What is closing capacity?
  • Closing capacity is the maximal lung volume at which airway closure can be detected in the dependent parts of the lungs
  • It can also be defined as the volume at which transition from Phase III to Phase IV occurs during an inert gas washout measurement. 

The closing capacity is a capacity of the lungs, which by convention means that it is a composite space, created by the combination of residual volume and closing volume. The latter is the volume of gas which represents the difference between closing capacity and residual volume. The best way to represent this is probably by a diagram:

What are the components which make up closing capacity?
  • Closing capacity is composed of residual volume (RV) and closing volume. 
Why does airway closure occur? What is the physiological basis of closing capacity?
  • The peripheral small airways (terminal bronchioles and alveolar ducts) constantly tend to collapse, partly due to the Law of Laplace and partly because they are largely devoid of rigidity-enhancing cartilage.
  • During normal respiration, these airways are kept splinted open by the stretch of alveolar septal elastic tissue
  • Thus, as the lung volume decreases, so the airway diameter decreases
  • Therefore there is a lung volume at which the stretch can no longer oppose the forces acting to collapse the airway, and the airway closes, trapping some of the gas.
  • Because of the effects of gravity on the lung, the airways in the dependent regions of lung are the smallest, and therefore the most prone to collapse.  
What factors alter closing capacity?
  • Expiratory air flow: (higher flow = higher CC)
  • Expiratory effort (more effort = higher CC)
  • Small airways disease, eg. asthma or COPD
  • Increased pulmonary blood volume, eg in CCF
  • Decreased pulmonary surfactant
  • Parenchymal lung disease, eg. emphysema
  • Age (increasing age = increased closing capacity)
What is the clinical significance of closing capacity?
  • Higher CC decreases the effect of pre-anaesthetic preoxygenation
  • Higher CC increases dependent atelectasis
  • It is responsible for the age-related decrease in  oxygenation, because of shunt
  • It aggravates lung injury through cyclic atelectasis 
What is the effect of age on closing capacity? What specific ages are important for closing capacity?
  • At age 44, supine FRC is lower than closing capacity
  • At age 66, erect FRC is lower than closing capacity
What are the methods of measuring closing capacity?
  • Gas bolus measurement, where a subject inhales a small bolus of tracer gas, starting at RV
  • Resident gas method, where a subject inhales a TLC of oxygen, starting from RV
  • Both methods produce a graph of gas concentration over volume, which has four distinct phases.
Explain the gas bolus method of measuring closing capacity
  • The subject exhales maximally, i.e. they are at their residual volume
  • The subject then starts inhaling slowly up to TLC (over 5-10 seconds)
  • As they start doing this, you quickly give them a small bolus of tracer gas (Dollfuss et al only needed about 2-4ml of radioactive xenon, or about 37 megabequerels, deliver over less than 1 second)
  • Because at RV the small distal airways in the dependent lung regions are closed, the upper alveoli get all the tracer gas.
  • After filling their lungs, the subject then exhales slowly, back down to RV.
  • As the subject exhales, the tracer gas concentration comes out in four distinct phases:
    • First, dead space gas comes out, which has no tracer gas in it (Phase I)
    • Next, tracer gas concentration increases as alveolar gas comes out (Phase II)
    • Then, a plateau of tracer concentration is reached, as the tracer content of these "middle" alveoli will be relatively even (Phase III)
    • Finally, as closing capacity is reached, the dependent (tracerless) alveoli close, and only the open tracer-rich alveoli continue with the exhalation. As this happens, the tracer concentration being exhaled is no longer diluted by the air of these dependent alveoli. The effect of this is an increase in the measured tracer concentration. This is conventionally referred to as Phase IV.

measurement of closing capacity by xenon bolus from Dollfuss et al (1967)

Explain the resident gas method of measuring closing capacity
  • The subject exhales to RV
  • At this volume, the upper lobe alveoli are well-open and full of nitrogen-rich air, and the dependent lung should be fairly collapsed.
  • Pure oxygen is then inhaled until the subject can inhale no more (i.e. up to TLC)
  • This fills the lung with pure oxygen, except for the upper lobe alveoli, where some nitrogen still remains and therefore dilutes the inspired oxygen
  • The subject then exhales through a nitrogen sensor
  • As with the gas bolus method, initially there is no nitrogen in the exhaled gas (this represents Phase I, the dead space volume)
  • Then, nitrogen begins to leak out, and the nitrogen concentration detected by the sensor increases. At this stage, both the nitrogen-rich upper alveoli and the nitrogen-poor dependent alveoli are emptying into the airway, and the nitrogen concentration detected by the sensor remains relatively stable.
  • At the end of expiration, as closing capacity is encountered, the dependent airways close and now the only gas being exhaled comes from the nitrogen-rich upper lobe alveoli, which increases the expired concentration of nitrogen.
  • On a N2 concentration/volume graph, the point at which the expired concentration of nitrogen suddenly increases is therefore the closing volume.

single breath nitrogen washout measurement from Robinson et al, 2013.jpg

References

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