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at all, but of muscular strength.

      The effects of disease on maximum flow rate

      In asthma (see Chapter 10), airway narrowing occurs, leading to a greater resistance between point A (the alveolus) and point B. The pressure drop, A to B, for any given flow rate will therefore be greater than in the healthy lung, and the critical (maximal) flow rate (when the pressure difference between A and B is just enough to overcome the retractile force of the lung) will be lower. You may have known for some time that peak expiratory flow is reduced in asthma, but now you understand why.

      In COPD (see Chapter 11), the loss of alveolar walls (emphysema) reduces the elastic recoil of the lung. There is therefore less protective retractile force on the airway wall and the critical pressure drop along the airway required to cause airway collapse will occur at a lower flow rate. Thus, maximum expiratory flow is also reduced in COPD.

      Airway resistance and lung volume

      It can easily be seen in the model that, as lung volume decreases, lung elastic recoil (tension within the springs) diminishes, providing less and less support for the floppy airway. It is clear, therefore, that the maximum flow rate achievable is dependent on lung volume and is reduced as lung volume is reduced. For any given lung volume, there will be a maximum expiratory flow that cannot be exceeded, no matter what the effort. You can confirm this by inspecting the shape of a flow loop, which is effectively a graph of the maximal flow rate achievable at each lung volume (see Chapter 3). A true PEFR can only be achieved by beginning forced expiration from a position of full inspiration. I would suggest you’ve been aware of this fact for longer than you realise. Immediately prior to blowing out the candles on your second birthday cake, you probably took a big breath in. At the age of 2, you had an intuitive understanding of the volume dependence of maximal expiratory flow rate.

      Lung volume and site of maximal airway resistance

      As we have already discussed, the greater part of airway resistance resides in the central airways. These airways are well supported by cartilage and so generally maintain their calibre even at low lung volumes. The calibre of the small airways, without cartilaginous support, is heavily dependent on lung volume. At lower lung volumes, their calibre is reduced, and resistance is increased. During expiration, therefore, as lung volume declines, the site of principal resistance moves from the large central airways to the small peripheral airways. The PEFR (see Chapter 3) tests expiratory flow at high lung volume and is therefore determined largely by the central airways. The forced expiratory volume in 1 second (FEV₁; see Chapter 3) is also heavily influenced by the central airway, though not as much as PEFR. Specialised lung function tests that measure expiratory flow at lower lung volumes (e.g. FEF _25‐75 and ; see Chapter 3) therefore provide more information about the smaller airways.

      Gas exchange

      The lung is ventilated by air and perfused by blood. For gas exchange, to occur these two elements must come into intimate contact.

       Where does the air go?

      An inspired breath brings air into the lung. That air does not distribute itself evenly, however. Some parts of the lung are more compliant than others, and are therefore more accommodating. This variability in compliance occurs on a gross scale across the lungs (upper zones verses lower zones) and also on a very small scale in a more random pattern. At the gross level, the lungs can be imagined as ‘hanging’ inside the thorax and resting on the diaphragm; the effect of gravity means that the upper parts of the lungs are under considerable stretch, whilst the bases sit relatively compressed on the diaphragm. During inspiration (as the diaphragm descends) the upper parts of the lung, which were already stretched, cannot expand much more to accommodate the incoming air; the bases, on the other hand, are ripe for inflation. Therefore, far more of each inspired breath ends up in the lower zones than the upper zones.

      On a small scale, adjacent lobules or even alveoli may not have the same compliance. Airway anatomy is not precisely uniform either, and airway resistance between individual lung units will vary. It can therefore be seen that ventilation will vary in an apparently random fashion on a small scale throughout the lung. This phenomenon may be rather modest in health, but is likely to be exaggerated in many lung diseases in which airway resistance or lung compliance is affected.

       Where does the blood go?

The pulmonary circulation operates under much lower pressure than the systemic circulation. At rest, the driving pressure is only on the order of 15 mmHg. In the upright posture, therefore, there is barely enough pressure to fill the upper parts of the system and the apices of the lung receive very little perfusion at all from the pulmonary circulation. The relative over perfusion of the bases mirrors the pattern seen with ventilation (which is fortunate, if our aim is to bring blood and air into contact), but the disparity is even greater in the case of perfusion. Thus, at the bases of the lungs, perfusion exceeds ventilation, while, at the apices, ventilation exceeds perfusion.

      The distribution of perfusion is also heavily influenced by another factor: hypoxia. By a mechanism we do not fully understand, low oxygen levels in a region of the lung have a direct vasoconstrictor effect on the pulmonary artery supplying that region. This has the beneficial effect of diverting blood away from the areas of lung that are poorly ventilated towards the well‐ventilated areas. This ‘automatic’ ventilation/perfusion (V/Q) matching system aims to maximise the contact between air and blood and is critically important to gas exchange.

       Relationship between the partial pressures of O2 and CO2

      During steady‐state conditions, the relationship between the amount of carbon dioxide produced by the body and the amount of oxygen absorbed depends upon the metabolic activity of the body. This is referred to as the ‘respiratory quotient’ (RQ).

      The actual value varies from 0.7 during pure fat metabolism to 1.0 during pure carbohydrate metabolism. The RQ is usually about 0.8, and it is assumed to be such for everyday clinical calculations.

       Carbon dioxide

      If carbon dioxide is being produced by the body at a constant rate then the partial pressure of CO₂ (PCO₂) of alveolar air (written P_ACO₂) depends only upon the amount of outside air with which the carbon dioxide is mixed in the alveoli; that is, it depends only upon alveolar ventilation. If alveolar ventilation increases, P_ACO₂ will fall; if alveolar ventilation decreases, P_ACO₂ will rise. P_ACO₂ (as well as arterial PCO₂, written P_aCO₂) is a sensitive index of alveolar ventilation.

       Oxygen

      The partial pressure of alveolar O₂ (P_AO₂) also varies with alveolar ventilation. If alveolar ventilation increases greatly then P_AO₂ will rise and begin to approach the PO₂

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