SECTION IV THE RESPIRATORY SYSTEM

Pulmonary Edema

A 50-year-old woman is in intensive care for treatment of pulmonary edema caused by heart failure. Edema
fluid is in both the interstitial and alveolar spaces of her lungs. For the moment she is breathing on her own,
(i.e., she is not connected to a mechanical ventilator). Her respiratory rate is 30 per minute. Previously, she
had normal lungs.

1. Based on this limited information, how would you characterize the following parameters as high, low, or
normal? State your reasons.

Total lung capacity

Surface tension
Lung compliance
Work of breathing
Airway resistance

After a few hours her condition deteriorates, and she is mechanically ventilated. The ventilator delivers
12 breaths/min, and tidal volume is 500 ml. The ventilator measures airway pressure at the end of each
delivered tidal volume, at a point of "no air flow"; at this point, airway pressure is 30 cm H2O. The
ventilator then allows her to passively exhale, and airway pressure returns to zero (atmospheric).

Total lung capacity (TLC) would probably be reduced. TLC is the amount of air contained within the
lungs at the point of maximal inhalation. If there is something, such as edema fluid, occupying or
obliterating the alveolar spaces, the volume of air at TLC probably will be lower than normal. Thus in
pulmonary edema and all other space-occupying disturbances of the lungs, the TLC will be reduced.

Surface tension would be increased. The edema fluid in the alveolar spaces washes away surfactant,
the complex phospholipid that reduces surface tension at the air¨Calveolar wall interface. As a result,
the patient's alveoli tend to collapse as she exhales, further worsening her lung compliance and overall
clinical condition. (The infant respiratory distress syndrome is characterized by pulmonary edema,
which is caused by lack of surfactant at birth.)

Lung compliance would be reduced. The edema fluid not only washes away surfactant, but it also
infiltrates the interstitium and makes the lungs stiffer than normal. Hence, a greater translung pressure
is required to inflate them, and the patient must work harder than normal to breathe. At some point, if
the pulmonary edema does not respond to treatment, the patient will tire and require mechanical
ventilation (as happened to this patient).

Her work of breathing, for the reasons just described, is increased.

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 Airway resistance would be reduced, although less than the fall in compliance and TLC. Most of the
airway resistance arises from the larger airways (i.e., those with a cross-sectional diameter greater
than 2 mm). Airways less than 2 mm diameter, while more numerous than larger airways, provide only
about 20% of the respiratory tract's total airway resistance. Even if these "small airways" are narrowed
50% by edema fluid, the impact on the total measured airway resistance may not be easily discernible.

On the other hand, if edema fluid enters the interstitium surrounding the larger airways and causes
them to constrict (as sometimes happens), their narrowing should cause a more obvious increase in
airway resistance. Some patients with pulmonary edema actually wheeze and sound "asthmatic"; they
definitely have increased airway resistance.

2. What is her thoracic compliance (state the units)? Is this a measurement of lung, chest wall, or lung plus
chest wall compliance? In measuring thoracic compliance, what is the importance of obtaining the peak
pressure at a point of no air flow?

The machine has taken over her breathing. She has a measured tidal volume of 500 ml and a translung
pressure difference of 30 - 0 cm H2O. Thoracic compliance, the change in thoracic volume over change
in pressure, is 600 ml/30 cm H2O, or 20 ml/cm H2O. This is the compliance of her lungs and chest wall
together, because the ventilator must expand both in delivering this tidal volume.

Compliance is a measurement of how much pressure is required to overcome the elastic forces of a
structure (lungs, chest wall, lungs and chest wall, etc.). If pressure is being exerted to overcome
airway resistance as well, you will not obtain a true compliance measurement. For this reason, lung
compliance measurements must always be made at a point of no air flow, so that airway resistance
does not affect the pressure being measured. Asthma exemplifies this point. The pressure volume
curve in asthma is close to normal or is shifted slightly to the left (i.e., the lungs have normal or
slightly elevated compliance). If pressure to distend the lungs is measured during breathing (i.e.,
during air flow), the increased resistance of asthmatic airways will give a higher pressure than at a
point of no air flow; the resulting "compliance" measurement will be artificially low, and the
asthmatic patient's lungs will appear stiffer than they really are.

3. A separate set of measurements is taken during air flow. During inhalation she has an airway opening
pressure (PaO) of 35 cm H2O, an alveolar pressure (PA) of 25 cm H2O, and an air flow of 1 L/sec. What
is the calculated airway resistance? Is this a normal value? Do you think this measurement reflects her
true airway resistance?

The patient recovers completely. Two months later she returns to the pulmonary function
laboratory. She is asked to inhale fully, then exhale as forcefully and fully as possible, and then
resume normal breathing. During the test, the volume of air exhaled and the rate of air flow are
measured.

Airway resistance = change in pressure over air flow. Pressure change is the difference between Pao,
the airway pressure at the mouth, and PA, the alveolar pressure. Airway resistance is not easy to

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 measure in a nonintubated patient because there is no simple way to obtain both pressures. (Airway
resistance can be measured with body plethysmography.) In an intubated patient the measurement is
easy to accomplish, but it will include the increased resistance of the endotracheal tube and will thereby
confound the patient's true airway resistance.

For a patient who is connected to a mechanical ventilator, Pao is the peak airway pressure measured
during air flow. PA is obtained by briefly occluding the airway at the point of peak airway pressure (e.g.,
0.5 second); during occlusion, air does not flow, and the pressure will equal PA. From the data
provided,

Raw = (Pao ¨C PA)/flow = (35 ¨C 25 cm H2O)/1 L/sec 35 = 10/1 = 10 cm H2O/L/sec

Her resistance in the airway (Raw) is elevated, but most of this elevation can be attributed to her
endotracheal tube. Her true pulmonary resistance cannot be determined.

4. What is the term for the volume of air that is (a) in her lungs at the point of maximal inhalation; (b)
exhaled from full inhalation to full exhalation; and (c) in her lungs at the point of full exhalation?

a. Total lung capacity (TLC); b. Forced vital capacity (FVC); c. Residual volume (RV)

5. At what point in this maneuver is her air flow the fastest? If she did not inhale maximally before
commencing this maneuver, would her maximal air flow be the same, higher, or lower than maximal
inhalation? Explain your answer.

In the FVC maneuver, maximal air flow occurs shortly after exhalation begins, well within the first
second; this fastest rate of flow is called the peak expiratory flow rate, or "peak flow." Peak flow (see
Fig. 34-14 in Physiology 3rd ed.) is the highest point on the expiratory flow volume curve. Peak flow is
dependent on the lung capacity at which the exhalation effort begins; the higher the initial lung
capacity, the higher the potential peak flow. Expanding the lungs fully maximizes the cross-sectional
diameter of the large airways and reduces their air flow resistance; thus peak flow exceeds that
achievable at lower lung volumes. If she did not inhale maximally before commencing this maneuver,
her peak flow would be less than the flow she could achieve starting from TLC.

6. What is the term for the volume of air in her lungs at the end of quiet, normal breathing? How does it
compare with a typical normal value? What is her intrapleural pressure at this point, relative to
atmospheric pressure (negative or positive)? Explain the elastic recoil forces acting at this point. If one
side of her chest wall is punctured, what will happen to the lung on that side, and why?

Functional residual capacity (FRC). A typical normal value for FRC is about 3.5 L.

Intrapleural pressure at FRC is negative because, at FRC, the elastic recoil of the chest wall, which
tends to expand that structure outward, is balanced by the elastic recoil of the lungs, which tends to
contract them.

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 If the chest wall is punctured, as long as there is a communication between the atmosphere and
intrapleural space, air will rush in until the intrapleural pressure equals the atmospheric pressure. As a
result, the elastic recoil of the lung on that side will no longer be opposed by the chest wall elastic
recoil, and the lung will collapse. This condition is called a pneumothorax.

Emphysema Pulmonary fibrosis

Elastic recoil D I
Compliance I D
TLC I D
FRC I D
FVC D D
RV I I
E V V
PaO2 (rest) V V
PaCO2 (rest) V V

7. Patients with recurrent episodes of pulmonary edema sometimes don't recover fully, but may develop
pulmonary fibrosis, or chronic lung scarring. Fibrotic lungs differ from emphysematous lungs. How do
each of the following parameters compare to normal (increased, decreased, or no change)?

D = decreased, I = increased, V = variable

Emphysema is a chronic lung condition characterized by loss of alveolar-capillary membranes and
supporting elastic tissue; it usually occurs from long-term cigarette smoking. The loss of elastic tissue
makes the lungs more easily distensible than normal (increased compliance), and allows them to
expand outward against the chest wall (increased TLC). At the same time, airways close earlier than
normal during expiration and thus the FRC and RV are increased. For the same reason, FVC tends to be
decreased. Minute ventilation increases as a consequence of the increase in dead space. Arterial blood
gases can be normal or abnormal in emphysema. If the increased minute ventilation goes to the
increased dead space and provides enough alveolar ventilation to wash out the patient's CO 2, PaCO2 will
stay in the normal range. In advanced emphysema, however, the respiratory muscles may be too weak
to perform the increased work of breathing, and PaCO2 may rise. As for PaO2, there may be enough
alveolar units with normal or near normal V/Q ratios to keep PaO 2 in the normal range, at least at rest.
However, in advanced stages of emphysema, V/Q imbalance may be so severe that PaO2 is reduced.

Pulmonary fibrosis, a chronic lung condition caused by accumulation of scar tissue in the lung
interstitium, can occur from many different causes; in some cases the cause is unknown. Pulmonary
fibrosis presents completely different mechanical problems than emphysema: increased lung recoil,
decreased lung compliance, and small lung volumes. As in emphysema, resting arterial blood gases are
also variable. In mild stages of fibrosis, blood gases may be normal at rest, but in advanced stages
hypercapnia and hypoxemia may prevail.

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