Page 1
Over the past 30 years, pulmonary
function testing has come into widespread use. This has been
facilitated by several developments:
Miniaturization and advances in
computer technology, microprocessor devices have become portable and
automated with fewer moving parts.
Testing equipment, patient
maneuvers, and testing technique have become widely standardized
throughout the world through the efforts of professional societies.
Widely accepted normative parameters
have been established.
DEFINITION
Pulmonary function testing is a
valuable tool for the evaluation of the respiratory system, representing
an important adjunct to the patient history, various lung imaging
studies, and invasive testing such as bronchoscopy and open-lung biopsy.
The overall approach is to compare the measured values for an individual
patient at any particular point in time with normative values derived
from population studies. Therefore, the percent predicted normal is used
to define normal and abnormal as well as to grade the severity of the
abnormality. Practicing clinicians must become familiar with pulmonary
function testing because it is frequently used in clinical medicine for
evaluation of respiratory symptoms such as dyspnea and cough, for
preoperative risk stratification, and for diagnostic purposes for common
diseases such as asthma and chronic obstructive pulmonary disease.
Pulmonary function tests (PFTs) is a
generic term used to indicate a battery of studies or maneuvers that may
be performed using standardized equipment to measure lung function. PFTs
may include simple screening spirometry, formal lung volume measurement,
diffusing capacity for carbon monoxide, and arterial blood gases. These
studies may collectively be referred to as a complete pulmonary function
survey.
Before a spirogram can be
meaningfully interpreted, one needs to inspect the graphic data (i.e.,
volume-time curve and the flow-volume loop) to ascertain whether the
study meets certain well-defined acceptability and reproducibility
standards. The interpretative strategy usually involves establishing a
pattern of abnormality (obstructive, restrictive, or mixed), grading the
severity of the abnormality, and assessing trends over time. A variety
of algorithms are available. Automated spirometry systems usually have
built-in software that can generate a preliminary interpretation,
especially for spirometry; however, algorithms for other pulmonary
function studies are not as well established and necessitate appropriate
clinical correlation and physician oversight.

PHYSIOLOGY
Basic concepts of normal pulmonary
physiology that are involved in pulmonary function testing include
mechanics (airflows and lung volumes), the ventilation-perfusion
interrelationship, diffusion/gas exchange, and respiratory muscle or
bellows strength. Ventilation is the process of generating the forces
necessary to move the appropriate volumes of air from the atmosphere to
the alveoli to meet the metabolic needs of the body under a variety of
conditions. Simply, the thoracic muscles generate negative pressure in
the chest and pleural space, favoring flow of air into the airways and
lungs (inspiration). When the pressures equilibrate, the muscles relax
and contract, increasing intrathoracic pressure and forcing air out of
the lungs (expiration).
With exhalation, the early portion
of the maneuver is characterized by high flows, mostly from large
airways, and the latter portion is characterized by low flows with a
larger contribution from the smaller airways. Inspiration is generally
not flow limited and is a function of overall muscular effort. In
contrast, a variety of factors affect expiratory flow, including the
overall driving pressure (which is the pressure head at the alveolus, or
PALV: the arithmetic sum of pleural pressure, or PPL; plus pressure from
lung elastic recoil, or PELAST), airway diameter, overall dispensability
of lung and chest wall, dynamic airway collapse (i.e., from a
flow-limiting segment), and muscular effort. So:
PALV = PPL + PELAST
The mechanism for the maximal
expiratory airflow limitation seen in normal airways is due to two
factors: the gradual pressure drop along the airways as well as dynamic
airway compression, with intrathoracic airways downstream becoming
narrowed distally to a choke point or equal pressure point. At maximal
airflow or during the early part of the expiratory maneuver, the main
driving pressure is the intrinsic elastic recoil of the lungs.
BATTERY OF MANEUVERS
Pulmonary function studies use a
variety of maneuvers to measure and record the properties of four lung
components. These include the airways (both large and small), lung
parenchyma (alveoli, interstitium), pulmonary vasculature, and the
bellows-pump mechanism. Various diseases can affect each of these
components.
Spirometry:
Spirometry is the most commonly used
lung function screening study. It generally should be the clinician's
first option, with other studies being reserved for specific
indications. Most patients can easily perform spirometry when coached by
an appropriately trained technician or other health care provider. The
test can be administered in the ambulatory setting, physician's office,
emergency department, or inpatient setting. The indications for
spirometry are diverse. It can be used for diagnosing and monitoring
respiratory symptoms and disease, for preoperative risk stratification,
and as a tool in epidemiologic and other research studies.
Spirometry requires a voluntary
maneuver in which a seated patient inhales maximally from tidal
respiration to total lung capacity (TLC) and then rapidly exhales to the
fullest extent until no further volume is exhaled at residual volume
(RV) . The maneuver may be performed in a forceful manner to generate a
forced vital capacity (FVC) or in a more relaxed manner to generate a
slow vital capacity (SVC). In normal individuals, the inspiratory vital
capacity, the expiratory SVC, and expiratory FVC are essentially equal.
However, in patients with obstructive airways disease, the expiratory
SVC is generally higher than the FVC.
A spirometer, including the
waterless, rolling seal type, and Stead-Wells water seal type is an
instrument that directly measures the volume of air displaced or
measures airflow by a flow sensing device, such as a pneumotachometer or
a tube containing a fixed resistance to flow (Table 2). Today, most
clinical pulmonary function testing laboratories use a
microprocessor-driven pneumotachometer to measure air flow directly and
then to mathematically derive volume.
|
Table 2: |
|
Types of Spirometers |
|
Volume |
Flow Sensing
(Pneumotach) |
|
Bellows
Rolling Seal
Water
Dry |
Fleisch
Screen
Hot-Wire
Turbine |
|
Adapted from reference
2 |
A spirogram is a graphic
representation of bulk air movement depicted as a volume-time tracing or
as a flow-volume tracing. Values generated from a simple spirogram
provide important graphic and numeric data regarding the mechanical
properties of the lungs, including airflow (forced expiratory volume in
1 second, or FEV1, along with other timed volumes) and exhaled lung
volume (FVC or SVC). The measurement is typically expressed in liters
for volumes or in liters per second for flows and is corrected for body
temperature and pressure of gas that is saturated with water vapor. Data
from a spirogram provides important clues to help distinguish
obstructive pulmonary disorders that typically reduce airflow, such as
asthma and emphysema, from restrictive disorders that typically reduce
total lung volumes, including pulmonary fibrosis and neuromuscular
disease.
A number of spirometry standards
have been developed over the years. The American Thoracic Society
standardization guidelines for acceptability and reproducibility
criteria are shown in. A well-trained pulmonary function technician
usually coaches the patient through the procedure so that the
measurement represents the best possible measure of lung function.
Forced Expiratory Volume In 1 Second
The FEV1 is the most widely used
parameter to measure the mechanical properties of the lungs. FEV1
accounts for the greatest part of the exhaled volume from a spirometric
maneuver and reflects mechanical properties of both the large airways
and medium-sized airways. In a normal flow-volume loop, the FEV1 occurs
at about 75% of the FVC. This parameter is reduced in both obstructive
and restrictive disorders. In obstructive diseases, FEV1 is reduced
disproportionately to the FVC and is an indicator of flow limitation. In
restrictive disorders, the FEV1, FVC, and total lung volume are all
reduced, and in this setting FEV1 is a measure of volume rather than
flow.
Forced Vital Capacity
FVC is a measure of lung volume and
is usually reduced in diseases that cause the lungs to be "smaller."
Such processes are generally termed restrictive and may include
disorders of the lung parenchyma, such as pulmonary fibrosis, or of the
bellows, including kyphoscoliosis, neuromuscular disease, and pleural
effusion. However, a reduction in FVC is not always due to reduced total
volumes and may occur in the setting of "large lungs" hyperinflated due
to severe airflow obstruction and air trapping, as in emphysema. In this
setting, the FVC is decreased due to reduced airflow, air trapping, and
increased residual volume, a phenomenon referred to as pseudorestriction.
Reduced FVC may occur despite a normal or increased total lung volume.
Therefore, FVC is not a reliable indicator of TLC or restriction,
especially in the setting of airflow obstruction. The overall accuracy
of the FVC for restriction is about 60%.
Volume-time Tracing and Flow-volume Loop
The volume-time tracing and
flow-volume loop ascertain the technical adequacy of a maneuver and
therefore the quality of the data as well as identify the anatomic
location of airflow obstruction. The volume-time tracing is most useful
in assessing whether the end-of-test criteria have been met, whereas the
flow-volume loop is most valuable in evaluating the start-of-test
criteria. The zero time point on the volume-time tracing has been
carefully defined and extrapolated to provide a uniform start point for
measurement. It corrects for a possible delayed start that may not
actually reflect airflow.
The shape of the flow-volume loop
may indicate the location of airflow limitation, such as the large upper
airways or smaller distal airways. With common obstructive airflow
disorders, such as asthma or emphysema, the disease generally affects
the expiratory limb and may reduce the effort-dependent peak expiratory
flow as well as subsequent airflows that are effort-independent. The
descending limb of the expiratory loop is typically concave. In
contrast, several unusual anatomic disorders that narrow the large
airways may produce a variety of patterns of truncation or flattening of
either one limb of the loop (variable upper airway obstruction) or both
limbs of the loop (fixed upper airway obstruction).
Additional Tests
A variety of parameters selectively
reflect small airways. These include measures of flow from a spirogram,
such as the maximal midexpiratory flow (MMEF) or forced expiratory flow
at 25% to 75% vital capacity (FEF25-75). The FEF25-75 is the slope of
the spirogram between the 25th and the 75th percentile of an FVC
maneuver. The closing volume from a single-breath N2 test and
frequency-dependent dynamic lung compliance also can be used to detect
small airway disease. It is believed that small airways dysfunction may
precede and exist separately in the setting of a normal FEV1 and FVC.
The hypothesis is that smokers may have isolated small airways
dysfunction and that there is an obligatory passage through a "silent
period" during which only sensitive tests are impaired. However, there
is a greater coefficient of variation for these tests of small airways
function. In addition, because these measures are vitally influenced by
lung volumes, they cannot be interpreted separately without volume
correction. Therefore, in practice, these tests have not been
particularly helpful to practicing clinicians, and the American Thoracic
Society does not recommend their use for detecting small airways
disease.6
Bronchoprovocation:
To define whether nonspecific airway
hyperreactivity is a mechanism for atypical chest symptoms of unclear
etiology, inhalational challenge tests are often used in the pulmonary
function laboratory.7
Methacholine and histamine are the agents most often used with this
procedure, although other agents may also be useful. Methacholine is
considered safe, can be used in outpatient clinics, and has no systemic
side effects.
When the baseline spirogram is
relatively normal, inhalational challenge may be performed by
aerosolizing progressive concentrations of methacholine by a dosimeter.
This is typically performed as a five-stage procedure with five
different concentrations. After each stage, the patient performs a
spirometry. When there is a 20% reduction in the FEV1, the test is
terminated and is considered positive for airway hyperreactivity. The
provocative dosage level of the inhalational agent required to produce a
20% reduction in the FEV1 is labeled as PD20. If the drop in FEV1 is
less than 20% after five stages of this procedure, the challenge test is
considered negative for the presence of airway hyperreactivity.
Bronchial hyperreactivity, as
assessed by this inhalational challenge procedure, is very sensitive for
the presence of active or current asthma. A positive test is strongly
suggestive of bronchial asthma. However, this test may be falsely
positive by a variety of conditions, including chronic obstructive
pulmonary disease, parenchymal respiratory disorders, congestive heart
failure, recent upper respiratory tract infection, and allergic
rhinitis. For practical purposes, a negative inhalational challenge with
methacholine or histamine excludes active symptomatic asthma as a cause
for the patient's chest symptoms.
Lung Volumes:
Because spirometry is an expiratory
maneuver, it measures exhaled volume or vital capacity but does not
measure residual volume, functional residual capacity (or the resting
lung volume), or TLC. Vital capacity is a simple measure of lung volume
that is usually reduced in restrictive disorders; however, vital
capacity is only an indirect measure of other lung volumes. Because
residual volume is not exhaled through the mouth, it is not measured by
a spirometer.
Other pulmonary function methodology
is required to formally measure TLC, which is derived from the addition
of FRC to inspiratory capacity obtained from spirometry. FRC is usually
measured by a gas dilution technique or body plethysmography. Gas
dilution techniques are based on a simple principle, are widely used,
and provide a good measurement of all air in the lungs that communicates
with the airways. A limitation of this technique is that it does not
measure air in "noncommunicating" bullae and, therefore, may
underestimate TLC, especially in patients with severe emphysema.
Gas dilution techniques use either
closed-circuit helium dilution or open-circuit nitrogen washout. They
are based on the inhalation of a known concentration and volume of an
inert tracer gas, such as helium, followed by equilibration of 7 to 10
minutes in the closed-circuit helium dilution technique. The final
exhaled helium concentration is diluted in proportion to the unknown
volume of air in the patient's chest (RV). Usually the patient is
connected at the end-tidal position of the spirometer; therefore, the
lung volume measured is FRC. In the nitrogen-washout technique, the
patient breathes 100% oxygen and all the nitrogen in the lung is "washed
out." The exhaled volume and the nitrogen concentration in that volume
are measured. The difference in nitrogen volume at the initial
concentration and at the final exhaled concentration allows a
calculation of intrathoracic volume, usually FRC.
Body plethysmography is an
alterative method of measuring lung volume that takes advantage of the
principle of Boyle's law, which states that the volume of gas at a
constant temperature varies inversely with the pressure applied to it.
The primary advantage of body plethysmography is that it can measure the
total volume of air in the chest, including gas trapped in bullae.
Another advantage is that this test can be performed quickly. Drawbacks
include the complexity of the equipment as well as the need for a
patient to sit in a small enclosed space. A patient is placed in a
sitting position in a closed "body box" with a known volume. From the
FRC, the patient pants against a closed shutter to produce changes in
the box pressure proportionate to the volume of air in the chest. The
volume measured by this technique is referred to as thoracic gas volume
(TGV) and represents the lung volume at which the shutter was closed,
typically FRC.
Diffusing Capacity:
Understanding gas diffusion through
the lungs requires recognition of the basics of the gas exchange
interface and of the various forces at work by which oxygen and carbon
dioxide move by molecular diffusion. Diffusion is limited by the surface
area in which diffusion occurs, capillary blood volume, hemoglobin
concentration, and the properties of the lung parenchyma that separate
the alveolar gas from the red blood cell with the capillary.
Because all lung volume is not
exchanged, most gas exchange occurs as a function of diffusion
independent of bulk flow. The role of ventilation is to reset
concentration of the bulk flow of gas with the ambient air and to
provide a constant gradient for oxygen and carbon dioxide. As spirometry
measures the components of this bulk flow exchange, diffusing capacity
measures the forces at work in molecular movement with its concentration
gradient from the alveolar surface through to the hemoglobin molecule.
The clinical test diffusing capacity of the lung (DL) most commonly uses
carbon monoxide (CO) as the tracer gas for measurement because of its
high affinity for binding to the hemoglobin molecule. This property
allows a better measurement of pure diffusion, such that the movement of
the CO is in essence only dependent on the properties of the diffusion
barrier and the amount of hemoglobin. The properties of oxygen and its
relatively lower affinity for hemoglobin compared with CO also make it
more perfusion dependent; thus, cardiac output may influence actual
measurement of oxygen diffusion measurements.
Diffusing capacity for CO (DLCO) is
the measure of CO transfer. In Europe, it is called the transfer factor
of CO, which describes the process more accurately. DLCO is a measure of
the interaction of alveolar surface area, alveolar capillary perfusion,
the physical properties of the alveolar capillary interface, capillary
volume, hemoglobin concentration, and the reaction rate of CO and
hemoglobin. After a number of simplifications, the commonly used
clinical tests to measure DLCO are based on a ratio between the uptake
of CO in mL per minute divided by the average alveolar pressure of CO.
Overall, DLCO is expressed as the uptake of CO in mL of gas STPD
(standard temperature and pressure, dry) per minute and per mm Hg
driving pressure of CO. In principle, the total diffusing capacity of
the whole lung is the sum of the diffusing capacity of the pulmonary
membrane component and the capacity of the pulmonary capillary blood
volume.
All methods for measuring diffusing
capacity in clinical practice rely on measuring the rate of CO uptake
and estimating CO driving pressure. The most widely used and
standardized technique is referred to as the single-breath
breath-holding technique. This technique relies on a subject inhaling a
known volume of test gas that usually contains 10% helium, 0.3% CO, 21%
oxygen, and the remainder nitrogen. The patient inhales the test gas and
holds his or her breath for 10 seconds. Exhalation is then performed to
"wash out" mechanical and anatomic dead space. Subsequently, an alveolar
sample is collected. DLCO is calculated from the total volume of the
lung, breath-hold time, and the initial and final alveolar
concentrations of CO. Alveolar volume is estimated by the helium
dilution and the initial alveolar concentration of CO. The driving
pressure is assumed to be the initial alveolar pressure of CO.
Hemoglobin concentration is a very
important measurement in interpreting reductions in DLCO. Because the
hemoglobin present in the alveolar capillaries serves as a CO sink such
that oxygen and CO are removed from dissolved gases, the concentration
gradient from alveolar to arterial blood remains relatively constant in
favor of dissolved gas flow toward the arterial circulation. In this
way, a DLCO may be decreased when the patient is anemic. Because the
level of hemoglobin present in the blood and diffusing capacity are
directly related, a correction for anemic patients (DLCOc.) is used to
further delineate whether a DLCO is decreased due to anemia or due to
parenchymal or interface limitation. If alveolar volume is low and the
patient is anemic, both corrections may be performed and reported as the
DLVAc.
Diseases such as interstitial
pulmonary fibrosis or any interstitial lung disease may make the DLCO
abnormal long before spirometry or volume abnormalities are present. Low
DLCO is not only an abnormality of restrictive interstitial lung disease
but may also occur in the presence of emphysema. In emphysema, the lung
volumes may be normal or hyperinflated; therefore, the DLVA is not
useful. Additionally, the loss of alveolar surface area, the pathologic
lesion of emphysema, is not proportionate to volume. As such, one can
understand that other obstructive entities that predominantly affect the
airways can have similar spirometry, but a low DLCO implies a loss of
alveolar surface area consistent with emphysema. Unfortunately, it is
not always this simple. Some forms of interstitial lung disease may have
components of restrictive physiologies, such as low lung volume and
clear evidence of decreased diffusion, but may also have airway flow
limitation. Sarcoidosis and Wegener's granulomatosis may have an
endobronchial component of airway webs or strictures, limiting flow
before overt volume loss and still have enough interstitial
granulomatous inflammation to reduce the DLCO.
On the other end of the spectrum,
alveolar hemorrhage or congested capillary beds may actually increase
the DLCO. The presence of trapped hemoglobin in proximity to alveolar
gas will absorb CO despite the actual severe limitation of gas exchange
and oxygen delivery.
As for spirometry, predicted
formulas have been established for DLCO and DLVA. It is important to
note, however, that differences in race have been observed in normal
subjects, and a race correction of 7% is allowed for African-American
patients.
EQUIPMENT
A detailed discussion of equipment
is beyond the scope of this chapter. The American Thoracic Society has
gone to great lengths to standardize and publish detailed
recommendations regarding spirometry, lung volumes, and diffusing
capacity. These guidelines include the selection of equipment, important
technical considerations for variability, and standardization between
laboratories for the maneuver. Table 5 lists the suggested performance
standards for an office spirometer.
|
Table 5: |
|
Performance
Standards for an Office Spirometer |
|
A Volume Spirometer
Should:
Accumulate volume
for greater than 30 s
Accommodate volumes
of up to 7 liters
Be accurate to
within 3% or 50 ml of a "test" volume
A Flow-Sensing
Spirometer Should:
Be able to measure
flows up to 12L/s
Be accurate to
within 5% or 0.2 L/s
Both Need:
Regular maintenance
Routine checks of
accuracy of the spirometer and the computer |
|
NORMALITY AND PREDICTED EQUATIONS
Studies from a healthy population
indicate that parameters of lung function, such as FEV1 or FVC, are
affected most significantly by standing height, age, gender, race, and
to a lesser extent, by weight. If we assume that lung function has a
normal Gaussian distribution, then a wide range of values may be
considered normal. Because there is no absolute cut-off point for what
is normal in biologic systems, an arbitrary statistical approach is
widely used to define the lowest 5% of the population, or abnormal. Over
the years, many regression equations have been generated by several
investigators using different methodologies to study a variety of
population cohorts. The recommendation is for clinical labs to choose a
published reference standard that is most similar to the typical patient
population at a given institution as well as the testing methods used.
The most commonly used standards include Morris et al, Crapo et al,
Knudson et al, and most recently, National Health and Nutrition
Examination Survey (NHANES III). These reference standards are based on
a cohort of normal people of similar age, height, and race, with normal
being defined as individuals without a history of smoking or disease
that may impact lung function.
Many approaches have been developed
over the years to determine the normal range of spirometry. These
approaches have included using a fixed percentage of predicted (i.e.,
75%) and a fixed FEV1-to-FVC ratio, (i.e., >0.70), although both of
these approaches have no statistical basis and are not recommended.
The American Thoracic Society
recommends using the concept of lower limit of normal by identifying the
lowest 5% of a population, or patients that fall outside the limits of
1.64 standard deviations from the mean. This value may be calculated by
multiplying 1.65 times the standard error of estimate (1.65 x SEE).
Weight is less important as a predictor of lung function. Obese patients
may have abnormal spirometry (i.e., decrease in FVC) based on the
diaphragm's ability to displace the intra-abdominal fat. Body weight has
little impact on intrathoracic volume. Race plays an important role in
determining normal lung function, as it has been recognized that
individuals of different races for any given height and age have
proportionately different lung volumes. Specifically, based on
anthropometric differences, the lung function for African-Americans is
systematically lower compared with Caucasians. The American Thoracic
Society recommends a 12% correction for African-Americans for FEV1, FVC,
and TLC. The FEV1-to-FVC ratio in African-Americans may be slightly
higher compared with Caucasians. A 7% correction for lower values is
recommended for FRC and residual volume. However, race-specific
reference standards are preferred. Over time, the NHANES III reference
equations will likely become the standard in most pulmonary function
testing laboratories around the country. The methodologies and the
sample size are most robust for this data set, as well as being
representative of the American population.
CLINICAL INTERPRETATIVE STRATEGIES
Spirometry:
In 1991, the American Thoracic
Society issued a position statement regarding interpretative strategies,
which forms the basis for PFT interpretation in practice. As previously
discussed, spirometry is the most widely used screening test of lung
function or pulmonary function studies. It is usually the first test to
be performed and interpreted. Supplemental studies may be conducted as
needed, such as a formal lung volume measurement, diffusing capacity,
methacholine provocation test, or cardiopulmonary exercise studies.
Spirometry is usually adequate for preoperative risk assessment and
stratification. It is also often adequate for rotated obstructive lung
disease, such as emphysema or asthma. However, when a patient's symptoms
or clinical history cannot be explained by findings on spirometry or
when multiple coexisting processes (i.e., dyspnea with both heart and
lung disease) are present, then further testing is usually warranted.
In a simplistic way, respiratory
disease can be classified as obstructive or restrictive processes.
Obstructive disorders, such as emphysema or asthma, are characterized by
airflow limitation, have increased lung volumes with air trapping, and
have normal or increased compliance (based on pressure volume profile).
In contrast, restrictive disorders such as pulmonary fibrosis are
characterized by reduced lung volumes and an increase in overall
stiffness of the lungs (with reduced compliance). Once the technical
adequacy of the spirogram has been established, the next step is to
classify whether the study is normal, has an obstructive pattern, a
restrictive pattern, or a mixed obstructive/restrictive pattern. In
general, the measured values are compared with the lower limits of
normal predicted values from one of the published studies. Airflow
obstruction exists, by definition, when the FEV1-to-FVC ratio is below
the lower limits of normal. When this ratio is above the lower limits of
normal, obstruction is usually excluded. However, occasionally, early
termination or short expiratory time can artifactually reduce FVC and
falsely normalize the FEV1-to-FVC ratio to mask obstruction. Once the
presence of airflow obstruction is established, then a typical approach
in the laboratory is to administer two puffs of inhaled albuterol and
repeat the spirogram after 15 minutes to establish bronchodilator
responsiveness. Lack of bronchodilator response certainly does not
exclude asthma, and the result needs to be used in the context of a
patient's clinical history.
Lung Volumes:
Because the FVC is not a reliable
measure of TLC, spirometry can only be suggestive of a restrictive
process and, in general, should be followed up by lung volume
measurement. When spirometry suggests a restrictive process or when the
abnormalities seen on the spirogram do not adequately explain a
patient's clinical history, then formal measurements of lung volume are
helpful. TLC can be particularly helpful when a patient has severe
airflow obstruction and has a reduction in FVC. In this case, a normal
or increased TLC would exclude an associated restrictive process, and
the reduction in FVC would actually be a pseudorestriction.
DLCO:
Diffusing capacity is a pulmonary
function test that is commonly performed to help further characterize
abnormalities in spirometry or lung volume measurements. The DLCO is a
test that has greater degrees of variability between laboratories and
that it is a study that requires some level of expertise to perform
reliably. Several processes can affect diffusing capacity. If diffusing
capacity is reduced proportionately to airflow obstruction (a
proportionate reduction in FEV1 and DLCO), then this is a pattern
typical for emphysema. If the DLCO is reduced proportionately to a
reduction in TLC in the context of restrictive abnormalities, then this
would be suggestive of a parenchymal process such as pulmonary fibrosis.
If there is an isolated or disproportionate reduction in diffusing
capacity along with either normal or fairly well-preserved mechanics,
then this would be suggestive of predominantly a pulmonary vascular
process such as primary pulmonary hypertension or thromboembolic
disease. Note that anemia or carboxyhemoglobinemia (from smoking) could
affect the measured DLCO. The concept of a reduced DLCO that normalizes
after correction for a lung volume measurement is often used to describe
an extrathoracic or extraparenchymal disease process such as resection,
obesity, or neuromuscular disease. However, this approach has many
limitations.
Notes
Pulmonary Function Interpretation
Identify the indications for pulmonary function testing:
According to the AARC CPG, PFT need
to be done to:
1.
diagnosis restrictive defects,
2.
to differentiate between restrictive and obstructive defects,
3.
assess the patient’s response to interventions
4.
pre-op assessment of patients at risk for pulmonary limitations
5.
evaluate pulmonary disability
6.
Quantify air trapping; is it getting worse, better
Identify the contraindications of pulmonary function testing:
According to the AARC CPG, the
relative contraindications include
·
untreated pneumothorax
·
hemoptysis
·
unstable hemodynamics
·
aneurysms.
If persons have claustrophobia,
upper body paralysis or cast that makes the ‘body box’ impossible, this
single test may be deferred.
Identify the hazards of pulmonary function testing:
·
PFT that add supplementary 02 can cause 02-induced hypoventilation
·
cross-contamination
·
hypoxemia due to removal of supplementary 02 or increased WOB during
certain maneuvers
·
hypercapnia
List the effects of gender and age and other issues on the patient
normal pulmonary function values.
·
The most important factor for prediction of normal values is the
height of the patient.
·
Sex: Adult men tend to have better values for all parameters than
adult women
·
The age of a person has a inverse effect on values, the older the
patient the lower the normal values. Peak values are found in the
person in their mid-twenties and then start to drop.
·
BSA: body surface area [height and weight together] because some
weight gain is in muscle mass, values will rise, but when weight
gain is due to increased body fat, the values fall.
·
Race has a small effect on pulmonary function study results [Madama
pp. 153] normal values for volumes may be smaller for Asian and
black person than European although the flows may not be that
different. Studies are going on all over the world to find normal
PFT values for different populations.
Quantifying PFT results:
Because normal values are based on
gender, age, size and general conditions, absolute normal values vary so
much that it is easier to look at these values as “percent of predicted”
--- % predicted.
The normal parameters are as a rule
considered normal if within +/- 20%, so a person with a value that is
79% of predicted has decreased values, and the person with 121% has
increased values.
·
deranged measurements between 65-79% or 121-135% are mild
·
deranged measurements between 50-64% or 136-150% are moderate
·
deranged measurements between 35-49% or 151-165% are severe
·
deranged measurements between less than 35% predicted more than 165%
predicted are very severe
List & discuss those PFTs that measure and quantify lung volumes and
capacities.

The 4 lung volumes are used to
document the presence of restrictive defects. In the case of a
restrictive defect, all or most of the volumes will be decreased.
We don’t worry about increased
volumes unless it is the residual volume [RV], which is a problem
because higher than normal RV imply there is air-trapping due to
obstructive defect.
1.
VT: tidal volume measured via spirometry; the normal VT is
monitored at the bedside and during PFT.
·
The VT is about 10% of the TLC & may or may not be decreased in
restrictive & obstructive defects
·
For accuracy, at the bedside, we need collect the VE and RR then
calculate the VT. An average is better than one or two single
breaths
·
In the PFT lab we will collect 3 minutes for our average
·
The VT is a fairly unhelpful measurement in of itself & is
frequently not even reported outside of discussions about weaning
patients from or placing patients on mechanical ventilation.
2.
IRV: inspiratory reserve volume the amount of gas that is inhaled
after a normal exhalation, the IRV is about 50% of the TLC.
·
In the case of restrictive defect, this figure will be less than 80%
predicted.
·
In case of obstructive defect, this might be normal or decreased
3.
ERV: expiratory reserve volume the amount of gas that is exhaled at
the end of a normal exhalation. The ERV is about 20% of the TLC
·
In the case of restrictive defect, this measurement will be less
than 80% predicted
·
In the case of obstructive defect, the ERV is normal or decreased
4.
RV: residual volume: volume of gas that stays in the lung after a
maximal exhalation. Because this gas cannot be exhales, it cannot be
measured via spirometry, so indirect means such as the body box or
He dilution are used to measure this gas. The normal RV is about 20%
of the TLC.
·
In obstruction, the RV may be more than 120% predicted due to
air-trapping
·
In restrictive defects the RV is lower than 80% of predicted
The 4 lung capacities:
A lung capacity is the sum of 2 or
more lung volumes. Lung capacities that include RV will have to be
measured indirectly.
1.
TLC = ERV + RV + VT + IRV. This is all the volume in the patient’s
lungs including that air that cannot exit the lungs [RV]
·
Decreased TLC implies there is a restrictive defect
·
TLC more than 120% predicted implies that air trapping has become
‘emphysema.’
·
A variation of the indirect measurement of TLC by He dilution or N2
washout is the measurement of the thoracic gas volume [TGV] via the
body plethysmograph.
·
When there is a large difference between the TLC measured by He
dilution & N2 washout and the Thoraic Gas Volume by body box, this
result implies that this patient might have areas of RV that are
completely obstructed so that they don’t connect to the airways. In
this case the TLC will be lower than the TGV.
·
In a healthy person the TLC and the TGV are identical [and both
within 20% of predicted]
2.
VC = ERV + VT + IRV: The maximal amount of gas that is inhaled after
a maximal exhalation. This is the most gas a person can move. It
should be 80% of TLC.
·
The VC can be slow SVC or forced [FVC] in which the patient inhales
and exhales as quickly as possible
·
The SVC will be decreased in restrictive defects
·
When there is a marked difference between the same person’s SVC and
FVC, we know this patient has the decreased flow rates associated
with obstructive defects.
·
When both the SVC & the FVC are decreased, we have restrictive
defect
3.
IC = VT + IRV: The maximal amount of gas that is inhaled after a
normal exhalation
·
is decreased in restrictive defects
·
if the patient has severe obstruction, this may be decreased because
the FRC is raised so high above normal
4.
FRC = ERV + RV
·
The combination of the normal exhaled reserve volume, plus the RV
that cannot be removed
·
Are decreased in restrictive defects
·
May be increased in obstructive defects associated with air-trapping
·
The “FRC point” at the end of a normal exhalation is considered the
point at which most PFT tracings will start
List & discuss those PFT that monitor flow characteristics & problems
with RAW associated with obstructive defects

The volumes associated with
obstruction include the FRC, the RV and the TLC. [see above lecture]
Assessment of patient’s flow rates
at various points will track the presence, location and degree of airway
obstruction.
Assessment of these flow before and
after bronchodilator administration should give the RCP an idea about
the reversibly of the obstructive defect.
Because FVC technique is so
effort-dependent, a good PFT lab will collect several different types of
flow measurement.
FVC measured with simple spirometry
can yield the following information:
1.
FEV1 : the volume of gas a person can exhale in the first second
during an FVC. This number is generally compared to the FVC.
Because we are measuring volume against time we are more or less
measuring the flow rates
·
Decreased values of FEV1 imply there is an obstructive defect, but
it could also be down in a person with restriction because the FRC
is down.
·
We need to compare the FEV1 to the FVC
2.
FEV1/FVC the person with normal RAW will be able to exhale at least
70% of the FVC within the first second of exhalation.
·
Anything less than this implies there is an obstructive component to
the lung disease.
·
A person with a decreased FVC due to a restrictive defect, may has a
normal FEV1 because he has no obstruction… his FEV1/FVC maybe be
abnormally large. So…oddly enough, high FEV1/FVC can, sometimes,
imply restrictive defects.
3.
FEF 200-1200 the average flow is measured between the first 200 ml
and the 1200 ml point. This is the average flow rate in the larger
airways. Decreased flows imply obstructive disorders
4.
FEF25% the volume exhaled at the point of the first 25% of the FVC
is a flow rate that can be decreased in obstructions in the larger
airways. Decreased flows imply obstructive disorders
5.
FEF 25-75% the average flow rate of the smaller airways. This is
measured between the first 25% of the FVC and the last 25%. This is
the average flow rate in the smaller airways Decreased flows imply
obstructive disorders
6.
FEF 50% the volume exhaled at the mid-point the FVC is a flow rate
that can be decreased in obstructions in the smaller airways
7.
FEF 75-85% the average flow rate of the smallest airways and will be
decreased with obstruction of the smallest airways.
8.
FEF 75% the volume exhaled at the last 25% of the FVC& it is a flow
rate that is decreased in obstruction in the smallest airways
The MVV – maximal voluntary ventilation in which the patient breaths
as fast and as deeply as he can for at least [10-15]12 seconds with
the results extrapolated to 1 minute. The units are LPM. This is a
nonspecific test of the patient’s over-all ventilatory function.

·
Both obstructive defects and restrictive defects will have lower
numbers
·
In the case of the obstructive defect, the actual shape of the
tracing will change. The base line will move up from FRC point
·
The most important function of the MVV is its ability to predict the
patient’s ability to withstand pulmonary rehabilitation. A person
with a MVV less than 50% of predicted cannot handle the rigors of
pulmonary rehabilitation
Flow/Volume loop the patient
performs a FVC but the computer displays the values in a flow/volume
graphic. Once the inspiratory flows are separated from the expiratory
flows we can start measuring:

·
PIFR: peak inspiratory flow rates- most of the concern with PIFR is
the patient’s ability to get inhaled medication via DPI
·
PEFR: peak expiratory flow rates: easily measured gage of
bronchodilation. Most effort dependent- better to look at FEV1 for
comparisons of various broncho-active agents
Shape of the flow/volume loop: in
the normal flow-volume loop we see the inspiratory flow pattern as a
sine wave while the expiratory flow rate is a descending curve.
|
Patients with restrictive disorders
will have a normal flow but decreased volume-- tall narrow loop
|
 |
|
Patients with small airway
obstruction such as asthma or COPD will have slower expiratory
flows with a scooped out expiratory tracing
|
 |
|
Patients with large fixed
obstructions [such as ET tubes] will have squared off
inspiratory and expiratory flows [kinda box-looking]
|
 |
|
Patients with intra-thoracic large
airway obstruction will have a squared off expiratory flow with
a slower sine wave on inspiration. This can be seen in persons
with a tumor in the central airways or compression of the
central airways.
|
 |
|
Patients with an extra-thoracic
large airway obstruction will show normal shape of the
expiratory flow but decreased inspiratory flow. This would be
seen in persons with tumors or other problems in the area of the
larynx.
|
 |
Measurement of the RV in order to calculate the TLC
Because we cannot exhale the
residual volume, measurement of this data is a little tricky.
There are two basic ways to do this:
[1] by dilution of a gas and [2] by changes in thoracic volume inside a
body plethysmograph
He dilution test [also called closed circuit method]:
Because He gas is rare in ambient air; we can use this gas to measure
the RV indirectly.

·
The patient inhales a known percentage of He into a known volume of
gas—usually quite large-- about 30 Liters.
·
The patient has an unknown volume of gas inside his RV, but a known
He percentage of zero [because He is so rare]
·
Over several minutes, the patient inhales and exhales into the huge
spirometer [holds almost 30 Liters] and after a few minutes the
percentage of He is measured.
·
Knowing that the He will have diffused throughout container that
includes the spirometer and the patient’s own lungs, we can
calculate the actual RV.
·
The change in He percentage is directly proportional to the amount
of the patient’s FRC volume added to the circuit volume.
·
Once we figure out the FRC, we can subtract the ERV to get the RV
·
Note that this technique of He dilution works only if all the
patient’s airways are patent. If there are significant areas of
completely collapsed airways, this measurement will be lower than
the actual FRC.
·
Because He dilution involves the patient rebreathing from the
container, we must add a soda lime canister to absorb the exhaled
C02 to prevent rebreathing C02.
·
Extra 02 can be added before the test starts so the patient doesn’t
become hypoxemia.
·
Towards the end of the test, if the supplementary 02 runs low the
patient might become hypoxemia
N2 washout study [or open circuit]
Another way to indirectly measure RV is to washout the patient’s
N2 with breathing 100% for several minutes [max 7 minutes].
·
The exhaled gases are collected and the N2 percentage measured. The
known volume of gas and known percentage of alveolar N2 [.75] at the
start of the test is compared to the final N2 percentage so that the
FRC can be calculated. Again once the FRC is measured, we subtract
the ERV to get the RV
·
Needless to say, COPD patients with hypoxic drives require another
means of RV, because they cannot handle the high Fi02.
·
Because the patient doesn’t rebreathe his Co2, the N2 washout test
is a open-circuit method
Body plethysmography used to measure
thoracic gas volume. The patient is placed inside the body boy and asked
to pant for a second or two, then the shutter valve closes and the
patient continues to pant. Because there is no flow, we can assume that
the mouth pressure is equal to the alveolar pressure.
·
Because the patient is sealed inside an airtight box, the changes of
pressure-- caused by the patient’s chest wall getting larger during
inspiration--can be measured and with various formulae turned into
thoracic gas volume.
·
Thoracic gas volume includes trapped gas that is not in contact with
the airways.
·
If there is a large difference between the RV found during He
dilution and that discovered during the TGV, we know that this
patient has significant areas of airways that are completely
collapsed.
·
RAW directly measured by body plethysmography
·
At the same time the patient is panting for the TGV measurement, we
can also measure the airway resistance of the patient because while
the shutter is closed we can measure the alveolar pressure.
·
Normal RAW determined this way is .6 to 2.8 cmH20/L/second
·
As we already know, increased RAW are signs of obstructive defect
List & discuss PFT that measure gas diffusion
We must measure the patient’s
ability to diffuse gas for a complete picture of his lung disease.
Anyone who has a disease that causes
hypoxemia most likely has some degree of diffusion defect, but we need
to investigate further
While a person with a restrictive
would have decreased alveolar ventilation which would limit diffuse of
gases and a person with severe obstruction would also have limited
alveolar ventilation thus diffusion- there is another class of patient.
If a person had no flow or volume
problems but still had decreased gas diffusion, we could diagnosis a
pure diffusion problem such as pulmonary embolism [common] or pulmonary
vascular edema, pulmonary vasculitis [both very rare.]
Normal diffusion of CO is 20-30
ml/minute/mmHg. This is called DLCO diffusion of CO -.
When we multiply the DLCO by 1.23 we
get the DLO2
Increased diffusion
While we expect diffusion to be down
in almost everyone who is significantly hypoxemic, occasionally we may
find that a patient has increased gas diffusion due to polycythemia
[more RBC with more Hb] or LV failure in which blood stays in the
pulmonary bed too long.
Persons who live at high altitudes
will have increased diffusion.
Diffusion increases during supine
positioning and during exercise
To perform gas diffusion studies,
the patient will inhale a small, known amount of carbon monoxide [CO].
Because the CO will bind with Hb, we
know that there will be zero CO dissolved in the plasma [PcapillaryC0]
so that we know that the PACo-PaC02 gradient is equal to the PACO
CO diffusion can be performed in a
single breath study of .3%CO or during a steady-state inhalation of 0.1%
CO over several minutes
Pulmonary function studies of gas distribution
We need to study the patient’s
physiological VD to get an understanding of the patient’s actual
alveolar ventilation.
While the anatomical VD stays the
same unless the patient gets a tracheostomy, the alveolar VD varies with
disease processes. So measurements of physiological VD gives us all the
information we need.
Gas distribution: the basal areas
fill first, then empty first
Single-breath N2 elimination

1.
N2 starts at zero because we are at the start of exhalation. This is
pure VD
2.
mixture of central airways and alveolar gases as patient starts to
exhale; so still exhaling VD gases
3.
pure alveolar gases
4.
Closing volume; small airways close so that there is no more gas out
of the basal portion of the lung. Now we have mostly gas flow out of
the apical areas which have more N2 because this is where air
trapping occurs.
Interpretation of single-breath N2 washout
·
We can calculate the VD alveolar and the VD/VT ratio from these
measurements as well as monitor the gas distribution.
·
Normal VD/VT ratio is .20 to .40 with VD anatomical and VD basically
the same figure