Age-related changes in respiratory physiology

This chapter is not relevant to any specific Section from the 2017 CICM Primary Syllabus, because there is no specific entry which directs the candidates to learn extreme geriatric pulmonology, but the college has certainly snuck a section into their "important to note" section in the Learning Objectives, which solemnly warns that "for all sections of the Syllabus an understanding of normal physiology, and physiology at the extremes of age, obesity, pregnancy (including foetal) and disease (particularly critical illness) is expected". So far the extremes of age have been represented mainly by Question 19 from the first paper of 2019, which asked the candidates to "describe the effects of ageing on the respiratory system". Though many age-related changes are associated with the diseases we pick up in the course of our maturing, the college examiners warn us that the mention of any such diseases will earn no marks, and only "normal" age-associated changes are accepted.

The best article to offer as a peer-reviewed reference was Sharma & Goodwin (2006). One really has no need for anything else, but if one for some reason wants another recommendation, one would be well served by Janssens et al (1999) or Sprung et al (2006). All of these are freely available and in many ways superior to the offical textbooks (for one, their bibliography is better). 

In summary:

Age-related Changes in the Respiratory System, 
and their Various Effects

Age-related changes	Effect of these changes
Airway function and structure Increased airway reactivity Decreased ciliary number and activity Diminished airway reflexes	Higher risk of bronchospasm Bronchospasm requires a lesser stimulus Clearance of secretions is impaired Increased propensity towards pharyngeal collapse
Structural properties of the chest wall: Calcification of costal ligaments Thoracic vertebral height loss Kyphosis	Decreased chest wall compliance Higher residual volume (RV) Higher FRC Lower vital capacity (VC) Unchanged total lung capacity (TLC)
Function of respiratory muscles: Decreased total muscle mass Decreased muscle strength Decreased proportion of fast-twitch fibres	Decreased MIP (maximum inspiratory pressure) Decreased FEV1 Decreased maximum minute ventilation Fatigue develops more rapidly Exercise capacity is decreased
Structure of the lungs "Senile emphysema"- hyperinflation Degeneration of elastic fibres Reduction in supporting tissue around small airways	Increased lung compliance Decreased elastic recoil Decreased diaphragmatic excursion Increased dead space ventilation Increased closing volume due to premature small airway closure, increasing the risk of gas trapping
Gas exchange Increased alveolar–capillary membrane thickness	Decline in DLCO
Control of ventilation Decrease in efferent neural output to respiratory muscles	50% reduction in response to hypoxia 40% reduction in response to hypercarbia
Immunological changes Increased immunoglobulin content Decreased alveolar macrophage population	Increased susceptibility to bronchospasm Increased susceptibility to infection Slower recovery from infection

Airway problems

Growing older is treacherous, and your own pharynx conspires to kill you in your sleep by growing lax and complacent. Once proud pharyngeal muscles find themselves less inclined to maintain their tone in old age, and upper airway reflexes are blunted. Malhotra et al (2006) found a significant decrease in the negative pressure reflex in the over-50s. To make matters worse, the soft palate lengthens, and the pharyngeal fat pad increases (which is not something associated with obesity, i.e. you can't diet-and-exercise away your pharyngeal fat pad).

Beyond the upper airway, the trachea and bronchi become more reactive, and more prone to spasm with slighter provocation. Using methacholine as the aforementioned provocation, Hopp et al (1985) found that the dose necessary to drop the FEV₁/FVC by 20% changes significantly (exponentially decreases!) with age. As the age at which this really becomes a problem (70) is well beyond one's normal reproductive timeframe, one might expect that this is bug rather than a feature (i.e. it has no protective effect and is probably due to some sort of degenerative dysregulation of immune function).

Structural properties of the chest wall and diaphragm

Multiple age-related changes occur in the chest wall, all of which can be described as "normal" and age-related even though they might sound suspiciously like something disease-related:

• Increased calcification of costal ligaments
• Decreased range of motion for thoracic rib articulations
• Kyphosis due to gradual loss of vertebral height
• Increased anteroposterior chest diameter
• Decreased elasticity of intercostal muscles
• Flattened curvature of the diaphragm

All of that causes decreased chest wall compliance and increased chest wall resistance. Logically, it makes sense that it should take more effort to stretch open an old calcified ribcage, rather than a supple young ribcage. Mittman et al (1964) captured several elders and demonstrated experimentally that the lung compliance was exxentially halved between the ages of 20 and 70.

Lung volumes in the elderly

The many degenerative processes taking place in old age all conspire to produce the following changes to the lung volumes:

• Higher residual volume (RV)
• Higher FRC
• Lower vital capacity (VC)
• Unchanged total lung capacity (TLC)
• Higher closing capacity

One might summarise these in the form of a graph (this one is from Stocks & Quanjer, 1995):

Decreased elastic fibre content in the lung needs to be emhasised. There is a gradual degradation in the elastin content of the lung parenchyma, which leads to the decrease of lung recoil. That recoil is the force which promotes a decrease in lung volume, and according to Turner et al (1968) it decreases at a rate of around 0.1 cm H₂O every year, starting probably from the age of 50. The outcome of this is an increase in the FRC. 

The increase of closing capacity with age also needs to be emphasised, as it has impact on the propensity of the elderly lung to collapse. Without revisiting the content of the chapter on closing capacity, it will suffice to say that closing capacity increases faster than the FRC (FRC also increases with age), such that the closing capacity exceeds supine FRC at around 44 years of age, and exceeds erect FRC at 66 years.

Function of respiratory muscles

In summary, everything gets weaker and more intolerant of workload.

• Loss of type II fast-twitch muscle fibres leads to decreased contractility, particulalry of the diaphragm. In the 70-year-old, electromyographic activity is reduced by 50%  (Polkey et al, 1997), leading to a decreased maximal transdiaphragmatic pressure. Clinically, this translates to weaker cough and poorer voluntary inspiratory effort. The ICU physiotherapist would be very disappointed.
• Decreased respiratory muscle mass,  which is just a reflection of the globally reduced muscle mass in old age, gives rise to a poorer tolerance of increased respiratory effort. Add this to poorer lung compliance and increased resistance, and one can imagine how the elderly patient will fatigue more easily during periods of respiratory distress.

These are two major elements which conspire with malnutrition and increased work of breathing to make weaning from mechanical ventilation more difficult.

Changes in ventilation and perfusion

The changes in V/Q characteristics which one can  expect in their old age can be summarised by this diagram from Wagner et al (1974), where a relatively young (44 year old) person already demonstrates V/Q mismatch in their MIGET traces:

Thus, in summary, there is:

• Increased shunt, even in healthy lungs, due to lung collapse (from the abovementoned changes in closing capacity)
• Increased V/Q scatter, therefore more venous admixture in arterial blood (mainly because of poorly ventilated basal regions of lung which receive a disporportionately large fraction of the total pulmonary blood flow). 
• Increased alveolar dead space, and therefore lower efficiency of ventilation. Tenney & Millar (1956) found that in the elderly, physiological dead space was about 235ml, whereas it was only around 150ml for young controls. In other words, the young people just had some normal anatomical dead space, and the elderly also had some added alveolar dead space.

Age-related changes in gas diffusion 

In short, everything is the fault of a smaller surface area. The gas exchange membrane, presumably, remains as thin as ever, but there's just less of it. In summary, with age there is:

• Decreased gas exchange surface area: Air spaces enlarge homogeneously over the course of a lifetime. As a result, the total gas exchange surface area decreases from 75 m² at age 30 to 60 m² at age 70 (Sprung et al, 2006).
• Decreased DLCO (diffusing capacity for carbon monoxide): Stam et al (1994) determined that this decline was faster in men, and was essentially linear in its relationship with the decreasing gas exchange surface area. Where young adult males had a DLCO in the range of 200-250 s^-1kPa^-1, men in their 70s had values closer to 150-200 s^-1kPa^-1