Pulmonary Function Tests - pediagenosis
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Thursday, December 6, 2018

Pulmonary Function Tests

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.

Pulmonary Function Tests

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.

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