Airway Resistance

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Measurement of Airway Resistance:

  • The pressure difference between the alveoli and the mouth divided by the flow rate
  • Mouth pressure measured using a manometer
  • Alveolar pressure measured using a body plethysmograph:
  • During inspiration, alveolar gas is expanded increasing box pressure, allowing calculation of alveolar pressure using Boyle's law
  • Boyle's law: Pressure and volume of a gas are constant at a set temperature in a closed system
  • The difference between alveolar pressure and mouth pressure divided by flow gives airway resistance
  • Can also measure airway resistance using intrapleural pressure record from an oesophageal balloon, however this includes tissue viscous resistance as well
  • Intrapleural pressure records includes elastic recoil of the lung and resistance to air/tissue flow, therefore elastic recoil must be subtracted

Pressures During the Breathing Cycle:

  • Intrapleural pressure is -5 at the beginning of inspiration, but elastic recoil of the lungs balances this and equalizes to give alveolar pressure of 0

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  • Alveolar pressure only drops ~1 cm of water in normal breathing
  • Intrapleural pressure falls for 2 reasons - because of increased lung elastic recoil, and because of decreasing alveolar pressure
  • Intrapleural pressure - lung elastic recoil = alveolar pressure
  • On expiration, intrapleural pressure rises as alveolar pressure is now positive
  • Alveolar pressure tracing is the same as the flow tracing if airway resistance remains constant throughout the cycle
  • Intrapleural pressure curve ABC would be the same shape as the volume tracing if lung compliance remained constant

What Determines Airway Resistance:

  • Major site of airway resistance is the medium-sized bronchi up to the 7th generation
  • Very little resistance in airways <2mm diameter due to the massive number of them
  • Lung volume is very important in airway resistance - bronchi are supported by radial traction and their calibre increases as lung expands
  • The reciprocal of resistance (conductance) is linearly proportional to lung volume

Things causing small airway obstruction:

  • Congestion/inflammation/oedema of mucosa/bronchioles, mucous/foreign bodies/oedema plugging, cohesion of mucosal surfaces, fibrosis of bronchioles, collapse of bronchioles due to loss of normal traction by alveolar elastic fibres
  • Physical factors - lung volume, closing volume, coughing, fixed obstructive lesions
  • At very low lung volumes, some airways close completely
  • Patients with increased airway resistance often breathe at high lung volumes to help reduce their airway resistance
  • Coughing - forced expiration against a closed glottis, then glottis suddenly opens with rapid expulsion of gas and tracheal narrowing to slits to force contents out
  • Nervous factors - cholinergic, adrenergic
  • Contraction of bronchial smooth muscle narrows airways and increases airway resistance
  • Occurs reflexly through stimulation of receptors in the trachea and large bronchi by irritants
  • Motor innervation is by the vagus nerve, and stimulation of adrenergic receptors causes bronchodilatation, as do epinephrine and isoproterenol
  • B2-adrenergic receptors relax smooth muscle in the bronchi, blood vessels and uterus, B2 agonists used to treat asthma
  • Chemical factors:
  • Endogenous - histamine, 5HT, bradykinin
  • Exogenous - sympathomimetics, anticholinergics, steroids, irritants
  • Injection of histamine into the pulmonary artery causes constriction of smooth muscle in alveolar ducts
  • Viscosity/density of inspired gas affects resistance - eg. high during a deep dive due to increased pressure, lower when a helium-O2 mixture is breathed
  • Fall of PO2 in alveolar gas

Dynamic Airway Compression:

  • Flow volume envelopes for forced expiration rapidly rise to a very high value, then decline at a constant rate which is impossible to overcome

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  • The gradient of the flow/volume envelope ends the same way regardless of the effort put into it - it is effort independent
  • This is due to airway compression by intrathoracic pressure making flow determined by alveolar pressure minus pleural pressure, and therefore indepenent of effort
  • Maximal flow is therefore dependent on lung volume, and decreases with it
  • This is exaggerated if:
  • Resistance in peripheral airways is increased
  • Lung volume is low - reducing alveolar pressure
  • Elastic recoil pressure of lung is reduced, eg. in emphysema. Radial traction is also reduced in emphysema
  • FEV1/FVC% is a good marker for this, and is significantly reduced in obstructive diseases
  • In Restrictive diseases, both FEV and FVC are reduced, but FEV1/FVC% is normal or high