Flashcards in Six Deck (17):
Describe what happens in a pneumothorax with both static recoil and chest wall forces. What does this mean concerning P(IT) and P(B) during exhalation past FRC toward RV and during inhalation towards TLC? What does this mean concerning the potential energies involved in inhalation and exhalation?
The chest wall and diaphragm normally oppose the recoil
forces of lung tissue elasticity and surface tension. Thus, the
negative PI P at functional residual capacity (FRC) (see Fig.
4.6) represents the equilibrium when these musculoskeletal
elements are bowed inwardly by lung recoil. Since this balance
is not intuitive, consider a bilateral pneumothorax when
PI P = PB (Fig. 6.2). When PI P increases from −5 to 0 cm H2O,
healthy lungs recoil toward their minimal volume, while the
chest walls spring outward and the diaphragm drops toward
the abdominal viscera. Indeed, the volume of the open chest
when PI P = PB is about 80% of a subject’s normal total lung
capacity (TLC), implying that musculoskeletal elements will
oppose all forces attempting to make the chest either larger or
smaller than about 80% of TLC.
When subjects who are at FRC expire toward RV, their PIT
is less than PB and a sensation of suction is felt as the thoracic
structures are increasingly deviated inward from their preferred
resting positions seen with a pneumothorax. Conversely, when
the subject inspires to lung volumes above FRC and toward
TLC, PIT exceeds PB and a sensation of chest compression
develops as lung elastic and tension recoil forces increase.
Indeed, the subject’s sensation of chest tightness will maximize
at lung volumes >80% of TLC (ie, the size of the thoracic space
after a pneumothorax) since the chest wall and diaphragm will
also then be exerting inwardly directed positive pressures that
augment the positive pressure created by lung recoil.
From this explanation, it becomes apparent that if a subject
breathes at lung volumes between FRC and about 80% of
TLC, each inhalation to infl ate the lungs is achieved in part
by utilizing potential energy stored in the chest wall and diaphragm
as they were pulled inward during the preceding exhalation.
By the same argument, every exhalation uses potential
energy stored in the infl ated lungs to expel the tidal breath,
while simultaneously storing potential energy in musculoskeletal
elements being bowed inward. Thus, it is not accurate
to consider normal inhalation to be entirely “active” or normal
exhalation to be entirely “passive”. Rather, normal breathing is carefully controlled to oscillate around the midrange of available
lung volumes so that inhalation consumes less energy
than one might think, but exhalation also costs energy.
Explain what happens during emphysema concerning TLC, chest wall forces, static forces, etc.
In contrast to this normal pattern, many patients with
obstructive lung diseases (eg, emphysema, asthma) will
struggle to exhale fully between breaths. They may become
hyper-infl ated, still breathing tidally but much closer to their
TLC. Their work of breathing is vastly increased, since every
inhalation will require distending both the lung tissues
and the thoracic elements surrounding them. You can
experience this phenomenon by fi rst taking a deep breath,
and then resume taking small tidal breaths but without
allowing yourself to exhale to FRC each time.
What is dynamic airway resistance? Where is it greater, lesser? Why?
additional resistance to ventilation also occurs in the airways
during fl ow, only to disappear under no-fl ow conditions such
as FRC. Such dynamic airway resistance is nevertheless
a powerful determinant of the pattern, energetic cost, and
overall effi ciency of ventilation. Thus, dynamic airway
compliance measurements are made to directly determine
in-line resistances due to the airways. Such measurements
have shown that most dynamic airway resistance resides in
the upper airways (generations 1-7) because their fl ow rates
tend to be high, their end-to-end pressure changes are large,
and their aggregate cross-sectional areas are small. By the same
argument, the smaller peripheral airways usually contribute less
resistance despite having smaller individual diameters, due
to their shorter lengths and their exponentially larger crosssectional
areas (Fig. 6.4).
To appreciate the role
Describe dynamic airway resistance using Ohms Law and Poiseuille's law.
To appreciate the role that airway dimensions play in creating
resistance to ventilation and thereby add to the work of
breathing, recall Ohm’s law:
I = ΔV/ R
where I = current, ΔV = voltage potential, and R =
In airways and other tubes, this becomes a generalized
fl ux equation:
Air Flow = ΔP/ R
where ΔP = pressure differential, either end-to-end or
R = resistance due to airway dimensions and gas viscosity,
R = (8 · η · l)/(π · r 4)
where r = airway radius, η = viscosity, and l = airway
Substituting terms gives the well-known Poiseuille
Air fl ow = (ΔP · π · r 4)/(8 · η · l)
Considering the dependence of resistance on radius to the
fourth power, the importance of even a small change in airway
radius is apparent. It will be shown in later chapters that many
respiratory diseases pivot on this aspect of airway resistance,
versus a lesser dependence on airway length or viscosity.
What kind of flow patterns exist in the airways?
Applying the Poiseuille equation to human ventilation
presumes an idealized laminar fl ow pattern, but evidence is
not persuasive as to how often and how distally such fl ow
exists in the airways (Fig. 6.5). Most bronchial airways are too
wide, too frequently bifurcated, or too short before branching
to promote consistent laminar fl ow. Rather, it seems likely
transitional fl ow patterns predominate at rest, that deteriorate to turbulent patterns during exercise and other events associated
How is airway resistance calculated clinically? When these calculations are plotted, how does the data compare with in vitro plotting? What does this mean?
Clinically, airway resistance is calculated using the pressure
gradient from trachea to alveolus divided by fl ow rate; the subject’s tracheal pressure and fl ow rate are estimated at the mouth by anemometer, and alveolar pressure by esophageal
transducer or plethysmography (Chap. 16). When the in vivo
volume/pressure changes are plotted for such a dynamic compliance
maneuver, the area between the infl ation and defl ation
curves representing hysteresis is larger than for excised lungs of the same size (see Fig. 5.2). Most importantly, this increased
area represents additional nonrecoverable work during both
infl ation and defl ation to overcome airway resistance.
Describe the 3 resistances that must be overcome to breath and what percentage each represents of the total resistance in a healthy adult.
In summary, the total work of breathing in a healthy adult
can be partitioned into energy that must be applied to overcome:
• Static lung resistance caused by tissue elasticity and
surface tension forces that must be overcome regardless
of dynamic resistance, normally 65%-70% but higher
when pathologies involving surfactant or the respiratory
parenchyma are present;
• Dynamic airway resistance that exists only when gas is
moving, normally 25%-30% and mostly in the upper 10
generations, but much higher in patients with obstructive
• Tissue viscous drag due to physical abrasion and friction
between pleural surfaces of the lung and chest,
normally 5% but can become fatally high if adhesions,
congenital anomalies, or effusions are present.
Describe both obstructive airway disease and restrictive lung disease. Gives etiologies of both including restrictive chest wall disease.
The rationale for devoting such attention to the work of breathing
and determination of lung compliance is that most respiratory
diseases arise in patients who present with impaired ventilation
characterized as an obstructive airway disease or a restrictive
lung disease. In general, a disease is obstructive if there is an
increased resistance to airfl ow, most evident during expiration
but also detectable upon inspiration. Specifi c examples include
asthma, bronchitis, and emphysema. Patients with restrictive lung
diseases do not necessarily show airfl ow obstruction, but their
ventilation is impaired due to restrictions in the maximal size or
movement of the lungs or chest wall (or both). Restrictive chest
wall diseases include kyphoscoliosis, neuromuscular disorders,
and spinal trauma. Restrictive lung diseases include interstitial
fi brosis, sarcoidosis, scarring after pneumonia or tuberculosis,
bronchopulmonary dysplasia, and alveolar edema due to congestive
heart failure. Patients can show features of both obstructive
and restrictive lung diseases.
Describe what FEV1, FEV2, FEV3, and FVC are and how they're measured? What are some standard values in a healthy adult?
In Chap. 4, procedures to measure forced vital capacity
(FVC) and forced expiratory volume (FEV) were introduced,
in which patients on a spirometer or fl owmeter inhale to TLC
and then exhale as quickly as possible as volume and fl ow rate
are recorded (Fig. 6.6). Exhaled volumes are reported as FVC
(= TLC − RV) in liters, and as percentages of the actual FVC
that are expired within the fi rst second (FEV1), fi rst two seconds
(FEV2), and fi rst three seconds (FEV3) of the maneuver. For a
healthy adult with FVC = 6 L, an FEV1 = 5 L or 83% FVC
would be normal; an FEV2 of ~95% and FEV3 of ~99% would
also be expected.
Describe the FEV1 and FVC and TLC in someone with obst. airway disease. What clinical implications does this have?
In patients with obstructive airway diseases (Fig. 6.6), both
FVC and FEV1 are lower than predicted based on age, gender,
and size. However, the patient’s TLC is often larger than predicted
because low expiratory fl ow rates lead to peripheral gas
trapping that increases RV. As RV expands with disease severity,
such patients will be forced to use their principal ventilatory
muscles at distinct mechanical disadvantages. Indeed, the resulting
hyperinfl ation of the chest as RV and FRC increase eventually
fl attens the diaphragm, so that its contraction fails to increase
Describe the FEV1 and FVC and TLC in someone with Restr. lung disease.
In contrast, a patient with restrictive lung
disease shows lower FVC and TLC than predicted by age, gender,
and size, due to physical limits imposed on lung and/or chest volumes
(Fig. 6.6). Of note, given the smaller lung or thoracic volumes
in such patients, the FEV1 may be normal or even increased
as a percent of FVC unless airway obstruction is also present.
How is flow rate measured? Describe the expiratory flow rate in healthy subjects? What does the term effort independent mean?
Flow rate (in L/sec) is measured at the mouth continuously
during an FVC test to obtain an expiratory fl ow-volume loop,
with airfl ow plotted versus lung volume from TLC to RV on
the abscissa (Fig. 6.7). The expiratory fl ow rate in healthy
subjects quickly reaches a maximum that corresponds to the
steepest portion of a conventional spirometer tracing
(Fig. 6.6). Despite continued maximal effort by the subject, airways
with high fl ow rates begin to collapse because pressures
within parenchyma surrounding the airways soon exceed airway
pressures themselves. This effect can be explained by principles
developed by the mathematician and physician Bernoulli. The
eventual decline in fl ow rate as a forceful exhalation proceeds is
termed effort-independent: no matter how forcefully the subject
attempts to exhale, their volume-dependent airway compression
during dynamic conditions limits maximal fl ow rate.
In fact, even if subjects exert a submaximal effort initially and
then a maximal effort later, the effort-independent portion of their
fl ow-volume loop is not displaced upward or to the right.
What is the expiratory flow volume rate like in someone with Obstr. airway disease?
When compared to healthy subjects, individuals with
obstructive or restrictive disease patterns show distinctive
shapes for their fl ow-volume loops (Fig. 6.8). Patients with
obstructive airway disease often begin an FEV maneuver at
an abnormally higher TLC due to hyperinfl ation, and end the
maneuver at a substantially increased RV. Such patients also
take longer to achieve maximal fl ow rates, which are lower than
expected, and their effort-independent region may be distinctly
concave as they approach RV.
What is the expiratory flow volume rate like in someone with Restr. lung disease?
Patients with restrictive lung or
chest disease have a low or normal RV, depending on the nature
of their disorder. By defi nition, such patients have abnormally
low total lung capacities. However, their peak fl ow rates often
resemble the effort-independent portion of normal subjects, if
airway caliber is not a prominent feature of their disease.
What ventilation differences exist between the top and bottom of the lung? Why? What alveolar differences exist between the top and the bottom of the lung? Why? What are P(IT) and P(A) like from the top and bottom of the lung? Why? What implications does this have on alveolar compliance from the top to the bottom of the lung? Why?
It has been assumed to this point that the lungs are uniformly
ventilated, and that their compliance shows no regional heterogeneity.
However, lungs are air-fi lled organs suspended in
a partial vacuum within a body cavity susceptible to the effects
of gravity. Lungs also have progressively smaller airways and
blood vessels, moving distally from the trachea and pulmonary
artery. These anatomical and physical conditions create
a situation that is far from ideal. Indeed, when an upright
subject breathes air containing trace amounts of 133Xenon [which, like helium (He), is poorly soluble in fl uid] while the
chest is scanned with appropriate detectors, it is found that more
inhaled 133Xe goes to the lung base than to its apex. This result is
not due simply to the greater volume of the lung bases. Rather,
the inhaled tracer is always observed to distribute preferentially
to dependent lung zones, defi ned as those regions lowest in the
gravitational fi eld. So when subjects inhale 133Xe while standing
on their head or lying supine, the tracer preferentially enters
apical alveoli or those nearest the spine, respectively.
These nonintuitive results occur because at any instant, PIP
is not uniform for the entire lung but varies from the gravitational
top of the lungs to their bottom within the thoracic space.
When upright, PIP is most negative at the thoracic apex, due to the
hanging weight of the lungs as they maintain contact with adjacent
apical pleural surfaces. In the same upright position, PIP at
the lung base is less negative or may even be positive, because
here the lungs pull less on basal pleural membranes, or may even
push against them. Such gradients in PIP exist for a subject in any
assumed body position and persist throughout a ventilation cycle.
Thus, individual alveoli in more dependent regions are smaller at
any lung volume, due to the less negative PIP they are experiencing
versus alveoli above them that are more distended due to the more
negative PIP adjacent to them in the same gravitational fi eld.
At the same time, all alveoli in the lung still experience
nearly identical levels of PI T and PA throughout a ventilation
cycle since they are connected via common airways from primary
bronchi to the most distal airspaces (Fig. 6.9). Consequently,
all alveoli experience the same ΔPI T and ΔPA during
inhalation, but those in the more dependent zones will infl ate
more easily because they are nearer to their own RV and thus
more compliant (see Fig. 4.6). At the same instant, alveoli in
gravitationally higher regions infl ate less since they are already
closer to their own TLC, and thus less compliant. Analogous
gravitational effects that act upon the pulmonary arteries and
the patency of alveolar capillaries will be discussed in Chap. 7.
What clinical consequences do the regional differences in ventilation have? How can they be prevented?
There are signifi cant clinical consequences to these
regional differences in ventilation. In a subject at FRC (Fig. 6.9),
basal alveoli are more easily ventilated because they are on the steepest portion of their individual compliance curves.
However, if the same lungs are studied at a low lung volume
like RV instead, perhaps in a comatose patient, the PIP at the
lung base is positive, and little or no alveolar expansion occurs
during a typical tidal breath of only 0.5-0.7 L. Such situations
also develop rather commonly in sedated patients, whose spontaneous
ventilation may not prevent collapse of their dependent
alveoli, particularly when an otherwise desirable increase in FIo2 accelerates this effect by absorption atelectasis (Chap. 30). In an awake and healthy subject, alveolar collapse is prevented or reversed by periodic sighs, with a sigh operationally defi ned as three times a subject’s normal tidal volume (VT).