be moved in and out of the lungs during breathing is highly dependent on age, sex, body build and level of fitness, making it difficult to quote a single, normal value for most of these measures.
Not all the gas can be expired from the lungs and the volume remaining after maximal expiration is called the residual volume. This cannot be measured directly using a spirometer but can be estimated from separate measures of the functional residual capacity (FRC) and the expiratory reserve volume (ERV).
1. TOTAL LUNG CAPACITY represents the sum of all the ventilatory volumes plus the residual volume.
2. VITAL CAPACITY is the sum of the ventilatory volumes (5 L in men and 3.5 L in women). Vital capacity depends on body build and body position, decreases with age.
3. FUNCTIONAL RESIDUAL CAPACITY is the volume of gas left in the lungs at the end of quiet expiration; this can be estimated using a variation of the indicator dilution technique (is typically about 3 L).
Not all the inspired air will actually reach the areas where gas exchange with the pulmonary circulation can take place. The volume which has to be ventilated but which does not participate in gas exchange is called the dead space .
The anatomical dead space includes all the airways down to the bronchiolar level. The air which enters these during inspiration is immediately expelled again at the beginning of the next expiration without contributing to pulmonary oxygenation.
In some areas of the lung, there may also be alveoli which are ventilated but receive very little pulmonary perfusion. These regions cannot contribute to gas exchange either, and when their volume is included, we refer to the physiological dead space.
THE MEASUREMENTS ARE COMMONLY MADE IN CLINICAL PRACTICE
FORCED VITAL CAPACITY (FVC) is the total volume of expired gas. This is similar to the vital capacity but is measured during forced expiration. The FVC is reduced in restrictive lung diseases (e.g. lung fibrosis).
FORCED EXPIRATORY VOLUME (FEV) is the volume of gas expelled in a given time; if this is measured for the first second it is called the forced expiratory volume in 1 second (FEV 1 ). This is limited by the speed with which gas can be forced through the airways and is decreased in obstructive lung disease. Since the actual magnitude of FEV1 is always reduced in parallel with any reduction in FVC, even in the absence of obstruction, it is the ratio of FEV1/FVC which is most useful diagnostically. This ratio should normally exceed 0.75 (75%) in healthy individuals but often falls below 0.5 (50%) when there is increased airways resistance (e.g. in asthma).
This is a simple test of ventilatory function which is widely used in clinical practice. The patient is simply asked to blow air out of their fully inflated lungs as rapidly as they can and the peak flow rate achieved is recorded with a flow meter.
Normal values are again very dependent on age, sex and build but are of the order of400 L/min. This may fall in cases of obstructive airways disease.
Obstructive airways disease is a diagnosis characterized by reductions in FEV 1 /FVC. It is seen in two main groups of patients, asthmatics and patients with chronic obstructive pulmonary disease (COPD).
Asthma is characterized by wheezing episodes caused by an acute increase in airways resistance. Between episodes lung function is often normal, especially in young patients.
In COPD airways resistance is persistently elevated but function deteriorates further during chest infections. COPD is often caused by smoking and atmospheric pollution and is associated with chronic bronchitis (cough with spit) and emphysema (destruction of alveolar tissue).