Abstract
A lung volume is measured directly, by a spirometer (Figure 12.1) or by a gas dilution technique (see p. ). A lung capacity is the sum of two or more lung volumes; it is therefore a derived value. There are four lung volumes and four lung capacities (values given are typical for a 70‑kg man when standing)
What is the difference between a lung volume and a lung capacity?
A lung volume is measured directly, by a spirometer (Figure 12.1) or by a gas dilution technique (see p. 52). A lung capacity is the sum of two or more lung volumes; it is therefore a derived value. There are four lung volumes and four lung capacities (values given are typical for a 70‑kg man when standing):
Four volumes:
– Tidal volume VT = 500 mL. VT is the volume of air inspired per breath during normal, quiet breathing.
– Inspiratory reserve volume IRV = 2500 mL. IRV is the volume of additional air that can be inspired over and above VT.
– Expiratory reserve volume ERV = 1500 mL. ERV is the volume of additional air that can be expired following normal tidal exhalation.
– Residual volume = 1500 mL. Residual volume is the volume of air that remains in the lungs following maximum expiration.
Four capacities:
– Functional residual capacity FRC = residual volume + ERV = 3000 mL.
– Vital capacity VC = ERV + VT + IRV = 4500 mL.
– Inspiratory capacity IC = VT + IRV = 3000 mL.
– Total lung capacity TLC = residual volume + ERV + VT + IRV = 6000 mL.
Figure 12.1 Spirometry trace with lung volumes and capacities.
Normal VT is typically around 500 mL for a 70‑kg adult, or 7 mL/kg. In mechanically ventilated patients, ventilator-associated lung injury can occur as a result of:
Volutrauma – diffuse alveolar damage caused by overdistension of the lung. Traditionally, tidal volumes of 12 mL/kg were delivered to mechanically ventilated patients. This high-volume ventilation strategy is now thought to cause volutrauma and lung damage. Most intensive care units have adopted a low-VT ventilation strategy (6 mL/kg), as it has been shown to reduce mortality in patients with acute respiratory distress syndrome (ARDS).
Barotrauma – damage to the lung as a result of high airway pressure. Strategies to prevent barotrauma include maintenance of peak airway pressure Ppeak below 35 cmH2O or plateau airway pressure Pplat below 30 cmH2O.
If a patient has particularly poor lung compliance (e.g. in ARDS), ventilation using lung-protective parameters (VT = 6 mL/kg and Pplat ≤ 30 cmH2O) may not achieve sufficient V̇A to maintain normocapnoea. In this situation, it is preferable to practice ‘permissive hypercapnoea’ rather than increase VT or inspiratory pressure, which may risk volutrauma or barotrauma, resulting in further lung damage. This is referred to as a lung-protective ventilation strategy.
What is the importance of the FRC?
FRC is the starting point of tidal breathing. At end-expiration, the inspiratory and expiratory muscles are relaxed – the inward elastic force of the lung parenchyma is exactly equal and opposite to the force with which the chest wall springs outwards (see Chapter 7, Figure 7.3).
FRC is physiologically important for three reasons:
O2 buffer. The air within the FRC acts as an O2 buffer during normal breathing. O2 continuously diffuses from the alveoli to the pulmonary capillaries. If FRC did not exist, there would be fewer aerated alveoli and therefore less O2 in the lungs – alveolar partial pressure of O2 (PAO2) would decrease during expiration. Pulmonary capillary blood would be intermittently oxygenated, only being fully oxygenated during inspiration.
Prevention of alveolar collapse. If FRC did not exist (i.e. expiration to residual volume), alveoli would collapse. Atelectasis would result in V̇/Q̇ mismatch and hypoxaemia. Re-expansion of atelectatic alveoli with every tidal breath would significantly increase the work of breathing.
Optimal lung compliance. Conveniently, lung compliance is at its highest at FRC. Pulmonary vascular resistance is also at its lowest (see Chapter 23).
FRC is of crucial importance to anaesthetists:
Apnoea. FRC not only buffers swings in PAO2 during tidal breathing, but also crucially acts as an O2 reservoir at times of apnoea, such as at induction of general anaesthesia.
Small airway closure. If FRC falls below a certain volume (the closing capacity, CC), small airways close, resulting in V̇/Q̇ mismatch and hypoxaemia.
Which factors affect FRC?
FRC is not fixed; its volume is affected by surgical, anaesthetic and patient factors:
FRC is reduced by:
– Position. FRC falls by 1000 mL just by the patient lying supine.
– Raised intra-abdominal pressure; for example, obesity, pregnancy, acute abdomen, laparoscopic surgery.
– Anaesthesia, irrespective of whether ventilation is spontaneous or controlled. The cause is not known, but is thought to be related to decreased thoracic cage muscle tone and loss of physiological positive end-expiratory pressure (PEEP).
– Younger age; that is, neonates, infants and young children.
– Lung disease; for example, pulmonary fibrosis, pulmonary oedema, atelectasis, ARDS.
FRC is increased by:
– PEEP, which is commonly used to maintain FRC intraoperatively, especially in paediatric anaesthesia and following intubation (where physiological PEEP has been lost – see Chapter 7).
– Emphysema. Lung elastic tissue is destroyed, resulting in reduced inward elastic recoil. The balance between the forces of inward elastic recoil and outward springing of the thoracic cage is found at a higher volume, resulting in patients having a ‘barrel chest’.
– Increasing age. The elderly have a reduced quantity of lung elastic tissue: FRC increases in a similar manner to emphysema.
– Asthma, caused by air trapping and high intrinsic PEEP.
