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 I. Airway Resistance
As you learned earlier, a parallel system of branching airways (including all bronchi and
bronchioles) that connects the atmosphere with the alveolar space is called conducting
airways. During inspiration, the air has to flow through the airways from the atmosphere
into the alveoli, and move in the opposite direction during expiration. Air volume passing
through the airways in a unit of time is called air flow (V). Driving force producing air flow is
the pressure difference between both ends of the airways. For expiration, this pressure
difference would be: Alveolar pressure (PA) minus pressure at airway opening (Pao).
Airway resistance (Raw) can be then obtained due to Hagen-Poiseuille law as shown
above.

Therefore, PA, Pao and airflow should be measured to use for the calculation of airway
resistance. Pao is zero (atmospheric pressure), and airway flow can easily be measured
with a pneumo-tachometer. A direct PA measurement is nearly impossible, because
alveolar space is not easily accessible for applying noninvasive methods. However,
techniques have been developed for indirect measurement of PA such as interrupter
method or the whole body plethysmography.

Changes in airway resistance induced by natural stimuli occur by changes in airway radius.
The principal changes are achieved either actively by alterations in the contraction of the
airway smooth muscle cells, or passively by changes in transmural pressure of airways.
Recall from geometry that cross sectional area of a tube is equal to πr2, so changes in
radius have magnified effects.

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 This slide shows that the volume of anatomic dead spsce (upper airways from
airway opening until terminal bronchioles; upper 16 bronching generations) is small
about 150 ml, whereas most of the volume (2.8 L) resides in peripheral airways
beyond bronching generation 16. Therefore, total diameter of airways is much larger
and their resistance much lower in peripheral airways beyond generation 16.

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 A. Distribution of airway resistance
Airways branch like a tree in 23 generations, so the total number of airways goes from one
to 223 or 8,388,608.

The radius of individual bronchi becomes smaller from generation 1 to 23, but the total
diameter of all bronchi within one generation decreases only in the first 4 generations. This
leads to the increase of total resistance in the early four dividing generations.

Thereafter total airway diameter increases rapidly from generation to generation toward
peripheral airways. As a result total airway resistance exhibits a sharp decrease toward
peripheral airways. Only 20% of the total airway resistance is then localized in the
peripheral airways beyond dividing generation 7, although very narrow airways are residing
in this region of the lung (diameter below 2 mm). Consequently the major site of airway
resistance is in upper airways, prior to division 7 (80%).

A disadvantage of this resistance distribution is called “silent lung disease”; i.e., even large
peripheral lung tumors do not constrict the large airway diameter of this region to a level
that could produce obstructive symptoms or to be detected by measurement of Raw. On the
other hand small obstruction in upper airways produces a significant change in Raw.

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 B. Five Factors influencing airway resistance

a) Density and viscosity of the repiratory air: The lower the density and viscosity
of the respiratory gas, the lower will be Raw. Thus, a helium-oxygen gas mixture
having a low density would help divers at extreme depths and patients with extreme
obstructive lung disease to breathe more comfortably.

b) Reduction in PCO2: A reduction in airway PCO2 causes bronchoconstriction and

thereby increases Raw. This effect plays a role in regional distribution of ventilation.
As a lung region becomes relatively hyperventilated and its PCO2 decreases, airway
resistance of that region increases to divert the ventilation to other hypoventilated
areas.

c) Sympathetic innervations. Sympathetic innervations and epinephrine produce

bronchodilation through stimulation of smooth muscle β- receptors.

d) Agents: such as histamine, thromboxane A2 and prostaglandin F2 are

bronchoconstrictors.

e) Lung volume

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 Factors influencing airway resistance

e) Lung volume: the higher the lung volume, the lower will be Raw. Bronchi and
bronchioles are residing within the lung tissue surrounded by alveoli. Their wall is
permanently pulled by the neighboring inward recoiling alveoli. Therefore, lung recoil
is a distending pressure for middle and small airways keeping them open.
Remember that lung recoil increases with lung volume, so that airway distending
pressure, and thereby airway diameter becomes larger at higher lung volume.
Consequently Raw drops as volume increases.

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 Assessing pulmonary function
Most of respiratory diseases are associated with changes in Raw or CRS. Measuring Raw and CRW is
not so easy and cannot be performed in every physicians office. What matters for a physician is to
be able to evaluate and observe changes in above parameters, but knowing their absolute values is
not essential. Therefore, several functional tests (easy to apply) have been developed to serve this
goal. These tests are introduced below:

I. Forced Expiratory Vital Capacity

To measure forced vital capacity the patient is asked to take a maximum breath in, hold it for a
second, then exhale as hard and fast as he/she can. The most important data derived from this
maneuver are:
1. Forced Expiratory Volume in 1 second (FEV1): It is the volume of air that is forcibly exhaled from
the lungs in the first second of a forced expiratory maneuver.
2. Forced Vital Capacity (FVC): After a maximal inspiration, the volume of air that is forcibly and
maximally exhaled until no more can be expired.
3. Ratio of FEV1/FVC which is normally 0.8 (80%).
4. Peak Expiratory Flow Rate (PEFR): The maximum flow rate achieved during the forced vital
capacity maneuver beginning after full inspiration and starting and ending with maximal
expiration.

These spirometry variables will be discussed later to help understand normal lung physiology and to
diagnose specific lung pathology.

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 II. Normal and abnormal spirograms
In the figure above, volume exhaled is plotted as a function of time during a single
forced expiration (the same maneuver as before). You can clearly see how the
pattern of flow changes from normal to that in obstructive lung diseases and
restrictive lung diseases.
In obstructive lung disease: Both FEV1 and FVC decrease in acute (asthma
attack) and chronic obstructive lung diseases (lung emphysema). The ratio of the
two, FEV1/FVC, decrease as well, which is an important parameter for
differentiation between obstructive and restrictive lung disease. FVC decreases
slightly, because some airways are closing during forced expiration (dynamic airway
obstruction) and the air from those regions is entrapped and can not be exhaled.
FEV1 decreases, because of high airway resistance and reduced FVC.
In restrictive lung disease: Both FEV1 and FVC are reduced, because of the small
TLC, but more importantly the ratio FEV1/ FVC is either normal or slightly enhanced.
It is because the recoil of the lung is increased in restrictive lung diseases such as
lung fibrosis.

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 III. Normal and abnormal flow volume loops
When the different slopes of the previous expired volume–time curves are calculated in units
of liters/second and plotted against corresponding lung volumes, or when expiratory flow is
directly measured during forced expiration and plotted against lung volume, you obtain a
“flow volume loop”. This is an important diagnostic tool for obstructive and restrictive lung
diseases. The following parameters are measured and analyzed by this test:
Peak Expiratory Flow Rate (PEFR): It is the highest obtained flow that is observed
immediately after the beginning of expiration. This parameter is dependent on the patient’s
effort. When patients do this with less effort they get a smaller peak flow but the lower part
of the flow volume curve coincides with curves obtained with greater effort (effort
independent region).
FEF 75: It is the forced expiratory flow at 75% of vital capacity. It means 25% of vital
capacity is exhaled with remaining 75% in the lung.
FEF 50: It is the forced expiratory flow at 50% of vital capacity. It means 50% of vital
capacity is expired with remaining 50% in the lung.
FEF 25: It is the forced expiratory flow at 25% of vital capacity. It means 75% of vital
capacity is exhaled with remaining 25% in the lung.
Absolute values of all above parameters are reduced by both obstructive lung disease
(because of high resistance) and restrictive lung disease (because of low lung volume).
Again these values relative to lung volume TLC are normal by restrictive lung diseases,
whereas they are reduced in obstructive lung disease.

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 Changes caused by chronic obstructive disease (Emphysema):
Compliance of the lung is increased and therefore, residual volume, functional
residual capacity and total lung capacities are increased. Increased compliance
causes obstruction of airways during expiration by shifting the equal pressure point
closer to alveoli. As a result of obstruction the peak expiratory flow during forced
expiration is reduced.
Changes caused by restrictive disease:
All lung volumes are proportionately smaller in a restrictive diseased lung, but
compliance of the lung is reduced and its recoiling force (for a given volume) is
increased. The peak expiratory flow during forced expiration is reduced, because
the vital capacity is much smaller than normal.

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 A. Dynamic compression of airways:
During forced expiration patients are using the accessory muscles of expiration,
abdominal and internal intercostal muscles. The contraction of these muscles
creates a positive pressure in the thorax (like the Valsalva maneuver). At the point
in an airway where this positive intrathoracic pressure is higher than the pressure
inside the airway, the airway becomes compressed. As voluntary effort increases,
the compression of the airway becomes stronger, so that the flow remains
independent of the effort.

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