Airway Resistance

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

• 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 P_O2 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

• 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