The respiratory system maintains normal levels of oxygen, carbon dioxide, and pH in the blood. Air enters the nose and travels through branching airways until reaching the alveoli in the lungs where gas exchange occurs. The lungs are kept inflated by the negative pressure between the visceral and parietal pleura, and contraction of the diaphragm and intercostal muscles during inhalation increases the thoracic cavity volume. Exhalation is a passive process as elastic forces cause lung deflation when the muscles relax.

1. R E S P I R A T O R Y S Y S T E M

2. RESPIRATORY SYSTEM The main homeostatic responsibility of the respiratory system is maintenance of normal levels of O 2 , CO 2 and pH within the systemic arterial blood. This blood is then distributed to actively metabolizing tissues by the circulation.

3. RELEVANT STRUCTURES Air enters the nose and is drawn through the nasopharynx into the lanynx. It passes through the glottis before entering the trachea, which divides into the right and left main bronchi going to the two lungs. The airways continue to branch, decreasing in diameter. Bronchi, which have cartilage in their walls, lead into bronchioles. The airways finally terminate in grape-like collections of alveoli, the main site of gas exchange.

4. BRONCHI AND ALVEOLI Bronchi and bronchioles contain smooth muscle and the airways are lined by mucus-secreting cells within a ciliated epithelium ( protective functions ) . The alveoli have a thin epithelial wall and are covered on their inner surface by a narrow layer of alveolar fluid. Pulmonary connective tissue contains a large amount of elastic tissue, which is stretched beyond its passive resting length.

5. BRONCHI AND ALVEOLI BRONCHI ALVEOLI

6. FUNCTIONS OF THE AIRWAYS 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.

7. FUNCTIONS OF THE AIRWAYS 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.

8. 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).

9. PLEURA 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.

10. FORCES ACTING ON THE LUNG 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.

11. CLINICAL NOTE: PNEUMOTHORAX The term pneumothorax indicates the presence of gas in the intrapleural space. This gas may either have escaped from ruptured alveoli or entered from the atmosphere following traumatic damage to the chest wall. In each case the negative intrapleural pressure which normally keeps the lungs inflated is lost and the lung collapses.

12. SURFACTANT AND ALVEOLAR STABILITY 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.

14. EXHALATION - INHALATION The outer surface of the lung is forced to follow the movements of the diaphragm and chest wall so that lung volume increases and decreases as thoracic volume changes.

15. MUSCLES OF RESPIRATION 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.

16. EXHALATION - INHALATION

17. WORK OF BREATHING Three elements contribute to work of breathing : 1) Compliance work is necessary to expand the lungs against elastic and surface tension forces. 2) Airways resistance to airflow has to be overcome. This is usually very low but may be markedly increased in certain pulmonary diseases. 3) Tissue resistance results from frictional forces, which oppose the movement of one layer of pulmonary and pleural tissue past another during chest expansion. Under normal conditions, the relative magnitudes of these components are: Compliance work -> Airways resistance -> Tissue resistance.

18. LUNG VOLUMES 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.

20. VENTILATORY VOLUMES The gas movement during ventilation can be recorded using a device called a spirometer.This measures functionally important changes in lung volume. 1) Tidal volume (TV) is the amplitude of the oscillation in lung volume during quiet respiration. It is usually about 400-500 ml. 2) Inspiratory reserve volume (IRV) is the maximum volume of air, which can be inspired in excess of normal inspiration ( 3.6 L). It is about 30% lower in females than males. 3) Expiratory reserve volume (ERV) is the maximum volume of air, which can be expired in excess of normal expiration (1.2 L).

22. RESIDUAL VOLUME (RV) 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). Residual volume = functional residual capacity (FRC) - expiratory reserve volume (ERV) This gives a value in the region of 1-2 L, but this tends to increase, with age.

23. LUNG CAPACITIES 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). 4. INSPIRATORY CAPACITY equals tidal volume plus inspiratory reserve volume (4.0 L).

25. VENTILATION RATES AND MINUTE VOLUMES The respiratory minute volume is the amount of new air being brought into the lungs each minute and can be calculated from the respiratory rate (about 12-15/min) and the tidal volume (450 ml). Respiratory minute volume - 5.85 L/min.

26. DEAD SPACE 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. Normally the dead space is about 150 ml .

27. ALVEOLAR VENTILATION RATE The purpose of ventilation is to regulate alveolar gas concentrations. The rate at which the gas in the alveoli is renewed is determined by the alveolar ventilation rate where: Alveolar ventilation rate = (Tidal volume - Dead space) x Respiratory rate = (450 -150) x 13 = 3.9 L / min

29. 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).

31. PEAK EXPIRATORY FLOW RATE (PEFR) 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.

32. CLINICAL NOTE: OBSTRUCTIVE PULMONARY 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).

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