Lung Mechanics: Airway Resistance - pediagenosis
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Sunday, September 16, 2018

Lung Mechanics: Airway Resistance


Lung Mechanics: Airway Resistance
Airflow is driven by the mouth-alveolar pressure gradient generated by the respiratory muscles (Chapters 2 and 3).
In laminar flow, gas particles move parallel to the walls, with centre layers moving faster than outer ones, creating a cone-shaped front (Fig. 7a). The factors affecting laminar flow of a flui of viscosity, η, in smooth straight tubes of length, l, and radius, r, are described in Poiseuille’s equation:

Halving the radius of an airway increases its resistance 16-fold. However, although the resistance of an individual bronchiole is high, there are thousands in parallel. The total resistance of each generation of peripheral airways is normally low, and the overall resistance of lung airways is dominated by the larger airways. Outside the lung, the nose and pharynx contribute substantial resistance, which can be reduced by mouth breathing, for example, during exercise. Peripheral airways are often affected by disease, but because their resistance must increase considerably to measurably affect airway resistance (RAW), they are known as the silent zone.
At higher linear velocities, especially in wide airways and near branch points, flow may become turbulent. With turbulence, the wave front is square and f ow L'l P (not L'l P), reflectin the dissipation of energy in the formation of eddies. Normally, at rest, fl w is laminar throughout the airways, but in exercise it may become turbulent, especially in the trachea, generating characteristic harsh breath sounds.

Lung Mechanics: Airway Resistance, Factors Affecting Airway Resistance, RAW in disease


Factors Affecting Airway Resistance
Bronchial smooth muscle and epithelium
Bronchial smooth muscle (Fig. 7b) receives a parasympathetic bronchoconstrictor nerve supply, acting via acetylcholine and muscarinic type 3 receptors, which forms the efferent limb of a reflex from air- way irritant receptors (rapidly adapting receptors). The smooth muscle also contains β2-adrenergic receptors, which cause relaxation when stimulated by circulating epinephrine (adrenaline) or drugs such as salbutamol. Sympathetic innervation of the airways is sparse in humans and has little effect on airway smooth muscle. Airways are also supplied with excitatory and inhibitory non-adrenergic non-cholinergic (NANC) nerves, the former acting via the transmitters substance P and neurokinins, and the latter via nitric oxide (NO) and/or VIP (vasoactive intestinal peptide). Parasympathetic bronchoconstriction is inhibited by activation of airway stretch receptors (slowly adapting receptors), and CO2 has a direct bronchodilator effect. Pollutants (e.g. sulphur dioxide and ozone) and substances released from mast cells and eosinophils can increase RAW via bronchoconstriction, mucosal oedema, mucus hypersecretion, mucus plugging and epithelial shedding - all of which are important in asthma (Chapter 24). Airway resistance can also be increased by chronic mucosal hypertrophy in chronic obstructive pulmonary disease (COPD) (Chapter 26) and by material within the air- ways, such as inhaled foreign bodies or tumours (Chapter 40).

Transmural (airway–intrapleural) pressure gradient
The pressure difference across airways can have important effects on their calibre, and this underlies the effects of effort on airflow, illustrated in Fig. 7c. Airflow is measured continuously and plotted against lung volume as the subject breathes between residual volume (RV) and total lung capacity (TLC). The inspiratory airflow at any volume increases progressively with increasing effort (1 = minimum effort, 6 maximum effort). The f ow-volume curves for progressively increasing expiratory efforts (upper traces 1-6) are more complicated. In the early part of expiration from TLC, flow is effort-dependent, but towards the end of the breath, as volume declines, the traces produced at different effort levels come together. Expiratory airflow towards the end of a breath is effort-independent and determined by lung volume.
Peak expiratory flow rate (PEFR) is seen to be reduced (B in Fig. 7c) if the lungs are only partially fille at the start of the forced expiration. Effort-independent airflow is explained by dynamic compression of airways. Before the start of inspiration (Fig. 7d, upper panel) the pressure along the airways is zero, intrapleural pressure is negative (Chapter 3) and transmural pressure acts to hold airways open. Intrapleural pressure is negative during both quiet and forced inspiration and it remains negative in quiet expiration, so transmural pressure holds airways open. In a forced expiration, however, expiratory muscle con- traction raises intrapleural pressure well above atmospheric pressure (e.g. 8 kPa, 60 mmHg), increasing the pressure gradient from alveoli to mouth. This would be expected to increase airflow, but the increased intrapleural pressure also acts to compress airways. Airway pressure falls progressively along the airway, and at some point - usually in the bronchi - the airway pressure will be suffciently below intrapleural pressure for the airway to collapse, despite its cartilaginous support. Pressure will then build up distally, opening the airways again. The resulting f uttering walls can be seen on bronchoscopy and produce the brassy note audible on forced expiration in healthy people.

RAW in disease
Increased airway resistance is important in many diseases and can be measured using a body plethysmograph. In healthy individuals, RAW is about 0.2 kPa/L per second (1.5 mmHg/L per second). More com- monly, airway resistance is assessed indirectly from forced expiratory measurements, such as forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC) and PEFR (Chapter 20). Especially useful is the forced expiratory ratio (FER FEV1/FVC), which is reduced when RAW is increased in obstructive pulmonary disease. High air- way resistance accentuates dynamic compression of airways by augmenting the pressure drop along airways. In addition, the airways may be less able to resist compression, in emphysema because of reduced radial traction and in asthma because of bronchoconstriction. Collapse of small airways may occur, leading to incomplete expiration, air trap- ping and increased functional residual capacity. Inability to produce high expiratory airflow impairs effective coughing, which can lead to a vicious cycle as secretions accumulate, further increasing RAW and further reducing peak flow. Expiratory wheezes (rhonchi), heard in asthma and other obstructive diseases, are probably generated by oscillations in opposing airway walls near their point of closure, like sounds from the reeds of an oboe. A reasonable airflow is needed to generate such sounds, and when constriction becomes very severe, they disappear to give the ominous silent chest seen in life-threatening asthma. Small airway collapse leads to characteristic shape of the maximum flow-volume curve in obstructive airway disease (Fig. 7e), which differs from that in upper airway obstruction and restrictive lung disease.

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