Pulmonary Function Tests
Accurate assessment of defects in
airflow, lung volume or gas exchange is essential to the diagnosis and
management of many respiratory disorders. It is important to note that these
tests characterize 'defects'; the clinician has to diagnose 'diseases'. The
normal range of many lung function tests is very wide, and it is essential to
compare measured values with those predicted for the subject's age, height and
sex by standard nomograms derived from large cross-sectional studies.
Airway resistance can be measured using a body plethysmograph (Chapter
7; Fig. 20c) to measure alveolar pressure. Lung compliance can be
measured using oesophageal pressure to assess intrapleural pressure (for
details see Chapter 6). More commonly, abnormalities of airway resistance (in
obstructive airway disease) are assessed indirectly from forced expiratory
manoeuvres, and abnormalities of compliance (in restrictive lung disease) are
assessed indirectly from lung volume measurements.
Forced expiratory tests
Peak expiratory flow rate (PEFR) is frequently measured, despite its inability to
distinguish between different types of ventilatory defect and its dependence on
patient effort (Fig. 7c). The subject breathes out as hard and fast as possible
from total lung capacity into a meter whose pointer records the maximum
momentary flow rate achieved during the expiration. Inexpensive versions of the
peak flow meter are available and used for home monitoring. It is reduced in
obstructive disease, respiratory muscle weakness and often in restrictive lung
disease (secondary to reduced volume). Its main value lies in monitoring
diseases, especially asthma, once the diagnosis has been made.
In contrast, plots of volume
against time (spirogram) or airflow against volume during a forced
expiration can help to distinguish between different types of defects. The
patient is asked to inhale to total lung capacity (TLC) and breathe out as hard
and fast as possible to residual volume (RV). A plot of volume against time
(Fig. 20a) can be produced by continuously measuring volume, either with a
spirometer or by integrating a flow meter output. If a flow meter is used, it is
also possible to compute a flow-volume plot from the same forced expiration
(Fig. 7c). Flow-volume plots show characteristic shapes with different defects
(Fig. 7e), such as the 'scooped out' appearance seen in obstructive airway
disease.
Forced vital capacity (FVC) and forced expiratory volume in ‘t’ seconds
(FEVt) can be read off the volume-time plot (Fig. 20a). FEVl
is extremely reproducible and correlates well with function and prognosis. It
is normal for FVC and FEVl to peak in adults in the third decade and
then decline by approximately 30 mL/year (Chapter 22).
Forced expiratory ratio (FER = FEVl/FVC)
is normally 0.75-0.90, but higher values may occur in healthy
children. FEVl/FVC helps distinguish between obstructive and
restrictive ventilatory defects. Typically, in obstructive lung diseases (e.g.
COPD and acute asthma), the FEVl/FVC is less than 0.70. If the
airway obstruction is due to asthma, FEVl, FVC and FEVl/FVC
may all increase after the inhalation of bronchodilators. In restrictive lung
disease (e.g. lung fibrosis) abso- lute values of FEVl and FVC are
reduced, but FEVl/FVC is normal or high.
Forced mid-expiratory flow (FEF25-75) is the average forced expiratory flow rate over the middle 50% of the FVC. It may be especially
affected by small airway disease, but the normal range is wide.
Maximal voluntary ventilation (MVV)
is measured by asking the subject
to breathe as hard and fast as possible into a spirometer for l5 seconds, with
the ventilation expressed in L/min. It is very dependent on effort and not very
reproducible, but it may correlate well with subjective dyspnoea.
Lung volumes
Typical values for lungs volumes are
given in Fig. 3, Table l, for an average-sized healthy young man. Lung volumes
are very variable and interpretation relies on comparison of the patient's
measured values with the predicted values for people of the patient's age,
height and gender, from nomograms constructed from large samples of healthy
individuals. Some volumes can be measured using simple spirometers and some
require more sophisticated techniques. Restrictive ventilatory defects
(RVDs) are characterized by a reduction in TLC. Lung volumes such as TLC,
RV and functional residual capacity (FRC) can be measured by helium dilution
(Fig. 20b) or by body plethysmography (Fig. 20c). The gas dilution
method is simpler for patients, but it is sensitive to gas leaks and will
underestimate TLC in the presence of extensive bullous or cystic lung disease.
RVDs may be caused by parenchymal lung disease (pulmonary fibrosis scleroderma,
pulmonary oedema), chest wall disease (kyphoscoliosis, massive obesity) or
weak respiratory muscles (myasthenia gravis, muscular dystrophy). RV and FRC
can help distinguish between these conditions, as FRC and RV are usually
reduced in lung disease; whereas FRC is usually normal in muscle weakness and
RV is elevated if it also affects expiratory muscles. FVC and TLC usually
decline in parallel; therefore, once a RVD has been established by measurement
of TLC, the progress of the disease may be followed with FVC from spirometry.
Measurement of lung compliance
(Chapter 6) and transdiaphragmatic pressure (Pdi) may
distinguish further between RVD due to parenchymal lung disease or muscle
weakness. By using two small balloon-tipped catheters, one measuring
oesophageal (Ppleural) pressure and the other gastric (Pabd)
pressure, Pdi ( = Pabd - Ppleural)
can be measured during a maximal inspiration or sniff from FRC. Typically, in
parenchymal lung disease lung compliance is low, elastic recoil pres- sure high
and Pdi normal; whereas in respiratory muscle weakness lung
compliance is relatively normal, elastic recoil pressure low and Pdi
low. Diffusing capacity, DL ( = transfer factor, TL),
is a measure of the ability of gas to diffuse from the alveolus into pulmonary
capillary blood. As discussed in Chapter 5, DLco is used as a
surrogate for DLo2, since it is simple to measure
and carbon monoxide diffuses across the lung in a fashion similar to oxygen. It
often helps interpretation to normalize DLco to the alveolar
volume (VA) by calculating the coeffi cient, KCO = DLco/VA.
DLco is reduced by reduced alveolar surface area, thickened
alveolar-capillary membrane, reduced capillary blood volume or anaemia.
Reductions in the DLco can be caused by a variety of
parenchymal diseases (idiopathic pulmonary fibrosis emphysema, pneumonia) or
vascular diseases (pulmonary hypertension, pulmonary oedema), such that the
test is sensitive but not specific Reductions in the DLco
below 50% predicted for age, sex and height are often associated with oxygen
desaturation during exercise. Severe reductions in
DLco
(<20% predicted) may result in resting hypoxaemia.
Arterial blood gases (Pao2, Paco2
and pHa) and arterial oxygen saturation are important tests of
respiratory system function and are discussed in Chapters 23 and 43.
