Respiratory Medicine. Stephen J. Bourke

      Lung perfusion

The lungs receive a blood supply from both the pulmonary circulation and the systemic circulation, via bronchial arteries. The purpose of the pulmonary circulation is to take the entire circulating volume of (deoxygenated) blood through the lungs in order to pick up oxygen and offload carbon dioxide. The bronchial arteries carry oxygenated blood from the systemic circulation to supply the tissues of the lung.

Figure 1.1 Diagram of bronchopulmonary segments. LING, lingula; LL, lower lobe; ML, middle lobe; UL, upper lobe.

Figure 1.2 Surface anatomy. (a) Anterior view of the lungs. (b) Lateral view of the right side of the chest at resting end‐expiratory position. LLL, left lower lobe; LUL, left upper lobe; RLL, right lower lobe; RML, right middle lobe; RUL, right upper lobe.

      The pulmonary artery arises from the right ventricle and divides into left and right pulmonary arteries, which further divide into branches accompanying the bronchial tree. The pulmonary capillary network in the alveolar walls is very dense and provides a very large surface area for gas exchange. The pulmonary venules drain laterally to the periphery of lung lobules and then pass centrally into the interlobular and intersegmental septa, ultimately joining together to form the four main pulmonary veins, which empty into the left atrium.

Several small bronchial arteries usually arise from the descending aorta and travel in the outer layers of the bronchi and bronchioles, supplying the tissues of the airways down to the level of the respiratory bronchiole. Most of the blood drains into radicles of the pulmonary vein, contributing a small amount of desaturated blood, which accounts for part of the ‘physiological shunt’ (blood passing through the lungs without being oxygenated) observed in normal individuals. The bronchial arteries may undergo hypertrophy when there is chronic pulmonary inflammation, and major haemoptysis in diseases such as bronchiectasis or aspergilloma usually arises from the bronchial rather than the pulmonary arteries and may be treated by therapeutic bronchial artery embolisation. The pulmonary circulation normally offers a much lower resistance and operates at a lower perfusion pressure than the systemic circulation. The pulmonary capillaries may be compressed as they pass through the alveolar walls if alveolar pressure rises above capillary pressure.

Figure 1.3 Structure of the alveolar wall as revealed by electron microscopy. la, type I pneumocyte; lb, flattened extension of type I pneumocyte covering most of the internal surface of the alveolus; II, type II pneumocyte with lamellar inclusion bodies, which are probably the site of surfactant formation; IS, interstitial space; RBC, red blood corpuscle. Pneumocytes and endothelial cells rest upon thin continuous basement membranes, which are not shown.

Physiology

      The core business of the lungs is to bring oxygen into the body and to take carbon dioxide out. The deceptively simple act of ‘breathing’ comprises two quite distinct processes.

      1 Ventilation. The movement of air in and out of the lungs (between the outside world and the alveoli).

      2 Gas exchange. The exchange of oxygen and carbon dioxide between the airspace of the alveoli and the blood.

      Ventilation continues throughout life, largely unconsciously, coordinated by a centre in the brain stem. The factors that regulate the process, ‘the control of breathing’, will also be considered here. Gas exchange happens automatically (by diffusion) if blood and inspired air are brought into close proximity.

      Ventilation

      To understand this process, we need to consider the muscles that ‘drive the pump’ and the resistive forces they have to overcome. These forces include the inherent elastic property of the lungs and the resistance to airflow through the bronchi (airway resistance).

       The muscles that drive the pump

Inspiration requires muscular work. The diaphragm is the principal muscle of inspiration. At the end of an expiration, the diaphragm sits in a high, domed position in the thorax (Fig. 1.4). To inspire, the strong muscular sheet contracts, stiffens and tends to push the abdominal contents down. There is variable resistance to this downward pressure by the abdomen, which means that in order to accommodate the new shape of the diaphragm, the lower ribs (to which it is attached) also move upwards and outwards. (When airway resistance is present, as in asthma or chronic obstructive pulmonary disease [COPD], the situation is very different; see Chapters 2 & 11.) The degree of resistance the abdomen presents can be voluntarily increased by contracting the abdominal muscles; inspiration then leads to a visible expansion of the thorax, rather than a distension of the abdomen (try it). The resistance may also be increased by abdominal obesity. In such circumstances, there is an involuntary limitation to the downward excursion of the diaphragm and, as the potential for upward movement of the ribs is limited, the capacity for full inspiration is diminished. This inability to fully inflate the lungs is an example of a restrictive ventilatory defect (see Chapter 3).

Figure 1.4 Effect of diaphragmatic contraction. Diagram of the ribcage, abdominal cavity and diaphragm showing the position at the end of resting expiration (a). As the diaphragm contracts, it pushes the abdominal contents down (the abdominal wall moves outwards) and reduces pressure within the thorax, which ‘sucks’ air in through the mouth (inspiration). (b) As the diaphragm shortens and descends, it also stiffens. The diaphragm meets a variable degree of resistance to downward discursion, which forces the lower ribs to move up and outward to accommodate its new position.

      Other muscles are also involved in inspiration. The scalene muscles elevate the upper ribs and sternum. These were once considered, along with the sternocleidomastoids, to be ‘accessory muscles of respiration’, only brought into play during the exaggerated ventilatory effort of acute respiratory distress. Electromyographic studies, however, have demonstrated that these muscles are active even in quiet breathing, although less obviously so.

      The intercostal muscles bind the ribs to ensure the integrity of the chest wall. They therefore transfer the effects of actions on the upper or lower ribs to the whole ribcage. They also brace the chest wall, resisting the bulging or in‐drawing effect of changes in pleural pressure during breathing. This bracing effect can be overcome to some extent by the exaggerated pressure changes seen during periods of more extreme respiratory effort, and in slim individuals intercostal recession may be observed as a sign of respiratory distress.

      Whilst inspiration is the result of active muscular effort, quiet expiration is a more passive process. The inspiratory muscles steadily release their contraction and the elastic recoil of the lungs brings the tidal breathing