This chapter is most relevant to Section F3(viii) from the 2017 CICM Primary Syllabus, which expects the exam candidates to "explain the relationship between resistance and respiratory gas flow". This topic has appeared multiple times in the Part One written papers, always as some variation on the theme of "which factors affect airway resistance".
- Question 6 from the second paper of 2016
- Question 23 from the second paper of 2013
- Question 6(p.2) from the first paper of 2009
Specifically, airway resistance is always asked for, with the implication that no marks would be awarded to any discussion of factors such as tissue resistance and respiratory inertance. In that spirit, this chapter mainly focuses on physiological and pathological factors which affect airway resistance.
Factors which affect airway resistance
- Gas properties which affect the type of flow
- Gas density (increased density leads to increased turbulence and hence increased resistance)
- Gas viscosity (increased viscosity promotes laminar flow and hence decreases resistance)
- Factors which affect airway diameter
- Lung volume (resistance decreases with higher volume)
- Physiological variation in airway diameter
- Pathological conditions which
- Factors which affect flow rate
- Respiratory rate (increased respiratory rate produces an increase in the flow rate for each breath)
- Inspiratory and expiratory work (eg. voluntary forced expiration for spirometry)
- Inspiratory flow pattern generated by a mechanical ventilator
Other factors which affect respiratory resistance as a whole:
- Resistance from deformation of the tissues (important at all flow rates)
- Tissue resistance from lung parenchyma (~70%)
- Tissue resistance from chest wall (~30% )
- Inertance of air and thoracic tissues (important at high respiratory rates)
- Compression of intrathoracic gas (important mainly with high respiratory pressures)
In terms of published material, Nunn's usually has a section in every edition which is typically titled "Factors affecting respiratory resistance" (p. 37 of the 8th ed). Beyond this resource, and other textbook chapters of its kind, there is nothing collected in a bundle - it appears that one must scour the physiology literature of the 1960s to find satisfactory references for this topic. A reader is left with the distinct desire to publish their own review.
Relationship of lung volume and airway resistance
As the lung expands, the airways also expand, as the elastic tissue of the parenchyma stretches them open. Resistance decreases on a hyperbolic curve, as airway diameter is an important factor in the resistance to both turbulent and laminar flow. Moreover, bronchi are stretched by lung expansion, and this increase in length promotes the development of laminar flow (the so-called "entrance length").
Any viva-like discussion of this seems to lead to the need to sketch a graph, which classically takes this shape:
It is probably not essential to reproduce the precise dimensions of this diagram; or at least that seems to be the attitude of most publishers. Truly, its value is in the shape of the lines rather than accuracy of contained data. The most important matters to communicate are that airway resistance decreases exponentially, and airway conductance increases linearly. Obviously, specific airway conductance is always going to be a flat straight line on these graphs, as it is conductance divided by thoracic gas volume.
The earliest examples of this graphical representation probably come from such classical papers as Briscoe & Dubois (1958). The investigators selected a series of normal subjects ("laboratory workers, or the relations of laboratory workers, except for a circus dwarf") and subjected them to body plethysmography, plotting their airway resistance and conductance along an x-axis with lung volume:
This relationship obviously breaks down in certain pathological scenarios. For example, Nakagawa et al (2015) were able to demonstrate that among COPD patients with tachypnoea, the effect of increasing lung volume (by dynamic hyperinflation) actually led to increased airway resistance. There was no anchoring of the airways to expanded lung tissue (because the connective tissue of the lungs had been destroyed by emphysema), and there was compression of the smaller airways by the surrounding hyperinflated lung parenchyma (where gas trapping had occurred).
Factors which affect airway resistance by affecting flow rate
So as not to recapitulate the contents of the respiratory resistance chapter, it will suffice to say that:
- Airway resistance is constant where flow is laminar
- Airway resistance increases exponentially with increasing flow where flow is turbulent
- Under most normal conditions the airflow in human airways is mainly laminar because the flow rates ar relatively low
- With increasing flow, flow in the airways may transition from laminar to turbulent flow
The effects of increasing flow rate on airway resistance at different points in the airway was computed by Pedley et al (1970). If one wanted to, one could also plot the (almost linear) relationship of flow and resistance next to the authors' original data.
In some dark timeline it may become necessary to extend this even further for an SAQ answer, for example if one were asked for some examples of the specific scenarios in which flow may be a serious influence on airway resistance. These would probably fall into three groups:
- Factors which change the respiratory rate: increased respiratory rate produces an increase in the flow rate for each breath, provided tidal volumes remain the same. Respiratory resistance increases as a consequence.
- Factors which change the pleural-atmospheric pressure gradient: which sounds fancy and scientific, but in reality means "inhaling or exhaling harder and with more force". Into this category, one might fit all those unnatural spirometry manoeuvres where one instructs a patient to blow as hard and as fast as they can into the measurement device.
- Scenarios where inspiratory flow is artificially increased. A good exaple of this is the inspiratory flow pattern generated by a mechanical ventilator. For instance, the decelerating ramp flow waveform used to generate a "square" pressure contour in a pressure control mode starts with quite a high flow.
Factors which affect airway resistance by affecting airway diameter
These are obviously numerous. Nunn's goes into overmuch detail regarding the sympathetic control of the airway smooth muscle, which has importance for bronchodilator therapy. There are of course numerous other factors. In answering a question like "which factors affect airway diameter", the trainee's bigger problem will not be coming up with factors but classifying them in a way which appears measured and thoughtful.
- Effects of bronchial smooth muscle tone:
- Increased smooth muscle tone
- Irritants, eg. histamine
- Parasympathetic nervous system agonists
- Decreased smooth muscle tone
- Sympathetic nervous system agonists
- Increased smooth muscle tone
- Decreased internal crossection
- Mucosal or smooth muscle hypertrophy
- Encrusted secretions
- Mechanical obstruction or compression
- Extrinsic, eg. by tumour
- Dynamic compression, eg. due to gas trapping or forceful expiratory effort
- Artificial airways and their complications, eg. endotracheal tube becoming kinked
Special considerations in infancy
"The differences in infants earned extra marks", remarked the examiners in their comment Question 6(p.2) from the first paper of 2009. Which differences did they mean? Well. Basically, it's higher. Airway resistance decreases markedly with growth from infancy to adulthood. Marciniak (2019) lists a resistance of 19 to 28 cm H2O/L per second in neonates, whereas the figure is closer to 2 cm H2O/L per second in adults.