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.
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 airway 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 contraction 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 commonly, 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 airway
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.
