This chapter is most relevant to Section F4(ii) from the 2017 CICM Primary Syllabus, which expects the exam candidates to be able to "state the normal values of lung volumes and capacities". Specifically, the focus here will be on the Functional residual capacity (FRC)  because a) it is important physiologically, and b) because the college examiners seem to love asking questions about it. Of the seven or so historical CICM Part One questions on lung volumes, four SAQs discussed the FRC and its measurement. These were:

• Question 2 from the second paper of 2020
• Question 24 from the second paper of 2017
• Question 4  from the second paper of 2015
• Question 8 from the first paper of 2017
• Question 15 from the second paper of 2010

Therefore, the exam-wise candidate will have a detailed knowledge of the FRC, and to hell with ERV IC and TLC. This is a sensible approach because no other lung volume has such far-reaching influence.

In summary:

For this sort of topic, one would be best served by a resource which does away with pointless frills and addresses the main point quickly and ideally in some sort of memorable pointform fashion. Hopkins & Sharma (2019) fits some of this description. There is little else out there; nobody has ever published an ode to the FRC for us to refer to. Multiple sources had to be scraped together and remixed to fashion this chapter.

Definition of the FRC

The FRC is composed of ERV and RV, and represents the volume of gas left behind in the chest at the end of expiration during some sort of normal tidal breath. In an anaesthetised patient, one might say that this is the volume of intrathoracic gas measured when the apnoeic patient is disconnected from the ventilator and the alveolar pressure equilibrates with atmospheric pressure. 

This volume represents the point at which elastic recoil of the lung (always tending to collapse) is in equilibrium with the elastic recoil of the chest (always tending to expand). This is explored well enough in the chapter on lung compliance, and here it will suffice to say that at FRC the positive pressure of the collapsing lung (5 cm H₂O) is balanced with the negative pressure of the chest wall (-5 cm H₂O) and so the net pressure is zero. 

Physiological importance: functions of the FRC

There's a reason this volume was not called called PRC (pointless residual capacity). These specific functions were called upon in Question 2 from the second paper of 2020, for 70% of the marks (i.e. these were the bulk of the question). In short, this gas volume is very important physiologically:

• It keeps small airways open. At FRC, the small airways are kept splinted open by the tension of the surrounding lung tissue. If the FRC is reduced below the closing capacity, there will be gas trapping and atelectasis. 
• It is representative of compliance. Any decrease in lung compliance (i.e. due to decreased chest wall compliance or due to decreased lung tissue compliance) causes a decrease in FRC (this is developed in greater detail in the chapter on the work of breathing and its components)
• It represents optimal compliance. At FRC, the pressure-volume curve which represents compliance is at its steepest, which means the work of breathing required to inflate the lung from FRC is at its minimum. In other words, ventilating tidal volumes which start and end at FRC is the most energy-efficient form of breathing
• It keeps a gas reserve between breaths. Breathing is an intermittent phenomenon, during two-thirds of which there is no fresh gas entering the chest. If there was no FRC (i.e. hypothetically if the lung collapsed completely during expiration) there would be no gas exchange and the pulmonary circulation would return deoxygenated blood to the left atrium for the majority of the respiratory cycle. This, clearly, is unsatisfactory from the standpoint of ongoing survival. Because some residual gas remains in the lung, gas exchange can carry on during the entire respiratory cycle. The most important implication of this, of course, is during induction of anaesthesia, where one's peri-intubation fiddling time is entirely dependent on the oxygen stores in the FRC.
• It keeps pulmonary vascular resistance at a minimum.   The alveolar and extra-alveolar vessels change their resistance characteristics as lung volume changes.  It makes sense: at small lung volumes everything is compressed, some of the lung is collapsed and so pulmonary vascular resistance is high because pulmonary arteries are narrowed. As the lung inflates to FRC, arteries can increase in diameter and the resistance decreases.  As the lung inflates further, expanding alveoli compress small interalveolar vessels and increase pulmonary vascular resistance again. Ergo, FRC is where pulmonary vascular resistance is at its lowest, representing the bottom of the U-shaped PVR-volume curve first described by Simmons et al in 1961.
• Relationship between FRC and closing capacity influences the development of atelectasis and shunt, as discussed elsewhere.

Factors which influence the FRC

The normal FRC volume is said to be approximately 30-35ml/kg, or 2100-2400 ml in an average sized person. It varies considerably depending on body size, and obviously changes according to changes in the mechanical properties of the respiratory system. In the event one is ever asked to describe the factors which influence the FRC, these numerous factors could be summarised in a tabulated format:

Consequences of a decreased FRC

Question 8 from the first paper of 2017 and Question 15 from the second paper of 2010 both asked about what might happen if the FRC decreases by 1000ml. Being able to answer such a question relies on the trainee's ability to know what the FRC does, and extrapolating what might happen if it stops doing that.

Effects of decreased FRC on lung mechanics

• Decreased lung compliance: the decreasing size of alveoli at lower FRCs results in a decreased rate of 
• Increased airway resistance: because airway resistance is relatively low at FRC, it is going to increase as the FRC decreases. This is due to the fact that collapsing alveoli tend to stop providing the radial traction which keeps the small airways open.
• Increased work of breathing, owing to the above.
• Decreased tidal volume and increased respiratory rate, due to decreased lung compliance 
• Decreased tolerance of position changes, i.e. with a low baseline FRc in the upriht position a patient will not tolerate being supine for very long, as the FRC will drop yet further 

Effect of decreased FRC on gas exchange

• Decreased oxygen reserves: because the FRC acts as the main oxygen reservoir, the loss of volume here will give rise to an increased fluctuation in the bloodstream oxygen contentbetween breaths, and during episodes of apnoea.
• Increased atelectasis: Decreasing the FRC to below the closing capacity tends to produce resorption atelectasis, as small airways close in expiration.
• Increased shunt:  The consequence of abovementioned atelectasis will be shunt, i.e regions of lung which do not participate in gas exchange because they are not ventilated.

Effects of decreased FRC on the pulmonary circulation

• Increased pulmonary vascular resistance, partly due to the effect of narrowed alveoli on perialveolar vessel caliber and partly owing to the inevitable increase in collapsed hypoxic lung regions which promote hypoxic pulmonary vasoconstriction.
• Increased right ventricular afterload, which is due to the increase in pulmonary pressure