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Pulmonary Function Tests in Clinical Practice
Pulmonary Function Tests in Clinical Practice
Ali Altalag, Jeremy Road, and Pearce Wilcox
Ali Altalag, MD Respirologist and Critical Care Fellow University of Toronto Toronto General Hospital 585 University Ave, 11C-1170 Toronto, ON, M5G 2N2 Canada
Jeremy Road, MD Professor of Medicine University of British Columbia Medical Director of Pulmonary Function Lab Vancouver General Hospital 2775 Laurel Street, 7th Floor Vancouver, BC, V5Z 1M9 Canada
Pearce Wilcox, MD Associate Professor of Medicine University of British Columbia Medical Director of Pulmonary Function Lab St. Paul’s Hospital 1081 Burrard Street Vancouver, BC, V6Z 1Y6 Canada ISBN 978-1-84882-230-6 e-ISBN 978-1-84882-231-3 DOI 10.1007/978-1-84882-231-3
British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Control Number: © Springer-Verlag London Limited 2009 Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or transmitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of reprographic reproduction in accordance with the terms of licences issued by the Copyright Licensing Agency. Enquiries concerning reproduction outside those terms should be sent to the publishers. The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a speciﬁc statement, that such names are exempt from the relevant laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. In every individual case the respective user must check its accuracy by consulting other pharmaceutical literature. Printed on acid-free paper springer.com
The volume of expelled air is believed to have been first measured by Galen in about 150 AD. However, it was not until the mid-1800s that Hutchinson designed a spirometer, very similar to the ones used today, which allowed routine measurement of exhaled lung volume. Finally, in 1969 Dubois designed the plethysmograph, which allowed a measure of the complete lung volume, which included the residual volume. Nowadays measuring spirometry has become routine with the advent of the pneumotachograph and computers. Although the technology is widely available and not excessive in cost, spirometry or the measurement of exhaled gas volume is still underutilized. To detect disease and assess its severity lung volume measures are extremely useful, indeed one might say mandatory, so the reason for this underutilization remains obscure. We hope that this book, which is aimed at the clinician, helps to explain the basics of lung volume measurement and hence increases its utility. The text also includes an overview of exercise and respiratory sleep diagnostic tests for the clinician. Ali Altalag Jeremy Road Pearce Wilcox Toronto, ON Vancouver, BC Vancouver, BC
Jennifer Wilson. A special acknowledgment to Dr. John Marshall. Dr. Abdulaziz Alsaif. and Dr. Dr. Peter Paré. Mark Fitzgerald. Dr. and Dr. Najib Ayas. John Fleetham. Dr.Acknowledgements We acknowledge everyone who helped in producing this book. Dr. Dr. Dr. John Granton. We also acknowledge Dr. vii . Turki Altassan. Raja Abboud. A special thanks to Bernice Robillard. Majdi Idris.
. . . . . . . . . . . . . . . . . . . . . . 1. . . 4. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Approach to PFT Interpretation . . . . . . v vii 1 37 59 71 81 91 107 133 157 217 265 271 275 277 Appendix 1. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Index . . . . . . . . . . . 9. . . . 10. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lung Volumes . . . 3. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6. . . . . . . Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8. . . . . . .Contents Preface . . . . . . . . . . . . . . . . . . . Appendix 3. . . . . . . . . . . . . . . . . 5. . Bronchial Challenge Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix . . . . . Appendix 2. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gas Transfer . . . . . Respiratory Muscle Function and Other Pulmonary Function Studies . . . . . . . . . . . . . . . . . . . . . Spirometry . . . . . . . . . . . . 2. . . . . . . . . . . . Diagnostic Tests for Sleep Disorders. . . . . . . . . . . . . . . . . . . . . . . . 7. . . . . . . . . . . . . . . . . . . . Exercise Testing . . . . . . . . . . . . . . . . . . . . . . . . Arterial Blood Gas Interpretation . . . . . Illustrative Cases on PFT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
• The inspiratory vital capacity (IVC) is the VC measured during inspiration rather than expiration.. but the exhalation is slow rather than being as rapid as possible as in the FVC. The IVC should equal the expiratory VC.Chapter 1 Spirometry Spirometry is the most essential part of any pulmonary function study and provides the most information.1007/978-1-84882-231-3_1. the SVC is usually larger than the FVC.3 while in patients with an obstructive lung disorder (see Table 1. the SVC usually equals the FVC. in obstructive lung disorders. the airways tend to collapse and close prematurely because of the increased positive intrathoracic pressure during a forceful expiration. © Springer-Verlag London Limited 2009 . The two most important dynamic lung volumes measured are the forced vital capacity (FVC) and the forced expiratory volume in the 1st second (FEV1). In spirometry. FVC is unique and reproducible for a given subject. Figure 1.1 for definition). The reason for this is that. a machine called a spirometer is used to measure certain lung volumes. Accordingly. Pulmonary Function Tests in Clinical Practice. • The slow vital capacity (SVC) – also called the vital capacity (VC) – is similar to the FVC. 2 Forced Vital Capacity • Is the volume of air in liters that can be forcefully and maximally exhaled after a maximal inspiration. DOI: 10. In a normal subject. called dynamic lung volumes. If it does not.1. a significantly higher SVC compared with FVC suggests air-trapping. DEFINITIONS1. This increased pressure leads to air trapping. This section deals with the definitions of these and other terms. poor effort or an air leak could be 1 Ali Altalag et al.
IVC may be larger than the expiratory VC in patients with significant airway obstruction.8 The changes in the elderly probably reflect the decrease in elastic recoil of the lungs that occurs with aging. see Table 1.1 for definitions. however. indicating air trapping.7. • Normally. responsible. SVC is larger than FVC.7) with normal aging. the ratio is either normal or even increased as the drop in FVC is either proportional to or more marked than the drop in FEV1. FVC and SVC are compared with each other in a normal subject (a) and in a patient with an obstructive disorder (b). and it normally represents ~80% of the FVC.7 In children. In case of airway obstruction. it is higher and can reach as high as 0. In obstructive disorders. In other words. but it decreases (to values <0. while in restrictive disorders. it is the volume of air that is exhaled in the 1st second of the FVC. 5 Narrowed airways reduce airflow and hence the amount of exhaled air. • FEV6 is similarly defined as the volume of air exhaled in the first 6 s of the FVC and its only significance is that it can sometimes substitute the FVC in patients who fail to exhale completely. .4.2 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 1.9. the FEV1/FVC ratio is greater than 0. as opposed to the narrowing of airways during exhalation as the intrathoracic pressure becomes positive. FEV1 drops much more significantly than FVC and the ratio will be low. as in this case the increased negative intrathoracic pressure opens the airways facilitating inspiration.1.6 FEV1/FVC Ratio • This ratio is used to differentiate obstructive from restrictive lung disorders. Forced Expiratory Volume in the 1st Second • Is the volume of air in liters that can be forcefully and maximally exhaled in the 1st second after a maximal inspiration.
1. and 75% of the FVC.g.g.SPIROMETRY 3 TABLE 1.10 Peak Expiratory Flow • Is the maximum flow (in liters per second) of air during a forceful exhalation.. They are abbreviated as FEF25. it takes place immediately after the start of the exhalation and it is effort-dependent. namely at 25.2b. however. bronchial asthma.9 Collectively.11 Their usefulness is limited. however.. Normally.10. restrictive disorders. Definitions of obstructive and restrictive disorders Obstructive disorders Are characterized by diffuse airway narrowing secondary to different mechanisms [immune related. they are considered more sensitive (but non-specific) in detecting early airway obstruction. FEF50. PEF drops with a poor initial effort and in obstructive and. FEF75) and the Maximum Mid-Expiratory Flow (MMEF or FEF25–75) • The instantaneous forced expiratory flow (FEF) represents the flow of the exhaled air measured (in liters per second) at different points of the FVC. and FEF75. The maximum mid-expiratory flow (MMEF) or FEF25–75. . 50. which tends to take place at lower lung volumes. FEF50. is the average flow during the middle half of the FVC (25–75% of FVC). chronic obstructive pulmonary disease (COPD)] Restrictive disorders Are a group of disorders characterized by abnormal reduction of the lung volumes. or environmental. because of the wide range of normal values. to a lesser extent. e. either because of alteration in the lung parenchyma or because of a disease of the pleura.2c. These variables represent the effort-independent part of the FVC. e. PEF measured in the laboratory is similar to the peak expiratory flow (PEF) rate (in liters per minute) that is measured routinely at the bedside to monitor asthmatic patients. see Figure 1. Figure 1. respectively. chest wall or due to muscle weakness The Instantaneous Forced Expiratory Flow (FEF25.
4 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE .
Figure 1. which needs to be at least 6 s for the study to be clinically reliable. • If a postbronchodilator study is done. FEF25–75 represents the slope of the curve at those two points.2a. see Figure 1. duration of the study (the forced expiratory time or FET) can be determined from the time axis. Note that this method represents a rough determination of FEFs. FEV1/FVC ratio can be estimated by looking at where the FEV1 stands in relation to the FVC in the volume axis. b. One curve will represent the initial (prebronchodilator) study whereas the second will represent the postbronchodilator study. • You can extract from this curve both the FVC and FEV1. Dividing the volumes (a. FIGURE 1. Quality control will be explained in more detail later in this chapter.SPIROMETRY 5 SPIROMETRIC CURVES The Volume–Time Curve (The Spirogram) • Is simply the FVC plotted as volume in liters against time in seconds. FEF75. FEF50. if any. then there will be two discrete curves. B. FEF50. c.2. In addition. Looking at how the two curves compare to each other gives an idea about the degree of the response to bronchodilator therapy. Figure 1.75 can be roughly determined by dividing the volume axis into four quarters and determining the corresponding time for each quarter from the time axis. as in case of suspected bronchial asthma. and c) by the corresponding time (A. (b) FEF25. The volume–time curve (spirogram). as it shows the duration of the exhalation [the forced expiratory time (FET)]. and C) gives the value of each FEF (FEF25.2a. (c) FEF25–75 can be roughly determined by dividing the volume during the middle half of the FVC (c–a) by the corresponding time (C–A). The following data can be acquired: (a) FVC is the highest point in the curve. .16. Figure 1.2b. respectively). The FEFs (FEF25. FEV1 is plotted in the volume axis opposite to the point in the curve corresponding to 1 s.50. as FEFs are actually measured instantaneously by the spirometer and not calculated. • This curve also provides an idea about the quality of the spirometry.16. FEF75) and MMEF (FEF25–75) can also be roughly estimated from the curve as shown in Figure 1. the curve’s shape helps in determining that ratio: a decreased ratio will necessarily make the curve look flatter and less steep than normal. 6 s in this curve.
as different diseases produce distinct curve shapes.* This curve is more informative and easier to interpret. Either method allows expression of the ﬂow– volume curve. * The ﬂow can be measured directly by a pneumotachograph. . Alternatively.3. a volume sensing device (spirometer) measures volume and the ﬂow is derived by differentiating the volume signal. Figure 1.6 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE The Expiratory Flow–Volume Curve (FV Curve) • Is determined by plotting FVC as flow (in liters per second) against volume (in liters). The volume is obtained by integration of the ﬂow signal.
• The curve starts at full inspiration (at the total lung capacity or TLC: the total amount of air in the lungs at maximal inhalation; Figure 1.3a) with 0 flow (just before the patient starts exhaling), then the flow or speed of the exhaled air increases exponentially and rapidly reaches its maximum, which is the PEF. The curve then starts sloping down in an almost linear way until just before reaching the volume axis when it curves less steeply giving a small upward concavity. The curve then ends in that way at the residual volume or RV (the amount of air that remains in the lungs after a maximal exhalation) by touching the volume axis, i.e., a flow of 0 (or within 0.1 L/s)8 when no more air can be exhaled; Figure 1.3a. • As you notice, there is no time axis in this curve, and the only way to determine the FEV1 is by the reading device making a 1st second mark on the curve, which is normally located at ~ 80% of the FVC. See Figure 1.3a. • Other data can be extracted from this curve including FEF25, 50, 75 as shown in Figure 1.3b. FEF25–75 cannot be determined from this curve. • In summary, every part of the curve represents something; Figure 1.3: – The leftmost end of the curve represents TLC. – The curve’s rightmost end represents RV. – Its width represents FVC. – Its height represents PEF. – The distance from TLC to the 1-s mark represents FEV1. – The descending slope reflects the FEFs. • Remember that we cannot measure RV and hence TLC with spirometry alone, because we cannot measure the air remaining in the lung after a full exhalation with this method. Methods that can measure RV are discussed in the next chapter. • The morphology of the curve is as important as the other values. It provides information about the quality of the study as well as being able to recognize certain disease states from its shape. These will be explained in detail later in this chapter.
FIGURE 1.3. (a) The flow–volume curve: the following data can be extracted: (1) TLC is represented by the leftmost end of the curve (cannot be measured by spirometry); (2) RV is represented by the rightmost end of the curve (cannot be measured by spirometry); (3) FVC is represented by the width of the curve; (4) PEF is represented by the height of the curve; (5) FEV1 is the distance from TLC to the 1st second mark. (b) The flow– volume curve demonstrating the effort-dependent and the effort-independent parts. Instantaneous FEFs are directly determined from the curve by dividing the FVC into four quarters and getting the corresponding flow for the first, second, and third quarters representing FEF25,50,75, respectively as shown. The FEFs represent the slope of the FV curve.
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
• Two curves are often shown in different colors (blue and red) to depict pre- and postbronchodilator studies, respectively, if a postbronchodilator study was done; Figure 1.15b. The Maximal Flow–Volume Loop • Combining the expiratory flow–volume curve, discussed earlier, with the inspiratory curve (that measures the IVC) produces the maximal flow–volume loop, with the expiratory curve forming the upper and the inspiratory curve forming the lower parts of that loop; see Figure 1.4. • This loop is even more informative than the expiratory flow– volume curve alone, as it also provides information about the inspiratory portion of the breathing cycle. For example, extrathoracic upper airway obstruction, which occurs during inspiration, can now be detected. • This loop commonly includes a tidal flow–volume loop too, shown in the center of the maximal flow–volume loop as a small circle; Figure 1.4. This loop represents quiet breathing. Additional useful data can be acquired from this tidal loop when compared with the maximal flow–volume loop. These useful data include the expiratory reserve volume (ERV) and the inspiratory capacity (IC); Figure 1.4b – see next chapter for definitions. The values of ERV and IC estimated from this curve might be slightly different from the lung volume study measurements, where the SVC is measured instead of the FVC as these (FVC and SVC) can be different in some disorders such as obstructive disorders, as was discussed earlier. More details about these measurements will be discussed in the following chapter. TECHNIQUE OF SPIROMETRY1 • The spirometer – the machine used to record spirometry – has to be calibrated every morning to ensure that it records accurate values before it is used. The temperature and barometric pressure are entered into the spirometer every morning, as variation in these measures does affect the final results†.12–14 • The patient must be clinically stable, should sit straight, with head erect, nose clip in place, and holding the mouthpiece tightly between the lips. Initially, he or she should breathe in and
As air in the lungs is at BTPS (body temperature pressure standard) but collected at ATPS (ambient temperature pressure standard), a correction factor has to be applied to obtain the BTPS volumes as these are the reported volumes.
FIGURE 1.4. (a) Represents the steps in data measurement during spirometry. (b) Demonstrates the ERV and IC in relation to the tidal flow–volume loop (VT stands for tidal volume).
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
out at the tidal volume (VT: normal quiet breathing) to record the tidal flow–volume loop; Figure 1.4a, No. 1. Then, when the patient is ready, the technician instructs him/her to inhale maximally to TLC (Figure 1.4a, No. 2), and then exhale as fast and as completely as possible to record the FVC (Figure 1.4a, No. 4). The point at which no more air can be exhaled is the RV (Figure 1.4a, No. 3). The patient is then instructed to inhale fully to TLC again in order to record the IVC (Figure 1.4a, No. 5). This test is then repeated to ensure reproducibility in order to meet quality control criteria (American Thoracic Society or ATS criteria); see next section. • If a bronchodilator study is needed, then the test is repeated in the same way 10 min after giving the patient a short-acting b2 agonist (usually 2–4 puffs of salbutamol through a spacer chamber). The ATS criteria should be met in the postbronchodilator study too. • The spirometer will produce the volume as absolute numbers and as curves. • The technician should make a note to the interpreting doctor of any technical difficulty that may have influenced the quality of the study. Technician’s comments are important as are the ATS criteria in the final report. THE ATS GUIDELINES1,2 The ATS criteria are easy to remember. They include both acceptability and reproducibility criteria. This means that each individual study should meet certain criteria to be accepted, and the accepted studies should not vary more than predefined limits to ensure reproducibility. If either of the criteria are not met, then the study is rejected as it may give a false impression of either normal or abnormal lung function. Of course, bedside tests or field testing, e.g., in the emergency department, do not, in many instances, meet the ATS criteria that are required for measures in an accredited laboratory. Acceptability1,2 The ATS mandates three acceptable maneuvers. The number of trials that can be performed on an individual should not exceed 8. An acceptable trial should have a good start, a good end, and absence of artifacts. 1. Good start of the test: • If the study needs back extrapolation, the extrapolation volume should not exceed 5% of FVC or 150 ml, whichever is larger. See Figure 1.5.1,2,15–19
FIGURE 1.5. Extrapolation volume of 150 ml or 5% of FVC (whichever is larger) (with permission from American Thoracic Society2).
Note: Back extrapolation applies to the VT curve and means that if the start of the test is not optimal, correction can be made by shifting the time axis forward, provided that the extrapolation volume is within either one of the limits mentioned earlier. To simplify this, consider that a patient’s FVC is 2 L and the study requires a back extrapolation correction, and 5% of the FVC (2 L) is 100 ml. Because 150 ml is larger than 5% of the patient’s FVC (100 ml), 150 ml should be used as the upper limit of extrapolated volume. Then, if the measured extrapolated volume is greater than 150 ml, the result cannot be accepted. Note: A good start of the study can be identified qualitatively on the FV curve as a rapid rise of flow to PEF from the baseline (0 point), with the PEF being sharp and rounded. The FEV1 can be over- or underestimated with submaximal effort, which may mimic lung disorders such as those due to airway obstruction or lung restriction; see later.2,20 2. Smooth flow–volume (FV) curve, free of artifacts1,2: These artifacts will show in both volume–time (VT) and FV curves but will be more pronounced in the FV curve. These artifacts include the following: (a) Cough during the 1st second of exhalation may significantly affect FEV1. The FV curve is sensitive in detecting this artifact; Figure 1.6. Coughing after the 1st second is less likely to make a significant difference in the FVC and so it is accepted provided that it does not distort the shape of the FV curve (judged by the technician).1
Variable effort: any study with a variable effort is rejected (with permission from American Thoracic Society2).8. Figure 1. Figure 1. FIGURE 1. (d) Early termination of effort.6.8. FIGURE 1. It is much clearer in the FV curve than in the VT curve as indicated by the arrows (with permission from American Thoracic Society2). . FIGURE 1.7.12 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE (b) Variable effort. Cough in the 1st second.7. (c) Glottis closure. Glottis closure (with permission from American Thoracic Society2).
the continuation of the curve will be plotted from the beginning of the time axis (with permission from American Thoracic Society2). Good end of the test (demonstrated in the VT curve): (a) Plateau of VT curve of at least 1 s.e. Figure 1. OR FIGURE 1.16.9. more commonly.e. by applying the tongue through the mouthpiece or biting it with the teeth. . i. Air leak can be detected from the FV loop. volume is not changing much with time indicating that the patient is approaching the residual volume (RV).9.2. however. Normal individuals.SPIROMETRY 13 (e) Obstructed mouthpiece.2: • Six seconds is the minimum accepted duration (3 s for children1). when the curve exceeds the limit of the time axis. Notice that.11e. can empty their lung (i. i...e.1 Patients with obstructive disorders can exhale for more than 40 s before reaching their RV. reach a plateau) within 4 s.21: • The air leak source could be due to loose tube connections or.2 OR (b) Reasonable duration of effort (FET)1. Mild airway obstruction. with prolonged duration of exhalation (20 s). before reaching a plateau in the VT curve. 3. because the patient weakly applies lips around the mouthpiece. • Ten seconds is the optimal.1. (f) Air leak1.. Figure 1.22 • FET of >15 s is unlikely to change the clinical decision and may result in the patient’s exhaustion.
11 shows the morphology of FV curve in acceptable and unacceptable maneuvers. This poor technique may result in underestimation of the FVC.1.10. the following reproducibility criteria should be applied: – The two largest values of FVC must be within 150 ml of each other.10. • If the studies are not reproducible. A downward concavity. indicates that the patient either stopped exhaling (prematurely) or started inhaling before reaching the RV.2 • After obtaining three acceptable maneuvers. however.2 FIGURE 1. Poor end in comparison to good end (small upward concavity) of FV curve.1. Reproducibility1. Figure 1. then the studies should be repeated until the ATS criteria are met or a total of eight trials are completed or the patient either cannot or should not continue testing. A poor end (downward concavity) indicates premature termination of exhalation (before 0 flow).10 • Figure 1.14 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE (c) The patient cannot or should not continue to exhale.2 Note: A good end of the study can be shown in the FV curve as an upward concavity at the end of the curve. – The two largest values of FEV1 must be within 150 ml of each other. .
11. (c) Shows a cough in the 1st second. (e) Shows air leak. with good start. (b) Shows a poor start. good end. (d) Shows a poor end. . and free from artifacts.SPIROMETRY 15 FIGURE 1. (a) An acceptable FV curve.
12.2 FIGURE 1. – The other flow parameters should be taken from the best test curve (which is the curve with the highest sum of FVC + FEV1).12 and 1.16 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • The final values should be chosen based on the following1. because the patient may not produce maximum effort in all trials. – If reproducibility cannot be achieved after eight trials. Acceptable and reproducible trials (with permission from American Thoracic Society2). . acceptable trials are not necessarily reproducible. the best test curve (the highest acceptable trial) should be reported. Figures 1. Acceptable but not reproducible trials (With permission from: American Thoracic Society2).13 give some useful examples.2: – FEV1 and FVC should be reported as the highest values from any acceptable/reproducible trial (not necessarily from the same trial). FIGURE 1. The technician should comment on this deviation from protocol so that the interpreting physician understands that the results may not be accurate.13. • Finally.
27 • The available reference values apply only to Caucasians on whom the original studies were performed. by looking at any FV curve.e. Figure 1. while interpreting the lung functions of a black American.29.14. If it is difficult to measure the height. The 5th percentile (1. Table 1. although they are usually taller. An adjustment factor of 0. you need to make race-specific corrections to the standard predicted values. because blacks have higher leg length to torso length ratios.14.11a: Good start with sharp and rounded PEF Smooth continuous decline free from artifacts Good end with a small upward concavity at or near the 0 flow The ideal VT curve should either have a plateau for 1 s or show an effort of at least 6 s • Now.10.28) – A fourth important variable is race (Caucasians have bigger lungs than Africans and Asians). Keep in mind that the lack of any of these features may indicate a lung disorder rather than a poor study. you should be able to tell whether or not it reflects an acceptable study.2 summarizes the features of the ideal FV and VT curves.23–27 • The reference values for the PFT have a wide range of normal as the lung size varies considerably in the normal subjects.94 is recommended for Asian Americans. as in kyphoscoliosis. smaller lungs. Figure 1. used to define the lower limit of the reference range for that given sex.) – Height (Tall people have bigger lungs. Table 1. then. REFERENCE VALUES10. age. and race. Figure 1.SPIROMETRY 17 TABLE 1. height.65 standard deviations) is. related to differing body proportions (legs to torso) • Spirometric measurements from a group of healthy subjects with a given sex. then the arm span can be measured instead. Features of the ideal FV and VT curves The ideal FV curve should have the following features.30 . Blacks are well studied too. So. height.2. These values depend on certain variables: – Sex (Men have bigger lungs than women. age.. and they generally have lower predicted values than the Caucasians.27 • Asians also have lower values than the standard predicted values. and race usually exhibit a normal distribution curve. i.3.10.14.) – Age (The spirometric values drop with age.
The predicted values used (reference equations) should be representative of the population being tested.10.88 0. then his/her values should roughly lie within 80–120% of predicted values.‡ When you interpret a PFT.65 standard deviations (the 5th percentile) to define the lower limit of normal will include 95% of that population. Applying 1.93 1 (i.18 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Figure 1. . If the patient is normal. The predicted values for a group of normal subjects at a given height.. DLCO FEV1/FVC ratio Correction factor 0. no correction needed) Blacks have smaller lungs than Caucasians and their lung function values need to be adjusted by multiplying these correction factors by the reference values acquired from Caucasian studies. TLC RV.* ‡ Using a ﬁxed value of the lower limit of normal (80%) may be accepted in children but may lead to some errors in adults.e. Correction factors for the PFT of Black Americans Variable FEV1. age. Many software programs for lung function testing can display the LLN and interpreting physicians may use this to determine normality. Values outside this range are then below the limit of normal (LLN).27 *As can be seen in ﬁgure 1.). FVC.14 the 95% conﬁdence limit may be used for normality as well.27 • The standard normal values roughly range from 80 to 120% of the predicted values that are derived from Caucasian studies. and sex form a normal distribution curve.14. TABLE 1. you should always look at the patient’s results as percentage of the predicted values for that particular patient (written in the report as % pred.3.
or mixed). patients are advised to stop taking any short-acting β2 agonists or anticholinergic agents within 4 h of testing. and the value of FEV1 is used to determine severity27.4. Response to bronchodilators suggests asthma.4.SPIROMETRY 19 • The absolute value for each variable has some significance. which optimizes the delivery of salbutamol. you will know that this is far below the expected for an average young adult and will warrant some attention.10 The traditional way of grading severity of obstructive and restrictive disorders involve the following: – In obstructive disorders. • Recently. chronic obstructive pulmonary disease (COPD). but other obstructive lung disorders can respond to bronchodilators as well.1 Long-acting β2 agonists (like formoterol and salmeterol) and oral aminophylline should be stopped at least 12 h before the test.36.§38–45 • For the test to be accurate. The ATS suggested using the TLC to grade the severity of restrictive disorders. FVC may be used to make that grading.35.27. but if somebody tells you that your patient’s FVC is 1 L. Table 1.1 Smoking should be avoided for ≥1 h prior to testing § A spacer is an attachment to the MDI. restrictive.e. which cannot be measured in simple spirometry.37 The bronchodilator of choice is salbutamol delivered by metered dose inhaler (MDI).27 Where only spirometry is available. FVC equals roughly 5 L in an average young adult.34.31–33.4. but this change is not considered significant. As an example. . the FEV1/FVC ratio should be <0. FEV1 has been selected to grade severity of any spirometric abnormality (obstructive.. GRADING OF SEVERITY • Different variables and values were used to grade severity of different pulmonary disorders10. however.7. however. – In restrictive disorders. i. through a spacer. BRONCHODILATOR RESPONSE • Bronchodilators can be used in selected patients following the initial spirometry. Normal subjects can also respond to bronchodilators by as much as 8% increase in FVC and FEV1. FEV1/FVC ratio is normal and the TLC is less than 80% predicted. should be known before confidently diagnosing a restrictive disorder27. This number could vary significantly among normal individuals. Table 1. Table 1.27 The TLC.
) Moderate 60–69 Severe <60 Restrictive disorder (based on FVC.1.20 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 1. restrictive. Methods of grading the severity of obstructive and restrictive disorders (A) Grading of severity of any spirometric abnormality based on FEV110 After determining the pattern to be obstructive.27 ● Obstructive disorder (based on FEV1) – Ratio < 0.7 FEV1 ³100 (% pred.8 The technicians’ comment should indicate if a patient has just had a bronchodilator prior to the study. they do not need to be stopped. in case no lung volume study is available) Mild Moderate Moderately severe Severe Very severe FVC > 70 (% pred.) 60–69 50–59 35–49 May be a physiologic variant ● ● <35 *This is a widely used grading system but different organizations use different systems of grading.4. . FEV1 is used to grade severity: Mild Moderate Moderately Severe Severe Very severe FEV1 > 70 (% pred. preferred) Mild TLC > 70 (% pred. and so. Inhaled or systemic steroids do not interfere with the test results. and throughout the procedure.14 Caffeine-containing substances should be avoided the day of testing.) 60–69 50–59 35–49 <35 (B) Traditional method of grading the severity of obstructive and restrictive disorders*. or mixed.) Mild 70–100 Moderate 60–69 Moderately severe 50–59 Severe 35–49 Very severe <35 Restrictive disorder (based on TLC.
These features include the following: – The height of the curve (PEF) is much less than predicted.10 FEV1 may be reduced too and is used to define the severity of obstruction. these components are also shown in this table. – The descending limb is concave (scooped). SPIROMETRIC PATTERN OF COMMON DISORDERS In this section. ¶ Increments of as high as 8% or 150 ml in FEV1 or FVC are likely to be within the variability of the measurement. as it has a distinct shape in such disorders.46 COMPONENTS OF SPIROMETRY • Table 1. we will discuss the PFT pattern of some common disorders. see Table 1. you may see multiple other parameters that are not discussed here and have little or even no clinical usefulness. Figure 1. FVC may be reduced in obstructive disorders but usually not to the same degree as FEV1. In any spirometry report.15. The slope of the descending limb that represents MMEF and FEFs is reduced due to airflow limitation at low lung volumes. with the outward concavity being more pronounced with more severe obstruction.5 summarizes the causes of abnormal spirometric components.6 summarizes the effects of different lung disorders on every component of spirometry. • Table 1.¶10. Obstructive Disorders • The two major obstructive disorders are bronchial asthma and COPD. The key to the diagnosis of these disorders is the drop in FEV1/FVC ratio.18.104.22.168 . Table 1.7. For the purpose of completeness.SPIROMETRY 21 • The definition of a significant response to bronchodilators according to ATS & ERS (European Respiratory Society) is increase in FEV1 or FVC by >12% and >200 ml in the postbronchodilator study. • The features of obstructive disorders are summarized in Table 1. • The flow–volume curve can be used alone to confidently make the diagnosis of obstructive disorders.
50.48–50 This sign.47 (associated with flattening of the expiratory curve of the flow–volume loop) Restrictive disorders other than pulmonary fibrosis FEF(25. 25–75) Decreased in obstructive and restrictive disorders Decreased also in variable extrathoracic or fixed upper airway obstruction Reduction in FEF75 and/or FEF25–75 may be the earliest sign of airflow obstruction in small airways. see also Table 1.5. 75. is not specific for small airway disease.11 FET (forced expiratory time) May be increased in obstructive disorders PIF (peak inspiratory flow) Decreased in variable extrathoracic or fixed upper airway obstruction FIF50 (forced inspiratory flow at 50% of FIVC) Decreased in variable extrathoracic or fixed upper airway obstruction FIVC (forced inspiratory vital capacity) Its main use is to check for the quality of the study (for air leak) FIF50/FEF50 Increased in variable intrathoracic upper airway obstruction (>1)10 Decreased in variable extrathoracic upper airway obstruction (<1).10 .6 FEV1 Decreased in obstructive and. Table 1.10. Causes of abnormal spirometric components FVC Increased in acromegaly8 Decreased in restrictive disorders (most important) and obstructive disorders.9.22 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 1. restrictive disorders FEV1/FVC ratio Increased in interstitial lung diseases (ILD) such as pulmonary fibrosis (because of increased elastic recoil that results in a relatively preserved FEV1) Decreased in obstructive disorders (asthma and COPD) PEF May be increased in pulmonary fibrosis (because of increased elastic recoil) Decreased in the following: Obstructive disorders (COPD. however. asthma) Intrathoracic or fixed upper airway obstruction10. to a lesser extent.46.
e.g. muscular dystrophy. large pleural tumor) . obesity) Obesity (restricting chest wall movement) Loss of air spaces: Resection (lobectomy. Causes of obstructive and restrictive disorders Causes of obstructive disorders Bronchial asthma (usually responsive to bronchodilators) COPD Causes of restrictive disorders Parenchymal disease as pulmonary fibrosis and other interstitial lung diseases (ILD) Pleural disease as pleural fibrosis (uncommon) Chest wall restriction: Musculoskeletal disorders (MSD).1 for more detail. FEF75.SPIROMETRY 23 TABLE 1. Diaphragmatic distention (pregnancy.6. Features of obstructive and restrictive disorders Features of obstructive disorders Diagnostic features: ↓ FEV1/FVC ratio Other features: ↓ FEV1 ↓ FVC (can be normal) ↓ FEFs and MMEF (FEF25. but it can be normal ↓ MMEF PEF: normal.g. FEF50. severe kyphoscoliosis Neuromuscular disorders (NMD). pneumonectomy) Atelectasis Tumors (filling or compressing alveolar spaces) Pulmonary edema (alveolar spaces become filled with fluid) Pleural cavity disease (pleural effusion. e. old poliomyelitis. extensive cardiomegaly. see Table 5. FEF25–75) ↓ PEF ↓ FET Significant bronchodilator response Scooped (concave) descending limb of FV curve Features of restrictive disorders Most important features: ↓ FVC and normal or ↑ FEV1/FVC ratio Other features: ↓ FEV1 (proportional to FVC). or decreased Steep descending limb of FV curve TABLE 1.7. amyotrophic lateral sclerosis (ALS). increased. paralyzed diaphragm. ascites.
most likely bronchial asthma. and FVC]. There are five features that make the diagnosis of a significant airway obstruction definite. FEV1/FVC ratio. Reversibility in the correct clinical context (i. Obstructive disorders (FV curve): (a) The FV curve looks technically acceptable. 1 – Decreased PEF when compared to the predicted curve. 3 – The 1st second mark is almost in the middle of the curve indicating that the FEV1 and FEV1/FVC ratio are significantly decreased.16. 2 – Scooping of the curve after PEF. – The width of the curve (FVC) as seen in the volume axis may be decreased compared with that of the predicted curve. .24 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 1. based on this curve alone.15b. Figure 1. with good start and end. – Decreased FEV1 and FEV1/FVC ratio are easily noted by identifying the 1st second mark (FEV1) and where it lies in relation to the FVC. FEV1. Lack of bronchodilator response does not exclude bronchial asthma as responsiveness can vary over time. – A postbronchodilator study. Figure 1. excluding a central airway obstruction. 5 – The inspiratory component of the curve is normal. 4 – FVC is decreased when compared to the predicted curve.e. indicating airflow limitation. represented by the red curve. young nonsmoker) supports the diagnosis of asthma. Similarly many patients with COPD can show reversibility. (b) There is a clear response to bronchodilators indicating reversibility and supporting the diagnosis of an obstructive disorder. the curve’s outward concavity (FEF).15. • The VT curve similarly has its distinct features of obstructive disorders. and absence of artifacts in the 1st second. namely asthma. demonstrates an improvement in all of the aforementioned variables [PEF. These improvements strongly suggest a specific obstructive disorder.
The FEV1/FVC ratio has to be preserved or increased. however.35 • Table 1. 2 – FEV1 and the FEV1/FVC ratio are decreased in the black curve.48–50 Another clue is the prolonged FET evident in the VT curve. with subsequent improvement of FEV1. as the distal upward concavity may show to be more pronounced and prolonged. The morphology of the FV curve can give a clue. the key to the diagnosis is the drop in FVC. the clinical significance of these mild changes is unknown. Remember that normal FVC or VC excludes lung restriction.9 Restrictive Disorders • In restrictive disorders. such as pulmonary fibrosis.18. the airways tend to collapse significantly at low lung volumes. . giving a characteristic “dog-leg” appearance in FV curve. indicated by the slope of the curve. Figure 1. However.10 To make a confident diagnosis of a restrictive disorder. FVC.35 So. Feature of obstructive disorders in VT curve: 1 – The black curve (prebronchodilator study) is less steep compared with the dashed curve (the predicted).34. based on spirometry alone. as the volume of the air spaces is significantly lower than normal. 6 – The curve morphology improves following bronchodilator therapy (the gray curve).6 summarizes the features of a restrictive disorder in spirometry and Table 1.7 summarizes the etiology.16. 3 – The FVC is also decreased.17. 5 – MMEF is also decreased.34.17. – In emphysema and because of loss of supportive tissues. • Special Conditions – In mild (or early) airway obstruction. the earlier features are reported as suggestive (not diagnostic) of a restrictive disorder. 4 – A prolonged FET (length of the curve) suggests airway obstruction. the classic reduction in FEV1 and FEV1/FVC ratio may not be seen.SPIROMETRY 25 FIGURE 1.27. the TLC should be measured and should be low. Figure 1. Figure 1. The lung elasticity increases and the lungs retract. and FEV1/FVC ratio.
. • FV curve features of restrictive disorders are described as follows: – For parenchymal lung disease (e. FIGURE 1.26 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 1. . Dog-leg appearance typical of emphysema.17. Mild airway obstruction (with permission from American Thoracic Society2).18.19a: (a) The PEF can be normal or high because of the increased elastic recoil that increases the initial flow of exhaled air.g. Figure 1. pulmonary fibrosis).
The reduction in MMEF. i. . PEF may be low as the disease progresses due to the reduced volumes exhaled. (c) NMD (or poor effort study) producing a convex curve..19. (b) chest wall restriction (excluding NMD). in this case. FIGURE 1.e. fewer liters per second. low MMEF).SPIROMETRY 27 However. does not indicate airflow obstruction and is related to the reduced volumes. (b) The width of the curve (FVC) is decreased and the 1st second mark (FEV1) on the descending limb of the curve is close to the residual volume indicating a normal or high FEV1/FVC ratio.. (c) The slope of the descending limb of the curve is steeper than usual due to high lung recoil or elastance (i.e. FV curve features of different forms of restriction: (a) ILD with witch’s hat appearance.
e. the obstruction will be more pronounced during expiration. Figure 1. Figure 1. • The volume–time (VT) curve will maintain the normal morphology but will be smaller than the predicted curve in restrictive disorders. Patm) and hence flow is reduced (flattened curve) during the inspiratory limb of the FV curve. a wheezy sound during inspiration.19b: (a) PEF is decreased as the elastic recoil of the lung is not increased here. diaphragmatic distention. extrathoracic portion of trachea) is relatively negative during inspiration compared with the pressure outside the airways (atmospheric pressure. 2. The MMEF is similarly decreased. Variable extrathoracic obstruction (above the level of sternal notch) (a) The word variable means that the obstruction comes and goes during a maximum inspiratory or expiratory effort. The obstruction has to be mobile or dynamic to follow this pattern. In variable extrathoracic obstruction. This is because the pressure inside the airways (larynx.20a. these disorders must be advanced to allow detection by this technique. and obesity). making the whole curve looking like the predicted curve but smaller. pharynx. There are three types of upper airway obstruction recognizable in the FV curve: 1. airway obstruction takes place during inspiration. The central intrathoracic airways (intrathoracic trachea and main bronchi) narrow when they are compressed . Variable intrathoracic obstruction (below the sternal notch) (a) In this case. Patients with such lesions develop stridor. – For neuromuscular disorders (this pattern is also seen in poor effort study).. (b) The MMEF is low. Figure 1.19c: (a) The PEF is low and not sharp (the curve is convex in shape). However. (b) The slope of the curve is parallel to the predicted curve. Upper Airway Obstruction51–55 The morphology of the flow–volume curve is very useful in identifying upper airway disorders. unlike a fixed obstruction that never changes with forced efforts. i.28 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE (d) The steep descending limb and the narrow width of the FV curve together with the relatively preserved PEF may produce a distinct shape of the curve typical for parenchymal lung fibrosis referred to as the witch’s hat appearance. – For chest wall restriction (including musculoskeletal disorders.
SPIROMETRY FIGURE 1.20. (c) Fixed upper airway obstruction. (b) Variable intrathoracic obstruction. 29 . Upper airway obstruction: (a) variable extrathoracic obstruction.
Figure 1. which is significantly reduced. starting right from the PEF. A variable lesion. but with time you will find that it is useful . Figure 1.20b. e. In these cases you may hear expiratory wheezes with the stethoscope placed in the midline over the upper chest. So. Another way is to think of the intrathoracic obstruction taking place during the ex-piration. tracheomalacia. while extra. Flattening of the lower part of the loop will then indicate a variable extrathoracic lesion and vice versa.20b.30 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE by the increased intrathoracic pressure that occurs during expiration. Figure 1.will take ex-.will take in-.g. (b) Unlike the obstruction in the lower airways (as in asthma and COPD). A way to remember which part of the curve is deformed in either forms of variable upper airway obstruction. in the upper airways will compress easily when the pressure outside exceeds the pressure inside the airways. think of the upper airways oriented upside down beside the FV loop with the horizontal (volume) axis at the level of the sternal notch.21. FIGURE 1. Figure 1. Central tumors can also preferentially reduce expiratory flow. the expiratory component of the FV loop in intrathoracic upper airway obstruction is deformed throughout its entire length. . while the extrathoracic during the in-spiration. intra. (c) To remember which part of the FV loop is affected by a variable upper airway obstruction.21..21. This way of remembering the different types of obstruction may sound odd.
by retrosternal goiter) Fixed lesions (lesions at any level in the major airways) Non-dynamic tumors at any level of upper airways Fibrotic stricture of upper airways TABLE 1. Fixed upper airway obstruction (above or below the sternal notch) (a) This type of obstruction does not change with inspiration or expiration (not dynamic). by goiter) Variable intrathoracic lesions (lesions below the sternal notch) Dynamic tumors of the lower trachea Tracheomalacia Dynamic tracheal strictures Chronic inflammatory disorders of the upper airways (e. it will not matter whether it is located in the intra. relapsing polychondritis) External compression of lower trachea (e. respectively & they stand for the maximal inspiratory ﬂow at 50% of FIVC and the maximal expiratory ﬂow at 50% of FVC. Note: In the absence of FV loop.8 for causes of upper airway obstruction.g.8.9. respectively...SPIROMETRY 31 3. Wegener granulomatosis.20c (c) See Table 1. see Table 1. both the inspiratory and the expiratory components of the FV loop are flattened. (b) As a result.g. Causes of upper airway obstruction8 Variable extrathoracic lesions (lesions above the sternal notch) Dynamic tumors of hypopharynx or upper trachea Vocal cord paralysis Dynamic subglottic stenosis External compression of upper trachea (e. you can still identify the different types of upper airway obstruction numerically using PEF.or extrathoracic compartment of the upper airways..51 ↓ <1 Variable intrathoracic ↓ Not applicable ↓ or normal >1 **MIF50 & MEF50 are sometimes used to describe FIF50 & FEF50. and FIF50/FEF50 ratio. . Figure 1.9. Differentiating types of upper airway obstruction numerically10 Fixed UAO PEF PEF/FEV1 FIF50 FIF50/FEF50 ↓ Not applicable ↓ ~1 Variable extrathoracic ↓ or normal <847.** TABLE 1.g. FIF50. PEF/ FEV1 ratio. and hence.
2. This variant is very common and is sometimes referred to as the knee variant. Am J Respir Crit Care Med 1995. Figure 1.26:319–338. et al. PEF is reduced. Paoletti P. Pistelli G. Bull Eur Physiopathol Respir 1986. it is recognized as a normal variant.22. Hankinson J. Miller MR. 3... Pellegrino R. the PEF is actually preserved compared to the predicted curve.152:1107–1136. Eur Respir J 2005. however.22. Vital capacities during acute and chronic bronchoconstriction: dependence on flow and volume histories. Normal variant. Brusasco V. 1994 update.32 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 1.22 References 1. Reference values for vital capacity and flow–volume curves from a general population study. 4. et al. A normal variant that mimics a variable intrathoracic upper airway obstruction. .22:451–459. knee.8. Standardization of spirometry. In variable intrathoracic upper airway obstruction. Rodarte JR. Eur Respir J 1997. American Thoracic Society. Note that the PEF is normal.10:1316–1320. when this curve is highly reproducible. Although the peak of the FV curve in this condition is flattened suggesting upper airway obstruction. Brusasco V. • The key to differentiating this normal variant from a variable intrathoracic upper airway obstruction is the preserved PEF. • Acceptability criteria may be questioned here (suggesting a poor start). Fazzi P. Standardisation of spirometry.
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• Therefore. and their clinical implications. © Springer-Verlag London Limited 2009 . DEFINITIONS. Pulmonary Function Tests in Clinical Practice.1 An abnormal increase in RV is called air trapping. These volumes are termed the static lung volumes.1 Total lung capacity (TLC) • Is the volume of air (in liters) that a subject’s lungs can contain at the end of a maximal inspiration. as this volume cannot be exhaled to be measured. Figure 2. 37 A.1 Residual volume (RV) • Is the volume of air that remains in the lungs at the end of a maximal exhalation. The techniques used to measure lung volumes are primarily designed to measure the residual volume. The rest of the lung volumes can then be measured by simple spirometry.1007/978-1-84882-231-3_2. how they are measured. DOI: 10. Altalag et al. SEE FIGURE 2. The TLC can then be calculated by adding RV to VC or functional residual capacity (FRC) to inspiratory capacity (IC).Chapter 2 Lung Volumes Measuring lung volumes helps characterize certain disease states. This chapter will discuss these lung volumes. while spirometry measures the dynamic volumes. using the SVC rather than the FVC..1. spirometry is an essential part of any lung volume study.
1. • The FRC is the sum of the expiratory reserve volume (ERV) and the RV and is ∼50% of TLC. when the respiratory muscles are at rest. Functional residual capacity • Is the volume of air that remains in the lungs at the end of a tidal exhalation. the FRC decreases. when the elastic recoil of the lungs decreases as in emphysema.e. the FRC increases (hyperinflation)..38 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 2. the resting negative intrathoracic pressure produced by the chest wall (rib cage and diaphragm) wanting to expand is balanced by the elastic recoil force of the lungs. which naturally want to contract. i. A volume spirogram showing the different lung volumes (on the left) and capacities (on the right).1 This means that at FRC. while when the elastic recoil increases as in pulmonary fibrosis. . Therefore.
The Terms “Volume” and “Capacity”.6. • FRC has important functions: – Aids the mixed venous blood oxygenation during expiration and before the next inspiration.1 Indeed. FRC is the volume measured by all the volume measuring techniques and RV is then determined by subtracting ERV. . Tidal volume (VT) • Is the volume of air that we normally inhale or exhale while at rest. a tremendous force will be needed to reinflate them.LUNG VOLUMES 39 • FRC measured using body plethysmography (discussed later) is sometimes referred to as the thoracic gas volume (TGV or VTG) at FRC or VFRC. See Figure 2.13 • The term “volume” refers to the lung volumes that cannot be broken down into smaller components (RV. Figure 2. IC equals the IRV + tidal volume (VT). and equals roughly 0. SVC or VC • Was discussed in Chapter 1. – Decreases the energy required to reinflate the lungs during inspiration.1 Inspiratory reserve volume (IRV) • Is similarly defined as the maximum volume of air that can be inhaled following a tidal inhalation. for example.1 Accordingly. and IRV). ERV.1 Inspiratory capacity (IC) • Is the maximum volume of air that can be inhaled after a normal exhalation. If.2 Expiratory reserve volume (ERV) • Is the maximum volume of air that can be exhaled at the end of a tidal exhalation and can be measured by simple spirometry.5 L in an average adult and increases with exercise. VT. Such effort would soon result in exhaustion and respiratory failure. the lungs want to go to the fully collapsed position. each time the patient exhales.
TLC.1).2. in addition to allowing measures of the ERV and the SVC. and VC). The other. The only three lung volumes that spirometry cannot measure are RV. and the radiographic method. in addition to its other uses.2. and TLC. and the disadvantages of each method. the inert gas dilution technique. less widely used. the FV curve may be rotated 90° clockwise and placed beside the volume spirogram. the advantages. The primary goal is to measure the FRC by the body box. METHODS FOR MEASURING THE STATIC LUNG VOLUMES • There are different ways of measuring the lung volumes. Figure 2. To aid in understanding lung volumes as they relate to the FV curve. among which the most accurate and widely used is the body box or body plethysmography. • The term “capacity” refers to the lung volumes that can be broken down into other smaller components (IC. FVC. methods are the nitrogen washout method. The RV and TLC . • This section will discuss the principles. FRC. – IC = IRV + VT – FVC = ERV + RV – VC = IC + ERV – TLC = VC + RV Correlation with the FV Curve • FV curve can be used as a volume spirogram (seen in Figure 2.40 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 2. Body Plethysmography (Body Box) • Is an ingenious way of measuring the lung volumes.
° V1 is the FRC (VFRC) that is the volume of air in the lungs at the beginning of the test. ° Similarly. We can now apply the new pressure and volume on the second part of the same equation.. we will get: (continued) . a valve (shutter) will close and the patient will perform a panting maneuver through an occluded airway where the change in pressure will be measured (ΔP). At FRC. which states that the product of pressure and volume of a gas TABLE 2.1..4. with a clip placed on the nose. where: ° P1 is the pressure of air in the lungs at FRC (the beginning of the test).5. after the valve closure) will equal the initial pressure (P1) minus the change in pressure (ΔP). resulting in a change in lung volume. V2 = (V1 + ΔV) ° By substituting these values in the original equation (P1 × V1 = P2 × V2). The patient is then instructed to breathe at the resting tidal volume (VT). where: ° P2 (the pressure of air in the lungs when the air gets decompressed as a result of the negative pressure produced by the inspiratory muscles during the panting maneuver. TLC = RV + SVC).e.e. Principle of body plethesmography1. The first part of the earlier equation (Boyle’s law) can then be applied at the patient’s FRC (the end of a normal exhalation). V2 (the volume of air in the lungs after it gets decompressed) will equal the sum of the initial volume of the lung (V1 or VFRC) plus the change in volume (ΔV). The air in the lungs will get compressed and decompressed as a result of the change in pressure. which equals the barometric pressure (760 cmH2O.7. see Figure 2. which states that the product of pressure and volume (P × V) of a gas is constant under constant temperature conditions (which is the case in the lungs): Therefore: P1 × V1 = P2 × V2 The patient is put in the plethysmograph (an airtight box with a known volume). i.3. and the mouth tightly applied around a mouthpiece. • The principle of body plethysmography depends on Boyle’s law.1. at sea level).LUNG VOLUMES 41 can then be calculated from these three variables (RV = FRC − ERV.8 The principle of body plethysmography depends on Boyle’s law. P2 = (P1 − ΔP). see Figure 2. earlier. a change in FRC (ΔV). i. So.
In plethysmography. multiplying (P1 − ΔP) by (V1 + ΔV): P1 × V1 = (P1 × V1) + (P1 × ΔV) − (ΔP × V1) − (ΔP × ΔV). as discussed earlier. the FRC is sometimes referred to as the thoracic gas volume (TGV or VTG). as a computer does all the measurements and calculations. After determining the FRC. adding (ΔP × V1) to both sides: (ΔP × V1) = (P1 × ΔV) − (ΔP × ΔV).1. the final equation can be simplified as follows: V1 = (ΔV × P1)/ΔP or VFRC = (ΔV × P1)/ΔP. as P1 is the barometric pressure. Then.42 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 2. subtracting (P1 × V1) from both sides: 0 = (P1 × ΔV) − (ΔP × V1) − (ΔP × ΔV). Principle of body plethesmography (the body box) . then we can accept: P1 − ΔP = P1. each of ΔP and ΔV are measured by the plethysmograph. dividing by ΔP (ΔP × V1)/ΔP = [(P1 × ΔV) − (ΔP × ΔV)]/ΔP or V1 = [ΔV × (P1 − ΔP)]/ΔP As ΔP is too small compared with P1 (20 cmH2O compared with a barometric pressure of 760 cm H2O). (continued) P1 × V1 = (P1 − ΔP) × (V1 + ΔV). You do not need to worry about all of this. but it is still good to know how it does all that.3. FIGURE 2. the RV and TLC can be calculated.
The equation of the concentration (C) and volume (V) can then be applied: C1 × V1 = C2 × V2.LUNG VOLUMES 43 is constant at a constant temperature. until almost all the nitrogen in the lungs is exhaled into that container. Nitrogen washout method1. 80%). The patient will continue this process.1 (Figure 2. Inert Gas Dilution Technique1.4. He/she will inhale 100% O2 and exhale into a separate container with a known volume. • The plethysmograph is the most popular way of measuring the lung volumes. The test is normally terminated after 7 min. more time (20 min) than usual is needed to washout N2 from the poorly ventilated areas. In obstructive disorders. which then can be washed out to determine the volume.2. A significant increase in TLC measured by plethysmography compared with that measured by N2 washout method suggests air trapping commonly seen in obstructive disorders (COPD). One is to account for the N2 that remains in the lungs at the end of the test and the second is to account for the N2 that is continuously released from the circulation into the lungs during the test. Keep in mind that two correction factors are made for accurate results.10 while body plethysmography is usually carried out over less than a minute.5. See Table 2. but it is the most expensive too.6 Nitrogen Washout Method1. This technique is less accurate and more time consuming (at least 7 min10).9 • Is another way of determining FRC. 5 For the details of how this law is applied in the body box to get the FRC.11. the patient will breathe into a closed system.4) for details. the inert gas technique is less accurate TABLE 2.2 (Figure 2. As in N2 washout method.3). resulting in underestimation of the lung volumes. . A comparison between the methods for measuring the lung volumes is shown in Table 2. The nitrogen concentration in the container is then determined.9 At FRC (the end of a normal exhalation). see Table 2.4.12 • An inert gas is a gas that is not absorbable in the air spaces. Its principle is related to the concentration of nitrogen in the lungs (which is the concentration of the atmospheric nitrogen. as it is the fastest and probably the most accurate. where: ° ° ° ° C1 V1 C2 V2 is is is is the the the the N2 concentration in the lungs at FRC (80%) FRC (unknown) N2 concentration in the container (known) volume of air in the collecting container (known) The FRC can then be determined.
11. TABLE 2. Inert gas dilution technique1.4. the patient will breathe into a closed system with a known volume (V1) and concentration (C1) of an inert gas [helium (He)].5. Principle of Inert Gas (Helium) Dilution Technique. therefore: C1 × V1 = C2 × (V1 + FRC) FRC = [(C1 × V1)/C2] − (V1) =V1 × [(C1/C2) − 1] = V1 × [(C1/C2) − (C2/C2)] = V1 × (C1 − C2)/C2 FIGURE 2. The patient will continue breathing the helium until concentration equilibrium is reached and measured by a helium analyzer (C2).44 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 2. V2 will be the sum of the original volume of helium (V1) and the initial lung volume (FRC). Principle of Nitrogen washout method. where V2 = (V1 + FRC). The equation of the concentration (C) and volume (V) can be applied to get the FRC as follows: ° C1 × V1 = C2 × V2. .12 At FRC (the end of a normal exhalation).3.
1. more time is required for the lungs to equilibrate and to clear inert gas in the dilution technique. TECHNIQUE FOR BODY PLETHYSMOGRAPHY • The plethysmograph should be calibrated daily to ensure accuracy.5) for details.4. large size.13 The test is too long1. Less accurate Underestimates FRC in obstructive disorders More accurate Slightly overestimates FRC in obstructive disorders5 Difficult to test patients on wheel chairs or stretchers or patients attached to i.LUNG VOLUMES 45 (underestimates lung volumes in airway obstruction) and is more time consuming.v. with the door closed.1. • The patient sits comfortably inside the body box.4. and complex Possible to test patients on wheel chairs or stretchers Cheap and small . pumps Expensive. See Table 2. a nose clip applied.3 (Figure 2. all the aforementioned methods should give similar values for the lung volumes. Table 2.20–22 The temperature and barometric pressure should be entered every morning. It is an invasive method that is not used routinely. This method may yield a lower TLC by >10% compared with plethysmography.1 It is only in disease state. and the mouth tightly applied to a mouthpiece. due to the unnecessary exposure to radiation.6 Plethysmography Fast Readily repeatable for reproducibility N2 washout method/Inert gas dilution technique Time consuming Difficult to repeat. when the values will vary between the different methods. if done properly. TABLE 2.17–19 • In a normal subject. Comparison between the common methods for measuring lung volumes5. Radiographic Method (Planimetry or Geometry) • The TLC and RV are estimated by doing posteroanterior (PA) and lateral chest radiographs during full inspiration (TLC) and full expiration (RV).14–16 CT scan and MRI are more accurate than plane radiography in determining TLC but they are more costly.
then (step 3) deep. Notice that SVC is used instead of FVC. – The physical calibration is done every morning and includes calibrating the mouth pressure transducer and the volume signal of the plethysmograph. as shown in Figure 2.6. The volume calibration is FIGURE 2.6. Technique for plethysmography.46 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • The patient should breathe normally at the VT until three or four stable tidal breaths are achieved. Figure 2. .* • The test is then repeated for reproducibility as ATS criteria should also be met in the measurements. where the plethysmograph measures the FRC. the patient is instructed to pant fast and shallowly23 against a closed valve (shutter). * In some labs. The difference between the two measurements of FRC and TLC should be within 10% and RV within 20%. • Step 2: the patient is then instructed to take a full inspiration (IC). The subsets of lung volumes can then be calculated. as explained earlier. Then (step1) at the end of the last tidal exhalation (FRC). the patient is instructed to exhale fully after the panting maneuver to measure ERV then to inhale fully to measure VC.1 • Physical and biological calibrations are also needed. slow expiration (SVC or VC) for at least 6 s.6. which is spirometry.
reference values are derived from Caucasian studies.1. • In restrictive disorders. Values above the fifth percentile are considered normal.1 CORRELATING THE FLOW–VOLUME CURVE WITH LUNG VOLUMES • When the FV curve is done while the patient is inside the body box. which means that the curve will shift to the right compared with the predicted (remember.LUNG VOLUMES 47 carried out using a container with a known volume (a 3-L lung model) where the container’s gas volume measurements should be within 50 ml or 3% of each other. normal.5 discusses the causes for abnormal lung volumes. . right = restrictive). see Figure 2. the TLC and RV are low. and corrections should be made in non-Caucasians. IC and IRV are not discussed as they have little diagnostic role. whichever is larger. COMPONENTS OF A LUNG VOLUME STUDY • The simple rule for lung volumes is that they increase in obstructive disorders and decrease in restrictive disorders.24–29 • As in spirometry.1 Measurements should not be significantly different from the previously acquired measurements in the same subjects (<10% for TLC and FRC and <20% for RV). the TLC and RV can be accurately plotted on the curve too. Table 2. TLC is represented by the leftmost point of the curve and RV by the rightmost point of the curve. CLINICAL SIGNIFICANCE OF FRC • A high FRC (as in emphysema) means that when the patient is not breathing in. Comparing these points with their equivalents in the predicted curve will indicate whether these lung volumes are decreased. REFERENCE VALUES1. The opposite is true in obstructive disorders. These reference values are related to body size.7.5 – Biological calibration should be done once a month on two reference subjects. As discussed in Chapter 1. see Appendix 2. TLC and RV are the most important for interpreting PTFs. or increased. with the height being the most important factor. at the same time as the lung volume study. The RV/ TLC ratio is similarly useful in interpreting lung volume studies. the lungs contain more air than normal.
(a) Represents the ideal curve. increases the effort of breathing. but at the same time.7. The increased effort noticed when breathing at high lung volumes is caused by two consequences of a high lung volume. Try that by taking a deep breath and try to talk and breathe at that lung volume and see for yourself. Breathing at that high lung volume helps prevent collapse of the airways and air trapping in emphysematous lungs. Firstly. As a result. more muscular activity is required to produce the pressure gradient that . This can be very uncomfortable and can lead to dyspnea. (b) represents an obstructive disorder with increased TLC and RV and shift of FV curve to the left.48 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 2. the breathing muscles are shortened and become at a mechanical disadvantage. (c) represents a restrictive disorder with decreased TLC and RV and shift of FV curve to the right.
swimmers ° ° TLC is usually normal in bronchial asthma.LUNG VOLUMES 49 TABLE 2.g. mainly lung fibrosis ° Obesity ° Supine position (abdominal organs push the diaphragm against the lungs) . but the RV is high because of air trapping Decreased in parenchymal restriction RV/TLC ratio Normal in parenchymal restriction2 Increased 30.. mainly emphysema 2 ° Acromegaly patients may have a high TLC. Causes of abnormal lung volumes TLC Increased in: ° COPD.7 for classification) RV Increased (air trapping) in obstructive disorders: ° COPD ° Bronchial asthma. e. as lung elastic recoil is normal32 Decreased in restrictive disorders30 (see Table 1.31 ° Mainly in obstructive disorders ° Can be increased in chest wall restriction (because of normal RV and low TLC) ERV Decreased in ° Restrictive disorders.5. which can be differentiated from emphysema by RV/TLC ratio (normal in acromegaly and high in emphysema31) TLC may be high in normal subjects with big lungs. although the TLC is normal. similar to TLC ° Obstructive disorders (because of the increased RV due to air trapping that occurs in these conditions) ° An isolated reduction in ERV is characteristic for obesity FRC Increased (hyperinflation) in ° Obstructive disorders. mainly emphysema due to loss of lung elastic recoil ° FRC increases slightly with aging Decreased in ° Restrictive disorders.
6 summarizes their usefulness. Figure 2.8. the patient cannot continue exercising. at which point. DISEASE PATTERNS The lung volumes are diagnostically useful in many ways. Note also that the expiratory phase decreases progressively with continued exercise indicating progressive air trapping.50 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE leads to airflow and tidal volume. The reduced expiratory time impairs lung emptying and leads to air trapping. their respiratory rate increases and the expiratory time decreases. . the lung compliance is reduced. Note that VT increases with exercise. as in pulmonary fibrosis and obesity. Table 2.8. can also increase the work of breathing. Secondly. In restrictive lung disorder. which means that more effort is needed to inflate the lungs. • When patients with emphysema exercise. which is discussed in more detail in this section: FIGURE 2. the lungs are less compliant as lung volume increases above FRC (more elastic recoil) and so more force is required to produce airflow. Dynamic hyperinflation in patients with emphysema during exercise. • Breathing at a low FRC. This phenomenon is called dynamic hyperinflation and is characteristic of patients with emphysema and is responsible for much of their exercise limitation. The air trapping results in a progressive increase in the FRC with each respiratory cycle. This process continues until the FRC approaches the TLC.
These volume changes indicate that the bronchodilators are clinically useful to such patients even though there is no change in FEV1. In this case. obstructive disorders (emphysema and asthma) result in increased RV (air trapping) due to airway narrowing while TLC is increased only in emphysema due to loss of elastic recoil.LUNG VOLUMES 51 TABLE 2. an increase in IC gives patients with emphysema more room or time to breathe before they develop dynamic hyperinflation to the point of stopping exercise.30 As a result.9. however. however. normal TLC. TLC and RV may be shown to decrease following bronchodilators.33 • Confirm the diagnosis of a restrictive disorder and differentiate its subtypes – A decreased TLC is essential to make the diagnosis of a restrictive disorder with confidence.31 – The RV/TLC ratio can be used also to differentiate an obstructive from a nonobstructive increase in TLC.20. Furthermore. even in the absence of a significant response in FEV1 and FVC. Figure 2. Additional information acquired by lung volume study compared with spirometry Differentiates the subtypes of obstructive disorders Confirms the diagnosis of a restrictive disorder and separates its subtypes Separates restrictive from obstructive disorders Helps in detecting combined. such as acromegaly (the RV/TLC ratio is normal).and postbronchodilator use. the RV and . where there is increased elastic recoil and loss of air space.2 – If lung volumes are measured pre.30.30 The RV and RV/TLC ratio. obstructive. Bronchial asthma. may be used to differentiate the subtypes of restriction: (a) In a parenchymal restriction (lung fibrosis). has normal elastic recoil and. much can be learned from looking at the behavior of TLC and RV before and after the use of bronchodilators. IC may increase as FRC may decrease more than TLC in response to bronchodilators. the RV/TLC ratio is increased in both emphysema and bronchial asthma. therefore. and restrictive disorders • Differentiate subtypes of obstructive disorders – Generally.6.
In NMD. Despite that BD can be of help to such patients because of the lung volume change.9. – Obesity and mild bronchial asthma can show a spirometric pattern consistent with mild restriction . and obesity). where the lung parenchyma is normal. musculoskeletal disease. (c) The diffusing capacity for carbon monoxide (DLCO) is a more reliable way of differentiation between parenchymal and chest wall restriction. Note that the change in TLC in this diagram is exaggerated. as will be discussed in the next chapter.2 (b) In chest wall restriction (NMD. the RV is usually normal (or increased) with an increased RV/TLC ratio (remember that TLC is low).52 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 2. The morphology of the curve has not changed indicating no improvement in FEV1 or FVC. Post-BD curve is closer to predicted curve indicating significant reduction in TLC and RV compared to that in the pre-BD curve. TLC are reduced with a normal RV/TLC ratio (both RV and TLC decrease proportionately). RV may be increased because the ERV can be very low due to weakness of the expiratory muscles. Maximal voluntary ventilation (MVV) and maximal respiratory pressures are measures to help differentiate the different types of chest wall restriction. paralyzed diaphragms.
The FV curve (combined with a tidal FV curve) can be used to make that distinction as shown in Figure 2. This ratio is normally 2–3:1. The technicians usually indicate in their comments if a poor effort is apparent. In this case a normal TLC can exclude restrictive disorders. • Separates obstructive from restrictive disorders – Obstructive and restrictive disorders are sometimes hard to separate based on spirometry alone.10.34 – Poor patient effort during spirometry may mimic a restrictive disorder. FIGURE 2. The way to differentiate parenchymal restriction from this pseudorestriction (caused by obesity or mild bronchial asthma) is by the IC/ERV ratio. . Lung volumes may provide additional clues as they are generally increased with obstructive and decreased with restrictive disorders. IC/ERV ratio is used to differentiate parenchymal restriction from pseudorestriction34. with low FVC and FEV1 and a normal FEV1/FVC ratio. The shape of the FV curve can also easily exclude a poor effort study (PEF is not sharp and is rounded in a poor effort study). This ratio decreases in parenchymal restriction to <2:1 and increases in pseudorestriction to >6:1.10.LUNG VOLUMES 53 (decreased FVC and normal FEV1/FVC ratio). as body plethysmography does not require much patient effort. the so-called pseudorestriction. In addition. the study is unlikely to be reproducible with a poor effort.
have a quick look at the FV curve and the rest of the PFT values. with low FEV1/FVC ratio. (d) If the TLC and RV are normal. • Detection of combined disorders – Combined disorders are hard to diagnose based on spirometry alone. Nakamura M. If all the values are decreased proportionately with a normal FV curve. – Keep in mind that an obstructive disorder (such as emphysema) with pulmonary resection (lobectomy or pneumonectomy) can give a similar pattern. Coates A. then consider in your report a normal person with relatively small lungs (racial variations). Spirometry coupled with a lung volume study is very useful: (a) An obstructive disorder should be clear in spirometry. • Chapter 6 discusses the approach to such PFTs in detail.26:511–522. a lung volume study may be of value: (a) If the TLC and RV are high. . then the study is most likely normal.54 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE – As an example. A bronchodilator study may show a significant response. Lippincott Williams & Wilkins. PA. Wanger J.35 The RV could be low. Second Edition. 2. Before you make such a conclusion. Standardisation of the measurement of lung volumes.1 – Combined defects can be seen in conditions such as sarcoidosis or coexisting COPD and lung fibrosis. then the reduced TLC suggests an additional restrictive disorder. (c) If the TLC is low. A Practical Guide. or high as airway obstruction may result in air trapping and increased RV. (b) If the TLC is normal and RV is mildly increased. then an obstructive disorder is the most likely (RV/TLC ratio is usually high). Interpretation of Pulmonary Function Tests. Clausen JL. provided that FVC is below the 5th percentile (a normal FVC rules out restriction36. References 1. Scanlon PD. with a normal FEV1/FVC ratio. when the FEV1 and FVC are at the lower limit of the normal range.37).30. If this airflow obstruction is seen with a reduced TLC. 2003. normal.2 In this case. et al. the airway obstruction is not severe enough to cause significant drop in FEV1 and the ratio. then a restrictive defect is likely to be the cause. Hyatt RE. Eur Respir J 2005. then a mild bronchial asthma and air trapping could be responsible (RV/TLC ratio is high). Philadelphia.
Corbeel LJ. Delmar. Crapo RO. Newth CJ. . Am J Respir Crit Care Med 1997. The volume of the lung determined by helium dilution. Thornton JC. Comparison between measurements of functional residual capacity and thoracic gas volume in chronic obstructive pulmonary disease. ATS Workshop on Lung Volume Measurements. Warshaw RH. Reference values for residual volume. 10. A method for the determination of the volume of air in the lungs: measurement in chronic obstructive pulmonary emphysema. New York.28:129–139. Richards DWJ. Cournand A. 1982. et al. Madama VC. Coxon HO.70:849–858. www. Stocks J.155:1649–1656. Studies on intrapulmonary mixture of gases. Eur Respir J 1997. Emmanuel G. Estimation of lung volumes from chest radiographs. Peslin R. 17. 5. Florence.pdf. Mayo JR. Darling RC. 15. Methods. Rodenstein D. IL. J Clin Invest 1956. Effect of pneumonectomy on the remaining lung in dogs.14:137–140. Briscoe WA. Accessed on July 19. Quanjer PH. Coates AL. 8. Kilburn KH. Eur Respir J 1997. 16.155–163. Marshall R.LUNG VOLUMES 55 3. Guidelines and Controversies. In: Clausen JL.10:2174–2185. J Clin Invest 1948. Baldwin ED. Bedell GN. Montague T. Miller A. Pulmonary Function Testing. IV. Northbrook. ed.10:1415–1427. Prog Respir Res 1969. Multiple breath nitrogen washout techniques: including measurements with patients on ventilators. Enright P. Invest Radiol 1979. 7. Thorax 1992. 2005. J Appl Physiol 1991.8:492–506. 4. Cassidy SS. Armstrong JD.20:329–337. Kaltreider NL. 18. 1993. Stocks J.20:681–689. Cournand A. and Normal Values. Johnson RL Jr. Consensus statement on measurement of lung volumes in humans. Comroe JH. J Clin Invest 1960.org/adobe/lungvolume. 2003. The significance of the pulmonary emptying rate and a simplified open circuit measurement of residual air. Johnson RL Jr. 11. Eur Respir J 1995. KY. 13. A rapid plethysmographic method for measuring thoracic gas volume: a comparison with a nitrogen washout method for measuring functional residual capacity in normal subjects. Meneely GR. Date last updated: December 30. NHLBI Workshop. Grover R. Pulmonary Function Testing and Cardiopulmonary Stress Testing.thoracic. 14. 6. Quantification of idiopathic pulmonary fibrosis using computed tomography and histology. Measurement of lung volumes by plethysmography. J Clin Invest 1941. Pulmonary Function Testing. Salzman SH. Hogg JC. Official Statement of the European Respiratory Society. Predictive equations for total lung capacity and residual volume calculated from radiographs in a random sample of the Michigan population. First edition.35:322–326. International symposium on body plethysmography. Equipment. functional residual capacity and total lung capacity. Thornton K. Botelho SY.4:194–204. 9. DuBois AB. ACCP Pulmonary Board Review Course. Inspiratory lung volumes achieved on routine chest films. 2005:297–320. Description of the method and comparison with other procedures. et al.47:518–523. Academic. 12.
Lung mechanics in disease. Eur Respir J 2005. Quanjer PH.27:1–79.152:1107–1136. In: Macklem PT. Pedersen OF. Cotes JE. Handbook of Physiology. 34. Bethesda. Kester MM. Roca J. Quanjer PH. Hankinson J. eds. Cotes JE. Assessing the reversibility of airway obstruction. Rodarte JR. Brusasco V. European Community for Steel and Coal and European Respiratory Society. Am Rev Respir Dis 1991. Standardization of spirometry. Yernault JC. Am Rev Respir Dis 1983. Reference values. Eur Respir J 1993. Lee TH. deKemp RA. Interpretative strategies for lung function tests. 32. 21. Physiology. Eur Respir J 1993. Stocks J. Godfrey S. Quanjer PH. Pedersen OF. Chest 1998. Yernault JC. Cotes JE.128:54–59. Enright PL. 1994 Update. Archer DC. Enright P. 31. Tammeling GJ. Grasbeck R. Mechanics of Breathing. Martin JG. 115:68–74. Miller MR. 27. 25. Norman G. London. Standardization of the measurement of transfer factor (diffusing capacity). Pride NB. Scanlon PD.26:319–338. Lung volumes and forced ventilatory flows. 28. Beck KC. Shore SA. Eur Respir J 2005. et al. Enright P.20:809–822. Salzman S. Pride NB. Peslin R. European Community for Steel and Coal. Peslin R. Eur Respir J 2005. 30. Vol. et al. Chapman and Hall. Report Working Party Standardization of Lung Function Tests. American Thoracic Society.6 Suppl 16:S5–S40. Effect of panting frequency on the plethysmographic determination of thoracic gas volume in chronic obstructive pulmonary disease.6 Suppl 16:S41–S52. functional residual capacity and total lung capacity. American Thoracic Society.659–692. Viegi G. Nahnmias C. Lung function testing: selection of reference values and interpretative strategies. Brusasco V.26:948–968. Pellegrino R. Eur Respir J 1993. Mead J. 23. 29. In: Clark TJH. Viegi G. MD. Asthma. Official Statement of the European Respiratory Society.188:835–838. Huk O. Chest 1999.8:492–506. Lung volumes in 4774 patients with obstructive lung disease. Third Edition. Report Working Party. Pulmonary function testing. American Physiological Society. Lung volumes and forced ventilatory flows. 33. Section 3. Quanjer PH. Eur Respir J 1995. 1992:14–72. Pellegrino R.144:1202–1218. Adv Clin Chem 1989. J Respir Dis 1999. Tammeling GJ. Dykstra BJ. Am J Respir Crit Care Med 1995. Chinn DJ. Macklem PT. Reference values for residual volume. European Community for Steel and Coal. Pellegrino R. Radiology 1993. Standardization of Lung Function Tests. 20. Coblenz CL. Automated in vivo quantification of emphysema. Standardisation of spirometry. 24. 1986. Official Statement of the European Respiratory Society. Official Statement of the European Respiratory Society.56 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE 19. Tips on how to interpret the results.26:948–968. III. 26. Mannix S. 35. The Respiratory System.6 Suppl 16:5–40. Report Working Party Standardization of Lung Function Tests.114:1607–1612. 22. Yernault JC. et al. . Interpretative strategies for lung function tests. Solberg HE. ATS Workshop on Lung Volume Measurements. eds. Part 2.
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1 59 A. no more diffusion will take place (no gradient for diffusion) until the capillary blood is replaced by fresh blood (perfusionlimited). Pulmonary Function Tests in Clinical Practice.*. which is impaired in many disorders. This feature makes the capillary backpressure for CO very low (almost zero). Altalag et al.and * In UK and Europe. DLCO is used to estimate gas transfer. A perfusionlimited gas such as acetylene.1 • CO is diffusion-limited as it is highly soluble and strongly binds to Hgb (CO affinity for Hgb is >200 times that for O2). Therefore. TLCO is used instead of DLCO and stands for lung transfer factor for carbon monoxide and is expressed in SI units (mmol/ min/Kilopascal). is so insoluble that if a small fraction of it diffuses to the capillary blood.. Oxygen is both diffusion.1007/978-1-84882-231-3_3. This property makes this gas useful in measuring the total pulmonary capillary blood flow (generally reflects the cardiac output) but not diffusion. © Springer-Verlag London Limited 2009 .Chapter 3 Gas Transfer DEFINITIONS Diffusing Capacity for Carbon Monoxide • Reflects the ability of carbon monoxide (CO) to diffuse into the blood through the alveolar capillary membrane. on the other hand. which allows the gas to diffuse freely to the capillary blood. DLCO stands for lung diffusing capacity for carbon monoxide and its traditional unit is ml/min/mmHg. DLCO measurement reflects the diffusing ability of the alveolo-capillary membrane of the lung. DOI: 10.
As an example. VA is measured simultaneously with the DLCO measurement using a single-breath technique. This ability makes it of great value in the diagnosis and follow-up of such conditions.3. • DLCO is determined by the amount of blood recruited in the alveolar capillary bed and the alveolo-capillary surface area available for diffusion.60 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE perfusion-limited. . a ratio represented as DLCO/VA. which makes it less accurate in estimating the TLC than the standard test. it is not suitable to measure the diffusing capacity. there is less time for equilibration. – VA calculated by He dilution corrects DLCO to the actual alveolar volume available for diffusion. – A third indirect use of VA is to roughly estimate the poorly ventilated volume of the lungs by subtracting VA from TLC (measured by body plethysmography). The result is expressed as “alveolar volume” (VA) rather than TLC. and VA should be less than TLC. Alveolar Volume (VA) • Represents an estimate of the TLC using a single-breath inert gas dilution technique. the DLCO level usually decreases before any drop in lung volume. which serves three important roles†: – Helium is used as an inert gas to calculate the initial alveolar CO concentration prior to diffusion of CO from the alveolar gas. and so TLC is underestimated. † Newer equipment use methane (CH4) instead of helium as it can be continuously analyzed together with CO using rapidly responding infrared gas analyzers. because in this technique. discussed in the previous chapter. in interstitial lung disorders (ILD). Therefore. DLCO may drop before the disease is obvious clinically or even radiologically.2 • DLCO measurement is very reliable and sensitive. therefore.4 (The standard inert gas dilution technique is performed over several minutes that are required for equilibration of the test gas). • The inert (nonabsorbable) gas used in this test is usually Helium (He).
• The test is repeated once more (after 4 minutes)1 for reproducibility & the results should lie within 10% or 3 ml/min/mmHg of each other. as the patient is instructed to keep a neutral pressure on a closed glottis.. and this will be recorded in the study as inspiratory vital capacity (IVC). ¶ Five consecutive DLCO measurements may increase CO-Hgb by ∼3.§.6 • Technique: After a full exhalation.3% of the gas mixture. steadystate.55 ‡ .e. CO & He.. intrabreath.9 The maximum number of trials is 5. which is discussed here. • The actual duration of breath-hold is recorded in the final report as breath-hold time (BHT).7 Then. It is available in some of the newer DLCO measuring devices and probably provides a more accurate measurement.15 § For most DLCO measuring devices. After the 10-second breath hold.8 This step is critical. in seconds. The three-equation method is a widely used way of calculating DLCO in the single-breath technique. 0. and N2. a VC of at least 1 L is required to produce an accurate measurement of DLCO. A mid-exhalation sample is required to avoid sampling the dead space gas.1. • The equipment used to measure DLCO should be calibrated every morning to ensure accuracy.¶.1 Don't worry about poisoning the patient with CO.‡ Other methods may be used to measure DLCO but they are less popular (e. O2. the patient inhales a mixture of CO.5% (i. only 0. as following that.5%.GAS TRANSFER 61 TECHNIQUE1 • The most popular method of measuring DLCO is the singlebreath technique. as the amount used for the test is too small. the patient exhales into the machine until a mid-exhalation (representing the alveolar gas) sample is analyzed for the concentration of both.7% per test). which will decrease the measured DLCO by ∼3–3. the retained CO in the blood from the previous trials will significantly interfere with test results.1. Figure 3.1 • For details of DLCO calculation using single-breath technique.5. He. The patient has to inhale to at least 85% of the previously measured VC. and rebreathing techniques).1. see Table 3. Blowing out (Valsalva maneuver) or sucking in (Muller maneuver) during this phase interferes with the results by altering pulmonary blood volume. the patient should hold his/her breath for 10 s to allow for diffusion.g. each with a known concentration.
62 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 3.). the equation can be simplified as follows: DLCO = Vco/PACO Vco can be calculated from the difference between the initial and the final CO concentration. VA is the alveolar volume measured by the single-breath helium dilution.1 With permission.1. as PACO is the partial pressure of alveolar CO and PcCO is the mean capillary partial pressure of CO. 0. and 47 is the partial pressure of water vapor at body temperature.7–1. Schematic of gas concentration during single-breath DLCO measurement. Dividing by the logarithmic mean of PACO results in the following equation: DLCO = VA/[T×(PB–47] × Ln (FACOI/FACOF) as FACOI is the initial alveolar CO concentration (before diffusion). while FACOI is calculated using the inert gas (He) measurements as follows: FACOI = FiCO × (FAHe/FiHe) as FiCO is the inspired CO concentration. FACOF is measured directly from the mid-exhalation breath sample (alveolar sample after discarding the dead-space washout. Calculating DLCO using single-breath technique1 The diffusing capacity for CO (DLCO) equals the rate of CO uptake (Vco) divided by its transfer pressure gradient (PACO − PcCO).0 L). and FAHe is the expired alveolar He concentration.1. which are all known. FiHe is the inspired He concentration. Notice that sample collection takes place after dead-space gas is exhaled (Modified from MacIntyre. This relation can be written as follows: DLCO = Vco/(PACO–PcCO) Because PcCO is negligible as CO almost completely binds to Hgb. . T is the breath-hold time (BHT) in minutes. FACOF is the final alveolar CO concentration (after diffusion). PB is the barometric pressure. TABLE 3.
− As an example. If the Hgb is not known. in patients who had lobectomy or pneumonectomy with an otherwise normal remaining lung tissue. a normal DLCO/VA cannot exclude ILD. • Adjustment to Hgb1. DLCO/VA determines whether the currently available alveolar spaces are functioning normally.7. DLCO /VA represents the diffusing capacity in the available alveolar spaces. VA is likely to be reduced too in such conditions (due to loss of lung tissue because of fibrosis). .1 Therefore. DLCO can be adjusted for VA (DLCO/VA ratio). The range (75–120% of the predicted value) is usually accepted as normal for DLCO.1 − DLCO is usually reduced in ILD. DLCO ADJUSTMENTS • Adjustment for alveolar volume (VA)1. however.GAS TRANSFER 63 REFERENCE VALUES10–13 • Are derived from Caucasian studies. − Correcting DLCO for Hgb is then essential for patients with anemia. anemia should be considered as a possible cause of any isolated or unexplained reduction in DLCO. The elevated DLCO/VA in these patients is due to the increased blood flow in the remaining lung tissue. The relation between Hgb level and DLCO value **LLN can be applied to appropriate reference equations to determine an abnormal result.14 − As discussed earlier. it will be normal or even high. emphysema) or pulmonary vascular disease (pulmonary hypertension). In other words. Accordingly. A decreased DLCO/VA is also seen in patients with anemia.e.16–20 − Anemia results in underestimation of DLCO because of the decreased Hgb available to uptake CO in the pulmonary capillary bed. See Chapter 6 for more details for the interpretation of abnormal DLCO measurements. If DLCO is then corrected for VA (i.. Similarly. A decreased DLCO/VA. which may result in a normal DLCO/VA.** On average. DLCO equals around 25 ml/min/mmHg. In simple terms. a normal or high DLCO/ VA indicates that the remaining lung tissue is functioning normally. as is discussed later. but. strongly suggests parenchymal lung disease (ILD. the absolute value for DLCO is expected to be reduced compared with the predicted values. at the same time. DLCO/VA). polycythemia will then overestimate DLCO.
27 Other more complicated equations may be used.26.2. and in fact. which is acquired from metabolic and environmental sources.|| − In healthy nonsmokers.1 − Average smokers have a CO-Hgb level of ∼4 or 5%.21 This is why smokers are advised to refrain from smoking for at least 8–10 h and preferably 24 h before the test. DLCO adjustment to Hgb Men (adjust to a Hgb value of 14.5 for men and ∼13. DLCO predicted for CO-Hgb = DLCO predicted × (102% − CO-Hgb%). if the Hgb is 3 g/dl less than normal.5 for women).21 Luckily.28–30.64 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE is not a linear relation. CO-Hgb level is ∼1–2%. the DL CO drops by ∼ 10%.1 . TABLE 3. but this can be as high as 10% in heavy smokers. For example. but will they comply? Some laboratories do measure the serum CO-Hgb level before DLCO measurement to be certain about the level. the DLCO drops by ∼30%.2. and decreasing the measured DLCO by 2% for each g/dl increase in Hgb from the reference (normal) levels.6 g/dl)1 DLCO adj = measured DLCO × [(10.” which results in a reduction in the amount of CO diffusing to the blood. a computer program does all the calculations if the Hgb value is entered.22 + Hgb)/(1. while if Hgb is 6 g/dl less than normal.7 × Hgb)] Women and children <15 years of age (adjust to a Hgb value of 13. Once the CO-Hgb level is known the DLCO can be easily estimated by decreasing the predicted DLCO by 1% for each 1% increase in the CO-Hgb level above 2%. These equations are summarized in Table 3.22 • Adjustment to carboxy-Hgb (CO-Hgb) − Increased CO-Hgb level tends to underestimate the DLCO because of (1) backpressure exerted by the CO-Hgb on the alveolar CO and (2) occupying Hgb binding sites producing an “anemia effect. there are equations to correct DLCO for Hgb.4 g/dl)1 DLCO adj = measured DLCO × [(9.38 + Hgb)/(1.7 × Hgb)] || Alveolar [CO] = (CO-Hgb/O2Hgb) × [(alveolar [O2])/210]25.1. − A rough way of quickly correcting DLCO for Hgb is by increasing the measured DLCO value by 4% for each 1 g/dl drop from the average (∼14.23–25 Patients who are suspected of smoking prior to the test can have their CO-Hgb levels measured.
42 Incorrect reference values Causes of low DLCO Decreased surface area available for diffusion Pulmonary resection (remaining lung tissue will have more blood supply (i. Table 3.g.3 summarizes the most important causes of abnormal DLCO. significant bronchial obstruction)1 Alveolo-capillary membrane disease ILD48.e.g..31–33 Hyperdynamic circulation (exercise31. however. A decreased DLCO. could be related to either reduced surface area of the lung available for diffusion or disease of the alveolarcapillary membrane. e. • Grading of severity for a reduced DLCO is shown in Table 3. TABLE 3. hypersensitivity pneumonitis. connective tissue disease. Causes of abnormal DLCO Causes of high DLCO Recruitment of blood in the alveolar capillary bed Supine position1.33.49 (IPF.34 and fever) Bronchial asthma35 Muller maneuver (inhaling against a closed glottis)36–38 Cardiac causes Left to right cardiac shunting1 Early congestive heart failure Miscellaneous conditions Polycythemia1 Alveolar hemorrhage (blood in alveolar space will take up CO)39 Obesity (uncertain mechanism)40 High altitude (due to a lower PIO2 at altitude increasing the CO binding to Hgb)1 Following bronchodilators in obstructive disorders (up to 6% increase)41. drugs) Pulmonary vascular disease.3.. ↑ DLCO/VA) but the overall DLCO will be low)1 Emphysema43–47 (actual functional alveolo-capillary surface area is reduced) VQ mismatch (e.4. pulmonary hypertension or acute pulmonary embolism1 (continued) ..GAS TRANSFER 65 CAUSES OF ABNORMAL DLCO • Anything that increases the blood flow or volume in the pulmonary capillary bed will result in elevation of DLCO. sarcoidosis.
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2001. Cotton DJ. Report Working Party Standardization of Lung Function Tests.26:948–968. Roca J. Begliomini E.111:225–240. Eur Respir J 2005. Mohsenifar Z. CO diffusing capacity in a general population sample: relationship with cigarette smoking and air-flow obstruction. The effect of abnormal levels of hematocrit on the single breath diffusing capacity. 2005:297–320. Roca J.65:56–62. Pistelli F. Clin Sci 1978.144:1202–1218. Northbrook. Sydney. Kane PB. Iron-deficiency anaemia: its effect on transfer factor for the lung (diffusing capacity) and ventilation and cardiac frequency during submaximal exercise. Carrozzi L. Viegi G. Enright P. Baldi S. Adjustment of DLCO for hemoglobin concentration. 12. Viegi G. 17. Reference values. Quanjer PH. McGraw-Hill.GAS TRANSFER 67 10. Pellegrino R. Elwood PC.155:236–241. Hall AM.27:1– 79.58:1319– 1325. Respiration 1998. 11. Tashkin DP. Hancox B. Dabbs JM. Cotes JE. Versprille A. Schnitzer B. Lung function testing: selection of reference values and interpretative strategies. Koerner SK. 18. Salzman SH.19:17–22. Considerations of the physiological variables that determine the blood carboxyhemoglobin concentration in man. IL.160:325–330. Stam H. Effect of breath-hold time on DLCO (SB) in patients with airway obstruction.54:627–631. Pocket Guide to Lung Function Tests. Whyte K. Effect of blood transfusion on the carbon monoxide transfer factor of the lung in man. ACCP Pulmonary Board Review Course. Brown HV. Respiration 1979. Pulmonary Function Testing. et al.60:155–161. 23. Clin Sci 1972. 19. Interpretative strategies for lung function tests. Prause JA. Am J Respir Crit Care Med 1997. Effect of carboxyhemoglobin on the single breath diffusing capacity: derivation of an empirical correction factor. 13. J Clin Invest 1965. American Thoracic Society. J Appl Physiol 1985. Comroe JH Jr. Ferdeghini EM. Official Statement of the European Respiratory Society. Grasbeck R. Hughes JMB.42:325–335. Lung 1982. Mohsenifar Z. Marrades RM. . Forster RE. Graham BL. Bogaard JM. European Community for Steel and Coal. 15. et al. 16. Chinn DJ. Respiration 1993. Am Rev Respir Dis 1975.6 Suppl 16:S41–S52. 14. 24. Solberg HE.37:185–191. Clark EH. 22. Coburn RF. Yernault JC. Pulmonary diffusing capacity for carbon monoxide (DLCO).44:1899–1910. Standardization of the measurement of transfer factor (diffusing capacity). et al. The components of the carbon monoxide diffusing capacity in man dependent on alveolar volume. 26. Mink JT. Adv Clin Chem 1989. 25. carbon dioxide. Diaz O. 20. Saunders MJ. Viegi G. Single breath diffusing capacity for carbon monoxide: effects of adjustment for inspired volume dead space. Paoletti P. Am Rev Respir Dis 1991. McDonald A. 21. Bull Eur Physiopath Respir 1983. First Edition. hemoglobin and carboxyhemoglobin. Cotes JE. Woods RL. Eur Respir J 1993.
68 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE 27. Johnson RL. Helms MI. J Appl Physiol 1960. Spicer WS.51:858–863.73:2623–2630.15:372–376. Cadigan JB. Askew J. Nejadnik B. J Appl Physiol 1992. Effect of lung volume and positional changes on pulmonary diffusing capacity and its components. 35. 39. Relative importance of diffusion and chemical reaction rates in determining rate of exchange of gases in the human lung. 28.60:507–512.110:1189–1193. 30. J Appl Physiol 1960. Rowley L. 31. 37. Njinou B.15:893–902. Effects of ventilation inhomogeneity on DLCO SB-3EQ in normal subjects. Effect of negative intraalveolar pressure on pulmonary diffusing capacity. Serial estimations of DLCO in intrapulmonary hemorrhage. Cotes JE. Cotton DJ. Chinn DJ. Sorensen T. Rankin J. Pulmonary diffusing capacity and the capillary bed during Valsalva and Muller maneuvers. Cadigan JB.2:1853–1854. Clin Sci 1981. 32. Effect of high negative inspiratory pressure on single breath CO diffusing capacity. Mink JT. Normal values for single exhalation diffusing capacity and pulmonary capillary blood flow in sitting. Versprille A. Shepard RH. Snidal DP. MacIntyre NR. Chest 1994.105:501–508. Collard P. A new method for rapid precise determination of carbon monoxide in blood. Measurement technique influences the response of transfer factor (TLCO) to salbutamol in patients with airflow obstruction. Roughton FJW. Wilputte JY. Cotes JE. Graham BL. Lung 1999. 43. Pulmonary capillary blood volume. Eur Respir J 1988. Marks A.27:826–833. Rapid method for estimation of carbon monoxide in blood. Frans A.1:15–21. supine positions and during mild exercise. 38. Gaensler EA. 40. Stam H. Respir Physiol 1983.49:945–957. 33. Forster RE.105:1426–1429. Hughes JMB. Ellicott MF. Apthorp CH. Rodenstein DO.51:553–564. Non-linear increases in diffusing capacity during exercise by seated and supine subjects. Br Med J 1960. 29. Stokes DL. 41. 36. Chest 1994. J Appl Physiol 1991. DLCO in stable asthma. Frans A. Kreuzer FJA. J Lab Clin Med 1958. J Appl Physiol 1957. Greening AP. Graham BL. Jones RH. with special reference to true diffusing capacity of pulmonary membrane and volume of blood in the lung capillaries. J Appl Physiol 1969. Iversen ET. The relationship between alveolar and blood carbon monoxide concentrations during breath-holding. Prabhu MB. J Appl Physiol 1981. Keyeux A. Nadel JA. Huang YC.11:290–302. Jones RH. The DLCO in obstructive sleep apnea and obesity. Forster RE. Jensen JI.71:1477–1488.177:263–271. Heckscher T. . Effect of terbutaline on exercise capacity and pulmonary function in patients with chronic obstructive pulmonary disease. 42. Collard P. Mink JT. flow and diffusing capacity during exercise.54:19–29. Ellicott MF. Cotton DJ. Smith TC. Gaensler EA. 34. J Lab Clin Med 1957. Bishop JM. Aubert G. MacIntyre NR. Henderson M. Chest 1996.
Frey TM. Lippincott Williams & Wilkins. Diurnal variation in pulmonary diffusing capacity for carbon monoxide. Determination of severe impairment (disability) in interstitial lung disease.11:21–32. 48. Kennell C. Comparison of single breath carbon monoxide diffusing capacity and pressure–volume curves in detecting emphysema.77:488–492.7:423–430. 46. Thomson ML. et al. Diurnal variation of the diffusing capacity of the lung: is it real? Am Rev Respir Dis 1987. Gelb AF. Am J Respir Crit Care Med 1995. Uptake of CO in health and emphysema. Bates DV. Crapo RO. Elliott CG. PA. Physiologic diagnosis of subclinical emphysema. 51. Am Rev Respir Dis 1989. Cinkotai FF. 50. The effects of acute ethanol ingestion on pulmonary diffusing capacity. Peavy HH. Epler GR. 53. Jensen RL. 47. Frey TM.21:539–542.139:1179–1187.136:1381– 1384.107:50–63. Elliott CG.GAS TRANSFER 69 44. Nordenfelt I. Hyatt RE. . Svensson G. Crapo RO. Chest 1980. Interpretation of Pulmonary Function Tests: A Practical Guide. Nakamura M. Philadelphia. 2003. Clin Sci 1952. Wright RR. Clin Physiol 1987. Ramadan F. The transfer factor (diffusing capacity) as a predictor of hypoxemia during exercise in restrictive and chronic obstructive pulmonary disease. Saber FA. Jensen RL. Morrison NJ. 54. 52. J Appl Physiol 1966. Sansores RH. Am Rev Respir Dis 1973. Prabhu MB. Gaensler EA. Bruch HR. Am Rev Respir Dis 1980. Summer WR. Second Edition. 55. Mink JT. Gurtner C. Abboud RT. J Appl Physiol 1993.75:927–932. Gold WM.136:1381– 1384. 45. Graham BL. Scanlon PD. Haynes N. Cotton DJ.121:647–659. The effect of menstruation on the pulmonary carbon monoxide diffusing capacity. Nadel JA. 49.151:381–384. Diurnal variation of the diffusing capacity of the lung: is it real? Am Rev Respir Dis 1987. Abboud RT. Effect of ventilation inhomogeneity on “intrabreath” measurements of diffusing capacity in normal subjects.
Chapter 4 Bronchial Challenge Testing DEFINITIONS Bronchial Challenge • Is a test used to help in diagnosing or excluding bronchial asthma by provoking a bronchoconstriction response to a controlled external stimulus. 71 A. Pulmonary Function Tests in Clinical Practice. • A significant bronchoconstrictive response is defined as a drop in FEV1 by ³20% of its baseline value. This will cause bronchoconstriction at low methacholine concentrations in asthmatics.. It could be a drug such as methacholine or a physical stimulus such as exercise or cold air. Altalag et al. *This test is sometimes called methacholine challenge test. DOI: 10. The external stimulus varies according to the type of asthma.1007/978-1-84882-231-3_4. Methacholine is an acetylcholine derivative that stimulates the cholinergic (muscarinic) receptors in the bronchial smooth muscle cells resulting in their contraction. © Springer-Verlag London Limited 2009 . The degree of airway reactivity is defined by the dose or concentration (PD20 or PC20) of methacholine resulting in bronchoconstriction. Methacholine • Is the most popular drug used in bronchial challenge*.
19 8h 24 h 48 h 48 h 8h 24 h Avoid on the study day No need to be stopped .. • Because methacholine responsiveness can be blocked by bronchodilators. formoterol)18. BACKGROUND • In asthmatics. ipratropium)17. salmeterol.g. salbutamol. Minimum time interval for drugs that may influence methacholine test result Inhaled Bronchodilators Short-acting agents (e. PD20 or PC20 is used to grade the severity of the provocative response. isoproterenol)21. the bronchial response to an allergen consists of two phases: – Immediate response. TABLE 4. • Different allergens may produce either one or both responses. the patient should be off these drugs to achieve the best results. This means that a drop of ³20% in FEV1 is required for the provocative test to be positive.1. which occurs 6–12h following exposure and is due to airway inflammation. – Delayed response. Methacholine produces only the immediate response but it is a good predictor of both responses caused by any allergen. the more severe the responsiveness is. respectively.72 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE PD20 or PC20 • Stands for provocative dose or provocative concentration. Table 4. 20.g.. If the provocative test is positive. This can be blocked by steroids.g.1. 42 Cromolyn sodium1 Leukotriene antagonists1 Caffeine-containing foods22 Inhaled or systemic steroids1. 39 Long-acting agents (e. that is. which occurs within few minutes of the exposure and is due to bronchial smooth muscle contraction (bronchospasm). This response can be blocked by bronchodilators or cromolyn sodium.. the dose or concentration of the drug at which a 20% decrease in FEV1 occurs.e. 38 Medium-acting agents (e.. the lower the concentration of methacholine in mg/ml). 40 Long-acting oral theophyllines41.1 The lower the PD20 or PC20 (i.
16 To protect the PFT laboratory staff from exposure. 8. • The test is started by doing a baseline spirometry to record the initial FEV1.1 . the patient is nebulized with normal saline. and the technician should be trained in how to deal with any unwanted response.8–15 Medical help should be readily available in rare case of a severe reaction though. • After spirometry.1 (usually 2 ml of 1–2 mg/ml solution) and delivered to the patient via a nebulizer over 2min. The results are plotted as a graph. such as severe bronchospasm or systemic reactions. nebulization is preferably performed in a negative pressure room. The technician will report this observation for the interpreter.2 The baseline spirometry tests need to be reproducible to allow comparison with later tests.BRONCHIAL CHALLENGE TESTING 73 TECHNIQUE • The patient should be clinically stable.2 lists indication for study termination.1. The patient should be observed until he or she is clinically stable and FEV1 is back to or near baseline. • Methacholine starting dose or concentration is then selected according to different dosing protocols†. These patients should not be tested with methacholine.27–35 FEV1 is then measured at 30s and 3min after nebulization.1.1 This test is done routinely in any standard pulmonary function laboratory or in specialized respiratory clinics and is generally safe. • The dose of methacholine is then doubled and the test is repeated in a stepwise fashion until the patient reaches the maximum concentration of methacholine allowed (16mg/ml) or the test becomes positive. If the spirometry reveals that the FEV1 is less than 1L or <50% of predicted value. Figure 4. • A short acting b2-agonist (2–4 puffs of salbutamol through a spacing device) is then given to subjects who develop bronchoconstriction and the spirometry is repeated 15min after that. • The test and the possible side effects should be explained to the patient. then the test should be abandoned because it is likely to cause trouble to the patient (very low baseline FEV1). Table 4. † Two major dosing protocols are widely used: (1) the 2-min tidal breathing method (the method discussed in this chapter) and (2) the five-breath dosimeter method. Some patients are so hyperresponsive that saline can precipitate a bronchospastic reaction.
The maximum dose was reached without a significant reduction in FEV1. (a) A negative bronchial challenge test.2. Two puffs of salbutamol resulted in restoration of FEV1. Indications for study termination Achieving the maximum dose or concentration allowed without a 20% or greater drop in FEV1 A positive test is achieved (drop in FEV1 by ³20% of baseline) Patient becomes unstable clinically (dyspnea. indicating a negative test. headache) FIGURE 4. as 2 mg/ml of methacholine resulted in a significant drop in FEV1 indicating a positive test. . (b) A positive bronchial challenge test. cough) Patient develops systemic reaction (flushing. wheezing.1.74 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 4. the y-axis represents the patient FEV1 as a percentage of the baseline FEV1 (before giving methacholine) and the x-axis represents the concentration of methacholine.
BRONCHIAL CHALLENGE TESTING 75 • Challenge testing can be done using other stimuli1: – Other drugs such as histamine – Exercise – in suspected exercise-induced asthma – Exposure to cold air – in cold air-induced asthma – Spirometry before and after work. Indications and contraindications for bronchial challenge Indications for bronchial challenge Unexplained dyspnea.3 summarizes the major indications and contraindications for bronchial challenge test. or episodic chest tightness Unexplained dyspnea with exercise or cold-air exposure A normal spirometry and bronchodilator response in a patient with a clinical picture suggestive of asthma Mild airflow obstruction without a bronchodilator response Absolute contraindications Severe airflow limitation (FEV1 <1 L or <50% predicted)2 A recent MI or CVA (within 3 months) Arterial aneurysm especially if advanced Hypertension (systolic >200 or diastolic >100 mmHg) Relative contraindications Moderate airflow limitation (FEV1 <1.3.5 L or <60% predicted)3. In many laboratories a positive response to bronchodilator negates the need for a methacholine challenge test. cough. . in suspected occupational asthma. 4 Clinical instability including a recent respiratory tract infection (test may be positive) Inability to perform acceptable-quality spirometry Pregnancy or nursing mothers Current use of cholinesterase inhibitors (for myasthenia gravis) Epilepsy ‡ Or by exposure to workplace allergens thought to cause occupational asthma.‡ INDICATIONS AND CONTRAINDICATIONS FOR BRONCHIAL CHALLENGE1 • The test is indicated when asthma is suspected but not obvious clinically or through spirometry as spirometry may be normal in stable asthmatics. Table 4. TABLE 4.
Methacholine challenge testing: safety of low starting FEV1. . Martin RJ. Wanger JS. it almost excludes active asthma.5. • Grading of severity of bronchial hyperresponsiveness based on PC20 is summarized in Table 4. Bartelson BB. Chest 1997.161:309– 329. 37 except if the patient took a bronchodilator prior to the test.112:53–56.1 gives examples of a negative and a positive methacholine challenge test. Grading of severity of bronchial hyperresponsiveness (based on PC20)1 Normal Borderline Mild Moderate–severe PC20>16mg/ml 4–16 1–4 <1 References 1.4. but the test may be normal if asthma is in remission. Am J Respir Crit Care Med 2000. A positive test can be seen in a variety of conditions.36. 2. which are summarized in Table 4. Table 4.1 Severe bronchial reactivity. and a negative test makes asthma very unlikely. Irvin CG.5. Cherniack RM. the Asthma Clinical Research Network (ACRN). Guidelines for methacholine and exercise challenge testing – 1999. a positive test should be reported as supportive of asthma. American Thoracic Society.5–7 Therefore. however.4.76 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE INTERPRETATION • This test is very sensitive but non-specific. may be considered diagnostic for bronchial asthma. Conditions associated with increase in bronchial reactivity5–7 Bronchial asthma Allergic rhinitis Sarcoidosis (up to 50% can have a positive test) COPD Cystic fibrosis Recent respiratory tract infection23–26 Table 4. This means that almost all subjects with active asthma will have a positive test.1 • Figure 4. If negative.
The Lung Health Study: airway responsiveness to inhaled methacholine in smokers with mild to moderate airflow limitation. Methacholine challenge testing: safety of low starting FEV. Am Rev Respir Dis 134:498–501. 13. J Allergy Clin Immunol 1992. 1986. Schouten JP. Bleecker ER. Am Rev Respir Dis 1982. The Lung Health Study: airway responsiveness to inhaled methacholine in smokers with mild to moderate airflow limitation. Mistretta A. Kanner RE. Ingram RH.145:301–310. Lee WW. Chest 1991. Wanger JS.143:317–322. Prevalence and nature of bronchial hyperresponsiveness in subjects with chronic obstructive pulmonary disease. Allergy 1992. 7. Yan K. Tashkin DP. Sterk PJ. Moser KM. the Lung Health Research Group. Malo JL. van der Lende R. Norman E. Characteristics of bronchial hyperresponsiveness in smokers with chronic air-flow limitation. 5. Am J Respir Crit Care Med 1996. Airway responsiveness: standardized challenge testing with pharmacological. Salome CM. Crimi N. 15. Bronchial responsiveness in a Norwegian community. for the American Academy of Allergy and Immunology Bronchoprovocation Committee. 16. Kanner RE. Am Rev Respir Dis 1992. Bartelson BB. Ramsdell JW. Shapiro GG. Weiss ST. 9. Connett JE. Protective effects of inhaled ipratropium bromide on bronchoconstriction . 6. Altose MD.47:188–189. Sundrum R. Wise R. Rosenhall L. Peat JK. Weiss JW. Airways responsiveness in a population sample of adults and children. Cherniack RM. 11. 4. Baste V. Irvin CG. Woolcock AJ. Bleecker ER. A survey of the current use and methods of analysis of bronchoprovocational challenges. 12. Scott GC. Chest 1997. Braun SR. 10. Du Toit JI. Tashkin DP. Am Rev Respir Dis 1988. 17. Wise R.BRONCHIAL CHALLENGE TESTING 77 3. Palermo F. Anderson SD. Salome CM. 1985.129:898–902.126(5): 829–832.137:826–832. the Lung Health Research Group. Polosa R. Speizer FE. Lee WW. Rijcken B. Martin RJ. Gulsvik A. Cockcroft DW.145:301–310. Fabbri LM. Weiss ST. O'Byme PM. Am Rev Respir Dis 1984. Tager IB. Settinieri I. Simon RA. Salome CM. Am Rev Respir Dis 132:25–29. The relationship between airway responsiveness to histamine and pulmonary function level in a random population sample. physical and sensitizing stimuli in adults. 14. On adjusting measurements of airway responsiveness for lung size and airway caliber.112:53–56. Connett JE. Woolcock AJ. Am Rev Respir Dis 1991. Black JL. Nachtwey FJ.16:53–83. Bronchoprovocation committee report.154:870–875. Munoz A. Altose MD. Bronchial hyperactivity in chronic obstructive bronchitis. Xuan W. 8. Am Rev Respir Dis 1992. Eur Respir J Suppl 1993. Baake PS. Quanjer PH.100: 322–328. Case report: development of increased airway responsiveness in two nurses performing methacholine and histamine challenge tests. Juniper EF. Lundgren R.89:775–778. Siiderberg M. Oliveri R. Statement of the European Respiratory Society. the Asthma Clinical Research Network (ACRN). Speizer FE.
Korobaeff M. Am Rev Respir Dis 1993. Newhouse MT. Tidal breathing method. deKlerk EPA. Salome CM. Cockcroft DW. Second Edition. Cockcroft DW. Killian DN. induced by adenosine and methacholine in asthma. 19. 20. and bronchial hyperresponsiveness in an epidemiological study. Interaction of inhaled Bz agonist and inhaled corticosteroid on airway responsiveness to allergen and methacholine. Douglas RG.118:295–303. Peat JK. Hargreave FE. O'Connell F. Astra Draco AB. In: Juniper EF. Cockcroft DW. 26. Cockcroft DW. 1994. Kauffmann F. Toelle BG. McMillan D. Airway hyperreactivity and peripheral airway dysfunction in influenza A infection. Histamine and Methacholine Inhalation Tests: Laboratory Procedure and Standardization. Prieto L. Berto JM. Am J Respir Crit Care Med 1995. Timmers MC. 25.5:560–565.147:1436–1441. Hargreave FE. Magnussen H. Ryan G.7:1845–1851. Berto JM. Clin Allergy 1977.78 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE 18. Speers DM. 30. Hargreave FE. Am J Respir Crit Care Med 1995. Effect of inhaled budesonide on seasonal changes in sensitivity and maximal response to methacholine in pollen-sensitive asthmatic subjects.133:735–739. Nowak D. Prieto JL. Greenspon LW. Comparison of the effects of salmeterol and formoterol on airway tone and responsiveness over 24 hours in bronchial asthma. Oroven-Frija E. Mudholkar GS. Spaan WJM. Thorax 1993. Neukirch F. Woolcock AJ. Lund.26:61–67. Rhinovirus inhalation causes long-lasting excessive airway narrowing in response to methacholine in asthmatic subjects in viva. Fuller RW. Sensitivity and maximal response to methacholine in perennial and seasonal allergic rhinitis. Dolovich MB. Henderson JC. Swystun VA.7:235–243. Oryszczyn M-P.48:824– 826.152:1485–1489. Am Rev Respir Dis 1986. Cheung D. Eur Respir J 1994. Dick EC. Dermand J. Patel K. Juniper EF. Sweden. Clin Exp Allergy 1996. Hargreave FE. Mellon JJ. 23. Bronchial reactivity to inhaled histamine: a method and clinical survey. Decrease of histamine induced bronchoconstriction by caffeine in mild asthma. Gutierrez V. Eur Respir J 1992. Rabe KF. 24. 28. Comparison of two epidemiological protocols for measuring airway responsiveness and allergic sensitivity in adults. Camps B. Roberts RS. Gutierrez V. Relationship of upper airways disorders [rhinitis] to FEV.7:1798–1804. Hall WJ. Sterk PJ. Factors that contribute to inhibition of methacholine-induced bronchoconstriction. 21. Eur Respir J 1992. Behr N. 27.152:1490–1496. 22. Am Rev Respir Dis 1978. Tornero C. Bhagat R. Crane J. eds. Annesi I. D'Souza W. 29. Jorres R. Standardization of inhalation provocation tests: .5:1104–1110. Morrissey WL. Juniper EF. Frith PA. Little JW. Eur Respir J 1994.
34. Comparison of histamine bronchial challenges with the Wright nebulizer and the dosimeter. Wisniewski A.BRONCHIAL CHALLENGE TESTING 79 31. Cooper S. Allergy Clin Immunol 1992.144:338–343.41:128–132. 42. 38. Howick J. Tattersfield AE. 40. Menendez R. Woolcock AJ. Bennett JB. Wachinger SL. two techniques of aerosol generation and inhalation compared. 35. Br J Dis Chest 1987. Kelley HW. Sensitivity and specificity of histamine PC-20 determination in a random selection of young college students. Weinberger MM. Coe C. Theophylline has a doserelated effect on the airway response to inhaled histamine and methacholine in asthmatics. Tattersfield AE. 36.81:252–259. 33. Bonham AC. I. . Salome CM. Malo JL. J Allergy Clin Immunol 1902. A comparison of the Yan and a dosimeter method for methacholine challenge in experienced and inexperienced subjects. Barnes PJ. The effect of inhaled salmeterol on methacholine responsiveness in subjects with asthma up to 12 hours.130:193–197. Am Rev Respir Dis 1984. Mortagy A. Green S. 39. Reuss G.136:1163–1167. Am Rev Respir Dis 1984. Gilbert R. Magnussen H.97:562–565. Berscheid BA.89:23–30. Eur J Respir Dis 1987. Murdock KY. Cockcroft DW. 41. A comparison of histamine and methacholine bronchial challenges using the DeVilbiss 646 nebulizer and the Rosenthal-French dosimeter. A method for comparing the peak intensity and duration of action of aerosolized bronchodilators using bronchoprovocation with methacholine. Am Rev Respir Dis 1987. Am Rev Respir Dis 1991. Ahrens RC. Effects of theophylline on inhaled methacholine and histamine in asthmatic children. Knox AJ. Gore BP.9: 575–583. Toelle BG. Jorres R. Davies RJ. Repeatability of histamine bronchial challenge and comparability with methacholine bronchial challenge in a population of Australian schoolchildren. Derom EY. Beaupre A.4:497–502. Maxwell GA. Am Rev Respir Dis 1981. Chest 1990. Van Der Straeten MEF. Pauwels RA. Thorax 1986. Britton J.89:81l–815. Peat JK.71:455–458. Bauman A.129:903–906. Wilson NM. 37. Clin Allergy 1979. Duration of protection by oxitropium bromide against cholinergic challenge. Histamine challenge testing: comparison of three methods. 32. McWilliams BC. Eur Respir J 1991. Auchincloss JH. Post-test probability of asthma following methacholine challenge.123:195–199.
The test is repeated * MIP and MEP are sometimes referred to as PImax and PEmax. the patient is instructed to exhale fully (to RV) and then inhale against a closed valve as hard as possible. respectively. Altalag et al.These pressures are generated by the respiratory muscles during a forceful inspiration and expiration. coexistent interstitial lung disease. Technique • To measure MIP.Chapter 5 Respiratory Muscle Function and Other Pulmonary Function Studies RESPIRATORY MUSCLE FUNCTION Maximal Respiratory Pressures The two self-explanatory tests used to assess the respiratory pressures are the maximal inspiratory pressure (MIP)* and the maximal expiratory pressure (MEP).. Indications • Assessment of respiratory muscle function: – In patients with known NMD – In patients with suspected early NMD (unexplained dyspnea or unexplained restrictive pattern in PFT) • Particularly helpful when lung mechanics are abnormal. DOI: 10. i. The resulting pressure should be sustained for 1 s. 81 A.. © Springer-Verlag London Limited 2009 . Pulmonary Function Tests in Clinical Practice.e.1007/978-1-84882-231-3_5. respectively.
Interpretation • The MIP is considered normal if it is below −70 cmH2O and MEP above +90 cmH2O in young adult males (lower values are reported in females and elderly). . the normal values vary signiﬁcantly with age and sex. the pressure has to be sustained for 1. For more details refer to the following references 2.2 Most laboratories use a flanged mouthpiece because it is easier to use as compared to the firmer rubber tube.1.3.3.e. TABLE 5.5 s and the highest reproducible pressure is reported.†. Similarly. which is considered a pressure transient.4 A small leak is introduced (a 2-mm hole in the tubing) to prevent glottic closure and use of the cheeks during MIP maneuver. • To measure MEP. Causes of NMD Neurogenic causes Motor neuron disease or amyotrophic lateral sclerosis (ALS) Guillain-barre syndrome Poliomyelitis Multiple sclerosis High spinal cord injury (quadriplegia) Phrenic nerve injury Neuromuscular junction causes Myasthenia gravis Eaton–Lambert syndrome Muscular causes Muscular dystrophy Myopathies (polymyositis. lupus. when the physical weakness is not clinically apparent. thyroid-related.82 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE for reproducibility and the highest reproducible pressure (i. inflammatory. biochemical) Malnutrition † There is a wide range of normal values in the same age and sex.1.5 Low MIP and MEP are seen in NMD even in early stages. For both MIP and MEP the maximum average pressure sustained for 1 s is recorded to avoid recording a brief peak.. steroid-induced.7–18. the patient inhales to TLC and then exhales against a closed valve as hard as possible. within 20%) is reported.2 For causes of NMD. see Table 5.
6 Limitations • There is a wide range of normal results. Shorter length leads to low ability to shorten and produce a pressure. • MIP can also be decreased in a poor-effort study and in patients with significant hyperinflation and air-trapping (like emphysema).RESPIRATORY MUSCLE FUNCTION 83 • Because the diaphragm is the major inspiratory muscle. 20 A negative pressure of >60 cmH2O excludes significant inspiratory muscle weakness. which represents a reasonable approximation of the esophageal pressure (Pes – used to reflect intrathoracic pressure). Sniff Tests • Are designed to assess the strength of the diaphragm and the other inspiratory muscles. sharp voluntary inspiratory maneuver performed through one or both unoccluded nostrils. in quadriparesis due to cord injury (below C3-5 where phrenic nerve originates). as the diaphragm is not affected. The same principle underlies the reason why MIP is measured at RV and MEP at TLC. sniffs need to be maximal. A sniff is a short.2 • Three sniff tests are available for clinical and research use: (a) Sniff nasal pressure (sniff Pnas) is the least invasive among the other sniff tests and most practical in the clinical setting. Sniffing with the unoccluded nostril and with mouth closed will generate a negative pressure in the nose. It is measured by placing a plug in one nostril and measuring the pressure in the nose via a pressure catheter passed through the plug.19.21 In COPD. To be useful as a test of respiratory muscle strength. but may require some practice.1. the MIP is usually low with a preserved MEP.2 The degree of air-trapping and hyperinflation is directly proportional to the degree of impairment of the respiratory pressures. the MEP is low with a relatively preserved MIP. This effect is a result of the reduction in diaphragm muscle length that occurs when lung volume increases. in bilateral diaphragmatic paralysis. • MEP of <40 is predictive of an ineffective cough. Most subjects achieve reproducible values within 5–10 attempts. and poor effort may mimic disease. making it sometimes difficult to separate normal from abnormal results. On the other hand. • The test is effort dependent. sniff Pnas tends to underestimate the esophageal pressure but . which is relatively easy for most willing subjects.
the electrical stimulation can be uncomfortable and does not always produce a supramaximal stimulation. and a supine fall in VC. Supramaximal stimulation can be performed resulting in maximal diaphragmatic contraction that can be measured as a transdiaphragmatic pressure (twitch Pdi) using gastric and esophageal balloons. malingering. 24 • The continuity of the phrenic nerve is assessed as the EMG of the diaphragm and is recorded using an esophageal electrode .84 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE can complement MIP in excluding significant inspiratory muscle weakness. all of which are highly diagnostic for diaphragmatic paralysis. again.24 • Although this test is effort-independent. • One or both hemidiaphragms may be stimulated at once (single pulse).22 (b) Sniff esophageal pressure (sniff Pes) is similarly measured by an esophageal balloon catheter system (a pressure sensing device on the end of a thin hollow tube) during maximal sniffs. transcutaneously at FRC using an electrode placed over the skin at the posterior border of the sternocledomastoid. • Magnetic stimulation of phrenic nerve may be used instead of the electrical stimulation..23 A negative pressure of >80 cmH2O in men and >70 cmH2O in women excludes significant inspiratory muscle weakness. e.25 Transcutaneous Electrical Phrenic Nerve Stimulation • Diaphragmatic function can be assessed nonvolitionally by stimulating the phrenic nerve(s).g. and is indicated when the sniff Pnas is inconclusive. A sniff Pdi of >100 cmH2O in men and >70 cmH2O in women excludes significant diaphragmatic weakness. assesses the global inspiratory muscles strength including the diaphragm. Magnetic stimulation is less uncomfortable but is less widely used because of high equipment costs. Sniff Pes.24 (c) Sniff transdiaphragmatic pressure (sniff Pdi) measurement is performed by passing an esophageal and a gastric balloon and measuring the pressure difference on both sides of the diaphragm (transdiaphragmatic pressure) during maximal sniffs.24 A sniff Pdi of <30 cmH2O is associated with orthopnea. A resultant twitch Pdi pressure of >10 cmH2O (unilateral) or >20 cmH2O (bilateral) excludes significant diaphragmatic weakness.2 This test is particularly useful in identifying muscle weakness when lack of effort is an issue. paradoxical abdominal motion. which can make it difficult to interpret subnormal results.2. Sniff Pdi specifically measures diaphragmatic strength.
‡. . ‡ Bilateral tetanic stimulation can give maximal Pdi but is uncomfortable and only used for research. • A drop in FVC of <10% of the sitting value is considered normal.5 ms).RESPIRATORY MUSCLE FUNCTION 85 or.26 Bilateral diaphragmatic paralysis is considered when FVC drops by >30% of the sitting value. Patients with low MEP can have a normal cough Pga. Cough Test • Is used to assess the expiratory muscle strength because cough is a natural maneuver that can produce MEP. a surface electrode placed in the seventh intercostal space at the midaxillary line (normal phrenic nerve conduction time is <9. which indicates that this test may be more reliable than MEP but is more invasive at the same time.2. 24 Peak cough flow rates are much less invasive and provide important information regarding airway clearance in patients suspected of having a weak cough.24 This test can substantiate diaphragmatic paralysis. This pressure is measured using a gastric balloon catheter and is referred to as cough gastric pressure (cough Pga). The FVC is significantly reduced in the supine position in such conditions because of elimination of gravity. Supine Spirometry • Is indicated when diaphragmatic weakness is suspected.35 Other Less Widely used Tests to Assess Respiratory Muscle Function • • • • Maximum mouth pressure Maximal static transdiaphragmatic pressure Abdominal muscle stimulation test Cough flow rates OTHER PULMONARY FUNCTION STUDIES Maximum Voluntary Ventilation (MVV) • Is the maximum volume of air that can be breathed in and out over 1 min (liters/minute). more commonly.
Because the lung volume at which . Airway Resistance (RAW) and Conductance (GAW) • RAW (L/s/cmH2O) is the amount of pressure (alveolar pressure over the mouth pressure or the transpulmonary pressure) required to generate a given airflow. 34 They are.e. prone to measurement and calculation errors.1. an important role in assessing the ventilatory function during exercise. while also measuring the lung volumes. The reciprocal of that is GAW. however. • MVV is a very nonspecific test and is usually reduced with any pulmonary disorder (obstructive or restrictive disorders including NMD). • These tests are not effort-dependent and are used in patients with suspected obstructive disorders who cannot produce good effort in spirometry. being more significantly lower in obstructive disorders. measured at the mouth. which limit their use. divided by the difference between alveolar and mouth pressures represents RAW.33. then this may suggest a poor effort.86 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 5. MVV is also reduced in poor effort test and in cardiac disease. see Figure 5. Measuring MVV in the laboratory. The flow.. the amount of airflow generated by a given alveolar pressure. The test is done over 12 s and the result is extrapolated to 60 s by multiplying by 5. • MVV has.1. and it can also be estimated by multiplying the patient’s FEV1 by 40 (some prefer 35). • Their measurement involves measuring the mouth and alveolar pressures in the body box at FRC. • MVV correlates very well with FEV1. as it correlates well with the maximal exercise capacity (see Chapter 9 for details). then the result is extrapolated to 1 min by multiplying that by 5. • It is measured in the laboratory by asking the patient to breathe as fast and as hard as possible for 12 s.27–32 If the measured MVV is significantly lower than the calculated one. however. while GAW (cmH2O/L/s) is the reciprocal of that. i.
ARDS). CLdyn decreases further as frequency of breathing increases. are recruited and these units are less compliant. the lung units with more rapid frequency response. • An increased RAW is likely to be due to an obstructive disorder. Lung Compliance (CL) • Is the change in lung volume for a given change in pressure or simply. It can only be reliably measured in ventilated and paralyzed patients where activity of the chest wall muscles is eliminated. Forced Oscillation Technique (Oscillometry) • Is the determination of the total pulmonary resistance by imposing known variations in flow at the mouth and measuring the resultant pressure changes. the ability of the lung to expand. § This reduction is caused by the effect of the increasing frequency of breathing on the lung units that are recruited. .e. static or dynamic lung compliance (CLstat and CLdyn): (a) CLstat is calculated by measuring the pressure when there is no flow at two different lung volumes. It is decreased in lung fibrosis (decreased ability of the lung to expand) and increased in emphysema. • CL can be expressed in two ways. It is decreased in disease of either the chest wall (ankylosing spondylitis) or the lungs (acute respiratory distress syndrome. • Its main use is in children who cannot generally perform spirometric maneuvers. i.24. • Because it measures the total resistance. it is hard to separate the upper from the lower airway resistance. § • Total thoracic compliance is the compliance of both the lungs and chest wall together. CLdyn is lower than CLstat in patients with airway obstruction. SGAW).RESPIRATORY MUSCLE FUNCTION 87 the flow is measured will influence the airway resistance. which limits its clinical usefulness. It is measured by simultaneous measurements of the lung volume and the elastic recoil pressure by an esophageal balloon (Pes). In these patients. (b) CLdyn is measured during tidal breathing (VT) by continuously measuring pressure and volume (CLdyn is represented as ΔP/ΔV).. shorter time constant. the results are corrected to that lung volume to generate the specific airway resistance and conductance (SRAW. As the frequency of breathing increases.
Keens TG. Enright PL. Polkey MI. Respiratory muscle strength in the elderly: correlates and reference values. Kronmal RA.66:750–754. Eur Respir J 1988. Nakamura M.1:863–867. Mills GH. Pardy RL. Fatigue of inspiratory muscles and their synergic behavior. Easton PA. Dixon GF. Eur Respir J 1995. 5. Green M. Am J Respir Crit Care Med 1994.9:241–247. 12. Road JD. Moreno RH. Inspiratory muscle conditioning using a threshold loading device.166:518–624. J Appl Physiol 1987. Wragg SD. Am Rev Respir Dis 1969. Manolio TA. Kyroussis D. 9. Comparison of two different mouthpieces for the measurement of PImax and PEmax in normal and weak subjects. Schenker MB. 13. Hyatt RE.135:919–923. Kyroussis D. 7. J Appl Physiol 1979. Grassino A. 1st Edition.8:463–466. Similowski T. 3. 16. Lincoln MJ. Moxham J. Philadelphia. Rodis A. Clanton TL. Moxham J. Fitting JW. Nickerson BG. 4.62:39–46.155:642–648. Diaphragmatic fatigue following voluntary hyperpnea. Diaphragm fatigue following maximal ventilation in man. Lippincott Williams & Wilkins. Hamnegard CH. Am J Respir Crit Care Med 1996. Tzelepis GE. Black L. Am J Respir Crit Care Med 1997.88 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE References 1. Interpretation of Pulmonary Function Tests: A Practical Guide. Koulouris N. Kikuchi Y. Goldman MD. 2nd Edition. Preferential fatigue of the rib cage muscles during inspiratory resistive loaded ventilation. Hyatt RE. Moxham J. Hershenson MB. 6. Green M.52: 768–772. Macklem PT. 15. Diaphragm performance during maximal voluntary ventilation in chronic obstructive pulmonary disease. Green M. Pocket Guide to Lung Function Tests. 8. Gross D.154:63–67. ATS/ERS statement on respiratory muscle testing: tests of respiratory muscle strength. PA. Roussos C. Martyn JB. Hancox B. Sydney. 17. 11. McGraw-Hill. . Eastwood PR. Drake J. Maximal respiratory pressures: normal values and relationship to age and sex. Diaz J. Gadek JE.46:897–904. Clanton TL. 10.149:430–438. Laroche CM.99:696–702. Green M. Sieck GC. Pare PD.87:62–66. Scanlon PD. Bradley TD. Mills GH. Mador JM. Eur Respir J 1996. Am J Respir Crit Care Med 2002. Bake B. Dixon G. Measurement of inspiratory muscle performance with incremental threshold loading. McCool D. Hughes PD.64:959–965. 2001. J Appl Physiol 1997. Polkey MI. Measuring ventilatory muscle endurance in humans as sustainable inspiratory pressure. Chest 1985. Whyte K. 2003. J Appl Physiol 1988. Am Rev Respir Dis 1987. Hamnegard CH. Hyatt R. Gadek JE. Road J. Drake J. A threshold loading device for testing of inspiratory muscle performance. 14. J Appl Physiol 1982. Dissociation between diaphragmatic and rib cage muscle fatigue. Moran J. Effects of swim training on lung volumes and inspiratory muscle conditioning. Mulvey DA. 2. Hillman DR.
McCumber TR. Grassino A . W. Handbook of Physiology. Lewis MI. Ameen K. Clanton TL. 19. Physiological Principles and Clinical Applications. 21. Rajagopal KR. Tubau J. Interpretative strategies for lung function tests. Evaluation of human diaphragm fatigue . J Appl Physiol 1988. Ries AL. Mador MJ.90:662–669. Hughes JMB . 30. Bethesda. B.132:230–235.64:1693–1699. Rahm F. Hunt B. Dillard TA. Green M. Heritier F. Szlachcic J. 27. et al. Dillard TA. Green M.26:948–968.53:1196–1206.147:870–875. W. 1986. Hnatiuk OW. Maximum intensity exercise training in patients with chronic obstructive pulmonary disease.RESPIRATORY MUSCLE FUNCTION 89 18. Topic N. 24. Brophy C. Section 3. J Appl Physiol 1982.154:448–453.20:433–436. B. Pride NB. Sniff nasal pressure. Mead J. Green M. 35. Am J Respir Crit Care Med 1994. 20. Comparison of cervical magnetic and transcutaneous phrenic nerve stimulation before and after threshold loading. Philadelphia. Cardiopulmonary exercise testing: physiologic principles and clinical applications. 23. Am Rev Respir Dis 1988.598–603. Eur Respir J 2005. 29. Fitting J-W. Respiratory muscle testing. Franciosa JA. Fall in vital capacity with posture. Prediction of ventilation at maximal exercise in chronic air-flow obstruction. Am J Cardiol 1985. Part 2. 22 . Rodis A.55:1037–1042. 25. American Physiological Society. Belman MJ. 32. Assessment of diaphragm weakness. Chest 1986.659–692. Moxham J. Kramer BL. Saunders. MD. Vol. Am Rev Respir Dis 1988. Br J Dis Chest 1995. Philadelphia. Pasche P. 33. Lack of correlation between exercise capacity and indexes of resting left ventricular performance in heart failure. Lung Function Tests. Pellegrino R. Bull Eur Physiol Respir 1984. Bellemare F. Piantadosi S. . First Edition. Am Rev Respir Dis 1993. Magalang UJ. III. 34. Allen SM. Mechanics of Breathing. Massie BM. Resistive breathing training in patients with chronic obstructive pulmonary disease. Green M. Ameredes BT.100:618–623. 31. Maximum voluntary ventilation: spirometric determinants in chronic obstructive pulmonary disease patients and normal subjects. eds. Pride NB.47:33–39. Lung mechanics in disease.79:267–271. Chest 1991. 26. Macklem PT. In: Macklem PT. Anon ivasive assessment of inspiratory muscle strength.150:1678–1683. Viegi G. Fatigue of the inspiratory muscle pump in humans: an isoflow approach. Am J Cardiol 1981. 1986. The value of sniff esophageal pressure in the assessment of global inspiratory muscle strength. Enright P. Punzal PA. Am Rev Respir Dis 1985. Am J Respir Crit Care Med 1996. Kaplan RM. Saunders. Correlates and prognostic implication of exercise capacity in chronic congestive heart failure.137:877–883. Levine TB. Mier A. Mier AK. Moxham H. Weber KT. Janicki JS. Scott GT. 28. Prewitt LM. Laaroche CM. 1999. Park M. The Respiratory System.
Chapter 6 Approach to PFT Interpretation APPROACH OUTLINE 1. Altalag et al. 91 A. Examine the volume–time curve: (a) Technical quality of the curve (b) Size and shape (c) Components (d) Postbronchodilator curve 3. and FEV1/FVC ratio. (b) Examine the postbronchodilator value of FVC. RV. DOI: 10. (c) Consider some special situations. and technician's comments 2. and RV/TLC ratio. © Springer-Verlag London Limited 2009 . (c) Examine MMEF and FEFs. (d) Examine the rest of the spirometry. (b) Examine the rest of the lung volumes (FRC. Review of clinical history provided. patient's demographics. and FEV1/FVC ratio. 5. FEV1.. (e) Consider some special situations. Lung volumes: (a) Examine TLC. ERV. Spirometry: (a) Examine FVC. FEV1. Pulmonary Function Tests in Clinical Practice.1007/978-1-84882-231-3_6. IC). Examine the flow–volume curve/loop: (a) Technical quality of the curve (b) Size and shape (c) Components (d) Location (e) Its relation to the tidal FV loop (f) Postbronchodilator curve 4.
REVIEW THE CLINICAL HISTORY PROVIDED. the presence of kyphoscoliosis. See also Table 6.92 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 6.. if available Examine the spirometry Examine the lung volumes Examine the gas transfer study Examine any additional test provided Compare the current study with previous ones. patient’s demographics. 7. if available Reaching a useful conclusion (based on spiromerty and lung volume study) Both are obstructive Both are restrictive Both are normal One is restrictive and the other is obstructive One is normal and the other is abnormal 6. (c) Examine the rest of the variables.1. • Technicians’ comments provide information about the quality of the study. . Technicians sometimes comment about the patient's condition. wheezing. The following is an abbreviated version of what we have reviewed in the previous chapters. e. Approach to PFT interpretation Approach outline Review: clinical history provided.g. • The patient's demographics also provide useful information. the patient's weight (obesity can lead to a restrictive pattern). consistency with the ATS guidelines. for example. (b) Examine DLCO/Hgb correction. AND TECHNICIAN'S COMMENTS • The clinical data provided in the requisition form are important to direct the interpreter's attention as well as the final report. Clinical data are extremely useful in helping to form your conclusion. Gas transfer study: (a) Examine DLCO and DLCO/VA ratio.1. and technician’s comments Examine the volume–time curve Examine the flow–volume curve/loop. and other tests provided 8. PATIENT'S DEMOGRAPHICS. ABG. Examine any additional test provided: (a) Methacholine challenge (b) Maximum respiratory pressures (c) Supine spirometry (d) MVV. and patient's effort. if available. Compare the current study with previous ones.
. which should be sharp and rounded) (b) Smooth curve free from artifacts (mainly in the 1st second) (c) Good end (slight upward concavity at the end of the curve) – The lack of any of these criteria affects the study quality. Improvement in the shape and slope of this curve compared to the original may indicate a response to bronchodilators. 2: (a) Good start (rapid climb to PEF.50. APPROACH TO THE FLOW–VOLUME (FV) CURVE/LOOP • Assess the technical quality of the study based on FV curve: – A good curve quality should have the following. APPROACH TO VOLUME–TIME (VT) CURVE • Examine the VT curve by observing: – The duration of the curve should be at least 6 s to meet the ATS criteria. if applicable (a) In patients with a suspected obstructive disorder. as the same curve may be seen in NMD and in children. and in the laboratory this is usually achievable. a post bronchodilator curve is also done (usually red in color). the results should then be interpreted with caution. Figure 1. Figure 1.11a1. The technician's comments address the patient's technique (if poor) and the study acceptability and reproducibility (which are impaired with a poor technique). Figure 6. Comparing the heights (FVC) and the volume corresponding to 1 second (FEV1) in both curves may help judging the response to bronchodilators more accurately.1f. – A morphologically poor start of the study should not prompt you to reject the study right away. – The size and shape of the curve compared with the predicted curve: (a) In obstructive disorder: the curve is less steep than the predicted curve. Therefore.16. (b) In restrictive disorder: the curve has a normal shape but is smaller than the predicted curve.APPROACH TO PFT INTERPRETATION 93 or stridor while testing.25–75 (extracted from the curve's slope) – Post bronchodilator curve. – The components of the curve help to distinguish restrictive from obstructive abnormalities: (a) FVC (the height of the curve) (b) FEV1 (the volume corresponding to 1 s) (c) FEF25.75. This information may not be provided in the clinical data.
(i) Fixed upper airway obstruction. (g) Variable intrathoracic upper airway obstruction. (c) Dog-leg obstructive curve. (f) NMD or poor initial effort (can also be seen in children).FIGURE 6. (e) Chest wall restriction (consider racial variations). . (d) Parenchymal restriction with a witch's hat appearance. typical for emphysema.1. Normal and most abnormal FV loops: (a) Normal. (h) Variable extrathoracic upper airway obstruction. (b) Obstructive loop.
1e.1.1b. including the normal variants such as the “knee” variant. (d) Small and parallel slope to the predicted curve: is seen in chest wall restriction (musculoskeletal disease. Figure 6. (c) Small and steep slope with a witch's hat shape: suggests parenchymal restriction. . (continued) • Examine the size and shape of the FV curve/loop: – The size and shape of the curve (after excluding poor quality curves) should fit one of the following. Figure 6. Figure 1.APPROACH TO PFT INTERPRETATION 95 FIGURE 6. c. (b) Small and concave or scooped: suggests obstructive disorder. Figure 6. Figure 6. and obesity) or normal patients with small lungs – racial variations.1: (a) Normal size and shape.22. Figure 6.1d. diaphragmatic distention.1a: indicates a normal study.
– This step is important in making a quick impression about the underlying disorder. it suggests a restrictive defect (remember: shift to the right → restriction). (c) If the curve is shifted to the left (↑TLC. think about that for a minute!). then RV/TLC ratio should be ↑. – Width (FVC) – if smaller than the predicted curve. size. – Then examine its shape.1f. This impression is usually correct. Figure 2. it suggests obstruction (If. If the red curve shows improvement in the shape. FVC is ↓. size.7: (a) If the curve runs along the predicted one. and location compared with the blue curve.. If low.96 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE (e) Small and convex shape (mimicking poor start. (f) Small and flat (suggests central airway obstruction): * Only the expiratory component is flat (variable intrathoracic obstruction). Figure 6.1g. in addition. it indicates a response to bronchodilators.e. • Examine the components of the curve: – Height (PEF) and slope (FEF25–75) – if low.1b.1h. If so. supporting obstruction.15. (b) If the curve is shifted to the right (↓TLC.1i. in NMD. – The 1st second mark (FEV1) – check how it compares to the whole width of the curve (FVC) to visually estimate the FEV1/ FVC ratio. then TLC and RV are normal. • Examine the location of the curve compared to the predicted: – This is only possible if spirometry is done in the body box while measuring lung volumes. – As mentioned earlier. suggests restrictive (mainly) or obstructive defect (to a lesser extent). * Both components are flat (fixed obstruction). • Examine postbronchodilator curve. ↑RV). which may be significant. – Quickly examine the technical quality of the red curve. ↓RV). Figure 6. Figure 6. Figure 1. Figure 6. then we can apply the following. if applicable. this may suggest an obstructive disorder. . it suggests obstruction. * Only the inspiratory component is flat (variable extrathoracic obstruction). and in children. Figure 6. while the postcurve is in red. and/or location compared with the blue curve. i. which is not sharp): is seen in a study with a poor effort. delayed and decreased PEF. a prebronchodilator curve is colored in blue.
Table 1. if available). – The response to bronchodilators can be as follows6. (b) Insignificant or no response – if it is less than that. FEV1 level (% pred.25–75 – These flows usually follow the FEV1. If excessively prolonged.. as it will be obvious in FV loop. Therefore.3 A normal FVC. rules out restriction. (c) Possibly restrictive – with ↓ FVC and a normal or ↑ FEV1/FVC ratio (confirm the restrictive nature of the disorder by measuring TLC.6. 8 • Have a quick look at the rest of the spirometry: – PEF decreases with the following: (a) Poor effort (as it is effort dependent) (b) Obstruction (mainly) (c) May decrease with restriction (such as NMD). and FEV1/FVC ratio: – There are four possibilities: (a) Normal – when all are normal. which should be low. – PIF and FIF50 – drop with poor effort or with variable extrathoracic obstruction (do not worry about this. the FEV1/FVC ratio is 65% and FVC is only 40% pred. Table 1. – FET – helps knowing the appropriate duration of exhalation (should be ≥6 s).50. This defect is not specific for small airways disease. • Examine the postbronchodilator value of FVC. (d) Combined obstructive and restrictive disorder – may be suggested if the reduction in FVC is out of proportion to the reduction in the FEV1/FVC ratio (e. if low. 7: (a) Significant response – 12% and 200 ml ↑ in FEV1 or FVC. 5 To be definite about the presence of a combined disorder. they suggest obstruction but can be low in restrictive disorders and upper airway obstruction. if available.4). FVC is used to grade severity. it may suggest a mild airway obstruction. . FEV1. the lung volumes need to be examined. (b) Clearly obstructive – defined by a ↓ FEV1/FVC ratio (FEV1 is usually ↓ and FVC is relatively preserved. it is usually preserved in parenchymal restriction.). however.) determines severity. Remember that spirometry with a poor effort may look restrictive.g. FEV1. • Examine FEF25. and FEV1/ FVC ratio.APPROACH TO PFT INTERPRETATION 97 APPROACH TO SPIROMETRY • Examine FVC.4.4). if TLC is not done.75.
Table 1.. Remember the causes of low DLCO (Table 3. • Examine the rest of the lung volumes (FRC. IC): – They usually follow the TLC and RV. the direction of obstruction or restriction. * ↑ RV indicates air trapping. suggesting obstruction. i. RV.3) and consider the most important ones: * Parenchymal lung disease . see next sections. so they are high in obstructive and low in restrictive disorders. APPROACH TO GAS TRANSFER STUDY • Examine DLCO and DLCO / VAratio: – For simplicity. (b) High volumes.3. and RV/TLC ratio (these are the most important lung volume variables): – They usually change in the same direction. TLC should be used to grade severity.98 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • Special situations – Isolated reduction in MMEF and FEFs indicates airflow limitation at low lung volumes.e. • Special situations: – Isolated reduction in ERV indicates obesity. check the patient's weight. The following are the possibilities: (a) Normal.4). – An isolated significant response to bronchodilators with normal flows at baseline strongly suggests bronchial asthma.6 APPROACH TO LUNG VOLUME STUDY • Examine TLC.6. ERV. when all are normal. consider combined disorders. * ↑ RV/TLC ratio reflects the degree of air trapping. 8–11 Lung volume study may be of help. if available. (c) DLCO/VA is low (regardless of the value of DLCO) – this indicates a gas-exchange abnormality. remember: * ↑ TLC usually indicates hyperinflation (hyperinflation is more accurately defined by ↑ FRC).6 (c) Low in restrictive disorders (↓TLC is essential to make a confident diagnosis of restriction6. (b) Both are high – seen in a variety of pulmonary and systemic disorders. consider four possibilities: (a) Both are normal – this indicates that there is no gasexchange abnormality. review Table 3. – When the lung volumes are incompatible with spirometry.
(b) IVC should be at least 85% of the patient's VC. Consider the following: * This could be an extraparenchymal disease (loss of alveolar spaces) such as lung resection or chest wall restriction (e.. you cannot conclude much from this. – If it does not correct to normal. it indicates that anemia is responsible for the reduction in DLCO. If less. plethysmography: if TLC is estimated with plethysmography and either N2 washout or gas dilution methods. DLCO is underestimated and vice versa.2. it normalizes if corrected to VA as the loss in VA is the predominant abnormality) – unfortunately.12 * Remember that gas-exchange abnormality like lung fibrosis cannot be excluded. If less.g. the difference between the two increases and roughly estimates the volume of the poorly ventilated air spaces. * Normal subjects who fail to take a deep enough breath or long enough breath-hold can show similar abnormalities. . • Examine DLCO/Hgb correction. then the difference between the two TLC measurements can estimate the volume of trapped air. then a gas-exchange abnormality rather than anemia is responsible. see next. From lung volume study: a high RV indicates air trapping. if Hgb is available:13–17 – If a low DLCO corrects to normal. NMD). – BHT and IVC help in determining the accuracy of DLCO study: (a) BHT should equal 10 s. DLCO is underestimated and vice versa.1 TABLE 6. N2 washout or gas dilution methods vs.e.. see also Table 6.2. Methods to identify the presence of air trapping and estimate its volume From spirometry: a significant difference between SVC and FVC indicates air trapping (SVC being larger than FVC). the difference between the measured and the predicted RV roughly estimates the volume of the trapped air. From gas transfer study: a significantly higher TLC compared with VA indicates air trapping.APPROACH TO PFT INTERPRETATION 99 * Pulmonary vascular disease * Anemia (d) DLCO is low with a normal or high DLCO/VA (i. In an obstructive disorder. • Examine the rest of the variables: – VA should roughly equal TLC and is usually less than TLC.
(b) A small curve with a parallel slope to the predicted curve suggests a chest wall restriction other than NMD.2: it is much higher in emphysema than in asthma. Both support a restrictive defect: • The final diagnosis is then a pure restrictive disorder. – Bronchial challenge: is more likely to be positive in asthma than in emphysema.21–26 – If you can estimate the degree of air trapping. Start by determining whether spirometry and lung volumes support the same diagnosis: If both (spirometry and lung volumes) support an obstructive defect: • The final diagnosis is then a pure obstructive disorder. – Lung volume study: (a) TLC is usually normal in asthma and ↑ in emphysema. • Remember that other obstructive disorders (such as bronchiectasis.1f) suggests NMD or poor effort study.100 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE REACHING A USEFUL CONCLUSION Combining spirometry. like ILD – Chest wall restriction (NMD. lung volumes and DLCO measurements helps reach an accurate conclusion. (b) RV/TLC ratio is increased in emphysema and in asthma. • You will need then to differentiate between the two major obstructive disorders – asthma and emphysema: – FV curve: a “dog-leg” appearance is characteristic for emphysema. . MSD. diaphragmatic paralysis and morbid obesity) • The following helps for the distinction: – FV curve: (a) A small curve with a steep slope suggests a parenchymal restriction. 20 – DLCO: ↓ in emphysema and normal or ↑ in asthma. (c) A convex curve (Figure 6. and chronic bronchitis) could be responsible.18 – Spirometry: a significant bronchodilator response is suggestive of asthma. • The two major groups of disorder involved are as follows: – Parenchymal restriction. see Table 6. obstructive bronchiolitis.19.
– DLCO12 (a) If low (DLCO/VA) – it supports parenchymal restriction. 8–11 . The RV/TLC ratio is invariably ↑ in chest wall restriction (it is mostly normal with parenchymal restriction).e. a BMI of >35 is compatible with obesity causing a restrictive pattern.6. this supports chest wall restriction.APPROACH TO PFT INTERPRETATION 101 – Lung volumes: (a) Although the TLC is ↓ in both disorders. then this supports parenchymal restriction. • To differentiate the types of chest wall restriction: – Obesity: (a) You can calculate the BMI.27 (b) The degree of the reduction in FVC compared with TLC: * If FVC and TLC are proportionally reduced. – NMD (such as ALS) (a) FV curve is usually convex in shape. – MSD (such as kyphoscoliosis): (a) Normal or reduced28 MIP and MEP (not such a large reduction as seen in NMD). (b) ERV is usually very low in obesity (c) Usually normal MIP and MEP. as discussed. (b) FVC is markedly reduced in supine position (drops by >30% from sitting FVC).. TLC is relatively preserved). (b) MIP and MEP are ↓.29 (c) Other tests (transdiaphragmatic pressure is reduced). RV is usually normal or ↑ in chest wall restriction and ↓ in parenchymal restriction. (b) Usually the history provided is suggestive of MSD. If both are normal: • Consider the isolated abnormalities before reporting the study as normal: – An isolated reduction of MMEF and FEFs: indicates a non-specific airflow limitation at low lung volumes. * If the reduction in FVC is out of proportion to the reduction in TLC (i. (b) If normal (DLCO and DLCO/VA) – it supports chest wall restriction (c) If DLCO is ↓ but DLCO/VA is normal or high – it supports chest wall restriction but cannot exclude a parenchymal restriction.28 – Diaphragmatic paralysis (a) MIP is ↓ with a normal MEP (normal expiratory muscles).
g. e. pulmonary vascular disease. consider early parenchymal lung disease (such as emphysema or ILD). a normal RV/TLC ratio is more likely with acromegaly than with obstruction.6 If one study (spirometry or lung volume study) is normal and the other is abnormal: • Normal spirometry with abnormal lung volume study – Normal spirometry with low lung volumes: (a) This is uncommon. – Isolated significant response to bronchodilators (with a normal prebronchodilator study): strongly suggests an obstructive defect6 (bronchial asthma). – Isolated reduction in DLCO/VA: indicates a gas exchange abnormality. Another clue is ↑ FVC. • Normal lung volume study with abnormal spirometry – Normal lung volumes with an obstructive spirometry: (a) A combined disorder .3. 6 (b) An obstructive disorder with pulmonary resection (history may help). – An obstructive disorder with severe air trapping or poor effort spirometry should be considered. or anemia. 4 – Normal spirometry with high lung volumes: (a) Obstructive disorder: * Emphysema with minimal airway disease.. * Mild asthma (if TLC is normal and RV is increased)27 (b) Another possibility is acromegaly. • A restrictive spirometry with high lung volumes: – May represent a combined abnormality.102 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE – Isolated reduction in ERV: is usually associated with obesity.27 Patients with large lungs. So.3. If the results of spirometry and lung volumes are opposite to each other: • An obstructive spirometry (↓ FEV1/FVC ratio) with low lung volumes (↓ TLC): – The two major possibilities are as follows: (a) A combined disorder. and may represent a lab error as normal VC from spirometry excludes the restrictive abnormality suggested by low lung volumes.12 An isolated reduction in DLCO with a normal DLCO/VA should be reported as abnormal and similar causes explored. swimmer may have similar values.
Standardisation of spirometry. et al.88:1989–1995. Mechanics of Breathing. Chest 2003. . 11. 1985. mild asthma.659–692. Pulmonary Function Testing. Cardinal P. How accurate is spirometry at predicting restrictive impairment. Flenley DC. Standardization of spirometry. 1994 update. Handbook of Physiology. 2. Lunau M.. bronchial asthma without air trapping) – Normal lung volumes with a restrictive spirometry: (a) Pure lung restriction is excluded because of a normal TLC. III. PA. et al. Viegi G. Mead J. 9. Philadelphia. Dales RE. A spirometry-based algorithm to direct lung function testing in the pulmonary function laboratory. Dales RE. 10.g. which simply means. Lung volumes in 4774 patients with obstructive lung disease. we do not know!27 * Consider a mild combined disorder. Am J Respir Crit Care Med 1995. et al. Scanlon PD. 8.115:68–74. Miller MR. 31. Bethesda. Pellegrino R. the following tests may be supportive: (1) ↑ Airway resistance (2) Significant bronchodilator response (3) Positive bronchial challenge * If not a poor effort study and there is no evidence of obstruction. Dis Mon 1988.123:1939–1946. Cerveri I. Orlando. Chest 1999. Dore R. Chronic obstructive pulmonary disease.115:869–873. Bates DV. FL. Aaron SD. 1989. WB Saunders. Pellegrino R. American Thoracic Society. sometimes called pseudorestriction (grade according to FEV1)30. Kester MM. Enright PL. Aaron SD. References 1.g.152:1107–1136. Dykstra BJ. Chest 1999. Eur Respir J 2005. Hankinson J. Beck KC. ed. Enright P. Glady CA. 5. MD.APPROACH TO PFT INTERPRETATION 103 (b) Obstructive disorder with pulmonary resection (review the history) (c) Pure obstructive disorder (e. Part 2. 7. Third Edition. Mechanisms for isolated volume response to a bronchodilator in patients with COPD. Grune & Stratton. e. report it as non-specific ventilatory limitation. Pride NB.34:537–599. Four possibilities could be considered: * Poor effort (examine the FV curve morphology and review technician's comments) * Mild obstructive disorder.. 1986. eds. In: Macklem PT. Lung mechanics in disease. Interpretative strategies for lung function tests. Eur Respir J 2005. Clinch J. Brusasco V. The Respiratory System. Macklem PT. J Appl Physiol 2000. Vol. 6.26:319–338. 4. American Physiological Society. Indications and Interpretations.26:948–968. Section 3. 3. Respiratory Function in Disease. Wilson AF.
Lung mechanics in disease. Eur Respir J 2005.54:627–631. Morrison NJ. Physiologic diagnosis of subclinical emphysema. ATS/ERS statement on respiratory muscle testing: tests of respiratory muscle strength. Chest 1994. Viegi G. 28. Nejadnik B. Njinou B. Mohsenifar Z. Clark EH. Single breath diffusing capacity for carbon monoxide: effects of adjustment for inspired volume dead space. Dabbs JM. Pocket Guide to Lung Function Tests. Handbook of Physiology. . Prabhu MB. 23. 20. MacIntyre N. Mechanics of Breathing. Pride NB. Graham BL. Clin Sci 1978. Effects of ventilation inhomogeneity on DLCO SB-3EQ in normal subjects. Diaz O. Uptake of CO in health and emphysema. First Edition. Hyatt RE. Cotton DJ. Cotes JE. 26. Hall AM. McDonald A. Standardisation of the singlebreath determination of carbon monoxide uptake in the lung. Brown HV. Marrades RM. Scanlon PD. Vol. Lung 1982. Hancox B. 21. Similowski T. carbon dioxide. Mink JT. Wright RR.26:948–968. Philadelphia. et al. The effect of abnormal levels of hematocrit on the single breath diffusing capacity. Elwood PC. Cotton DJ. 15.26:720–735. Mink JT.104 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE 12. Enright P. Road J. Interpretation of Pulmonary Function Tests. Am Rev Respir Dis 1989. Effect of ventilation inhomogeneity on “intrabreath” measurements of diffusing capacity in normal subjects.166:518–624. Sieck GC. Keyeux A. Hughes JMB. Viegi G. Gelb AF. Schnitzer B. DLCO in stable asthma. Whyte K.73:2623–2630. The Respiratory System.42:325–335. Collard P. Adjustment of DLCO for hemoglobin concentration. Abboud RT. Second Edition. Viegi G. J Appl Physiol 1993. Lippincott Williams & Wilkins. Baldi S. Mead J. Clin Sci 1972. Part 2. Koerner SK. et al. Prabhu MB. A Practical Guide. Green M. Roca J.65:56–62. et al.155:236–241. 14. 25. 22. Am Rev Respir Dis 1973. Sydney. 24. et al. Bethesda. III. 17.659–692.75:927–932. American Physiological Society. Pellegrino R. PA. Nakamura M. Crapo RO. 18. McGraw-Hill. Bates DV. eds. Eur Respir J 2005. 1986.139:1179–1187. 16. 27. 2001. Am J Respir Crit Care Med 2002. Ferdeghini EM. Effect of blood transfusion on the carbon monoxide transfer factor of the lung in man.105:1426–1429. Gold WM. In: Macklem PT.11: 21–32. Woods RL. J Appl Physiol 1992. Respiration 1998. Clin Sci 1952.107:50–63. Saunders MJ. Graham BL.160:325–330. Iron-deficiency anaemia: its effect on transfer factor for the lung (diffusing capacity) and ventilation and cardiac frequency during submaximal exercise. Bruch HR. Comparison of single breath carbon monoxide diffusing capacity and pressure–volume curves in detecting emphysema. hemoglobin and carboxyhemoglobin. Frans A. Interpretative strategies for lung function tests. Nadel JA. Pistelli F. 2003. MD. Begliomini E. Section 3. Ramadan F. Am J Respir Crit Care Med 1997. 13. Macklem PT. Prause JA. 19.
20:433–436. Bull Eur Physiol Respir 1984. 31. Green M. J Respir Dis 1999. Salzman S. Tips on how to interpret the results.20:809–822. Respiratory muscle testing. Gilbert R. 30. Auchincloss JH. What is a “restrictive” defect? Arch Intern Med 1986.APPROACH TO PFT INTERPRETATION 105 29. Pulmonary function testing.146:1779–1781. .
17 % Change 50 30 2. Spirometry (Figure 7. DOI: 10.52 5.82 3.34 2.11 4 % Pred.1) Pred. History of chronic dyspnea. 46 15 Post 2.31 0.41 0. Heavy smoker.4 1. 15 32 44 107 A. 1. Altalag et al. DLCO DLCO/VA VA 22.9 4.20 73% % Pred. Pulmonary Function Tests in Clinical Practice.86 36% Pre 7. 139 280 3.14 1.23 0.. TLC RV RV/TLC 5. CASE 1 A 52-year-old female.70 Pre 1.23 Pre 3. © Springer-Verlag London Limited 2009 .1007/978-1-84882-231-3_7.27 0.47 2.1 lists the normal values for the most important PFTs and their grading of severity. Diffusing capacity Pred.15 5. Caucasian.53 0.53 0. FVC FEV1 FEV1/FVC FEF25–75 2.Chapter 7 Illustrative Cases on PFT Table 7. Lung volumes Pred.31 % Pred.
) FEV1 80–120 80–120 FEV1/FVC ratio FEF25–75 >65% pred. Four puffs of salbutamol inhaler given.) Mild 70–100 Moderate 60–69 Moderately severe 50–59 Severe 35–49 Very severe <35 Restrictive disorder (based on TLC. but can be as low as 55% FEF25–75/FVC ratio >0. Q2: What is the most likely diagnosis? Q3: How can you estimate the volume of trapped air? .66 (more accurate) TLC 80–120 FRC 75–120 RV 75–120 80–120 DLCO MEP >90 cmH2O MIP <−70 cmH2O Supine FVC Within 10% of the sitting value. in case no lung volume study is available) Mild FVC >70 (% pred.) Moderate 60–69 Severe <60 Restrictive disorder (based on FVC.7 May be a physiologic variant FEV1 100 (% pred.1.) Moderate 60–69 Moderately severe 50–59 Severe 35–49 Very severe <35 *LLN can be applied to appropriate reference equations to determine an abnormal result Technician's comments: Data acceptable and reproducible. PFT normal values and grading of severity scale* Normal values (ATS) – apply mainly to young and middle ages FVC 80–120 (% pred. >30% drop suggests diaphragmatic paralysis Traditional method for grading the severity of obstructive and restrictive disorders Obstructive disorder (based on FEV1) – ratio <0.108 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 7. preferred) Mild TLC >70 (% pred. Q1: Interpret this PFT.
1. suggesting obstructive defect. (b) The postbronchodilator curve shows a better morphology indicating a degree of bronchodilator response that needs to be defined numerically. which supports the obstructive nature of the disorder. although patient did not take full inspiration while measuring the IVC. (a) VT curve.ILLUSTRATIVE CASES ON PFT 109 FIGURE 7. INTERPRETATION • Spirometry is obstructive: – VT curve: (a) Is flattened. (b) It is small and scooped out. . (b) FV curve. Notice that the FET (16 s) is prolonged. – FV loop: (a) Is of a reasonable quality. with a “dog-leg appearance” (suggesting emphysema).
It did not reach significance in FEV1 (120 ml and 30%). suggesting severe obstruction.34 L – This patient has severe emphysema clinically and radiologically. emphysema is the most likely but bronchial asthma cannot be excluded. – Spirometric data: (a) Severe obstructive disorder (↓ FEV1 of a very severe range and very ↓ FEV1/FVC ratio). both support obstruction. 1. • Lung volume study is obstructive: – TLC and RV are ↑ with a very ↑ RV/TLC ratio suggesting emphysema with hyperinflation and air-trapping (in asthma TLC is usually normal). (c) Partial but significant response to BD in FVC (780 ml and 50%). favoring emphysema. but emphysema is the most likely. Caucasian.84 L (b) RV (pred. (b) ↓ FEF25–75 supporting obstruction. Spirometry (Figure 7. (d) Post-BD curve is bigger and less scalloped (suggesting some response to BD). Given his smoking history and the dog-leg appearance in the FV curve. DLCO will be of help. as in asthma TLC is usually normal. – Air-trapping can be estimated by two ways: (a) TLC – VA = 4. • Conclusion: very severe obstructive disorder with significant reversibility and impaired gas exchange suggesting emphysema. • DLCO – DLCO/VA is extremely low suggesting a gas-exchange abnormality.110 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE (c) The 1st second mark is closer to the leftmost end of the curve indicating a very low FEV1 and FEV1/FVC ratio. CASE 2 A 74-year-old female. Based on spirometry alone.2) .) − RV (measured) = 3. the patient has a very severe obstructive defect with a significant response to bronchodilators. which is supported by the significant response to BDs. Based on spirometry and lung volumes.
ILLUSTRATIVE CASES ON PFT 111 FIGURE 7. 99 108 139 Technician's comments: Data acceptable and reproducible Q1: Interpret this spirometry.57 81 2.21 2. Q2: How would you describe the FV curve? . (a) VT curve. FVC FEV1 FEV1/FVC FEF25–75 1.38 Pre 3. (b) FV curve.91 3.65 % Pred. Pred.17 2.2.
FVC FEV1 FEV1/FVC FEF25–75 3. and ratio. There is no predicted curve to compare with.112 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Interpretation • Spirometry is normal: – VT curve looks normal. • Conclusion: spirometry is suggestive of a moderately severe restriction most likely due to an interstitial lung disease. – Spirometric data: (a) Normal FEV1.55 Pre 2. History of progressive dyspnea.27 4. • Conclusion: normal study (the knee variant).55 % Pred.79 1. A lung . Spirometry (Figure 7. ↓ FEF25–75 can be seen in restriction. – FV loop: (a) Is normal. suggesting a true restriction (IC:ERV ratio is clearly <2:1). Q1: Interpret this spirometry. Its width (FVC) is clearly reduced with a preserved ratio. CASE 3 A 65-year-old female. Q2: What is the most likely diagnosis? Interpretation • Spirometry is restrictive: – VT curve looks normal morphologically.56 3. Notice that PEF is normal. – FV loop: (a) Is small with a steep slope (witch's hat appearance). FVC. – Spirometric data: (a) Moderate restrictive disorder (Moderately reduced FVC with a normal ratio). (b) PEF is preserved suggesting a parenchymal restriction. with a knee.91 0.3) Pred. 53 54 47 Technician's comments: Data acceptable and reproducible. 1. (b) Normal FEF25–75.43 1. (c) The tidal FV loop is closer to the TLC. FET is ∼12 s. This is reproducible and considered a normal variant. Caucasian.
4) . volume study is indicated to confirm the restrictive nature of the disease (low TLC). (a) VT curve. Spirometry (Figure 7.ILLUSTRATIVE CASES ON PFT 113 FIGURE 7. 1. Asian. CASE 4 A 79-year-old male. • This patient has lung fibrosis secondary to IPF.3. (b) FV curve. History of dyspnea.
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
FIGURE 7.4. (a) VT curve; (b) FV curve. Pred. FVC FEV1 FEV1/FVC FEF25–75 1.65 3.02 2.34 Pre 1.37 0.61 48 0.23 % Pred. 45 26
Technician's comments: Data acceptable and reproducible. Q1: Interpret this spirometry. Interpretation • VT curve is very flat suggesting an obstructive disorder. • FV loop is small and flat. It has flat inspiratory and expiratory components suggesting a fixed upper airway obstruction. • This patient has a fibrotic tracheal stricture related to a previous tracheostomy.
ILLUSTRATIVE CASES ON PFT
CASE 5 A 54-year-old male, Caucasian. 1. Spirometry (Figure 7.5)
Pred. FVC FEV1 FEV1/FVC FEF25–75 1.92 5.11 4.03 Pre 4.70 3.64 78 0.94 49 % Pred. 90 89 Post 4.61 3.58 77 % Change −2 −1
2. Lung volumes
Pred. TLC RV RV/TLC ERV 7.31 2.21 31 1.58 Pre 7.63 2.58 34 0.78 % Pred. 104 117 110 50
3. Diffusing capacity
Pred. DLCO DLCO/VA VA 30.50 4.34 7.02 Pre 27.99 4.19 6.68 % Pred. 92 96
Technician's comments: Data not reproducible. Best values reported. Four puffs of salbutamol inhaler given. Q1: Interpret this PFT. Q2: What is the most likely diagnosis? Interpretation • Spirometry is normal: – FV loop: (a) The pre-BD curve is interrupted by a cough in its 1st second. The study is not reproducible. (b) The curve looks normal and slightly smaller than the predicted one. FVC and the ratio look normal. (c) Post-BD curve is smaller than the pre-BD curve indicating lack of response to BDs.
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
FIGURE 7.5. FV curve.
– Spirometric data: (a) FVC, FEV1, and the ratio are normal with no response to BD. (b) ↓ FEF75 (non-specific and may be seen in obesity) Based on spirometry alone, the patient has no significant obstructive or restrictive disorder despite the study quality. • Lung volume study is normal except for an isolated reduction in ERV suggesting obesity. • DLCO – DLCO and DLCO/VA are normal indicating that there is no gasexchange abnormality. • Conclusion: Normal PFT with isolated reduction in ERV suggestive of obesity. The patient's weight at the time of the test was 108 kg with a BMI of 33. CASE 6 A 48-year-old female with chronic dyspnea. Spirometry (shown in Figure 7.6) was done in Body Box. Technician's comments: Data acceptable and reproducible. Q1: Interpret this FV curve
ILLUSTRATIVE CASES ON PFT
FIGURE 7.6. FV curve.
Interpretation • • • • FV loop morphology looks acceptable. It is small and has a steep slope (witch's hat). Its width (FVC) is low with normal ratio suggesting restriction. It is shifted to the right compared with the predicted indicating decreased TLC and RV, which is consistent with a restrictive defect secondary to an interstitial lung disease. • This patient was found to have interstitial fibrosis secondary to sarcoidosis. CASE 7 An 84-year-old male, Caucasian. 1. Spirometry (Figure 7.7)
Pred. FVC FEV1 FEV1/FVC FEF25–75 1.44 2.94 2.09 Pre 1.90 0.77 41 0.22 15 % Pred. 64 37 Post 2.07 0.89 43 % Change 9 15
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
FIGURE 7.7. (a) VT curve; (b) FV curve.
Technician's comments: Data acceptable and reproducible. Four puffs of salbutamol inhaler given. Q1: Interpret this spirometry. Interpretation • VT curve is flat with increased FET suggesting obstruction. The post-BD study indicates some improvement.
Caucasian. The 1st second mark is very proximal indicating that FEV1 and its ratio are very low. DLCO DLCO/VA VA 20. – Curve is small and scalloped indicating obstruction.17 85 3. Lung volumes Pred. Diffusing capacity Pred.17 % Pred. CASE 8 A 61-year-old female.18 1. TLC RV RV/TLC 4.31 2.23 140 % Pred. 48. 87 94 Post 2.ILLUSTRATIVE CASES ON PFT 119 • FV loop: – Curve quality indicates either air leak or poor initial breath in the post-BD study.27 Pre 2. • Spirometric data: – FEV1 and the ratio are severely decreased indicating a severe obstructive defect.8 53. – Some improvement in the curve morphology following bronchodilators.85 2.71 41 % Pred. – ↓ FEF75 is very low supporting obstruction – There is 15% improvement in FEV1 but it is less than 200 ml (only 120 ml) indicating some response to BD that did not reach significance.5 88 . • Conclusion: Severe obstructive disorder with no response to BD.73 Pre 10. 1.1 2.52 4.42 4.47 2. FVC FEV1 FEV1/FVC FEF25–75 2. Unexplained SOB.06 -5 % Change 3 2 2.92 40 Pre 4. Spirometry Pred.7 4. 87 89 3.78 1.55 2.13 86 2.
. 79 130 3.28 1. Q1: Interpret this PFT.97 5. DLCO DLCO/VA VA 27. 79 108 73 Technician's comments: Data acceptable and reproducible. Four puffs of salbutamol inhaler given.15 21% Pre 4.66 88 2.41 4.10 2. or anemia.46 31 % Change 2 10 2. Lung volumes Pred.17 4.99 % Pred.02 2. TLC RV RV/TLC 5.43 1. Lung volume study is normal. • This patient has pulmonary hypertension with a pulmonary artery systolic pressure of 74 mmHg.93 94 3.65 60 % Pred. pulmonary vascular disease. Q1: Interpret this PFT. Conclusion: Isolated reduction in the diffusing capacity indicating an early parenchymal lung disease.72 Pre 3. 70 72 Post 3.42 5. Four puffs of salbutamol inhaler given.120 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Technician's comments: Data acceptable and reproducible. Spirometry Pred.50 35% % Pred. CASE 9 A 61-year-old female.46 Pre 21. Diffusing capacity Pred. 1.37 3.30 3. FVC FEV1 FEV1/FVC FEF25–75 4. Caucasian. DLCO/VA is extremely low suggesting a gas-exchange abnormality. Q2: What is the most likely diagnosis? Interpretation • • • • Spirometry is normal with no response to bronchodilators.
58 2. DLCO 24.ILLUSTRATIVE CASES ON PFT 121 Interpretation • Spirometry is suggestive of mild restriction with some but insignificant response to bronchodilators.73 3. 106 87 2. Lung volumes Pred.25 79 1. • This patient has emphysema and interstitial fibrosis.42 3. FVC FEV1 FEV1/FVC FEF25–75 FIF50 FEF50 4.44 0. CASE 10 A 55-year-old male.75 Pre 5.8) Pred.35 4. . • Conclusion: The spirometry is restrictive and the lung volume study is obstructive.19 Pre 6.80 0. 107 100 Technician's comments: Data acceptable and reproducible.91 2. Caucasian. Spirometry (Figure 7. 1.79 DLCO/VA 3.73 1. Q1: Interpret this PFT. • Diffusing capacity is normal. TLC RV 6. The possibilities are either a combined defect (most likely) or an obstructive disorder with a suboptimal spirometry (unlikely as data are reproducible). Diffusing capacity Pred.42 41 % Pred. weight 84 kg.21 % Pred. history of shortness of breath. 97 66 68 RV/TLC 0.73 % Pred.31 3.72 Pre 26.00 3. • Lung volume study is obstructive but with a low TLC (making restriction alone less likely) and evidence of air trapping (↑ RV).
• FV loop: – Curve quality looks suboptimal. (a) VT curve.8. . which could be due to a disease state. (b) FV curve.122 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 7. Interpretation • VT curve looks normal (no predicted curve to compare with).
82 1. Caucasian.37 Pre 14. . FEV1.38 Pre 2. 60 76 Technician's comments: Data acceptable and reproducible. Lung volume study: – Normal TLC with low RV.9) Pred.54 0. CASE 11 A 67-year-old male. DLCO and DLCO/VA are normal. weight 105 kg.75 DLCO/VA 3. Lung volumes Pred. 61 61 2. – FIF50/FEF50 is much less than 1 indicating a variable extrathoracic upper airway obstruction. Diffusing capacity Pred. This suggests a variable extrathoracic upper airway obstruction.82 47 % Pred.40 0. Spirometry (Figure 7. Q1: Interpret this PFT. Conclusion: The only significant abnormality is the flattened inspiratory component of FV loop and a very low FIF50/FEF50 ratio indicating a variable extrathoracic upper airway obstruction.36 3. – ↓ FEF25–75 is non-specific. This patient has laryngeal stenosis. Spirometric data: – Normal FVC. 71 64 92 3.78 2. and FEV1/FVC ratio.66 2. – The expiratory component of the curve is not significantly abnormal.32 % Pred.79 2.57 % Pred.ILLUSTRATIVE CASES ON PFT 123 • • • • – Curve is small with a flat inspiratory component.98 4. 1. FVC FEV1 FEV1/FVC FEF25–75 3.35 Pre 4.05 77 1. DLCO 24. TLC RV RV/TLC 6.
Interpretation • VT curve looks normal (no predicted curve to compare with). (b) FV curve.124 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 7.9. • FV loop: . (a) VT curve.
which corrects partially when VA is taken into consideration.38 1. – ↓ FEF25–75 is non-specific. DLCO is low. MIP: –27 cm water.40 % Pred. CASE 12 A 64-year-old male.95 4.ILLUSTRATIVE CASES ON PFT 125 • • • • – Curve quality looks suboptimal with multiple variable efforts.53 1.41 Pre 1. Lung volume study: – Slightly reduced TLC with low RV confirming a mild restrictive pattern.23 Pre 16.97 L. 60 112 Supine FVC: 0. Spirometry Pred. which still cannot exclude a gas-exchange abnormality.54 1.72 % Pred. 1. MEP: 229 cm water. The restrictive disorder noted is probably unrelated to Parkinson's disease. 50 64 61 3. 35 34 2. TLC RV RV/TLC 6.31 Pre 3. FVC FEV1 FEV1/FVC FEF25–75 3. DLCO DLCO/VA 26. Spirometric data: – Reduced FVC and FEV1 with a normal FEV1/FVC ratio suggesting a possible restriction. weight 120 kg. .87 22 % Pred.15 78 0. which explains the variable effort noticed in the FV loop. – The height (PEF) and width (FVC) of the curve are reduced.73 4. history of shortness of breath.40 2. Lung volumes Pred. Diffusing capacity Pred.70 2. Conclusion: Mild restrictive disorder.04 4. This patient has Parkinson's disease. Caucasian.36 3.
80 23 18 26 33 % Pred. Interpretation • Spirometric data: – Reduced FVC and FEV1 with a normal FEV1/FVC ratio suggesting a possible restriction. weight 81 kg. – ↓ FEF25–75 is non-specific. Q1: Interpret this PFT.38 5. Spirometry (Figure 7. which corrects when VA is taken into consideration. Caucasian. CASE 13 A 22-year-old male.37 72 1. • Lung volume study: – Significantly reduced TLC with a low RV confirming the restrictive nature of this disorder.09 % Pred.21 Pre 2.47 0. 36 30 2.68 1. which showed a low MIP and normal MEP indicating inspiratory muscle (diaphragmatic) weakness.73 1. FVC FEV1 FEV1/FVC FEF25–75 PEF FEF50 FIF50 4. This patient had a paralyzed diaphragm.23 0.73 5. TLC RV RV/TLC 6.24 5. 1.126 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Technician's comments: Data acceptable and reproducible. • Further tests to be done include MEP and MIP.14 1.38 4. • Conclusion: Severe restrictive disorder with a relatively preserved DLCO indicating a nonparenchymal cause of restriction.52 Pre 1.97 1. Supine FVC dropped significantly compared with the sitting value (>30% drop). • DLCO is low. history of shortness of breath.51 1.44 0.99 9. Lung volumes Pred.10) Pred. 36 16 43 . which still cannot exclude a gas-exchange abnormality.
which indicates a fixed upper airway obstruction. Q1: Interpret this PFT.46 Pre 20. and FIF50.10. 55 143 Technician's comments: Data acceptable and reproducible. FEF50. FV curve. FIF50/FEF50 ratio is around 1. – Reduced PEF. Interpretation • FV loop: – Is small and flat at both inspiratory and expiratory components. • Spirometric data: – Reduced FVC and FEV1 with a normal FEV1/FVC ratio suggesting a restrictive disease. suggesting fixed upper airway obstruction. .ILLUSTRATIVE CASES ON PFT 127 3. DLCO DLCO/VA 36. Diffusing capacity Pred.82 % Pred. FIGURE 7.67 5.34 7.
91 4.27 3. • DLCO is also low. 1.128 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • Lung volume study: – Lung volumes are all significantly reduced confirming severe restriction. . which possibly indicates that there is no significant parenchymal abnormality.26 3. FVC FEV1 FEV1/FVC FEF25–75 PEF 3.33 11. TLC RV RV/TLC 6.74 1.11) Pred. DLCO DLCO/VA 28. 64 58 2. 65 62 3.19 6. history of shortness of breath. Caucasian.28 Pre 18. which overcorrects when VA is taken into consideration. Q1: Interpret this PFT. Spirometry (Figure 7. He was also found to have large bilateral pleural effusions related to his lymphoma causing this lung restriction.19 38 141 % Pred.24 30 % Pred. Diffusing capacity Pred.98 72 1.51 7. 65 63 Technician's comments: Data acceptable and reproducible. • Conclusion: Fixed upper airway obstruction with severe restriction. CASE 14 A 54-year-old male.97 % Pred. Lung volumes Pred. weight 89 kg.01 32 Pre 4.45 Pre 2.07 1. This patient has lymphoma with significant paratracheal lymphadenopathy compressing the trachea.28 2.
ILLUSTRATIVE CASES ON PFT 129 FIGURE 7.11. (b) FT curve. . There is no predicted curve to compare with. Interpretation • Spirometry is restrictive: – VT curve looks normal morphologically. (a) VT curve.
06 3.51 38 Pre 5.80 Pre 10. 1.52 3. • Conclusion: Moderately severe restrictive disorder most likely due to a parenchymal disease. Its width (FVC) is clearly reduced.33 54 0.82 2. – PEF is increased suggesting a parenchymal restriction.70 7.67 2. weight 80 kg.88 16 65 % Pred. FVC FEV1 FEV1/FVC FEF25–75 PEF 2. 61 43 2.46 1. • Lung volumes: – Moderately reduced TLC and RV with a preserved RV/TLC ratio confirming moderately severe restriction.64 % Pred.00 2. TLC RV RV/TLC 6. DLCO DLCO/VA 23. • DLCO/VA is reduced going with a parenchymal restriction. 46 69 Technician's comments: Data acceptable and reproducible. • Spirometric data: – Reduced FVC and FEV1 with a normal FEV1/FVC ratio suggesting a restrictive disease. CASE 15 A 78-year-old male.42 48 % Pred.130 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • FV loop: – Is small with a steep slope (witch's hat appearance). 75 97 127 3. . Q1: Interpret this PFT. Diffusing capacity Pred. Lung volumes Pred. Caucasian.54 4.12) Pred. Spirometry (Figure 7.44 4.07 Pre 2.
ILLUSTRATIVE CASES ON PFT 131 FIGURE 7. (b) FV curve. .12. (a) VT curve.
FET is 9 s. • Lung volume study is restrictive: – Mildly reduced TLC with a normal RV and increased RV/TLC ratio. – Spirometric data: (a) Reduced FVC and FEV1 with a reduced FEV1/FVC ratio suggesting a severe obstructive disorder. – FV loop: (a) The expiratory curve is small and scooped out. The reduced TLC indicates a restrictive disorder. FEF25–75 is reduced going with an obstructive disorder. suggesting an obstructive disorder. which may be seen in both restrictive and obstructive disorders. This patient has emphysema and lung resection.132 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Interpretation • Spirometry is obstructive: – VT curve looks flat. • DLCO/VA is reduced. . • Conclusion: Severe obstructive disorder with a mild restriction.
Na+ (143 mg/dl). DEFINITIONS1 • Acidosis is a disturbance that lowers the extracellular fluid pH. and Cl− (98 mg/ dl). HCO3 (23 mmHg).38). • Alkalemia is an elevation of the final extracellular fluid pH. 133 A. PaCO2 (41 mmHg).. • Base excess (BE) is the amount of acid (+) or base (−) (in mEq/L) required to restore the pH of a liter of blood to the normal range at a PaCO2 of 40 mmHg. such as the one given above. • Alkalosis is a disturbance that raises the extracellular fluid pH. DOI: 10. how would you interpret it? • These values are all normal but the patient has significant acid– base disturbances that may be fatal.1007/978-1-84882-231-3_8. Accordingly an acidemia may result from a combination of different types of acidosis or a combination of acidosis and alkalosis. • The above ABG is discussed in case number 4. later. • Acidemia is a reduction of the final extracellular fluid pH. Pulmonary Function Tests in Clinical Practice. © Springer-Verlag London Limited 2009 . Table 8. Altalag et al.1 shows the normal values of the ABG components.Chapter 8 Arterial Blood Gas Interpretation INTRODUCTION • If you are given this ABG with pH (7. PaO2 (95). This chapter tries to introduce a simple approach to help solving any acid– base problem including the hidden ones. if untreated.
134 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 8. where K = 24. shown here: pH = pK + log ([HCO3]/[H2CO3]). and it can be easily calculated from pH.35–7. as K is the thermodynamic constant that varies with the temperature and ionic strength of the solution.5. therefore: [H+] = K × [H2CO3]/[HCO3−]. In this case K = 24. [HCO3 ] − By substituting PaCO2 for [H2CO3] that is measured from ABG. while Henderson– Hasselbalch equation is a logarithmic expression of Henderson equation. ABG normal values pH PaCO2 PaO2 HCO3 BE SaO2 Anion gap (AG) P(A–a)O2 7. the equation can be written in a more practical way2: [H + ] = K × Pa CO2 . where K = 24. * Henderson equation is the equation shown earlier. see Table 8.45 35–45 mmHg >80 mmHg 21–26 mmol/L (Average: ∼24) 0 to −2 mmol/L >95% 10 ± 4 (Average: ∼12) <15 To convert from KPa (Kilo-Pascal) to mmHg.1 † This equation is derived from the chemical reaction: H2CO3 ↔ H+ + HCO3−. − The rest of the variables can be acquired directly from the ABG. . HENDERSON EQUATION2 • This equation represents the relationship between the components of the ABG and may be written in different ways*: − A simple way is as follows†: [H + ] = K × [H 2 CO3 ] . which can be written as: [H+] ↔ [H2CO3]/[HCO3−].2.1. multiply by 7. [HCO3 ] − [H+] is the hydrogen ion (proton) concentration. • The purpose of this equation is as follows: − To ensure that the ABG values are accurately recorded. Solving the equation should result in equalization of its two sides.
ARTERIAL BLOOD GAS INTERPRETATION
TABLE 8.2 Calculating [H+] from pH2 When pH is within (7.30–7.50) pH of 7.40 ↔ [H+] = 40 nmol/L Then increasing or decreasing pH by 0.01 is equivalent to decreasing or increasing [H+] by 1 nmol/L, respectively (remember that [H+] changes in the opposite direction of pH; for instance, acidosis decreases pH but increases [H+]). So if pH is 7.35, then [H+] will equal 40 + 5 = 45 nmol/L. When pH is outside the range of 7.3–7.5, the following applies (Note, this technique can be applied when pH is within the above range too): pH of 7.00 ↔ [H+] = 100 nmol/L Then every increase or decrease of pH by 0.10 is equivalent to multiplying or dividing [H+] by 0.8. So if pH is 7.10, then [H+] will equal 100 × 0.8 = 80 nmol/L. If pH is 7.20, then [H+] will equal 100 × 0.8 × 0.8 = 64 nmol/L. If pH is 7.40, then [H+] = 100 × 0.84 = 40. If pH is 6.80, then [H+] = 100/(0.8 × 0.8) = 156. If you do not want to bother yourself with these boring calculations, the following table can be of help: pH 7.00 7.05 7.10 7.15 7.20 7.25 7.30 [H+] 100 89 79 71 63 56 50 pH 7.35 7.40 7.45 7.50 7.55 7.60 7.65 [H+] 45 40 35 32 28 25 22
− If one of the ABG values is missing, the equation can be solved to determine that missing value. Indeed this is usually done for ABG results. The pH and PaCO2 are actually measured in the blood sample and the HCO3 is calculated using this equation, e.g., pH 7.3 ([H+] = 50), PaCO2 = 50 mmHg, and HCO3 = unknown. − By applying Henderson equation: [H+] = K × (PaCO2 / [HCO3]), [50 = 24 × (50 / [HCO3]). Therefore, [HCO3] = 24.
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
METABOLIC ACIDOSIS Causes Metabolic acidosis can be classified – depending on the nature of the acid causing the disturbance – into anion gap (AG) and nonanion gap (NAG) metabolic acidosis.8,9 The NAG metabolic acidosis is also called hyperchloremic metabolic acidosis, because it is associated with high serum chloride. Table 8.3 summarizes these causes.
TABLE 8.3 Causes of metabolic acidosis Anion gap metabolic acidosis Uremia Ketoacidosis Diabetes Alcohol-induced Starvation Lactic acidosis Toxin ingestion Salicylates Methanol Ethylene glycol Paraldehyde Nonanion gap (hyperchloremic) metabolic acidosis GI loss of HCO3 Diarrhea Ileostomy or colostomy Uretero-segmoid fistula Pancreatic fistula Renal loss of HCO3 Renal tubular acidosis Proximal (type II) Distal (types I and IV) Carbonic anhydrase inhibitors/deficiency Hypoaldosteronism, aldosterone inhibitors Hyperkalemia Renal tubular disease Acute tubular necrosis (ATN) Chronic tubulointerstitial disease Iatrogenic Ammonium chloride (NH4Cl) Hydrochloric acid (HCl) therapy Hyperalimentation (with TPN lacking acetate buffer) Dilutional acidosis (caused by excessive isotonic saline infusion)
ARTERIAL BLOOD GAS INTERPRETATION
Approach to Metabolic Acidosis • In both types of metabolic acidosis, the primary disturbance is a drop in bicarbonate. Because the respiratory system is fast in its compensation, there is a rapid drop in PaCO2, which should always accompany a pure metabolic acidosis (remember that PaCO2 changes in the same direction as HCO3 in a pure metabolic disturbance).‡ Remember that normal bicarbonate does not exclude a metabolic disturbance as metabolic acidosis may coexist with metabolic alkalosis. • We suggest a protocol in interpreting ABG. Table 8.4 summarizes a useful one. • The first step is to determine the type of disturbance (acidemia or alkalemia) by looking at the pH. • Then determine the most likely primary disturbance. So, if a reduction in HCO3 is the predominant abnormality in the setting of acidemia, then the primary disturbance is a metabolic acidosis. • Determine the type of metabolic acidosis you are dealing with (AG or NAG) by calculating the AG18: AG = Na+– (Cl– + HCO3–). − If normal (£12), then this is a nonanion gap metabolic acidosis (NAGMA). Go to the next step. − If high (>12), then this is an anion gap metabolic acidosis (AGMA). In AGMA, you need to determine then whether
TABLE 8.4. Approach to ABG interpretation Determine whether the ABG data are accurate by quickly applying Henderson equation. Look at the pH and determine whether it is normal, acidemic, or alkalemic. Determine the most likely primary disturbance (by looking at HCO3 and PaCO2 and determining which one is largely responsible). If the primary disturbance is respiratory, determine whether it is acute or chronic. If the primary disturbance is metabolic, determine whether an appropriate respiratory compensation is present. Calculate the AG. Calculate the corrected HCO3, if applicable.
‡ PaCO2 in fact follows the pH (same direction as change in pH). Therefore, if PaCO2 fails to decrease (or if increased) in response to a decreased pH (e.g., secondary to metabolic acidosis), then a primary respiratory acidosis is diagnosed straight away.
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
another metabolic disturbance is present, by calculating the corrected HCO3: Corrected HCO3 = ΔG+measured HCO3 as ΔG = AG – 12. (a) If the corrected HCO3 is within the normal range of HCO3 (21–26), then there is no other metabolic disturbance, so go to the next step. (b) If the corrected HCO3 is higher than the normal range, then there is an additional metabolic alkalosis (corrected HCO3 is higher than it should be). (c) If the corrected HCO3 is lower than the range, then there is an additional NAG metabolic acidosis (NAGMA). • Determine whether there is a primary respiratory disturbance by initially looking at the PaCO2. − If PaCO2 is normal or high (opposite direction to HCO3), then there is a primary respiratory acidosis. Go to the next step.§ − If PaCO2 is low (same direction as HCO3), then calculate the expected PaCO2 range¶,10,11: Expected PaCO2 range = 1.5 x HCO3 + (8+2). (a) If the patient’s PaCO2 is within this range, then the patient has no respiratory disturbance (this is an appropriate compensation). (b) If the patient’s PaCO2 is above the range, then there is a primary respiratory acidosis (inadequate compensation). (c) If the patient’s PaCO2 is below the range, then there is a primary respiratory alkalosis (overcompensation). The lowest level PaCO2 can reach as a compensation for metabolic acidosis is 10–12 mmHg.15 • In NAGMA, determine whether the cause is of renal or nonrenal origin by calculating the urine anion gap (also called urine net charge or UNC)21: Urine gap = (UNa + Uk) – UCl. − If the urine gap is negative, then the kidney is appropriately compensating by secreting H+ in the form of ammonia
If in doubt, calculate the expected PaCO2 range shown in the next point.
This formula is sometimes called Winters’ equation.11 Other methods to determine the expected PaCO2 include: (1) PaCO2 = HCO3 + 15,15 (2) PaCO2 should approximate the last two digits of pH in a steady state metabolic acidosis,19 (3) or PaCO2 drops by ∼1 mmHg for each 1 mEq/L drop in HCO3.
ARTERIAL BLOOD GAS INTERPRETATION
TABLE 8.5. Approach to metabolic acidosis Quickly apply the Henderson equation. Look at the pH (normal, acidemia, or alkalemia). The reduction in HCO3 is the predominant abnormality → primary metabolic acidosis. Calculate the AG (AG = Na+ − (Cl− + HCO3)) If normal (∼12) → nonanion gap metabolic acidosis (NAGMA). If high (>12) → anion gap metabolic acidosis (AGMA). Calculate the corrected HCO3 (Corrected HCO3 = ΔG + measured HCO3 as ΔG = AG − 12): − If within normal range of HCO3 (21–26) → no other metabolic disturbance. − If >26 → primary metabolic alkalosis. − If <21 → primary nonanion gap metabolic acidosis. Look at PaCO2: If normal or high → primary respiratory acidosis. If in doubt, calculate expected PaCO2 range. If low → calculate the expected PaCO2 range, given by 1.5 × HCO3 + (8 ± 2): − If the patient’s PaCO2 is within this range → no respiratory disturbance. − If patient’s PaCO2 is above the range → primary respiratory acidosis. − If patient’s PaCO2 is below the range → primary respiratory alkalosis. In NAGMA, calculate urine anion gap (urine gap = (UNa+ UK) − UCl): If negative → extrarenal cause of metabolic acidosis. If positive → a renal cause of the metabolic acidosis (RTA).
(NH4+), which neutralizes this negative urine anion gap. An extrarenal cause of metabolic acidosis is the most likely. − If the urine gap is positive (or zero), then the kidneys are not secreting H+ appropriately, indicating a renal cause of the metabolic acidosis [renal tubular acidosis (RTA)]. • These steps are summarized in Table 8.5. METABOLIC ALKALOSIS Causes • Are classified into Cl−responsive and Cl−resistant alkaloses, which are summarized in Table 8.6. Approach to Metabolic Alkalosis • Similar to metabolic acidosis, metabolic alkalosis presents as a high HCO3, which is compensated for by an increase in
renin-secreting tumor) Iatrogenic Excessive NaHCO3 infusion Excessive citrate infusion (massive blood transfusion) Excessive acetate infusion (hyperalimentation with acetate-containing TPN) Excessive lactate infusion (Ringer’s lactate) Milk–alkali syndrome • • • • PaCO216.140 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 8.. Determine the type of disturbance (acidemia or alkalemia) by looking at the pH.6. then there is an additional primary AGMA. in this setting. So if the increase in HCO3 is the predominant abnormality rather than a decrease in PaCO2. then there is no primary metabolic acidosis. then the primary disturbance is metabolic alkalosis. . Causes of metabolic alkalosis Cl responsive: GI loss of H+ Vomiting. Then determine the most likely primary disturbance. Determine whether there is a primary respiratory disturbance by initially looking at the PaCO2. Determine whether a primary metabolic acidosis is present as well by calculating AG: − If normal (∼12). A normal or a low PaCO2 indicates a respiratory alkalosis. − If high (>12).17 (which rarely exceeds a level of 60 mmHg15).g. Go to the next step. nasogastric suctioning Cl−-rich diarrhea Villous adenoma Renal loss of H+ Diuretics Hypovolemia Posthypercapnia High-dose carbenicillin Cl resistant: Renal loss of H+ Primary hyperaldosteronism Increased corticosteroid activity Primary hypercortisolism Adrenocorticotropic hormone (ACTH) excess Drug-induced Licorice ingestion Hypokalemia Increased renin activity (e.
9 x HCO3 + (9 to 16). If >20 mmol/l → Cl− resistant metabolic alkalosis. then this is Cl− responsive (depleted) metabolic alkalosis.9 × HCO3 + (9 to 16): − If patient’s PaCO2 is within this range → no respiratory disturbance. − If patient’s PaCO2 is above the range → primary respiratory acidosis. or alkalemia). then there is a primary respiratory acidosis (overcompensation). Look at PaCO2: If normal or low → primary respiratory alkalosis. Check the urinary Cl− (UCl): If <20 mmol/l → Cl− responsive metabolic alkalosis.|| − If PaCO2 is high (same direction as HCO3). then the patient has no additional respiratory disturbance (this is an appropriate compensation). • Table 8. Go to next step.7 summarizes these steps. (a) If the patient’s PaCO2 is within this range. If in doubt. (c) If the patient’s PaCO2 is below the range. then there is a primary respiratory alkalosis. then calculate the expected PaCO2 range12–14: Expected PaCO2 range = 0. • Determine the type of metabolic alkalosis (Cl− responsive or Cl− resistant) by measuring the urinary Cl− (UCl)1: − If UCl is <20 mmol/l. Think of it as the body is trying to conserve Cl−. . Look at the pH (normal. The increase in HCO3 is the predominant abnormality → primary metabolic alkalosis. TABLE 8. acidemia. which is equal to 0.7.ARTERIAL BLOOD GAS INTERPRETATION 141 − If PaCO2 is normal or low (opposite direction to HCO3). || If in doubt. (b) If the patient’s PaCO2 is above the range. Calculate the AG (AG = Na+– (Cl− + HCO3)): If normal (∼12) → no primary metabolic acidosis. then this is Cl− resistant (expanded) metabolic alkalosis. If high (>12) → primary anion gap metabolic acidosis (AGMA). − If UCl is >20 mmol/l. calculate the expected PaCO2 range shown in the next point. If high → calculate the expected PaCO2 range. calculate expected PaCO2 range. then there is a primary respiratory alkalosis (inadequate compensation). Approach to metabolic alkalosis Quickly apply the Henderson equation. − If patient’s PaCO2 is below the range → primary respiratory alkalosis.
08.03 × Pa CO2 − 40 . secondary to sedative and narcotic drugs) (continued) . TABLE 8. pneumothorax) Pleural disease Hypoventilation Central (e.142 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE RESPIRATORY ACIDOSIS Types of Respiratory Acidosis • Because the body compensates slowly for a primary respiratory disturbance. • Tables 8. 10 − HCO3 increases by 3 mmol/L.8.g. • In chronic respiratory acidosis.. that is: pH = 0. for every 10 mmHg rise in PaCO23: − pH drops by 0.9 summarize the causes and steps of interpretation of respiratory acidosis.08 × Pa CO2 − 40 10 − HCO3 increases by 1 mmol/L. maximum level of HCO3 is ∼32 mmHg. maximum level of HCO3 is ∼45 mmHg. the latter is then classified into acute and chronic forms. Causes of respiratory acidosis Obstructive Disorders Upper airway obstruction Foreign body Laryngospasm Obstructed endotracheal tube Obstructive sleep apnea Lower airway obstruction Severe bronchospasm due to bronchial asthma or COPD Restrictive disorders (see Table 1. for every 10 mmHg rise in PaCO24: − pH drops by 0.8 and 8.03. that is: pH = 0. • In acute respiratory acidosis.7) ILD Chest wall restriction Loss of air spaces (pleural effusion. respectively. The following will highlight these forms.
If normal (∼12) → Look at HCO3. If ↓ or N → primary nonanion gap metabolic acidosis.8. HCO3 ↑ by 3 mmol/L (max ∼45). Determine whether acute or chronic Acute: pH ↓ by 0. If higher → metabolic alkalosis. for every 10 mmHg drop in PaCO25: − pH rises by 0.08 for every 10 mmHg ↑ in PaCO2. that is: pH = 0.08. shivering Hypermetabolism High carbohydrate diet Others Inappropriate ventilator settings Compensatory TABLE 8.08 × 40 − Pa CO2 10 . If applicable. Approach to respiratory acidosis Quickly apply the Henderson equation. acidemia.03 for every 10 mmHg ↑ in PaCO2. If ↑ → look at HCO3 and determine the type of respiratory acidosis: (HCO3 ↑ by 1 (acute) or 3 (chronic) for each 10 mmol/L ↑ in PaCO2) If within the expected → no primary metabolic disturbance. (continued) Obesity-hypoventilation syndrome Neuromuscular disease (Table 5. HCO3 ↑ by 1 mmol/L (max ∼32). or alkalemia). Calculate the AG (AG = Na+ − (Cl− + HCO3)) If high (>12) → primary anion gap metabolic acidosis (AGMA). The increase in PaCO2 is the predominant abnormality → primary respiratory acidosis. as in metabolic acidosis. calculate the Corrected HCO3.9. If lower → nonanion gap metabolic acidosis.1) Parenchymal lung disease (like ARDS) Increased CO2 production Fever. Chronic: pH ↓ by 0. Look at the pH (normal.ARTERIAL BLOOD GAS INTERPRETATION 143 TABLE 8. RESPIRATORY ALKALOSIS Types of Respiratory Alkalosis • In acute respiratory alkalosis.
. The drop in PaCO2 is the predominant abnormality → primary respiratory alkalosis. calculate the Corrected HCO3. progesterone) Pregnancy Others Inappropriate ventilator settings Compensatory TABLE 8. Sepsis.10. − HCO3 drops by 2 mmol/L. If normal (∼12) → Look at HCO3. Calculate the AG (AG = Na+ − (Cl− + HCO3)) If high (>12) → primary anion gap metabolic acidosis (AGMA). that is: pH = 0. If applicable.144 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 8. for every 10 mmHg drop in PaCO26. If within the expected → no primary metabolic disturbance. as in metabolic acidosis. infection Respiratory stimulants (e.03 (and HCO3 ↓ by 5–7 mmol/L) for every 10 mmHg ↓ in PaCO2. salicylates. psychogenic Liver failure with encephalopathy Fever.03 × 40 − Pa CO2 10 . or alkalemia). Approach to respiratory alkalosis Quickly apply the Henderson equation. Causes of respiratory alkalosis Increased hypoxemic drive Right-to-left shunt High altitude Pulmonary disease Emphysema Pulmonary embolism Pulmonary congestion Stimulation of respiratory center Anxiety. Look at the pH (normal. acidemia.7: − pH drops by 0.11. If ↓ → look at HCO3 and determine the type of respiratory alkalosis (HCO3 ↓ by 2 (acute) or 5–7 (chronic) for each 10 mmol/L ↓ in PaCO2). Determine whether acute or chronic Acute: pH ↑ by 0. • In chronic respiratory alkalosis. If ↑ or N → primary metabolic alkalosis. Chronic: pH ↑ by 0. If lower → nonanion gap metabolic acidosis If higher → metabolic alkalosis.g.03.08 (and HCO3 ↓ by 2 mmol/L) for every 10 mmHg ↓ in PaCO2. pain.
.ARTERIAL BLOOD GAS INTERPRETATION 145 − HCO3 increases by 5–7 mmol/L.. PACO2 is the CO2 tension in the alveoli. the calculated anion gap will be underestimated and a significant AGMA may be missed. RQ is the respiratory quotient. secondary to a critical illness or liver disease) will influence the AG level.5 − alb in g/dl)].g.25 × (45 − alb in g/L)]. †† Abbreviations: PAO2 is the O2 tension in the alveoli. • Tables 8. and PaCO2. 1 RQ ** This equation can also be written as follows: Adjusted AG = Calculated AG + [0.20 These are commonly referred to as Flenley’s acid–base nomograms. P(A–a)O2 is the alveolar–arterial O2 gradient. FIO2 is the fractional inspired O2. a drop in its level (e.11 summarize the causes and steps of interpretation of respiratory alkalosis. respectively. In this case. EFFECT OF A LOW ALBUMIN LEVEL ON AG • Because albumin is one of the unmeasured anions in the blood.5 × (4. where P O2 = F1O2 ( Patm − PH2 o ). the calculated AG should be adjusted for albumin**: Adjusted AG = Calculated AG + [2. ACID–BASE NOMOGRAM • The nomogram shown in Figure 8. • If this adjustment is ignored with a low albumin. THE ALVEOLAR–ARTERIAL (A–a) OXYGEN GRADIENT AND ALVEOLAR GAS EQUATION23 Alveolar Gas Equation†† • This equation allows us to estimate the O2 tension in the alveoli (PAO2): PA O2 = P O2 − 1 PaCO 2 . PH2O is the partial pressure of water vapor.10 and 8.1 is one of many acid–base nomograms developed to assist in solving difficult acid–base disturbances and involves plotting pH. PaO2 is the O2 tension in the arterial blood. HCO3. PIO2 is the O2 tension in the inspired air. PatmO2 is the O2 tension in the atmospheric air. PaCO2 is the CO2 tension in the arterial blood.
and pH (With permission from Goldberg et al.21 × 713 = 150 mmHg.21 × 760 = 160mmHg(at sea level).1. An acid–base nomogram. it does not equal PatmO2. − PIO2 is the O2 tension of inspired air.20) • To understand this equation it is good to go through certain definitions: − PatmO2 is the atmospheric O2 tension or partial pressure of O2.146 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 8. PaCO2. Because the inspired air contains water vapor. It is calculated by multiplying the atmospheric pressure (760 mmHg at sea level) by the percentage of O2 in the atmosphere (21%): PatmO2 = 0. The water vapor tension (PH2O) should then be extracted from the atmospheric pressure before applying the earlier equation: P O2 = F1O2 × ( Patm − PH2 o ) = 0. 1 (if breathing room air. at sea level) .21 × Patm = 0. used to interpret ABG by directly plotting HCO3.21 × (760 − 47) = 0.
however. PACO2 has to be subtracted from PIO2 to get PAO2. If breathing room air at sea level. i.ARTERIAL BLOOD GAS INTERPRETATION 147 − PAO2 is the alveolar O2 tension. which is assumed to be 0. This value changes if the patient is breathing through a nasal cannula or a face mask.8 = 150 − (40 × 1.8 RQ P CO = 150 − a 2 OR 150 − ( Pa CO 2 × 1. it equals 0. as RQ = 0. Accordingly. A–a Gradient (P(A–a)O2) • It is the difference between the alveolar and the arterial O2 tension. at sea level) − PaO2 is the arterial O2 tension that is measured in the ABG. Its calculation is now easy. in a normal individual (because we produce 0. CO2 diffuses from the circulation into the alveoli and hence reduces the PAO2.e. − FIO2 is the fractional inspired O2.8 mole of CO2 for each mole of O2 we consume while at rest).8 at rest. where PA O 2 = P O 2 − 1 or P CO ⎤ ⎡ P( A −a )O 2 = ⎢ P O 2 − a 2 ⎥ − Pa O 2 . (if breathing room air. then the equation can be simply written as follows: P CO ⎤ ⎡ P( A −a )O 2 = ⎢150 − a 2 ⎥ − Pa O 2 0.25). − RQ is the respiratory quotient and represents the amount of CO2 produced for a given amount of O2 consumed by our bodies. PaCO2 can be substituted for PACO2 (when taking the respiratory quotient (RQ) into consideration.8 ⎦ ⎣ Pa CO 2 RQ . Next chapter discusses this in more detail. the percentage of O2 in the inspired air. The RQ increases with exercise.21)..25) = 100 mm Hg.2: P( A −a )O 2 = PA O 2 − Pa O 2 . 0.8 while at rest): PA O2 = PI O2 − Pa CO 2 . It equals 0. 1 RQ ⎦ ⎣ • If at sea level and breathing room air (FIO2 of 0. see Figure 8.21.
25 × Pa CO 2 )] − Pa O 2 • P(A–a)O2 is normally £15 mmHg and increases with age. 23 These mechanisms can be classified into hypoxemia with a wide A−a gradient and hypoxemia with a normal A−a gradient: • Hypoxemia with a wide A−a gradient (P(A–a)O2 > 15) – Shunting. Breathing RA at sea level in a normal person.21 × age in years).148 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 8. . or P( A − a )O 2 = [150 − (1. the following is a popular one22: Normal P(A-a)O2 = 2. MECHANISMS OF HYPOXEMIA‡‡. This diagram summarizes the alveolar gas principles. Different formulas are used to determine the normal P(A–a)O2 in relation to age. like intracardiac shunts or pulmonary AV malformation – VQ mismatch.5 + (0.2. as in atelectasis – Decreased mixed venous O2 tension (PvO2) ¯ – Diffusion limitation (seen in severe ILD) ‡‡ Hypoxemia refers to a reduction in oxygen level in the blood while hypoxia refers to a reduction in oxygen at the tissue level.
e.. it dropped by 25 mmHg).3. §§ .# FIGURE 8.e. then PAO2 is calculated to be 75 mmHg using the alveolar gas equation (i. if the patient is breathing room air. – Hypoventilation. 50 mmHg. as in obesity hypoventilation syndrome. As the alveolar CO2 equals the arterial CO2. The reason for this hypoxemia is the elevated PACO2 (secondary to hypoventilation). even if the lungs are normal.§§. (a) Hypoventilation causes primarily hypercapnia because of impaired washout of CO2. This rule is true only if the patient is breathing room air. as in the case of high altitude. both PaCO2 and PACO2 will be equally elevated. Effects of hypoventilation on alveolar and arterial O2 and CO2 tension: This patient is breathing room air at sea level and has a normal A−a gradient but still has a severe hypoxemia (PaO2 of 45). So if PaCO2 is increased by 20 mmHg. at sea level. (b) Hypoventilation causes hypoxemia. # Another way of roughly predicting the degree of hypoxemia secondary to hypoventilation when the patient is breathing room air is the 130 rule. PAO2 drops by 25 mmHg. In general. In this case. at sea level.25×80) = 150 – 100 = 50 mm Hg. if PaCO2 is 80 mmHg then PaO2 should roughly be 130 – 80. Figure 8. It simply states that the sum of PaO2 & PaCO2 should always equal 130 if the patient is breathing room air.3. i.ARTERIAL BLOOD GAS INTERPRETATION 149 • Hypoxemia with a normal A−a gradient (P(A–a)O2 ≤ 15) – Low inspired O2 (↓ FIO2). which resulted in this degree of hypoxemia: P A O2 = 150 – (1. The PACO2 has increased by 40 mmHg resulting in a reduction in PAO 2 by 50 mmHg. Figure 8. as well. if PaCO2 increases by 20 mmHg.e. If PaCO2 is increased by 20 mmHg (i.3. PaCO2 of 60 mmHg).. So. the degree of hypoxemia can be predicted from the level of PaCO2 using the alveolar gas equation. PAO2 decreases by 25 mmHg.
150 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TYPES OF RESPIRATORY FAILURE 23 • Type I respiratory failure (hypoxemic respiratory failure) is characterized by hypoxemia and defined as an isolated reduction of PaO2 to <60 mmHg (the point at which the SaO2 drops steeply as shown in the O2 dissociation curve). PaCO2 (24).4. – pH is ↓. ILLUSTRATIVE CASES Case 1 • A 63-year-old man presented with generalized malaise. Cl− (101). SaO2 changes significantly with any given change in PaO2 .4. This type of respiratory failure is associated with an increased A−a gradient. so this is an acidemia. When PaO2 < 60 mmHg.4). His ABG showed pH (7.32). K− (5. • Type II respiratory failure (ventilatory failure) is characterized by hypoxemia and hypercapnia and defined as a PaCO2 of >50 mmHg. What type of acid–base disturbance this patient has? • Interpretation: – Applying Henderson equation: [H + ] = K ( Pa CO 2 / [HCO3 ]) ↔ 48 = 24(24 / 12) = 48. Na+ (135). The A−a gradient is normal. FIGURE 8. SaO2 changes slightly with any given change in PaO2. Figure 8. the equation proves that the values are accurate. – So. O2 dissociation curve: when PaO2 > 60 mmHg. HCO3 (12).
PaCO2 (16).5 × HCO3 + (8 ± 2) = 13. – So corrected HCO3 = 10 + 12 = 22. HCO3 (5). so there is no primary respiratory disturbance.5–17. This patient was found to have a creatinine of 500 mg/dl and so the unmeasured anions producing the gap were related to renal failure. Na+ (135). so we should calculate the expected PaCO2 range: – Expected PaCO2 range = 1. – ↓ pH → so this is acidemia.5 → the patient’s PaCO2 lies within this range. the expected PaCO2 range = 24–28. so there is no primary respiratory disturbance.ARTERIAL BLOOD GAS INTERPRETATION 151 – The predominant abnormality is the ↓ HCO3 → so this is primary metabolic acidosis. – By calculating the AG = Na+ − (Cl− + HCO3) = 22 (↑). – AG = Na+ − (Cl− + HCO3) = 10 (normal) → so this is a NAGMA.88). – ↓ HCO3 → so this is a primary metabolic acidosis. It is >12 → so this is an AGMA. so there is no other metabolic disturbance. This patient is a 74-year-old very anxious lady who presented with severe gastroenteritis (diarrhea). – ↓ HCO3 → so this is primary metabolic acidosis. Cl− (118). . – Conclusion: This patient has a pure AGMA. – Expected PaCO2 range = 1. – Corrected HCO3 = ΔG + measured HCO3 (as ΔG = AG − 12 = 10). Cl− (118).5 × HCO3 + (8 ± 2) – So. • Interpretation: – Applying Henderson equation indicates accurate results. PaCO2 (40). • Interpretation: – Applying Henderson equation indicates accurate results. Na+ (133). – ↓ pH → so this is an acidemia. – AG = Na+ − (Cl− + HCO3) = 10 (normal) → so this is a NAGMA. the patient’s PaCO2 lies within this range. – PaCO2 is low. Case 2 • Interpret the following ABG: pH (7. – Conclusion: The patient has a simple NAGMA. Case 3 • Interpret the following ABG: pH (6. it is within the normal range of HCO3 (21–26).11). HCO3 (7).
Cl− (98). • Interpretation: – Applying Henderson equation indicates accurate results. PaCO2 (49). – Expected PaCO2 range = 1. – Conclusion: A combined NAGMA and respiratory acidosis. PaO2 (95). PaCO2 (41). apply expected PaCO2 range). Cl− (84). HCO3 (42).5 × HCO3 + (8 ± 2) = 41–45 → the patient’s PaCO2 (41) lies within this range → so. – Corrected HCO3 = ΔG + measured HCO3 (ΔG = 22 − 12 = 10). a combined disturbance is present – AGMA and metabolic alkalosis. This is the same patient described in case 2 after she was sedated with a benzodiazepine that suppressed her respiratory center.5–20. Na+ (143). – So. – Normal pH → so no acidemia or alkalemia. His ABG showed pH (7. – AG = Na+ − (Cl− + HCO3) = 22 (↑) → so there is an AGMA. – PaCO2 is normal (so does the pH and HCO3. What type of acid–base disturbance this patient has? • Interpretation: – Applying Henderson equation indicates accurate results. If in doubt. Case 5 • Interpret this ABG: pH (7. – Conclusion: Although this ABG looked normal. the corrected HCO3 = 10+23 = 33 → it is higher than the normal range of HCO3 (21–26) → so there is an additional metabolic alkalosis.5 → the patient’s PaCO2 is higher than this range so there is primary respiratory acidosis. there is a primary respiratory acidosis. He had diabetic ketoacidosis responsible for his AGMA and vomiting caused his metabolic alkalosis. This patient was found to have a blood sugar of 510 mg/ dl and ketones in the urine. Case 4 • A 23-year-old man presented with generalized malaise and vomiting.55). there is no primary respiratory disturbance. . Sedation can be harmful in elderly patients. so this is appropriate. – Normal HCO3 → so no obvious metabolic abnormality.152 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE – PaCO2 is normal (it should be low in the face of a very low pH) → so. HCO3 (23).5 × HCO3 + (8 ± 2) = 16. Although unnecessary you can still apply the equation – expected PaCO2 range = 1. Na+ (148).38).
↑ PaCO2 (same direction as HCO3) → Expected PaCO2 range = 0. – PaCO2 is normal (it should be low) → there is a primary respiratory acidosis. AG = Na+ − (Cl− + HCO3) = 22 (↑) → so there is an AGMA. • Interpretation: – Applying Henderson equation: [H + ] = K × ( Pa CO 2 / [HCO3 ]) ↔ 28 24 × (44 / 45) = 21. Na+ (142). – Conclusion: A combined AGMA and metabolic alkalosis with an alkalemic pH.55). Cl− (112). Repeat ABG sampling is advised or check with the lab to ensure accurate calculation of HCO3 and recording of results. . – Conclusion: A combined AGMA. ↑ HCO3 → so there is a metabolic alkalosis.9 × HCO3 + (9 to 16) = 47–54 → the patient’s PaCO2 (49) lies within this range → so. metabolic alkalosis. He is not intubated yet but has an NG tube. the equation indicates that the values are incorrect. PaCO2 (40). HCO3 (7). What type of acid–base disturbance does this patient have? • Interpretation: – Applying the Henderson equation indicates accurate results. His respiratory acidosis is likely due to respiratory failure (COPD ± aspiration) and the metabolic alkalosis is due to gastric suction. – Corrected HCO3 = 30. PaCO2 (44). This patient’s metabolic acidosis is most likely related to sepsis. Case 7 • Interpret the following ABG: pH (7. – ↓ pH → so this is an acidemia. – ↓ HCO3 → so this is a primary metabolic acidosis. His ABG showed pH (6. – AG = Na+ − (Cl− + HCO3) = 35 (↑) → so this is an AGMA. and respiratory acidosis. Cl− (100).ARTERIAL BLOOD GAS INTERPRETATION 153 – – – – ↑ pH → so there is an alkalemia. it is higher than the normal range of HCO3 (21–26). Na+ (144).88). Case 6 • A 58-year-old man (heavy smoker) admitted to the ICU with sepsis. HCO3 (45). there is no primary respiratory disturbance. so there is an additional primary metabolic alkalosis. So.
HCO3 (31). at sea level? • Interpretation: – Applying Henderson equation indicates accurate results.154 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Case 8 • A 68-year-old man known to have COPD presented to the emergency department with increasing cough. PaCO2 (60). PaO2 (169). AG (10). – AG is normal and HCO3 is adequately increased → no metabolic disturbances. – AG is normal and HCO3 is adequately increased → no metabolic disturbances. Case 10 • The patient in the previous case was intubated and mechanically ventilated to protect his airways. His ABG showed pH (7. – pH is slightly low indicating a mild acidemia. .6 (0. PaO2 (60).3/10 mmHg of PaCO2) and an increase in HCO3 by ∼6 (3/10 mmHg of PaCO2). • Interpretation: – Applying Henderson equation indicates accurate results. A repeated ABG showed pH (7. which corresponds to a drop in pH by ∼0.15). This patient was given a highflow O2 (indicated by the high PaO2) unnecessarily resulting in retention of CO2 and severe acute respiratory acidosis. – Conclusion: Acute primary respiratory acidosis on top of a chronic respiratory acidosis. PaCO2 (96).34). A repeat ABG showed pH (7. – ↑ PaCO2 → so this is primary respiratory acidosis.55). – ↓ pH → acidemia. – ↑ PaCO2 → so this is a primary respiratory acidosis. – Metabolic compensation indicates an acute respiratory acidosis in addition to the chronic respiratory acidosis. HCO3 (33). AG (10). The acute increase in PaCO2 resulted in mental deterioration and unresponsiveness. – The A−a gradient = (150 − PaCO2 × 1. AG (11). PaCO2 (39).25) − PaO2 = 15 (normal) – Conclusion: Chronic primary respiratory acidosis. HCO3 (33). – Metabolic compensation indicates a chronic respiratory acidosis: PaCO2 increased by 20 mmHg. PaO2 (198). Case 9 • The patient in case 8 became drowsy and unresponsive 4 h after presentation. What is the acid–base disturbance? What is the A−a gradient provided that the patient was on room air.
van Ypersele de Strihou C. Ann Intern Med 1966. Frans A. Javaheri S.44:291. Dubose TD. Philadelphia.280:117. Herbert LA. Sixth Edition. Dyck RF. Bleich HL. Weil JV. 2000. Schwartz WB. J Clin Invest 1972.297:814. Handbook of Physiology. 10. Quantitative displacement of acid– base equilibrium in metabolic acidosis. N Engl J Med 1969. American Physiological Society. Clinical approach to the diagnosis of acid–base disorders.925–997. Rapid estimation of plasma carbon dioxide tension from pH and total carbon dioxide content. ed. 11. Fulop M. Lennon EJ. Section 3: The Respiratory System. J Clin Invest 1965. Schwartz WB. The nature of the renal adaptation to chronic hypocapnia. Characterization and clinical application of the “significance band” for acute respiratory alkalosis. MD. Oh MS. In: Brenner BM. Ann Intern Med 1967. Carroll HJ.56: 38–54. Gennari FJ.136:1101–1116. Narins RGL Clinical use of anion gap. The elevated HCO3 was primarily a compensatory mechanism for the respiratory acidosis. Effect of increasing degrees of acute hypercapnia on acid–base equilibrium.65:265. ed. Cohen JJ. 13.703–727. The ventilator should have been set to target a normal pH rather than a normal PaCO2. Arbus GS. Am Rev Respir Dis 1987. Carbon dioxide titration curve of normal man. 9. Clin Sci Mol Med 1973. Winters RW. Goldstein MB. – ↑ pH → alkalemia. 3. Brackett NC Jr. Lemann J Jr. Defense of hydrogen ion concentration in chronic metabolic acidosis. Bethesda. 8. . et al. Kazemi H.66:312. The respiratory response to metabolic alkalosis and acidosis in disease. – The elevated HCO3 indicates a metabolic alkalosis resulting from overcorrecting the chronic respiratory acidosis. A new evaluation of an old approach.51:1722.272:1067.120:173–182. 4. NY State J Med 1976. Ventilatory control at high altitude. N Engl J Med 1977.76:19. 5. Albert MD. The response of extracellular hydrogen ion concentration to graded degrees of chronic hypercapnia: the physiologic limits of the defense of pH. Medicine 1977. N Engl J Med 1965. PA. Cohen JJ. 2.272:6. Metabolic alkalosis and hypoventilation in humans.ARTERIAL BLOOD GAS INTERPRETATION 155 • Interpretation: – Applying the Henderson equation indicates accurate results. 12. In: Fishman AP. Sell RB. References 1.45:439. 14. The resulting metabolic acidosis is sometimes called posthypercapnic metabolic alkalosis. 6. 1986. Schwartz WB. N Engl J Med 1965. Levesque PR. The anion gap. Acid–base disorders. Emmett M. 7. Can Med Assoc J 1979. Hypercapnia in metabolic alkalosis. Kassirer JP. Bear RA. WB Saunders. 15. Brackett NC Jr. Brenner and Rector's The Kidney.
Simple and mixed acid–base disorders: a practical approach. Am J Nephrol 1997. Moss ML. 21. Cuomo AJ. 23.77:405. West JB. Ann Intern Med 1972. Marked hypercapnia secondary to severe metabolic alkalosis. 22. Cohen E. 20. Medicine 1980. Respiratory Physiology. et al: The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. . Acta Physiol Scand 1966. Seventh Edition. Fulop M. The alveolar-arterial oxygen difference: its size and components in normal man. Am J Med 1972. Philadelphia. Batlle D. 19.59:161–187. Emmett M. Severe alveolar hypoventilation in a patient with metabolic alkalosis. Lifschitz MD. Brasch R. Goldberg M. Hizon M.318:594. Mellemgaard K. Computer-based instruction and diagnosis of acid–base disorders: a systematic approach. A guide for predicting arterial CO2 tension in metabolic acidosis.52:817.223:266–275. 18. et al. N Engl J Med 1988. et al. Lippincott Williams & Wilkins. PA. 2004. Oliva PB. the Essentials. Green SB.67:10. 17. JAMA 1973. Narins RG.156 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE 16.17:421–424.
e.1. © Springer-Verlag London Limited 2009 .1 This test can also be used to assess the functional status and predict mortality and morbidity in such patients.1. Its main indication is to assess the response of patients with pulmonary or cardiac disorders to certain interventions. walker.1007/978-1-84882-231-3_9.36 The patient is allowed.g. Table 9. however. Altalag et al. pulmonary hypertension. leg cramps.. unassisted in carrying portable O2 cylinder if used..33. better tolerated. intolerable dyspnea. the patient should walk normally.1. unstable balance.Chapter 9 Exercise Testing THE 6-MIN WALK TEST • The 6MWT is similar to the 12MWT.g. 157 A. A distance of 30 m (~100 ft) is considered suitable and the laps are then counted.32–35 Under the supervision of the respiratory therapist.1 Technique • The technique and methodology of 6MWT used for prognostic studies must follow a standardized protocol. e. if the patient develops chest pain. to use any kind of assistance that he/she normally uses for daily activities. The 6MWT is generally safe. • The 6MWT is best performed in a building with unobstructed level corridors. During the test.2 • The 6MWT is a useful tool for both the clinical and research fields. DOI: 10. the patient may be encouraged only by standardized phrases. but the 6MWT is preferred because it is faster. or pale or ashen appearance. marked diaphoresis.27–32 The test should be immediately terminated.22.1. Pulmonary Function Tests in Clinical Practice.. however.1 summarizes the indications and contraindications to 6MWT.37 The patient is allowed to rest whenever needed. and more standardized.
It is usually reproducible and the largest achieved distance is reported.1. A significant reduction in the 6MWD.36 • The most important measurement is the 6MWD.34 Interpretation • Three measurements can be obtained from the 6MWT: the 6-min walk distance (6MWD).24.9 Drug therapy for COPD10–12 and heart failure (CHF)13. the degree of dyspnea and fatigue. which is normally ≥ 580 m in men and 500 m in women.16 CF. Indications & contraindications for the 6MWT Indications for 6MWT To assess outcome of therapy (test is done before and after therapy) Pulmonary hypertension1 Lung transplantation3. .7 Pulmonary rehabilitation8.14 To assess functional status in patients with: Lung disease (COPD.15.23 COPD. and musculoskeletal disease (arthritis) or even in normal subjects who perform a submaximal effort.1.26 To assess outcome parameters for research studies Contraindications1 Absolute Unstable angina or MI within the past month Relative Resting tachycardia (>120/min) Uncontrolled hypertension (systolic >180 and diastolic >100) A portable pulse oximeter may be used during the test but more important is the reporting of SPO2 at the start and the end of the test.1. heart disease.17.39 • The 6MWT is repeated after a sufficient resting period.158 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 9.25 and pulmonary hypertension4.30 A low 6MWD is nonspecific and nondiagnostic.22. and the SPO2.4 Lung resection5 Lung volume reduction surgery6. coupled with the appropriate clinical setting is useful to grade the exercise capacity and to evaluate response to therapy and predict the overall outcome.38. An unexplained reduction of the 6MWD should prompt a search for a possible cause.18 and pulmonary hypertension) Heart disease (CHF)19–21 To predict mortality and morbidity in patients with CHF. A low 6MWD may be seen in patients with lung disease.1.
38. given the low intrasubject variability. to assess disease progression or effect of therapy. which is a 12-level scale ranging from “no discomfort” to “maximal discomfort.EXERCISE TESTING 159 • The 6MWD varies significantly among normal individuals. however. FIGURE 9.1. may be used to grade the degree of dyspnea that the patient experiences during and at the end of the test. Factors such as age. • The modified Borg scale. make the test more useful.39 • Sometimes a walking (exercise) oximetry is done (without measuring the 6MWD) to assess SPO2 to determine the need for. may influence the accuracy of the SPO2. The modified Borg Scale.41 Artifacts related to signal recording during walking. weight.1. . This is often referred to as exercise oximetry and has nothing to do with the 6MWT.1. sex. supplemental O2 during exertion. or to titrate the level of. Any drop of >5% usually indicates a respiratory or possibly a cardiac disorder.1 Serial measurements of 6MWD in the same patient. and height independently influence the 6MWD in healthy adults.40 • SPO2 normally is unchanged with exercise.” Figure 9.
these organ systems interact and coordinate their functions together to achieve one goal. disorders of any of these organ systems result in FIGURE 9.2. Principles of Exercise Testing and Interpretation. Whipp BJ. The Wassermann's gears illustrate the interaction and coordination of the body organ systems to produce energy. Fourth Edition. Exercise normally prompts the delivery of the appropriate amount of O2 from the external environment to the red blood cells (the function of the pulmonary system). O2 is then transported to the muscle cells (the function of the cardiovascular system and blood) where oxidative phosphorylation takes place to produce energy (adenosine triphosphate or ATP) (the function of the mitochondria).). Hansen JE. . So. PA. Figure 9. as is illustrated by the Wassermann's gears. Philadelphia. Sue DY. • CO2 should then flow in the opposite direction through the same organ systems until it is exhaled to the external environment.160 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE CARDIOPULMONARY EXERCISE TESTING Introduction • The cardiopulmonary exercise test (CPET) is aimed at assessing the ability of the body organ systems to respond normally during exercise. Lippincott Williams & Wilkins. Failure of any of the organ systems results in failure of energy production (With permission from Wasserman K. Stringer WW. the production of energy needed for function. Therefore.2. 2004.
76) Evaluation for impairment/disability77–82 Other indications Diagnosis of exercise-induced asthma83–87 Identification of gas-exchange abnormalities42. Indications and contraindications for CPET Major indications To determine exercise capacity/impairment42 To identify the cause of exercise limitation43–52: If the patient has both cardiac and pulmonary diseases and unsure which is most responsible for the exercise limitation If no cause is apparent for exercise limitation after full evaluation Assessment of exercise capacity if resting data do not explain symptoms42. orthopedic impairment) .69–72 ILD.74 and CF75.. TABLE 9. pulmonary edema.94.52 Assessment of therapy selection and response (pulmonary rehabilitation. diastolic >120 mmHg) or pulmonary hypertension Hypertrophic obstructive cardiomyopathy Significant left main coronary artery stenosis (without acute symptoms) Others (moderate stenotic valvular heart disease. thyroid disease) Relative contraindications42.44. myocarditis.95 Active cardiac disease (acute MI.73. severe aortic stenosis. we aim to achieve two goals: detecting any exercise limitation and identifying the organ system(s) responsible for that limitation.62 medical therapy for lung diseases such as COPD.60 cardiac transplantation. active arrhythmias.88–93 Absolute contraindications91. where subjects are encouraged to achieve their maximum exercise capacity. acute PE or DVT) Hemodynamic instability or acute noncardiopulmonary disease affecting exercise performance (infection.61.59. respiratory failure.56–58 lung transplantation. unstable angina. endocarditis. inability to achieve the predicted maximum exercise capacity for a given individual.EXERCISE TESTING 161 exercise limitation. i. electrolyte abnormalities.63–68 pulmonary hypertension. aortic dissection. uncontrolled CHF. advanced pregnancy. • The indications and contraindications for exercise testing are listed in Table 9.53–55 lung resection.2.44 Titration of supplemental O2 rate during exercise64.72 Uncontrolled systemic (systolic >200 mmHg. pericarditis) Active pulmonary disease (uncontrolled asthma.e.2. • In exercise testing.
102–104 • Cardiovascular monitors: – Include baseline and continuous ECG monitoring throughout exercise. which monitors the heart rate (HR) and aids in detecting arrhythmias and ischemia. Technique • The CPET equipment must be calibrated before use to meet strict quality control parameters in order to ensure accurate measurements.107. more commonly.162 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Equipment • A cycle ergometer or a treadmill – Represents a way to apply a controlled quantifiable workload that can be steadily increased.97–99 – More invasive methods can be used (arterial line) to monitor the arterial blood gases (ABG for PaO2 and bicarbonate) and lactate.52 (b) A more linear and quantifiable workload can be achieved by the ergometer.42 • Respiratory system monitors: – Gas analyzers: measure the amounts of the exhaled O2 and CO2 throughout exercise.105. from which other useful data can be derived.42. Figure 9. intermittent (cuff system)106blood pressure (BP) monitoring is also done.100 – The modified Borg scale chart: can be used to grade the degree of discomfort the patient experiences in terms of breathlessness and leg fatigue during different stages of exercise.1. These measurements are not routinely needed.44.106 – Continuous (through an arterial line)42.109–115 • The technique involves asking the patient to pedal the cycle ergometer at a fixed speed with a progressive increase in the .52 (c) Ergometer is less expensive and occupies less space.101 Breathlessness and leg fatigue are the two major symptoms that limit exercise.42.108 or.42. which produce fewer artifacts in the recorded data. from which many exercise parameters are derived.42 – Pulse oximeter: is used to record SPO2 throughout exercise (its function is different from the gas analyzer that measures the amount of exhaled O2). – An ergometer is generally preferred over a treadmill because of the following: (a) Ergometer is associated with less body movements.106.42.96 – Airflow or volume recording device: is used to measure ventilation during exercise.
diastolic BP of >120 mmHg) Signs and symptoms of cardiovascular. respiratory failure) . • Continuous supervision by a properly trained technologist and a physician is mandatory throughout exercise. These instruments will feed data to a computer with software that can plot the results in both a graphic and numeric format. namely. whenever you encounter “VO2” remember that it represents WR used during the test. a mouthpiece for gas collection and flow and volume measurements. 44. high-grade AV blocks) BP instability (systolic BP of >250 mmHg or dropping by >20 mmHg from the highest value during CPET. Therefore. Significant degree of lactic acidosis → either HCO3 ↓ by 5 meq/L or ↑ in RER to 1. respiratory or CNS instability (sudden pallor. The patient is connected. – VO2 (in L/min) represents the internal metabolic work and is directly proportional to the external WR (in watts) applied through the cycle ergometer or treadmill.3. This section discusses the major concepts of VO2.42 O2 Uptake. 52. dizziness. mental confusion. arrhythmias. ABG may then be withdrawn (if arterial line is placed) and a recovery period starts. to a number of instruments. patients may be encouraged to continue exercising if they can. WR curve (but not reaching the predicted max HR42). throughout the test. and a blood pressure cuff. Definitions • VO2 (O2 uptake): – Is the amount of O2 in liters that the body consumes per minute (liters/minute). Indications for termination of exercise testing42.15120 Significant ECG changes (ischemia. syncope. loss of coordination. that is why VO2 is considered equivalent to WR. pulse oximeter.3 arise. ECG monitor.EXERCISE TESTING 163 resistance to pedaling (work rate or WR). Major Concepts • Understanding O2 uptake is the window to understanding the body's physiological changes in response to exercise. 116–119 Severe dyspnea or fatigue at peak exercise Ventilatory limitation or severe symptomatic desaturation (SPO2 £ 80%) Reaching a plateau of VO2 vs.42 • Maximum VO2 (VO2 max) (L/min): TABLE 9. The test is terminated once any of the factors listed in Table 9.
× (CaO2 − CvO2) ¯ Because C. = VO2/CaO2 − CvO2 ¯ SO : VO2 = C.42. • Measured peak VO2 (L/min): – Is the highest VO2 that a subject actually achieves during CPET.42.003) × (PaO2 ¯ ¯ − PvO2)] and because: [(0. HR is the heart rate. ¯ TABLE 9.34) × Hgb × (SaO2 − SvO2). and body size.O. and SvO2 is the mixed venous O2 saturation ¯ . then: VO2 = SV × HR × (CaO2 − CvO2) ¯ Because: (CaO2 − CvO2) = (1. SaO2 is the arterial O2 saturation.O. – It is determined by the patient’s age. = SV × HR. Figure 9. the measured peak VO2 usually equals predicted peak VO2 while in patients with heart or lung disease the measured peak VO2 is often less than predicted peak VO2.003) × (PaO2 − PvO2)] is negligible.34) × Hgb × (SaO2 − SvO2). Fick equation122 It states that the cardiac output equals the rate of O2 uptake divided by the difference in the arterial and mixed venous O2 content: C.34) × Hgb × (SaO2 − SvO2) + [(0.4): VO2 = SV × HR × (1. VO2 max can be detected when the VO2 plateaus in relation to the external workload (WR).O. where SV is the stroke ¯ volume. Hgb is the hemoglobin.122 which can be written as follows (for details see Table 9. sex. • VO2/kg (ml/min/kg): – Is the O2 consumption in milliliters/minute corrected for the body weight in kg. It is particularly useful in interpreting the test in obese individuals. · Factors Determining VO2 • These factors can be acquired from the Fick equation. • Predicted peak VO2 (L/min): – Is the highest VO2 (workload) that a subject is expected to achieve.11c.119 VO2 max represents the maximum exercise capacity for a given subject and is an indication for exercise termination.89.164 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE – Is the maximum achievable VO2 (workload).3. indicating that no further increase in VO2 can be achieved despite increasing WR.121 – In normal subjects. then the ¯ final equation can be written as follows: VO2 = SV × HR × (1.4. see Table 9.
pacemaker patients with fixed HR or patients on β-blockers) cannot increase their HR appropriately with exercise.. SV. the ability of muscle cells to extract O2 from the blood). with the exception of Hgb.124 – Patients with chronotropic disorders (e. C. the factors that determine VO2 are HR.g.3. In highly trained athletes.44 • Normally we are exercise-limited by our heart. with increasing WR (VO2). it is important to determine the predicted maximum HR so that we can define our cardiac limits to exercise.42. – Patients with muscle disease that impairs O2 extraction and utilization (e. Hgb.5.O. initially accomplished by increases in both SV and HR (to a lesser extent). Figure 9. SV plateaus.e..O. they are exercise limited.125–127 So. = SV × HR. the amount of O2 extracted from the blood (SaO2 − SvO2) is threefold higher than at the start of exer¯ cise.O. these factors progressively increase in response to the increased WR.65 × age). hence. C.44 Similarly.EXERCISE TESTING 165 • From this equation. and the difference between the arterial and mixed venous O2 content (i. can increase by up to fourfold at peak exercise by increasing HR and SV.g. however. are HR and SV.123 • Conditions that affect any of these factors will necessarily affect VO2 and hence the exercise capacity: – Patients with a cardiac disease (like cardiomyopathy) cannot increase their SV appropriately in response to exercise resulting in exercise limitation. the two components determining C. Figure 9.O. Then. that is.. mitochondrial disease) will have exercise limitation. V O2 Relationship with the Cardiac Output Components • As discussed earlier. at peak exercise. Assessing the Cardiovascular System . As an example. During exercise. • During exercise. at which time HR increases more rapidly. there is an augmented increase in SV in response to exercise resulting in a supranormal exercise capacity. • The predicted maximum HR depends on the age and can be derived from different formulae: – Max HR = 220 − age89 or Max HR = 210 − (0. – Patients with anemia (or carboxy-hemoglobinemia) may have low exercise capacity because of low O2 carrying capacity. we stop exercising when we achieve our maximum HR. there is a near linear increase in C.128 .
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
FIGURE 9.3. The relationship between VO2 and C.O. components. SV increases first then when it plateaus, HR increases more rapidly. This maintains a linear increase in C.O.
• The HR can be easily measured during exercise, while the SV generally requires a more invasive method (e.g., cardiac catheterization). A search for a noninvasive method to estimate SV resulted in the concept of the “O2 pulse.” . O2 Pulse (VO2/HR) • Is defined as the O2 uptake or consumption (in L/min) for each cardiac cycle, i.e., VO2 divided by the HR. The Fick equation can then be rearranged to calculate O2 pulse: O2 pulse or VO2 / HR = SV × 1.34 × Hgb × (SaO2 − SvO2). ¯ • Assuming that the variables in the right side of this equation are constant [Hgb and (SaO2 − Sv O2)], then O2 pulse becomes equiva¯ lent to SV. That is why, O2 pulse is used by some as a noninvasive surrogate marker for SV in exercise test interpretation.89,91 When O2 pulse is plotted against VO2, it produces a curve comparable ¯ to SV curve; Figure 9.3. The assumption that the a–v O2 saturation difference is constant is not always true. The O2 pulse is a more qualitative assessment of SV and must be viewed in this context for interpretation.
• When O2 pulse (SV) fails to increase appropriately with exercise, it may indicate cardiac disease, e.g., cardiomyopathy, as discussed earlier. As a result, the body will compensate by increasing HR to maintain an appropriate increase in C.O., which is required to continue exercising. The patient will end up reaching the maximum HR much earlier than expected, resulting in premature termination of exercise (i.e., a low peak VO2); see Figures 9.4 and 9.5.129 A low O2 pulse can also be seen in deconditioning.42 • By looking at the curves in Figure 9.4, we can make two comments: – There is a significant reduction in peak VO2 (i.e., exercise limitation). – The steep increase in HR with minimal increase in O2 pulse (SV) indicates a cardiovascular origin of exercise limitation. • Aerobic training, however, results in a higher SV for a given workload, thus a lower HR. A higher VO2 therefore, can be achieved (e.g., elite athletes may more than double their peak VO2); Figure 9.5.130
FIGURE 9.4. Heart disease, steep increase in HR with a flat O2 pulse (SV); peak VO2 is reduced.
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
FIGURE 9.5. HR reaches its peak early in heart disease and late in aerobic training resulting in a significant difference in peak VO2 in the two conditions.
• If peak exercise is reached before reaching the maximum HR, this is referred to as HR reserve: HR reserve = Pred. HR max − achieved HR at peak VO2. • HR reserve is increased in patients with pulmonary disease and those who cannot reach their peak exercise for other reasons (e.g., volitional, muscle fatigue). Definition of Other Exercise Parameters • V CO2: is the amount of CO2 produced by the body per minute (L/min). • Respiratory quotient (RQ): is the amount of CO2 the body produces for each liter (mole) of O2 it consumes, at the tissue level. Normally, at rest, we produce ∼0.8 mole of CO2 for each mole of O2 we consume (RQ = 0.8), but this increases with exercise as will be discussed. • Respiratory exchange ratio (RER): is the amount of CO2 produced per liter of O2 consumed as measured from the exhaled air at the mouth (VCO2/VO2). At steady state, RER equals RQ
allowing RER to be used as a rough index of RQ given the difficulty of measuring the later.42 • VE (minute ventilation): is the volume of air we breathe per minute. VE is the product of tidal volume (VT) and respiratory rate (RR): . VE = V T × RR. • PETO2: is the end-tidal O2 tension as measured from the exhaled air. • PETCO2: is the end-tidal CO2 tension as measured from the exhaled air. • Ventilatory equivalent for VO2 i.e., (VE/VO2): is the amount of VE for a given level of VO2 (WR). • Ventilatory equivalent for VCO2, i.e., (VE/VCO2): is the amount of VE at a given level of VCO2. Anaerobic Threshold (AT) • Is defined as the VO2 (in L/min) at which there is substantial transition to anaerobic metabolism to produce extra energy (ATP). This is aimed at supplementing aerobic metabolism, which becomes insufficient at higher levels of exercise (in healthy subjects AT takes place at ∼45–60% of predicted peak VO285,86). • AT is called anaerobic because this process is O2 independent. At the same time, it results in the production of lactic acid, which when accumulating, contributes to muscle fatigue leading to termination of exercise. This is why AT is sometimes called lactate threshold.131,132 The body buffers the rising levels of lactic acid in the blood with bicarbonate to stabilize the pH: Lactate + H + + HCO3 → H2CO3 → H2O + CO2. • As a result, extra CO2 is produced, unrelated to O2 consumed (VO2) resulting in the rise of RER during exercise, which often exceeds 1 (i.e., more CO2 is produced than the O2 consumed). Because of this accelerated rise in CO2 (VCO2) at AT, the respiratory system responds by eliminating the extra CO2, resulting in a rise in VE out of proportion to VO2 if they are plotted against each other; Figure 9.6a. The point at which the slope of VE curve changes is called the inflection point and corresponds to AT; Figure 9.6a.
PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE
FIGURE 9.6. (a) VE vs VO2 curve showing a steady increase in VE, then at AT it inflects upward. (b) VCO2 vs. VO2 curve. (c) VE/VO2 vs. VO2 curve and VE/VCO2 vs. VO2 curve. (d) PETO2 vs. VO2 curve and PETCO2 vs. VO2 curve.
• Methods to identify AT include the following: – VE vs. VO2 curve, as discussed earlier; Figure 9.6a. – VCO2 vs. VO2 curve; Figure 9.6b. As at AT, VCO2 rises.faster because of the increased CO2 production; this is called the V-slope.163 – Ventilatory equivalents for VO2 and VCO2 i.e., (VE/VO2 and VE/VCO2) vs. VO2 curve; Figure 9.6c42: (a) With exercise, VE/VO2 drops steadily as the increase in VO2 (denominator) exceeds the increase in VE (numera-
6d: (a) The expired O2 tension remains stable during exercise but inflects upward at AT in response to the increased VE. Figure 9.6c.138 or indeterminate139 as the patient is usually limited by ventilatory constraints. (b) This inflection point may be clearer in this curve than in the VE vs. (b) PETCO2 similarly remains stable at and beyond AT for some time before deflecting downward in response to the disproportionate increase in VE when a frank metabolic acidosis develops. Figure 9. if lactate or HCO3− is plotted against VO2. Other causes of reduced AT include deconditioning. and muscle oxidative disorders. does not increase appropriately during exercise. This means that in cardiovascular disease. VO2 curve. both the denominator (VCO2) and numerator (VE) increase proportionately initially. VO2 plot changes direction from downward to upward. not reached137. as the VE/VO2 vs. VO2 curve.134 So. the ventilatory equivalent for VCO2 (VE/VCO2) continues to decrease after VE/VO2 inflection point (AT) is reached. At AT. This downward slope of VE/VCO2 vs. as. reduction in O2 carrying capacity.42 – PETO2 and PETCO2 vs. the AT is generally low (<40% of peak VO2) and contributes to exercise limitation because of muscle fatigue (accumulation of lactate).42. (c) On the other hand. then the point at which the lactate starts rising or HCO3− starts dropping corresponds to the AT. the AT is either normal.133.135.42 In respiratory disease.7. at which point the curve changes direction upward.EXERCISE TESTING 171 tor).O. Figure 9. at AT.42 – AT can also be determined invasively by serial measurements of lactate or bicarbonate (ABG) during exercise. If C.136 • The AT is determined predominantly by the cardiovascular system. until AT is reached when the (VE/VO2) inflects upward due to the disproportionate increase in VE compared with that in VO2. it will result in impaired O2 delivery to the muscles and a faster transition to anaerobic metabolism. . VO2 curve continues beyond AT until VE disproportionately increases as a compensation when a frank metabolic acidosis develops. lactate rises and bicarbonate drops (to buffer the lactic acid) in the same ratio (they are equimolar).
. HCO3 starts to drop and lactate starts to rise.172 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 9.7. diastolic >100 mmHg) during exercise suggests abnormal sympathetic BP control. or ischemia) or circulatory disorder (pulmonary vascular disease or central pulmonary venous obstruction). • Failure of BP to rise with exercise suggests a cardiac disorder or abnormal sympathetic control of BP. At AT. Assessing the Respiratory System The respiratory system is assessed as two components: the ventilatory component and the gas-exchange component.O.g. the systolic BP increases with exercise because of increased C. and the diastolic BP remains unchanged or drops slightly because of decreased systemic vascular resistance in response to vasodilatation in the exercising muscles.140 • BP is another parameter used to assess cardiovascular function. Normally. Blood Pressure Response42. but may also be seen in patients with known resting hypertension. systolic >220 mmHg. aortic stenosis. Ventilatory Component Definitions • Maximal voluntary ventilation (MVV) . • A drop of BP with exercise should prompt exercise termination as it indicates either a serious cardiac disorder (CHF. • An excessive rise in BP (e..
EXERCISE TESTING 173 – Is the maximum minute ventilation that a subject can achieve. Figure 5.147 • Unlike HR. i.. V E. It can be determined mathematically as follows: (a) Calculated MVV: derived from the patient's FEV1.146.1. Figure 9.130.8. i. the VT increases initially rapidly and then plateaus. the equation will then be: MVV = FEV1 × 35.* Therefore. = MVV − VE max. and age by multiplying the predicted (not measured) FEV1 by 40.e. Major Concepts • The components of VE are RR and VT: VE = RR × VT. (b) Predicted MVV is calculated from the patient's height. then the result is extrapolated to 1 min by multiplying by 5. Calculated MVV is often referred to in the final CPET as the predicted VE max .89 . sex. If both measured and calculated MVV are done (which is unusual). • Ventilatory reserve = Predicted − measured VE max.141–145 which is the technique used by most clinical exercise laboratories*.52.53. in respiratory disease. • VE max: is the maximum VE that the patient achieves during CPET. the calculated MVV will often be less than the patient's predicted MVV.44.. ††: MVV = FEV1(L) × 40. †† .52.e. It is used as an estimation of the predicted VE at peak exercise (predicted VE max). allowing for some reserve in V E * Some laboratories use 35 instead of 40 as the conversion factor. see Chapter 5. • During exercise. † Measured MVV: is determined in the lab by measuring the patient's ventilation over 12 s during a maximal effort.89 • Breathing reserve (another way of expressing ventilatory reserve) = measured/predicted VE max. = VEmax/MVV. the maximum RR (50/min) is not reached normally at peak exercise (VO2). at which point the RR increases maintaining a linear increase in VE.44. †. the higher of the two is reported as the predicted VE max.
but they reach their VE max at a higher than predicted VO2.174 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE (∼30–40% of the predicted VEmax). . Behavior of VT and RR during exercise is similar to SV and HR. Figure 9.9. This can be expressed as either ventilatory or breathing reserve. Figure 9. This will lead to a left shift of the tidal flow–volume loops with the end-inspiratory lung volume approaching TLC and the tidal expiratory flow reaching or approaching the maximal expiratory envelope. • This means that if VE max is achieved during exercise. Note that VE and VO2 maintain a linear relationship. Figure 9. and stops exercise because of dyspnea.148–151 Dynamic hyperinflation is probably the main cause of breathlessness in patients with COPD (emphysema).64. FIGURE 9. see earlier definitions. This may indicate that elite athletes have such well-conditioned oxygen delivery from the lungs to the working muscle that they reach their VE max and may thus be exercise limited by their lungs! • Ventilatory limitation may also occur when dynamic hyperinflation is recognized in the tidal flow–volume loops recorded during exercise.8. • Elite athletes may achieve their VE max (MVV) during exercise.10.9. then the patient is generally exercise-limited by ventilatory parameters. This flow limitation and mechanical constraint increase the work of breathing and limit exercise capacity. Dynamic hyperinflation leads to a progressive rise in FRC during exercise.
Dead Space Fraction • At rest.EXERCISE TESTING 175 FIGURE 9. VT is normally ∼450 ml. The other two-thirds reach the gas-exchange units and are referred to as the alveolar volume (VA). both PaCO2 and PETCO2 can increase due to a relative hypoventilation. however. Patients with lung disease reach their predicted VEmax early. Elite athletes may approach their predicted MVV with a supranormal VO2. In some ventilatory disorders.e.9. • PaCO2 and PETCO2 normally remain stable until AT is reached. and RQ. one-third of which (150 ml) is wasted in the anatomic and physiologic dead spaces (dead space volume. . when they start to decrease due to the increased VE. notice that the calculated MVV (i. the predicted VE max) is less than the predicted MVV in patients with lung disease. so: VT = VD + VA. VD). they are considered also useful in assessing gas-exchange function as will be explained later. Although PaCO2 and PETCO2 may be used to assess ventilatory function. Gas-Exchange Component This is assessed by three ways: dead space fraction. ABG.
• Dead space fraction (VD/VT) is then the dead space volume expressed as a fraction of VT. a phenomenon called dynamic hyperinflation. This is due to a number of factors including exercise-induced bronchodilatation and distention of airways related to the increased lung volumes. It similarly equals V D/V E.167:211–277. the upper lobes of the lungs are not as well perfused as the bases but with exercise. shifting the tidal FV curves to the left. (With permission from ATS/ACCP Statement on Cardiopulmonary Exercise Testing.10.52 • At rest. Am J Respir Crit Care Med 2003. Normally. however. as discussed. this equation can be applied to the VE: V E = V D + V A.5 L with exercise.176 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 9. • Similarly. In emphysema.). In reality VD does not remain constant with exercise. perfusion improves to the upper ‡ § VT can reach as high as 2.152 . resulting in a reduction of dead space fraction from ∼1/3 to ∼1/5. VT increases to 800 ml or more‡ with a relatively constant dead space volume§. which improves gas exchange. which equals 1/3. dead space fraction is 150 ml/450 ml. the decreased expiratory time (because of increased RR during exercise) results in more air-trapping and increases the FRC. it increases slightly and may reach 200 ml. During exercise. • At rest. tidal flow–volume loops expand from both directions during exercise.
e.EXERCISE TESTING 177 lobes (because of increased blood flow) resulting in a more even V/Q distribution and hence better gas exchange. . ¯ where PE CO2 is the mixed expired CO2 measured in exhaled ¯ samples. • On the other hand. So.. the higher the PE CO2).(VD VT )⎤ ⎣ ⎦ – From this equation. This assumption can be applied near or at the AT. which states that the product of volume and concentration is the same under constant temperature. This may be done in two ways: – VD/VT can be measured from the dead space equation:153. where the stiff small lungs are incapable of increasing the VT appropriately in response to exercise.¶ VD/VT = (PaCO2 − PE CO2)/PaCO2. VD/VT remains unchanged or does not decrease as expected with exercise as the excessive increase in RR at a low VT increases the volume of wasted ventilation (dead space). • Estimating VD/VT allows for detection of such diseases. we normally improve our gas exchange during exercise by increasing alveolar ventilation more than dead space and improving overall V/Q matching. VCO 2 Pa CO 2 ⎡1. the lower the VD/VT. – The other way is using the mass balance equation that can be rearranged as follows52: VE 1 = K× . but not beyond that.52 • In summary. that is. Lung fibrosis is an example. The smaller the difference between PaCO2 and PE CO2 ¯ (i. diseases that interfere with dead space fraction during exercise result in an inefficient gas-exchange process and can contribute to premature termination of exercise. the ventilatory equivalent for VCO2 (VE/VCO2) can be used as a noninvasive surrogate marker for the dead space fraction (VD/VT) if PaCO2 remains constant. when PaCO2 drops in response to increased VE (to compensate for the lactic acidosis). ¶ This equation is derived from Bohr's law. To measure this parameter noninvasively PETCO2 is substituted for PaCO2. the ¯ more efficient the ventilation is.
94.155 – P(A–a)O2 can be calculated from the alveolar gas equation as follows (see Chapter 8 for details): P(A-a)O2 = [ PIO2 − PaCO2 ] − PaO2 . If so. it indicates a gas-exchange abnormality.3.42. The following are the major steps in interpreting such studies: Maximal Effort Determine whether a truly maximal effort was achieved. A drop in PaO2 indicates a gas-exchange abnormality.5 shows one suggestion). RER should not exceed 1. Approach to Exercise Test Interpretation In interpreting any cardiopulmonary exercise study. A maximal effort is achieved if one or more of the factors listed in Table 9. see Table 9. PaO2 – Remains stable or increases slightly with exercise. RQ • • • • – RQ is substituted for by RER that is measured simultaneously with PaO2 and PaCO2 during and at the end of exercise.154. SPO2 (pulse oximetry) or SaO2 (ABG) – SPO 2 is the standard measure of oxygenation used during exercise testing.15 generally indicates maximal effort). P(A–a)O2 is normally <10 mmHg and increases with exercise to >20 mmHg.120 PaCO2 and PETCO2 are increased in gas-exchange disorders. you have to apply a structured approach (Table 9.157 Both SPO2 and SaO2 should remain normal and stable with exercise.6 is .158 A significant symptomatic desaturation (<80%) during exercise indicates a significant gasexchange disorder and should prompt exercise cessation.156. Any drop of ³ 5% indicates a gas-exchange abnormality. as PAO2 normally increases with exercise and PaO2 remains normal. However. This is a useful measurement to determine if peak exercise is truly achieved (RER of ³1. any increase in P(A–a)O2 of >35 mmHg with exercise is considered abnormal and indicates a gas-exchange abnormality.3 at peak exercise. It may be less accurate than S aO 2 particularly at low levels and can be prone to artifact.178 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Other Methods for Assessing Gas Exchange • A–a gradient (P(A–a)O2) – At rest.
Examine the gas-exchange response: Examine the dead space fraction: VD/VT normally decreases with exercise Determine VE/VCO2 at AT (<34) – a surrogate marker for VD fraction Determine VE/VO2 at AT (<31) Check PETCO2 (and PaCO2) at peak exercise (it normally decreases) (continued) . Determine whether exercise capacity is normal: Determine the peak VO2 (should be >83% predicted). HR max (should be >90% of predicted) Calculate HR reserve = predicted − achieved HR (normal is ±15) HR curve (should be along the predicted curve) Examine O2 pulse at peak VO2 Determine the value of O2 pulse at peak exercise (>80% predicted) O2 pulse curve should run along the predicted curve Determine AT (>40% predicted VO2). VCO2.). it should run along the predicted curve.). Determine the severity of exercise limitation. Table 9. moderate (40–60% pred. Examine VO2 vs. graphically identify AT from: VE. Determine the type of exercise tool used (usually cycle ergometer) Report the reason for exercise termination (dyspnea. Report the BP (normally: 205 ± 25 over 100 ± 10. which can be graded according to VO2 max. WR curve. ↑ systolic and pulse pressures) Examine the ECG for arrhythmia and/or ischemia Examine the ventilatory response: Determine VE max (<70% of predicted MVV) Compare the calculated MVV to the predicted MVV. and severe (<40% pred. fatigue) Report the Borg scoring for dyspnea and leg discomfort at exercise termination.15) RR max (<50) Examine tidal FV loops for dynamic hyperinflation. WR curve.). Examine VE curve (should be along the predicted curve and should not reach MVV) Determine VE (ventilatory) reserve = calculated MVV − VE max (>15) Determine the breathing reserve = VE max/calculated MVV (0. Determine whether a truly maximal effort was achieved. Suggested steps in reading exercise testing Determine: The indication for CPET. this can be done numerically or through VO2 vs.5. Examine the cardiovascular response: Examine HR response (remember that max HR should be achieved at peak exercise).EXERCISE TESTING 179 TABLE 9. leg discomfort. Examine the base-line spirometry and maximal flow volume loop.5. Determine the maximum WR achieved (>80% predicted). as mild (60–83% pred.e. i.72 ± 0. VE/VO2 and PETO2 curves.
WR curve serves the same purpose. is severe). WR. A subnormal exercise capacity is indicated when the curve does not reach the predicted peak VO2 . is mild. VE max. WR curve. or submaximal effort. Figure 9. which could be cardiac disease. with or without an early plateau. is moderate. then the exercise capacity is normal. pulmonary disease. while failure to achieve the predicted WR indicates a decreased exercise capacity. Achieving predicted maximum HR. c.180 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 9. looking at VO2 vs. reduced oxygen carrying capacity.1–1.11a. If peak VO2 is normal.5 (continued) Determine RER at peak VO2 (1. • Achieving the predicted WR (in watts) also indicates a normal exercise capacity. moderate.3) Determine SPO2 (more accurately SaO2) at peak VO2 (it should not drop by >5%) ABG at the end of exercise PaO2 is unchanged normally with exercise P(A–a)O2 increases slightly but should not exceed 35 mmHg. then you are likely to be dealing with a normal subject. approaching or exceeding the calculated MVV.15. Patient exhaustion with a Borg scale rating of 9–10. If peak VO2 is reduced. then you need to determine the cause.119. Factors suggesting a maximal effort42. RER of ≥1. which may limit the usefulness of the CPET. . the conclusion TABLE 9. and <40% pred. deconditioning. Achieving predicted maximum WR. The degree of impairment of exercise capacity is graded into mild. and their relationship: • Peak VO2 should be more than 83% of the predicted peak VO2 (VO2 max). • Graphically. Lack of these factors indicates a submaximal effort. neuromuscular disease. Figure 9. If the curve reaches the predicted peak VO2. peak VO2 of 60–83% pred.6.g. and severe depending on peak VO2 (e.11b.. (are) present. 40–60% pred.120 Achieving predicted peak VO2 and/or a plateau is observed in VO2 vs. Exercise Capacity Determine whether the exercise capacity is normal by checking the peak VO2. Finally.
(c) Patient did not achieve the predicted max VO2 with an early plateau. This is because these patients cannot increase their stroke volume (SV) appropriately in response to exercise. the predicted HR max is usually not reached and their HR reserve is then increased. VO2 curve will generally have a steeper slope (left shift) compared with control. The HR vs. cannot increase HR appropriately). O2 pulse. Figure 9.. WR curve. and ECG.167:211–277.12a). VO2 vs. Figure 9. Am J Respir Crit Care Med 2003. VO2 vs. (a) Patient achieved predicted max VO2. In patients with lung disease.EXERCISE TESTING 181 Cardiovascular System Determine whether the cardiovascular response to exercise is normal by looking at the HR max. BP. • The predicted HR max is reached at the predicted peak VO2 in normal subjects (Figure 9. indicating reaching VO2 max and exercise limitation most likely related to a cardiovascular disease (With permission from ATS/ACCP Statement on Cardiopulmonary Exercise Testing. indicating exercise limitation. but is reached prematurely in patients with heart disease. Patients with chronotropic incompetence (i.11. those on β-blockers.12c. or patients with severe FIGURE 9.12b. WR curve. such as patients with pacemakers.e. (b) Patient did not achieve the predicted max VO2.) . the onset of AT.
11 (continued) HF.159 may have a high HR reserve but are still limited by their cardiovascular system.182 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 9.142.12b. Figure 9. which is representative of the SV. is generally decreased at peak exercise in patients with heart disease and its curve shows an early plateau. In normal patients . • The O2 pulse.
Am J Respir Crit Care Med 2003. the O2 pulse is usually normal. The AT is reached earlier than predicted (40–60% of predicted peak VO2) in patients with heart disease. however. or PETO2 curves.).12a. indeterminate.160. Figure 9. VE/VO2. Figure 9.. ↓ΔVO2/ΔWR ratio) also suggests a cardiovascular limitation to exercise. FIGURE 9. O2 pulse curve has an early plateau indicating a cardiac disease limiting exercise. Exercise-related significant ECG changes (arrhythmia or ischemia) suggest a cardiac disease. In patients with lung disease. (b) HR curve shifted to the left with steep slope. Figure 9. failure to rise or drop in BP) suggests a cardiovascular abnormality. WR curve (i. (a) HR and O2 pulse curves along the predicted curves. c.EXERCISE TESTING 183 • • • • and in patients with lung disease. HR and O2 pulse vs.161 An abnormal BP response (excessive rise. VO2 curves. however.11c. (c) HR and O2 pulse curves along the predicted curves but with increased HR reserve. AT can be determined from VE. indicating normal response to exercise. .4. it is normal. This pattern can be seen in submaximal effort and in respiratory disease (With permission from ATS/ACCP Statement on Cardiopulmonary Exercise Testing. An early plateau of the VO2 vs.167:211–277. VCO2.12. or not reached as the patient may stop prematurely due to ventilatory limitation.e.
184 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 9. RR and tidal FV loops: – The measured VE max is normally much less than the calculated MVV (the calculated MVV should equal or be close . (continued) Respiratory System • Ventilatory response: Determine whether the ventilatory response is normal by looking at VE max. breathing (and/or ventilatory) reserve.12.
There is normally a significant ventilatory (VE) reserve (calculated MVV − VE max). • Tables 9. while PaO2 remains stable normally during exercise. – RR often increases excessively in ventilatory disease. The calculated MVV itself is much reduced compared with the predicted MVV in these patients. which is shown as a shift to the left in VE curve. which is reduced in ventilatory disease. SPO2. Similarly. Figure 9. – VD/VT fails to drop as expected or even increases in patients with a gas-exchange abnormality in response to exercise. however. Figure 9. and the ABG at exercise termination (if measured).EXERCISE TESTING 185 to the predicted MVV in normal subjects). Table 9. • Gas-exchange response: Determine whether the gas-exchange response is normal by looking at VD/VT. In ventilatory disease. – A gas-exchange disorder can result in abnormal increase in PaCO2 and PETCO2 at peak exercise. SPO2 (and SaO2) is unchanged in most normal subjects during exercise but may drop in gas-exchange disturbances. – In patients with a gas-exchange abnormality. P(A–a)O2 may show a slight increase in normal subjects as a result of V /Q mismatching.10.8 show the classic findings in pure cardiac and pulmonary disease in a stepwise approach. . It may behave abnormally with exercise in patients with a significant cardiac disease because of impaired lung perfusion. and low mixed venous O2. – In COPD. while it decreases in normal subjects. O2 diffusion limitation. – The breathing reserve (VE max/calculated MVV) is usually close to 1 in patients with ventilatory disease and is much lower in normal subjects and in patients with a pure cardiac disease. PaO2 is reduced and P(A–a)O2 is increased (>35 mmHg) because of impaired gas exchange and V /Q mismatch. This is not seen normally or in patients with isolated heart disease.7 and 9. Figure 9. VE max approaches or even exceeds the calculated MVV. these variables increase with a ventilatory disease.13a. PETCO2 (and PaCO2).9 summarizes the exercise patterns of other common conditions.162 – Similarly.13b. while they normally decrease. evidence of dynamic hyperinflation in the tidal FV loops indicates a ventilatory limitation to exercise.
The calculated MVV (dashed horizontal line) is much lower than the predicted MVV (not shown in this figure). VO2 curve).) . (b) a patient with ventilatory limitation with a left shift of the curve compared with the predicted (dashed) curve. (a) a normal patient with normal curve (solid curve). along the predicted (dashed) curve. Am J Respir Crit Care Med 2003. VE vs. and there is no ventilatory reserve (With permission from ATS/ACCP Statement on Cardiopulmonary Exercise Testing. Note the significant ventilatory reserve.167:211–277. VCO2 curve (this curve serves the same purpose as VE vs.13. The calculated MVV (dashed horizontal line) here equals the predicted MMV.186 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 9.
SpO2 (and SaO2) at peak VO2 is normal. which is normal. Exercise capacity is reduced: ↓ peak VO2 (<83% predicted). but it could be dyspnea related to left ventricular failure. Ventilatory reserve is normal (>15). ECG may show arrhythmia or ischemia. Tidal FV loops show no evidence of dynamic hyperinflation. (continued) . PaO2 and P(A–a)O2 at the end of exercise are usually normal. The gas-exchange response is normal: Dead space fraction: VD/VT is reduced with exercise (which is normal) or slightly increased because of impaired lung perfusion.3). Pattern in pure cardiac disease such as cardiomyopathy The base-line spirometry and maximal flow volume loop are usually normal.EXERCISE TESTING 187 TABLE 9. The cardiovascular response is abnormal: HR response HR max is usually achieved early (>90% predicted) No HR reserve (<15) HR curve is steep (left shifted) O2 pulse at peak VO2 The value of O2 pulse is decreased (<80% predicted) O2 pulse curve shows an early plateau.1–1. Exercise capacity is reduced: ↓ peak VO2 (< 83% predicted) Maximum WR is usually ↓. RR max is normal (<50). VO2 vs. RER at peak VO2 is normal (1. reduced WR. The reason for exercise termination is usually fatigue because of early AT. Conclusion: reduced exercise capacity with impaired cardiovascular response indicating a cardiac origin of exercise limitation. AT has an early onset (<40% predicted). Breathing reserve is normal or even low because VE max is decreased (the patient stopped prematurely). The reason for exercise termination is usually dyspnea with ↑ Borg scale for dyspnea. Pattern in pure pulmonary disease such as COPD and ILD The base-line spirometry and flow volume loop are generally abnormal. TABLE 9. The calculated MVV usually equals or is close to the predicted MVV. VE curve is normal (along the predicted curve).8. The BP may show abnormal response to exercise (abnormally low). WR curve may show an early plateau. PETCO2 (and PaCO2) decrease at peak exercise. The ventilatory response is normal (understressed): VE max is normal (< predicted MVV).7.
can be >1. Large HR reserve (>15) HR curve is normal (along the predicted curve). including a chest X-ray. Breathing reserve (VE max/MVV) is increased. Illustrative Examples Case 1 A 37-year-old male. (continued) VE max approaching the calculated MVV (mainly with a ventilatory disease). Conclusion: reduced exercise capacity with impaired ventilatory. It may even increase. ECG. AT is normal (>40% predicted) or indeterminate if patient stops before reaching AT because of severe ventilatory limitation. PETCO2 and PaCO2 are increased at peak exercise. VE/VCO2 at AT is increased (>34). presented with shortness of breath.188 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Table 9. VE curve is shifted upward and to the left. In COPD.2 or more (mainly with a gas-exchange disorder). The initial investigations. The BP response is normal. SPO2 (and SaO2) at peak VO2 may be reduced (³5%). RR max is ↑ (typically very high in patients with ILD because of ↓ VT). ECG is usually normal. The cardiovascular response is normal (understressed): HR response HR max is not achieved (<90% predicted).8. Caucasian. O2 pulse curve is normal (along the predicted curve). RER of 1. tidal FV loops may show evidence of dynamic hyperinflation. The gas-exchange response is abnormal (typically in a gas-exchange disorder as ILD): Dead space fraction: VD/VT is ↑ at rest and only drops slightly with exercise. The calculated MVV is much less than the predicted MVV. O2 pulse at peak VO2 The value of O2 pulse is normal (>80% predicted). gas exchange. The ventilatory response is abnormal (typically in a ventilatory disease as COPD): VE max is high (reaching the calculated MVV). RER at peak VO2 may be increased. ABG at peak VO2 may show ↓PaO2 and ↑↑ P(A–a)O2 (>35). or both responses to exercise indicating a pulmonary origin of exercise limitation. No ventilatory reserve (<15). The history and the physical examination were unremarkable. and a detailed .
Ventilatory response is normal. Weight 70 kg. height 184 cm. Exercise test pattern in other common conditions Pulmonary hypertension Exercise capacity is ↓. . The cardiovascular response is abnormal (similar to pure cardiac disease). A CPET was performed to determine the cause of the patient's shortness of breath.EXERCISE TESTING 189 TABLE 9. Gas-exchange response is abnormal: ↑ resting VD/VT with minor drop or even increase with exercise. The cardiovascular response is normal. Obesity Exercise capacity is ↓ in L/min/kg but normal in l/min. The cardiovascular response is borderline – abnormal (HR max is reached earlier than normal and O2 pulse is not profoundly reduced and may course along the predicted curve. Gas-exchange response: normal. Malingering Exercise capacity is ↓ with no obvious reason. Gas-exchange response is normal. lung function study. P(A–a)O2 increases and PaO2 drops with exercise.9. Ventilatory response is normal. Gas-exchange response is normal. Deconditioning Exercise capacity is ↓. except that it does not reach its peak because of early exercise termination). Myopathy Exercise capacity is ↓. The cardiovascular response is abnormal (similar to pure cardiac disease). Ventilatory response is abnormal [similar to pure lung disease but without complete ventilatory limitation based on VE/MVV (it is <1 here)]. Gas-exchange response is normal. – Modified Borg scale: for dyspnea (8). Ventilatory response is normal. • Test details – Instrument: Cycle ergometer – Technique: Incremental – Reason for exercise termination: leg fatigue. AT is reduced. Ventilatory response may be normal (lung parenchyma is normal). for leg discomfort (9) – ECG: normal throughout exercise. WR curve is more upright than normal. The cardiovascular response is normal. The VO2 vs. were normal.
27 Measured % Pred.6 3.20 180/90 % Pred.05 250 181 19.) 4. V E (L/min) VT (liters) RR (cycle/min) Tidal FV loops 150 2.) 4.) • Resting data HR BP SPO2 VD/VT 80 bpm 116/76 mmHg 99% 0. 72 ** The conversion factor used in these cases is 35 (not 40).9 3. Measured PETCO2 (mmHg) VD/VT VE/VO2 at AT VE/VCO2 at AT SPO2 (%) RER 0.52 (pred.18 35 0.14 % Pred.60 (pred.190 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • Spirometry FVC FEV1 FEV1/FVC ratio MVV** 5. 92 61 2.0 1. O2/kg (ml/kg/min) O2 (L/min) WR (Watts) HR (BPM) O2 pulse (ml/beat) AT CO2 (L/min) BP (mmHg) 39.24 • Cardiovascular response at peak exercise Pred.0 3.13 27 25 99 1.19 96 29 normal throughout exercise • Gas-exchange response at peak exercise Pred.30 Measured 38.) 158 (pred.01 254 176 18. †† As a percentage of VO2 max. 96 101 98 102 101 65%†† 97 • Ventilatory response at peak exercise Pred. .30 (measured) 89% 150 (calculated) 86 (% pred.9 3.) 95 (% pred.84 (measured) 4.
The instrument used is a cycle ergometer with an incremental WR. • For the graphic representation of the patient's data. (c) VCO2 vs.14. . • Base-line spirometry was normal. VO2 curves.EXERCISE TESTING 191 FIGURE 9. see Figure 9. VO2 curve.14. Exercise was terminated because of leg discomfort that scored 9/12 in the modified Borg scale. (b) HR and O2 pulse vs. WR curve. VO2 curve. while dyspnea scored 8/12. (d) VE vs. (a) VO2 vs. Interpretation • The test was performed because the resting data could not explain the patient's symptoms.
14b.14a. (d) The breathing reserve was also normal (90/150 = 0.) and its curve is along the predicted one. – Similarly. Figure 9. (c) The ventilatory (VE) reserve was normal (150−90 = 60 which is >15). Figure 9.14b. Figure 9. Figure 9.192 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • The patient achieved a maximal effort as evident by – Achieving predicted VO2 max (101% pred.14a. – Therefore. which is normal). VO2 curve is along the predicted one. – Therefore. scoring 9/12 for leg discomfort in modified Borg scale at peak exercise.14a. – ECG and BP responses were normal.14a. – Tidal FV loops were normal with no evidence of dynamic hyperinflation.14b. see also Figure 9.14a. – Patient's exhaustion. was found to be 1. the predicted maximum WR had been achieved (98% pred. . – VO2 vs. WR curve is along the predicted curve.6). Figure 9. WR curve. (the normal is >90% pred. – Achieving predicted maximum WR (98% pred. Figure 9.). – RR at peak exercise was normal (29). as the peak VO2 approached the predicted VO2 max. – AT as determined from VCO2 vs.). Figure 9. VO2 curve.). Figure 9. respectively). (c) HR curve is along the predicted curve.14c. see also Figure 9. – Achieving predicted maximum HR (102% pred.): (a) The calculated and predicted MVV are almost identical (150 and 158 L. • The exercise capacity was normal as: – Peak VO2 was >83% of the predicted VO2 max. the ventilatory response was normal. the cardiovascular response was normal. Peak VO2 even exceeded the predicted value of VO2 max (101%).).9 L/min (65% of VO2 max). which is normally <70% pred. VO2 curve (V slope) and VE vs. (b) The VE vs.14d. • Cardiovascular response: – The HR response was normal as: (a) HR max was 102% pred.. d. (b) There was no HR reserve (176−181 = −5. This fact can also be shown in VO2 vs. – O2 pulse at peak exercise was normal (101% pred. • Ventilatory response: – VE max was normal (61% pred. which is normal (>40%).).
) 172 (pred. and P(A–a)O2 if ABG is available. • Spirometry FVC FEV1 FEV1/FVC ratio MVV 6. the gas-exchange response was normal. height 190 cm. respectively). The study is normal. Weight 121 kg. .24 (at rest) to 0.39 ‡‡ Comment on the ABG result before and after exercise especially PaO2. • Test details – Instrument: Cycle ergometer – Technique: Incremental – Reason for exercise termination: dyspnea. – PETCO2 at peak exercise was normal.09 (pred.) 45 (% pred.23 (measured) 52% 78 (calculated) 70 (% pred.EXERCISE TESTING 193 • Gas-exchange response: – Dead space fraction at peak exercise was normal: (a) VD/VT dropped from 0. Caucasian. PaCO2.13 (at peak exercise). (b) VE/VCO2 and VE/VO2 at AT were normal (25 and 27. which is normal.14.) 4. • Conclusion (a) There was no evidence of exercise limitation.‡‡ – Therefore.92 (pred. which is a normal response. – SPO2 had remained normal throughout exercise (99%).) 4. A CPET was performed to evaluate the results of this intervention. – RER at peak exercise was 1. a known case of pulmonary hypertension secondary to pulmonary thromboembolism has recently undergone thromboendarterectomy. Case 2 A 31-year-old male. The patient is also known to have significant emphysema secondary to alpha-1-anti-trypsin deficiency. for leg discomfort (9) – ECG: normal throughout exercise.29 (measured) 2. – Modified Borg scale: for dyspnea (9).) • Resting data HR BP SPO2 VD/VT 95 bpm 117/75 mmHg 100% 0.
4 0. . see Figure 9.9 1.3 180/90 % Pred.0 Measured 15.9 132 148 12. 121 90 • Gas-exchange response at peak exercise Pred. VO2/kg (ml/kg/min) VO2 (L/min) WR (Watts) HR (BPM) O2 pulse (ml/beat) AT VCO2 (L/min) BP (mmHg) 43 4. VE (L/min) VT (liters) RR (cycle/min) 78 2.18 Measured % Pred.5 287 181 21.0 47 % Pred.13 36 36 95 1.4 2. §§ As a percentage of VO2 max. PETCO2 (mmHg) VD/VT VE/VO2 at AT VE/VCO2 at AT SPO2 (%) RER 0.2 72 • For the graphic representation of the patient's data.2 Measured 95 2.15. 26. 37 42 46 82 61 29%§§ • Ventilatory response at peak exercise Pred.7 1.194 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • Cardiovascular response at peak exercise Pred.
(c) VCO2 vs. (a) VO2 vs. (b) HR and O2 pulse vs. VO2 curve. (d) VE vs. VO2 curves. WR curve.EXERCISE TESTING 195 a b c d e FIGURE 9. VO2 curve.15. (e) Tidal FV loops during exercise within the maximal FV loop .
cardiovascular response was normal. – ECG and BP responses were normal. Figure 9. • Cardiovascular response: – The HR response was normal although the patient did not achieve his maximum predicted HR as he needed to terminate exercise prematurely because of ventilatory limitation: (a) HR max was 82% pred. The early onset of AT could similarly be related to deconditioning or reduced O2 carrying capacity. – AT was low (1. WR curve is parallel to the predicted curve but VO2 is slightly lower than expected for any given WR. – Achieving a RER of 1. – Therefore. VO2 and VE vs. – VO2 vs. Figure 9. Exercise was terminated because of dyspnea that scored 9/12 in the modified Borg scale. The curve did not reach a plateau. The curve is showing an early plateau.15b. – Because the patient is obese (121 kg).4 or 29% of predicted VO2 max) as determined from VCO2 vs. – Exceeding the calculated MVV. – O2 pulse at peak exercise was low (61% pred. Figure 9.15a. which still indicates a marked reduction in exercise capacity (37%).).2. VO2 curves. These features are also noticed in the VO2 vs. (b) Increased HR reserve (181−148 = 33). it is important to correct VO2 for weight by examining VO2/kg. which is abnormally low (normal >90% pred.15d. WR curve.196 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Interpretation • Incremental CPET using a cycle ergometer was performed to assess the response to endarterectomy. The decreased stroke volume response could be due to deconditioning or reduced O2 carrying capacity. (c) HR curve is along the predicted curve. . Figure 9. and the achieved WR at peak exercise was only 46% of the predicted maximum WR.15b. Figure 9.15a.15c. see Figure 9. • The exercise capacity was moderately–severely reduced as follows: – Peak VO2 was only 42% of the predicted VO2 max.). d. • The patient achieved a maximal effort as evident by – Patient's exhaustion – scoring 9 for dyspnea and leg discomfort in the modified Borg scale.. • Base-line spirometry shows severe obstructive defect indicating that the patient's emphysema is severe. leg discomfort similarly scored 9/12.
underwent a CPET to assess the need for a cardiac transplant. (b) The VE/VO2 curve is shifted to the left indicating an abnormally increased ventilatory response. – No ABG was done. Case 3 A 25-year-old female. – Therefore. Caucasian. which could be attributed to the significant obstructive disorder (COPD). • Gas-exchange response: – Dead space fraction at peak exercise was normal: (a) VD/VT dropped from 0. there was no significant gas-exchange abnormality. Lack of an appropriate increase in HR response to compensate for the decreased stroke volume may indicate that the patient was on a β-blocking agent.EXERCISE TESTING 197 • Ventilatory response: – VE max was abnormally increased (112% pred. Weight 68 kg. which is a normal response. height 171 cm. – Therefore. (b) VE/VCO2(31) and VE/VO2(32) at AT were at the upper limit of normal.): (a) The calculated MVV was much lower than the predicted MVV indicating that the patient had a ventilatory abnormality. • Conclusion – Findings suggest moderate to severe exercise limitation associated with an abnormal ventilatory response. there was an abnormal ventilatory response to exercise. – Tidal FV loops showed dynamic hyperinflation. .39 (at rest) to 0.15e. (c) There was no ventilatory reserve (78−95 = −27. normal >15). which is normal. – PETCO2 at peak exercise was normal. – RER at peak exercise was 1. (d) The breathing reserve was also abnormally high (95/78 = 1. The patient had a normal HR response to exercise but the reduced O2 pulse and AT suggest deconditioning or reduced O2 carrying capacity. There was no significant gas-exchange abnormality as dead space fraction behaved normally with exercise as did the SPO2..2.22). – RR at peak exercise was increased (47). Figure 9. who is known to have an idiopathic cardiomyopathy.15d. Figure 9.13 (at peak exercise). – SPO2 remained normal throughout exercise (99–100%). normal <70% pred.
VO2/kg (ml/kg/min) VO2 (L/min) WR (Watts) HR (BPM) O2 pulse (ml/beat) AT VCO2 (L/min) BP (mmHg) 39 3.) 3.7 137/88 % Pred.9 Measured 21 1. • Spirometry FVC FEV1 FEV1/FVC ratio MVV 119 (pred. – ECG: normal throughout exercise.41 (pred.93 (measured) 86% 103 (Calculated) 80 (% pred.) 4.39 (measured) 2. – Modified Borg scale: for dyspnea (6).) • Resting data HR BP SPO2 VD /VT 94 bpm 123/78 mmHg 96% 0.) 81 (% pred.27 (pred.4 170 182 11.36 • Cardiovascular response at peak exercise Pred. for leg discomfort (9).1 0.) 3. 54 41 57 104 59 21% .74 1.198 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE • Test details – Instrument: Cycle ergometer – Technique: Incremental – Reason for exercise termination: fatigue.4 96 189 7.
16a.9 35 % Pred. • The exercise capacity was moderately to severely reduced as: .5 0.2 72 % Pred. – Achieving a RER of 1. 68 124 Gas-exchange response at peak exercise Pred. VE (L/min) VT (liters) RR (cycle/min) 103 1.2.13 31 36 95 1. Exercise was terminated because of fatigue. scoring 9/12 for both dyspnea and leg discomfort in modified Borg scale at peak exercise. Figure 9. – Achieving predicted maximum HR (102%). Interpretation • An incremental CPET using a cycle ergometer was performed to assess the need for a cardiac transplant. • For the graphic representation of the patient's data. WR curve.EXERCISE TESTING 199 • Ventilatory response at peak exercise Pred. The modified Borg score for dyspnea and leg discomfort was 9/12. • The patient achieved a maximal effort as evident by: – Patient's exhaustion. PETCO2 (mmHg) VD/VT VE/VO2 at AT VE/VCO2 at AT SPO2 (%) RER 0.16b. see Figure 9.18 Measured 31. • Base-line spirometry was normal.16.5 Measured 65 1. – Reaching a plateau in the VO2 vs. see also Figure 9.
WR curve. (b) HR and O2 pulse vs. .200 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE a b c d e FIGURE 9. (d) VE vs. (a) VO2 vs.16. VO2 curve. VO2 curve. VO2 curves. (e) Tidal FV loops during exercise within the maximal FV loop. (c) VCO2 vs.
16d.16a.). • Cardiovascular response: – The HR response was abnormally increased as: (a) The resting HR was increased (94/min).16a. respectively). indicating that exercise was terminated early. (b) Similarly. • Ventilatory response: – VE max was normal (61% pred. Figure 9. Figure 9. – These findings suggest that a cardiac disease is responsible for exercise limitation. with no HR reserve (189 − 182 = −7). The ECG was normal throughout exercise. – The tidal FV loops were way away from the maximal FV loop suggesting significant ventilatory reserve. – AT was achieved prematurely (0. which is high (>15). (b) The VE vs. Figure 9. Figure 9.13 (at peak exercise). (c) HR curve is steep and shifted to the left.) and its curve shows an early plateau. which should normally be <70% pred.63). WR curve. – VO2 vs.36 (at rest) to 0.16b. (c) Ventilatory reserve was 103 − 65 = 48.16a. VO2 curve was along the predicted one with a small shift to the left. Figure 9. WR curve demonstrates an early plateau (i.): (a) The calculated and predicted MVV were within the acceptable range of normal (103 and 119 L.74 L/min. – RR at peak exercise was 35/min.16b. (d) The breathing reserve was also high (65/103 = 0. (b) The maximum predicted HR was achieved prematurely. Figure 9.. An early AT suggests a cardiovascular compromise. the WR achieved was low (57% pred.EXERCISE TESTING 201 (a) Peak VO2 was 41% of the predicted VO2 max. see Figure 9.16c. d. ↓ΔVO2/ΔWR ratio). • Gas-exchange response: – Dead space fraction at peak exercise was normal: (a) VD/VT dropped from 0. – O2 pulse at peak exercise was reduced (59% pred. which is a normal response. . 21% of VO2 max).e. HR max was 104% pred. – BP response to exercise was abnormally low. see also VO2 vs. – The earlier findings suggest that the ventilatory system was understressed and its response to exercise was generally normal.
2). – SPO2 remained normal throughout exercise (95%).35 (measured) 68% 47 (calculated) 48 (% pred.34 . Findings also suggest some degree of gas-exchange abnormality. – RER at peak exercise was normal (1.97 (measured) 1.) 4. • Test details – Instrument: Cycle ergometer – Technique: Incremental – Reason for exercise termination: dyspnea – Modified Borg scale: for dyspnea (10).) 3.202 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE (b) VE/VCO2 and VE/VO2 at AT were elevated (36 and 36. The patient is on 24-h O2 therapy at 5 l/min through nasal prongs.) • Resting data HR BP SPO2 VD/VT 92 bpm 120/78 mmHg 98% (on 45% FIO2) 0. Weight 79 kg. respectively). height 168 cm. Case 4 A 62-year-old male. which may be explained by impaired pulmonary perfusion.10 (pred. • Conclusion – There was moderate to severe exercise limitation associated with an abnormal cardiovascular response.) 41 (% pred. Caucasian. – The slightly impaired gas exchange may suggest impaired lung perfusion secondary to cardiomyopathy. for leg discomfort (5) – ECG: normal throughout exercise • Spirometry FVC FEV1 FEV1/FVC ratio MVV 114 (pred.25 (pred.) 1. with known idiopathic pulmonary fibrosis (IPF) undergoing a CPET as part of lung transplant workup. – PETCO2 at peak exercise was normal.
2 70 114 11.17. • For the graphic representation of the patient's data.7 Indeterminate 1. VO2/kg (ml/kg/min) VO2 (L/min) WR (Watts) HR (BPM) O2 pulse (ml/beat) AT VCO2 (L/min) BP (mmHg) 25. VE (L/min) VT (liters) RR (cycle/min) 47 0.9 2.32 91 1.3 0.18 Measured 44.52 48 % Pred. • Base-line spirometry showed severe restriction with a mild obstructive component.EXERCISE TESTING 203 • Cardiovascular response at peak exercise Pred. see Figure 9.2 151 156 13. 79 74 • Gas-exchange response at peak exercise Pred. Exercise was terminated because of dyspnea.5 Measured 15. .4 177/98 % Pred. The modified Borg score for dyspnea was 10/12 and for leg discomfort was 5/12. 59 54 46 73 87 • Ventilatory response at peak exercise Pred.2 1. PETCO2 (mmHg) VD/VT SPO2 (%) RER 0.29 135 % Pred. Interpretation • An incremental CPET using a cycle ergometer was performed as part of lung transplant workup.68 Measured 37 0.
VO2 curve. . (e) Tidal FV loops during exercise within the maximal FV loop. (c) VCO2 vs.17. VO2 curves. WR curve. VO2 curve. (d) VE vs.a b c d e FIGURE 9. (b) HR and O2 pulse vs. (a) VO2 vs.
see also Figure 9. the cardiovascular response to exercise was normal. This . • Cardiovascular response: – The HR response was normal: (a) Although the resting HR was high (92/min). suggesting a ventilatory disturbance (47 and 114 L.. WR curve was normal. respectively). (b) HR curve is running along the predicted curve. – VE max approaching the calculated MVV (>70% of calculated MVV) – Achieving a RER of >1. (b) The VE vs.). – Similarly.17a.17a. – Therefore. • Ventilatory response: – VE max was high (79% pred.78). which is high. (c) Ventilatory reserve was reduced (47 − 37 = 10.17d. while the breathing reserve was normal (37/47 = 0. • The exercise capacity was moderately reduced as: – Peak VO2 was 54% of the predicted VO2 max.EXERCISE TESTING 205 • The patient achieved a maximal effort as evident by: – Patient's exhaustion. – RR at peak exercise was 48/min.17b. – O2 vs. which should be >15). – O2 pulse response was normal (87% pred. which should normally be <70% pred. Therefore. which may indicate that it had not been achieved as the cardiovascular system had not been stressed enough before exercise termination. scoring 10/12 for dyspnea in the modified Borg scale at peak exercise. see Figure 9. Figure 9. Figure 9.17c. VT at peak exercise was abnormally reduced. the maximum predicted HR had not been achieved at peak exercise (73% pred). Figure 9. Figure 9. VO2 curve is slightly shifted to the left. – The tidal FV loops were approximating the expiratory envelope of the maximal FV loop but did not show dynamic hyperinflation with shift to the left as is expected with emphysema. the WR achieved was reduced (46% pred. – AT could not be determined. d. Figure 9. This strongly supports a noncardiac cause for exercise limitation.) and its curve runs along the predicted one.15.17a.): (a) The calculated MVV was significantly reduced compared with the predicted one.17b. the HR reserve was high (156 − 114 = 42). – BP and ECG responses to exercise were normal.
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4.1007/978-1-84882-231-3_10. Parasomnias are characterized by abnormal behavioral events occurring during sleep such as sleepwalking.. Pulmonary Function Tests in Clinical Practice.2 OSA affects ∼9% of men and ∼4% of women. Parasomnias typically do not cause insomnia or excessive sleepiness. 2. Respiratory Sleep Disorders (Sleep-Disordered Breathing) Represent a group of sleep disorders caused by abnormal breathing patterns during sleep and may result in sleep fragmentation and excessive daytime sleepiness. There are two major respiratory sleep disorders: 1. Dyssomnias are characterized by insomnia and excessive daytime sleepiness (hypersomnolence).1 1. or psychiatric (mental) disorders. Proposed sleep disorders are sleep disorders that so far have no known key features to distinguish them from normal variants or other sleep disorders. 3. Altalag et al. neurologic. © Springer-Verlag London Limited 2009 . Obstructive sleep apnea/hypopnea (OSA or OSAH) • The most prevalent respiratory sleep disorder. The respiratory sleep disorders belong to this group. DOI: 10. Medical-psychiatric sleep disorders are directly caused by medical.3 It is characterized by repeated upper airway obstruction during sleep due to a 217 A.Chapter 10 Diagnostic Tests for Sleep Disorders SLEEP-RELATED DISORDERS The International Classification of Sleep Disorders classifies 84 distinct sleep disorders into four major categories.
repetitive in cycling. 34).5–10 coronary artery disease. The treatment of choice for OSA is continuous positive airway pressure (CPAP) applied through the nose and/or mouth during sleep. cerebrovascular disease. Several risk factors for OSA are identified.11–16 and arrhythmias17–22). Central sleep apnea syndrome (CSA) • Is classified into the following: – CSA with decreased respiratory drive as in sleep alveolar hypoventilation syndrome and neuromuscular disorders. 2.26–29 In addition.30–32 • The gold standard in the diagnosis of OSA is polysomnography (sleep study) but other tests may aid in making this diagnosis. • This chapter will mainly deal with tests used to diagnose OSA. and surgery (especially if there is an obvious cause for airway obstruction such as enlarged tonsils). Tracheostomy to bypass the upper airway is effective but is generally considered a last resort. 23 diabetes mellitus. This form of CSA is more common and is characterized by a hyperpneic phase of breathing (because of abnormally increased respiratory drive) followed by an apneic phase (due to respiratory alkalosis). Excessive sleepiness is a feature that these conditions share with OSA as do all dyssomnias.4 OSA is associated with cardiovascular disease (hypertension. Other modes of therapy include oral appliances. obesity being the most important. arousals are common in CSA but they take place during the hyperpneic phase rather than during the apneic phase.35 Conditions That May Mimic Respiratory Sleep Disorders • Patients with other conditions may present to the respiratory sleep disorders’ clinic and may even be misdiagnosed with OSA. – CSA with periodic breathing pattern as in Cheyne-Stokes respiration (seen mainly with heart failure33. • OSA is a significant cause of morbidity and mortality. weight reduction. as will be discussed later. Excessive sleepiness may be a consequence of the arousals. which add to the morbidity and mortality of untreated OSA.25 and pulmonary vascular disease.12–16.218 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE collapsible upper airway resulting in recurrent arousals and often daytime hypersomnolence. hypoxia of high altitude. These conditions may include . the excessive sleepiness caused by OSA is a potential cause of road traffic collisions and industrial accidents. and in diffuse neurological disorders. As in OSA.24 lipid abnormalities.
TABLE 10.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 219 narcolepsy. Conditions that may mimic respiratory sleep disorders Narcolepsy Incidence: 1/2. neurotransmitters responsible for promotion of wakefulness.g. the upper airway resistant syndrome. secondary to: iron deficiency anemia. equal prevalence in men and women38. The prevalence of moderate–severe form is 2. Treatment: similar to restless leg syndrome (RLS).00036. often frightening hallucinations that occur just as the patient is falling asleep or waking up. Starts at young age.. treated with stimulants.g. pregnancy. Major clinical features Daytime sleepiness: could be so severe that patient may doze off with little warning “sleep attacks. male:female ratio is 1:2. Sleep paralysis: is a complete inability to move for 1–2 min immediately after awakening. venous insufficiency).7%. Most patients with RLS also have PLMD. and anxiety.. worsens over few years and then persists for life. The distinction of these disorders is usually made on clinical grounds but specific testing may be necessary. creeping or crawling sensation in the legs while patient is sitting or lying with an irresistible urge to move the legs. excessive use of sedatives. venlafaxine) Diagnosis: clinical and polysomnography (PSG).39 May coexist with OSA. Diagnosis: clinical and with multiple sleep latency test (MSLT). PLMD is sometimes called nocturnal or sleep-related myoclonus. Periodic limb movement disorder (PLMD) is another condition that should be considered. incidence is unknown and can be caused by medications such as antidepressants (e.1. 37. More common in older age. which is a misnomer. It is usually associated with hypnagogic hallucinations or a feeling of suffocation. Etiology: loss of orexin A and B. connective tissue disease. Table 10. reduced sleep duration.40–71 (continued) . Parkinson’s disease.1. and excessive sleepiness. diabetes mellitus. Periodic limb movement disorder (PLMD) Repetitive leg jerks (mostly dorsiflexion of the feet) usually accompanied by arousals. sleep fragmentation. Restless leg syndrome (RLS) An unpleasant deep.” Hypnagogic hallucinations: are vivid. end-stage renal disease. Cataplexy: is unilateral or bilateral loss of muscle tone triggered usually by some form of excitement and leads to partial or complete collapse. depression. Etiology: Primary (idiopathic) and secondary (e. RLS commonly causes insomnia.
A minimum of 12 variables are acquired. Snoring and excessive daytime sleepiness (due to recurrent arousals) are common features. COPD. When considered.” UARS is commonly seen in women with certain craniofacial abnormalities. PSG is diagnostic but detecting high esophageal pressures prior to arousals using the esophageal balloon catheter system is pathognomonic. lack of adequate sleep POLYSOMNOGRAPHY Introduction • Polysomnography (PSG) is a comprehensive diagnostic procedure that allows simultaneous recording of a number of physiologic variables during sleep.72 Upper airway resistance syndrome (UARS)73. benzodiazepines. excessive alcohol intake.. which include the following: – Central and occipital electroencephalography (EEG) – Right and left electroocculography (EOG) – Chin electromyography (Chin EMG) – Right and left leg EMG – Electrocardiography (ECG) – Airflow – Chest movement and abdominal movement channels – Pulse oximetry (SPO2) . pulmonary fibrosis Psychiatric disorders: panic attacks. Diagnosis may be missed in the PSG unless attention is paid to an unexplained increase in arousal index. depression Neurological disorders: nocturnal seizures Others: Drugs (hypnotics). PSG may be helpful.g. Treatment is continuous positive airway pressure (CPAP) similar to OSA. Miscellaneous conditions GI disorders: gastroesophageal reflux disease (GERD). 74 Is caused by abnormal narrowing of the upper airways that results in increased resistance to airflow during sleep leading to the “respiratory effort related arousals.220 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE TABLE 10.1. swallowing disorders Respiratory disorders: nocturnal asthma. (continued) Diagnosis: clinical. Primary snoring is very common and PSG may be needed to exclude OSA. dopaminergic agents. Primary (habitual or continuous) snoring without sleep apnea Patients are typically asymptomatic and present due to complaints from their bed partners. and opioids (in resistant cases). treat iron deficiency anemia). anxiety. Treatment: correct the cause if any (e.
AROUSALS. and chin EMG are discussed separately in this section. The information in this section was acquired mainly from the standard manual. namely. Scoring converts the data into a meaningful summary that can be readily interpreted. arousals. Sleep stages. EEG Electrodes (Leads) • Six EEG electrodes are placed over the patient’s head. arousals. SLEEP STAGES.* These electrodes are central. The variables used to score sleep stages.75 Electroencephalography Used to record the brain electrical signals. . as will be discussed. and snoring. Each group of these variables is used to evaluate different aspects of the PSG: 1. Respiratory events (apneas or hypopneas) are scored using airflow. which is subclassified into the following: – Light sleep (stages 1 and 2) – Deep sleep (or slow wave sleep) (stages 3 and 4) • Relaxed wakefulness is the stage that immediately precedes sleep and is referred to as stage wake (W). Miscellaneous channels include ECG. and SpO2 channels. and wakefulness are scored using EEG. sleep position. 2. and chin EMG channels. and auricular * The standard EEG recording for detection of seizures requires more electrodes. 4. Periodic limb movements (PLMs) are scored using the leg EMG channel. Sleep is classified into the following: • Rapid eye movement (REM) sleep • Nonrapid eye movement (NREM) sleep. EEG.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 221 • Each of these variables is displayed on channels (computer display) and evaluated in a process called scoring of the PSG. AND WAKEFULNESS To discuss the scoring of these variables. three on each side. 3. which vary according to the sleep stage. EOG. occipital. which is subdivided into the following: – Stage W with eyes open – Stage W with eyes closed An arousal is a brief awakening that should meet certain criteria. and wakefulness. chest and abdominal movements. EOG. it is essential to know the sleep stages.
Optimal sleep staging requires two exploring electrodes (C and O) but a minimum of one central exploring electrode is needed for definition of sleep stages75 (central leads are good in capturing most EEG signals as will be discussed later76. C4 –A1 means the right central electrode is the exploring electrode and is referenced to the left auricular electrode.222 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE electrodes and are abbreviated as C.† amplitude. and O2–A1). Beta waves are not seen during sleep.2a–i. and/or shape. odd numbers (1 or 3) refer to the left side and even numbers (2 or 4) refer to the right side. Figure 10. 77). respectively..2b. † Also referred to as cycles per seconds or cps. • To magnify the amplitude (voltage difference) of the EEG signals. They continue to be seen in stage 1 sleep but with reduced numbers. Each of these letters is followed by a number (1–4) to indicate the side of the electrode.g.78 EEG Waves75 Distinct EEG waves are present and each is differentiated from one another by its frequency in seconds (Hertz or Hz). O1–A2. • The EEG in PSG is recorded only from one side while the leads in the opposite side are kept in place as a backup for cases of malfunction of the recoding side while the patient is asleep. – Alpha waves (8–13 Hz) are seen when the patient is awake and relaxed. the other electrode pairs will be C3–A2. and A. respectively. O.2c. therefore: – O1 and O2 are the left and right occipital electrodes. the exploring (recording) electrodes are usually referenced to the auricular electrodes of the opposite side (e. respectively. The following are the wave patterns in human sleep.2d. – Delta waves (<4 Hz) are seen in sleep stages 3 and 4. • The placement of the EEG leads is explained in Figure 10.1. – A1 and A2 are the left and right auricular electrodes.2a. respectively. – Theta waves (4–7 Hz) are mainly seen in sleep stages 1 and 2. . – C3 and C4 are the left and right central electrodes. Figure 10. Figure 10. see Figure 10. Figure 10. • Standard wave patterns: – Beta waves (>13 Hz) are seen when the patient is awake and alert or excited.
Schematic of the 10–20 EEG electrode placement system.5-s duration with an initial upward (negative) deflection ‡ Slow waves in older patients may not meet the voltage criteria but are still considered.1. Figure 10. Figure 10. 20% from the midline. The auricular leads are placed over the mastoid processes. Landmarks are the nasion (the bridge of the nose). inion (the prominence of the occiput).5 s.5–1. The occipital leads are placed over an imaginary circle as shown. They are seen in sleep stages 3 and 4. and the right and left preauricular points.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 223 FIGURE 10. – K complexes (Ks) are high-altitude. 10% from the midline. • Other EEG patterns: – Slow waves (<2 Hz) represent a slow form of delta waves with high amplitudes (voltage criteria for slow waves: trough to peak is ≥75 μV).‡ – Sleep spindles are oscillations of 12–14 Hz with duration of 0.2e. .2f.79 They are seen in stage 2 sleep but may persist into stage 3 and 4. biphasic waves of >0. The lines between nasion and inion and between the preauricular points are divided into 10 and 20% segments as shown. The central leads are placed over the preauricular line.
They are of theta frequency & may be notched.75. a concept that sometimes is referred to as “negative up” rule. h) Vertex sharp wave. § A positive voltage in EEG means a downward deflection and vice versa. It is clearly distinguishable from background EEG. A cardinal feature of K complexes is that they are clearly distinguishable from background EEG activity. f) Sleep Spindle (12-14 Hz. c) Theta waves (4-7 Hz) Sleep stages 1 & 2.2g. e) Slow waves (<2 Hz) Sleep stages 3 & 4. followed by a downward (positive) deflection§.2.¶.224 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE a) Beta waves (>13 Hz): Patient is awake & alert.5 sec). Wave Patterns in EEG. ¶ Slow waves may be thought of as a series of two or more K complexes. d) Delta waves (<4 Hz) Sleep stages 3 & 4. FIGURE 10. Sleep stage 2. b) Alpha waves Stages W & 1. g) K complex (high amplitude biphasic wave. Sleep spindles may be superimposed on K complexes. Seen near transition from stage 1 to stage 2 sleep. i) Saw tooth waves Seen in stage REM. Mainly stage 2 sleep.5-1. 0.5 sec duration). These waves are best captured by the occipital leads. duration 0. Figure 10. Notice the 1 second & 75 microvolt marks. Ks are seen in stage 2 sleep (may be seen in stages 3 and 4 but are then indistinguishable from background EEG75).80 .
Figure 10. – Saw-tooth waves are waves of theta frequency and may be notched. Because the eye has a potential difference (cornea is positive with respect to the retina).82 . then measuring this potential (polarity) difference makes it possible to record eye movements using ocular electrodes. This phenomenon is used to differentiate true eye movements from artifacts.. This will result in a downward (positive) deflection at ROC and an upward (negative) deflection at LOC.3a.e. This is why the central leads are essential for PSG recording. ** Some laboratories reference the ocular leads to the auricular leads in the same side.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 225 – Vertex sharp waves are narrow. ROC-A2 and LOC A2.3a. For example.. and spindles) are best recorded by the central leads. The same thing will happen if the eyes move upward.82 Right and left ocular electrodes are placed at the right outer canthus (ROC) and left outer canthus (LOC). The opposite thing should happen if the eyes move to the left or downward. Figure 10.81 • Alpha waves are best recorded by the occipital leads while the rest of EEG waves (including slow waves.75 Keeping the eyeball polarity in mind. respectively. in order to record vertical eye movements. i. • Remember that ROC and LOC deflections are out of phase when the eyes move.2i. These electrodes are placed at the right outer canthus (ROC) and the left outer canthus (LOC). Figure 10. with the right electrode placed slightly above and the left slightly below the eye level.**. ROC-A2 and LOC-A1 or to one auricular lead. which are essential to define stage REM sleep. high-amplitude negative (upward) waves seen in stage 1 and near transition from stage 1 to stage 2 sleep. to amplify the signals acquired from ROC and LOC.3d. Ks.e. They are seen in stage REM sleep but are not essential for REM definition.76. ocular leads may capture high-voltage EEG signals such as K complexes or slow waves but the deflections recorded at ROC and LOC will be in-phase (same direction) and should not be mistaken for an eye movement. 77 Electroocculography • Is used to record the eye movements. Figure 10. moving the eyes to the right will bring the cornea (relatively positive) of the right eye closer to the right ocular lead and the retina (relatively negative) of the left eye closer to the left ocular lead. • As in EEG. Figure 10. i. as the right ocular lead is at a higher level than the left one. which means that the deflections are out of phase (opposite direction).2h. the ocular leads are usually referenced to the opposite auricular leads and abbreviated as ROC-A1 and LOC-A2.
3a. chin EMG is usually low. 3. sharp waves with a usually flat baseline between movements. Figure 10.Seen in stage W with eyes closed especially before falling asleep. but still higher than that of REM sleep. The different eye movements. out of phase. but similar waves can be seen in stage W with the eyes open representing the normal eye movements. Eye blinks show usually as downward deflections at ROC only. the chin EMG becomes minimal during REM (equal to or lower than the lowest EMG amplitude in NREM sleep). Seen also in stage 1. Seen in REM sleep.3c. Typically. FIGURE 10. . in this case a K complex. Chin Electromyography • The main implication for chin EMG is to help in identifying REM sleep. REMs are seen typically in stage REM sleep.226 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE a)REM:Episodic sharp waves. c) Slow Rolling Eye Movements (SEMs): Slow undulations of the baseline. • Two distinct eye movements can be recorded through the ocular leads: – REMs are episodic. Convergence of the waves indicate eye movement to the right or upwards & vice versa. and 4. These movements are seen in stage W with eyes closed and in stage 1 and disappear in stages 2.3.75 Three EMG leads are placed at the mental and submental areas and the voltage between two of them is measured. the chin EMG activity drops with onset of REM sleep. Figure 10.3b.Seen in stage W with the eyes open. Figure 10. Chin EMG is highest during wakefulness. During deep sleep. b)Eye Blinks: result in downward deflection of ROC while LOC remains flat. The third lead is reserved for cases of malfunction of any other lead. d)Artifact: results from a high amplitude EEG signal. – Slow rolling eye movements (SEMs) appear as a smooth undulation of the tracing (baseline). • Because the body muscles normally relax during REM sleep.
• Remember that the wave frequency reflects the brain activity.‡‡ • In scoring sleep and wakefulness. Longitudinally.5-cm deflection.4b. ‡‡ In paper recording. see Figure 10.2a. Figure 10. Therefore. EOG may show REMs and blinks. Figure 10. and change the page or tracing format. the frequency is highest when the patient is awake but slows down as the patient gets to sleep and slows down further as he/she goes into deep sleep. PSG used to be recorded on paper with a standard paper speed of 10 mm/s. patient drowsy): – EEG here consists of low voltage. two faint horizontal lines are drawn at the EEG tracing where the distance between them is equivalent to 75 μV. Each epoch is divided horizontally into 1-s segments by means of vertical dashed lines to help in distinguishing EEG waves. EOG shows slow rolling eye movements and chin EMG is increased.‡ Currently. This makes 75-μV equivalent to 1. high-frequency waves with attenuated alpha activity. each epoch is scored independently and then the scoring of all epochs is added together and presented in the final report. and chin EMG activity is typically increased. ‡ Paper speed in recording EEG for detection of seizures is slower (15–30 mm/s). • Each 30 s of PSG recording (fit on one screen) represent a distinct time segment termed an epoch. • Stage W (eyes closed. because voltage criteria are required to define slow waves. a 50-μV stimulus results in a 1-cm longitudinal deflection. computers have made PSG recording and scoring easier with the ability to compress or decompress tracings. Scoring Sleep Based on EEG. scoring should be according to the predominant stage. and Arousal Before discussing the scoring technique. enlarge or contract scale. Wakefulness. EOG. Because an epoch may show more than one stage of sleep.4a. high-frequency waves with >50% alpha waves/epoch (alpha waves are not attenuated here). . it is important to discuss some concepts of PSG recording and scoring: Concepts of EEG Recording and Scoring • Before the era of computerized PSG recording.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 227 Scoring Sleep Stages. and Chin EMG75 • Stage W (eyes open. Slow waves have to cross these two lines to meet the voltage criteria. patient relaxed): – EEG in this stage shows low voltage.
• EOG: No eye movements. high frequency. high frequency. Figure 10. mixed frequency. e) Stage 3: • EEG: 20-50% slow wave activity. d) Stage 2: • EEG: Low voltage. • EOG: SEMs. Saw tooth waves may be seen. • Chin EMG: increased. • EOG: No eye movements. • Chin EMG: Usually low. g) Stage REM: • EEG: Low voltage. May see sharp waves near transition to stage 2. at least one spindle or K. • EOG: May see SEMs. <50% alpha activity. stage 1 does not have sleep spindles or K complexes. • EOG: Episodic REMs. blinks may be seen. FIGURE 10. mixed frequency. alpha wave activity >50%. • Chin EMG:Usually low. no spindles or Ks. EOG continues to show slow rolling eye movement with increased chin EMG activity. attenuated alpha activity. • Stage 1 sleep: – EEG shows low voltage. high frequency. • Chin EMG: Minimal. • Chin EMG: May be increased. mixed frequency waves (alpha and theta) with <50% alpha waves/epoch.4c. Sharp waves may be present near transition to stage 2. <20% slow waves. . • EOG: Flat. b) Stage W (eyes closed): • EEG: Low voltage. f) Stage 4: • EEG: >50% slow wave activity. Typically.4. • Chin EMG: May be increased. Sleep stages. • Chin EMG: increased. • EOG: REMs.228 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE a) Stage W (eyes open): • EEG: Low voltage. c) Stage 1: • EEG: Low voltage.
b. Figure 10. Figure 10. containing spindles or Ks) is less than 3 min and the intervening sleep would otherwise meet criteria for stage 1 (<50% alpha activity) with no evidence of intervening arousal. EOG shows no eye movements and chin EMG activity usually slows down during this stage.4d. • Stage 4 sleep: – EEG should show >50% slow wave activity/epoch. If that period is ≥3 min.§§ • Stage REM sleep: – Is identified mainly by the presence of REMs in EOG and minimal activity in chin EMG.. then this period of sleep is scored as stage 1. Additional Rules for Scoring Sleep • Because sleep spindles and K complexes (in stage 2) and eye movements (in stage REM) are episodic (i.e. EEG shows low voltage.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 229 • Stage 2 sleep: – EEG here is similar to stage 1 (low voltage. additional staging rules were introduced concerning these two sleep stages:75 – The 3-min rule for stage 2: (a) If no arousal is present: If a period of time between two epochs of unequivocal stage 2 (i. EOG shows no eye movements and chin EMG activity is usually low.4f. respectively).e. The presence of saw-tooth waves supports the definition of REM sleep but their absence does not exclude REM.. EOG should record no eye movements and chin EMG activity is still increased. • Stage 3 sleep: – EEG should show 20–50% slow wave activity/epoch. delta sleep.83 . mixed frequency) but it must show at least one sleep spindle or K complex with <20% slow wave activity/epoch. are not necessarily seen in every epoch of stage 2 or stage REM. Figure 10. mixed frequency waves with no spindles or Ks (as in stage 1) and may show saw-tooth waves.4g. (b) If arousal is present: If there is an arousal within the intervening sleep (<3 min). then the epochs following the arousal are scored according to their nature while the §§ The distinction between sleep stages 3 and 4 is not essential in interpreting PSG and some laboratories score stages 3 and 4 as deep sleep. Figure 10.5a. or slow wave sleep. then this period of sleep is scored as stage 2.4e. Figure 10.
epochs before the arousal will still be scored as stage 2. The 3-min rule for stage 2. then that section is scored as stage REM.¶¶ (b) If arousal is present. (c) In stage REM sleep. If the arousal is prolonged and/ or slow rolling eye movements or sharp waves are present following arousal.5. ( c ) Two Ks separated by <3 min but with an arousal. then that section is scored as stage 1. Scoring Arousals • An arousal in NREM sleep is defined as a brief awakening characterized by abrupt shift in EEG frequency. – The REM rule: (a) If no arousal is present: If any section of the record is contiguous with an unequivocal stage REM and has a chin EMG and EEG consistent with stage REM. . so epochs between the two Ks are staged as stage 1.5c. scorer scrolls backward and restudy the previous segment of sleep and rescore it according to this rule. epochs between the two Ks are staged as stage 2. epochs that exhibit REMs are sometimes referred to as phasic REM while those that do not exhibit REMs are referred to as tonic REM. epochs following arousal are staged according to their nature. Figure 10. which may include ¶¶ Once a REM sleep is identified. then the distinction is between stage 1 and REM: If the arousal is very brief and/or saw-tooth waves are present following the arousal. (a) Two Ks separated by <3 min without arousal. then that section should be scored as stage REM regardless of whether eye movements are present. in this case stage 1. (b) Two Ks separated by >3 min.230 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE a b c FIGURE 10.
Figure 10. FIGURE 10. Different techniques are used to measure airflow: – Temperature-sensitive devices are placed close to the nose and mouth to sense the change in temperature of the exhaled air.85 . Arousals. . • The number of arousals per hour of sleep is termed the arousal index.85.6b.6. Airflow • Is measured during PSG in order to detect apneas and hypopneas. An awakening. which is translated into a flow signal in the PSG record. Figure 10.86 • To be scored as an arousal. b)Arousal (REM): A burst of alpha waves has to be associated with increased chin EMG activity to be scored as an arousal in REM sleep. 84 • In REM sleep.6a. oximetric recording. alpha waves. is a complete change from any stage of sleep to wakefulness (at least an epoch of stage W). 87 RESPIRATORY EVENTS Respiratory events including apnea and hypopnea are scored using airflow.182 An elevated arousal index is associated with daytime sleepiness. such frequency change should be preceded by at least ten continuous seconds of any stage of sleep. however. theta waves. This is because bursts of alpha activity are seen normally in REM sleep. and/or frequencies >16 Hz (usually bursts of alpha waves). The sleep stage following an awakening can be different from that prior to the awakening. which is mostly the same sleep stage prior to arousal. abdominal and chest movements.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 231 a)Arousal (NREM): A burst of alpha activity of more than 3 seconds duration following stage 1 sleep (>10 seocnds). This method is a qualitative method that cannot accurately Another definition of a brief arousal is that of ≥ 2-s duration with no alteration of sleep stage. which is normally ≤20/h and increases with age. there must be a concurrent increase in chin EMG activity in addition. Usually there is a rapid return to a pattern consistent with sleep after an arousal. lasting 3 s or longer.
7b. chest and abdominal movement are adjusted in such a way that an upward deflection indicates inspiration and a downward deflection indicates expiration. therefore. Changes in the inductance (inductance plethysmography) of these coils due to chest and abdominal expansion during inspiration are recorded as deflections in the PSG traces. Nasal pressure can be measured by a pressure transducer connected to a nasal cannula. V-sum. Exhaled CO2 measurement by continuously sampling the exhaled air (rich in CO2) through a nasal/oral cannula connected to a CO2 analyzer. Pneumotachography is an accurate method of measuring airflow but is less comfortable as a mask covering the nose and mouth is needed to measure the pressure difference created by airflow. It is semiquantitative and is sometimes called effort sum. which makes it the most popular method. This method is convenient and is semiquantitative.232 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE – – – – detect the amount of flow and.88.90 Chest and Abdominal Movements • Are measured using bands with coils applied around the chest and abdomen. Nadir saturation is delayed by 6–8 s due to . Small expiratory puffs (again rich in CO2) that may take place during inspiratory apneas may be misinterpreted as airflow by the CO2 analyzer. which limits the use of this method. V-sum signal is derived from chest and abdominal movement. A computerized summation of the chest and abdominal movement signals is reported as V-sum. Two types of such devices are available: (a) Thermistor: change in temperature results in change in resistance of transducer. A time delay is expected for the transfer and analysis of the sampled air. which is considered a semiquantitative measurement of tidal volume (airflow). Pulse Oximetry • Is used to measure O2 saturation (SPO2) during sleep using a finger or ear probe. but are not usually. It may also falsely record airflow during apneic episodes if the transducer touches the body. Figure 10. 89 (b) Thermocouple: change in temperature results in change in voltage of transducer. • Tracings corresponding to airflow. makes detection of hypopnea problematic. calibrated for volume displacement. see next session. These can be.
e)Central Hypopnea: Decreased airflow is noted with decreased chest & abdominal movements. – Mixed apnea is when no chest or abdominal movements are detected initially followed by paradoxical movements of the chest and abdomen. b)Central Apnea: No airflow is noted & no chest or abdominal movements. Apnea is divided into the following: – Obstructive apnea is when chest and abdomen move paradoxically (out of phase tracing. Figure 10.7c. A desaturation is defined as a drop of SPO2 by 4% from the baseline. .7a). circulatory and instrumental delay.7. c)Mixed apnea: starts with central apnea followed by an obstructive apnea with paradoxical chest & abdominal movements. FIGURE 10. Figure 10. Scoring Respiratory Events (Apnea and Hyponea) • Apnea is defined arbitrarily as absence of airflow (or flattening of V-sum tracing) at the nose and mouth for 10 s or more. d)Obstructive hypopnea: Decreased airflow is noted with paradoxical chest & abdominal movements which are also decreased.7b. Figure 10. f)Respiratory effort related arousal:arousal is preceded by morphologic & size changes of airflow waves.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 233 a)Obstructive Apnea: No airflow is noted with paradoxical chest & abdominal movements. – Central apnea is when no chest or abdominal movements are detected. Respiratory events.
– Obstructive hypopnea is when chest and abdomen move paradoxically. 74. It may also take place before sleep onset resulting in sleep onset insomnia as in restless leg syndrome (RLS). 90. unexplained arousals. By consensus. It is sometimes called the respiratory disturbance index. The arousals (in the form of bursts of alpha waves) usually last for 3–14 s in UARS. otherwise.7e. RERA is characterized by change in shape and progressive increase in size (width) of the airflow inspiratory waves prior to the. • Apnea hypopnea index (AHI) is the average number of apnea and hypopnea per hour of sleep. – Central hypopnea is when chest and abdominal movements continue to be in-phase but with a lower amplitude.7f . PLMs are scored using leg EMG electrodes. SCORING PERIODIC LIMB MOVEMENTS OF SLEEP PLMs may be a cause for sleep fragmentation and daytime sleepiness (periodic limb movement disorder or PLMD). Apnea index (AI) and hypopnea index (HI) are similarly defined. Figure 10. 181 or ⅔91 from baseline for 10 s or more. Hypopneas can be obstructive or central. Figure 10. AHI is used to define the severity of sleep apnea (obstructive and central) as follows: – <5/h is normal and – 5–15/h is mild – 15–30/h is moderate and – >30/h is severe. Progressive inversed negative swings in esophageal pressure (using esophageal balloon system during PSG) prior to arousal are considered diagnostic but are not generally employed clinically. • Respiratory effort-related arousal (RERA) 73. . • Apnea and hypopnea are usually followed by an arousal that helps in their identification. Figure 10.7d. These changes are typically not associated with a decrease in S PO 2.234 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE – Hypopnea is defined as a reduction in airflow (or V-sum) by a ½ 89. 93 is seen in the upper airway resistance syndrome (UARS) and is not associated with apnea or hypopnea (UARS has a normal AHI of <5). Hypopneas are more difficult to detect and some experts mandate the presence of arterial desaturation (a drop SPO2 by 4%)92 together with the reduction in airflow to define hypopnea.
*** A leg movement will be recorded as a sudden increase in the leg electromyography (leg EMG) activity. Figure 10. On the other hand. a sequence of four or more leg movements should be present and each leg movement should be separated from the adjacent leg movements by 5–90s. A PLM arousal. simultaneous bilateral leg movements are counted as one. A PLM-I of <5 is considered normal. *** Some labs use a separate channel for each leg EMG tracing. FIGURE 10. and >50 is severe.180 The duration of each leg movement should be 0. In this case 5 seconds.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 235 Leg Electromyography • Right and left EMG leads are placed over the right and left tibialis anterior muscles and the signals acquired are fed to a single recording channel. follow the arousals and should not be counted as PLMs. 25–50 is moderate. Severe insomnia and/or excessive daytime sleepiness have been associated with a PLM-AI of >25/h. ††† Leg movements may be used to help identifying arousals. .5-5 seconds. in this case. arousals may trigger leg movements. a) A PLM with an arousal: The duration is 0. These arousals can result in sleep fragmentation and excessive daytime hypersomnolence associated with PLMD.8.5–5 s. which can be seen in EEG as a burst of alpha waves. which. In this case. snoring.178 • In PLMD. The number of PLMs per hour of sleep is the PLM index (PLM-I). PLMs usually take place in NREM sleep. This index is better in defining PLMD than PLM-I as it takes into consideration the arousals caused by PLMs. together with the other parameters.8a. leg movements may result in arousals.††† PLM arousal index (PLM-AI) refers to PLMs accompanied by arousal per hour of sleep. 5–25 is mild. b) Apnea with snoring channel: Notice that the snoring ceases during an apneic episode. For leg movements to be part of PLM of sleep.
Respiratory events related to OSA preferentially take place while in the supine position. – Checking eye movements and blinking: by asking the patient to keep the head still and look to the left. The most important arrhythmias encountered include bradycardias and ventricular asystole lasting longer than 10 s. CONCEPTS OF PSG INTERPRETATION Biocalibration • Is an essential procedure that should be performed prior to any sleep study (PSG). up. and down and then to blink.94–98 nonsustained SVT and VT. see Figure 10. atrial fibrillation. Snoring • A microphone may be used to record the snoring as a separate channel.99. Visual and Auditory Monitoring • Visual monitoring is done through a low-light video camera to monitor sleep position (as discussed) and to check for parasomnias.9a. Its role is to ensure appropriate technical function of the components of the polysomnograph in response to different biological stimuli. This may help to identify sleep onset (when the patient starts snoring at the beginning of the study) and the apneic episodes (snoring tracing disappears when there is no airflow). – Checking EEG: first with the eyes closed looking for alpha activity (and slow rolling eye movements in the EOG chan- .236 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE MISCELLANEOUS PSG CHANNELS Electrocardiography • Is used to detect arrhythmias during sleep especially during periods of obstructive apneas/hypopneas. Figure 10. Sleep Position • Is determined manually (using a video monitor) or using posture detecting devices. 100 and sinus arrhythmias. right.8b. which can be easily synchronized with the PSG. Auditory monitoring is required to provide assistance to the patient if needed.
to the left then blinks. chest and abdominal movements: by asking the patient to inhale and exhale and observing an appropriate deflection of all three channels that should be adjusted so that they have the same polarity with an upward deflection during inhalation. chest & abdominal movements: inhalation results in upward deflection in all 3 leads. e) Checking airflow. g) Checking leg EMG: wiggling the toes results in increased activity in this channel. – Checking airflow.9b and then with the eyes open looking for attenuation of alpha activity. nels) – Figure 10. Figure 10.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 237 a)Checking eye movements & blinks: Patient looks to the right (waves converge). ‡‡‡ . chest & abdominal mvts with breath holding: resulting in flat lines. as discussed earlier.9c. f) Checking airflow. Biocalibration. FIGURE 10. Figure 10. c) Checking EEG with the eyes open:Alpha activity becomes attenuated with REMs.‡‡‡ – Checking chin EMG: by asking the patient to grit the teeth and observing an appropriate increase in the chin EMG activity.9. The patient is then asked to take a deep breath and then hold to simulate apnea Patients who naturally have no or low alpha activity can be identified during biocalibration.9d. d) Checking Chin EMG: Gritting the teeth causes increased activity. b) Checking EEG with the eyes closed:Alpha activity with slow rolling eye movements. which helps anticipating the type of stage 1 sleep in them.
which results in recording a slow undulation of the baseline activity. which may conduct the ECG signals.238 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE that should be translated as flat lines on these three channels. Figure 10. the undulated baseline may be mistaken for slow §§§ The patient may be asked to breathe through the mouth. Figure 10. Sweat Artifact • Is caused by sweat getting in contact with a recording electrode altering its potential.10a. f . . as positive and negative ECG signals going to each auricular electrode will cancel each other out. ¶¶¶ If sweat artifact is synchronous (in-phase) with respiration. Switching to another electrode may be necessary.9e. Sixty-Cycle Artifact • Occurs when a recording electrode is disconnected or has high impedance. PSG Artifacts ECG Artifact • Is a very common and easily recognized artifact. Figure 10. it is called respiratory artifact. Figure 10. as chin EMG and EOG.10b. This artifact is minimized by placing the reference auricular electrode directly over the bone (mastoid process) and avoiding the neck soft tissue.§§§ – Checking leg movements: by asking the patient to wiggle the right and left toes resulting in appropriately increased leg EMG.¶¶¶ If EEG electrodes are affected. which results in recording a 60-Hz AC electrical activity from the power lines instead. which should show movement of chest and abdominal tracing but not the airflow tracing. Another way of overcoming this artifact is by referencing the exploring EEG electrode to both auricular electrodes. It can be minimized by proper placement of electrodes and by using certain filters in the AC amplifiers.9g. This artifact affects mainly the EEG and EOG leads. commonly seen in EEG tracings but can be seen in the other tracings too. It is made of periodic deflections corresponding to the QRS complexes and resembles them in shape.
FIGURE 10. high frequency signal (60 Hz) of the EEG tracing.10d.10.10c. . d) Electrode popping artifact: High-amplitude signals corresponding to body movements during respiration. This artifact may be minimized by lowering room temperature. This artifact is also called respiratory artifact because it is synchronous with respiration. uncovering the patient or using a fan especially in obese patients. Figure 10. It is corrected by switching to an alternative electrode. PSG Artifacts. b) 60 cycle artifact: Notice the symmetrical. ROC and LOC tracing. e) Unilateral artificial eye: REMs are seen in the right eye but not in the left(The left eye is an artificial eye). Figure 10. delta waves resulting in overestimation of sleep stages 3 and 4. Electrode Popping Artifact • Is caused by complete loss of signals from one electrode (as complete detachment from the skin or complete dryness of the conducting gel) resulting in high-amplitude signals corresponding to body movement during respiration. This artifact may be generalized (if patient is sweating heavily) or confined to the side that the patient is lying on. The electrode responsible in this case is A1.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 239 a) ECG artifact: QRS complexes can be seen clearly in the chin EMG. The offending electrode can be easily identified by looking for a common lead in the affected channels. c) Sweat artifact: Undulation of the baseline of most of the tracings.
Consider UARS if arousals are not explained on the bases of respiratory events and PLMs. Figure 10.240 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Unilateral Artificial Eye • Results in unilateral deflection of EOG during stage REM sleep leading. and AHI can then be determined. scoring different channels. Lights-out is the point in time at which lights are turned off to allow the patient to sleep. A computerized scoring program100–108 is currently available but does not replace manual scoring. The sleep architecture and the arousal index can then be determined. • Fourth round is for studying the ECG for arrhythmias especially during a respiratory event. the scorer should differentiate central from obstructive events and identify events associated with arousals. lights-on is when the patient is awakened in the morning. and wakefulness: by studying the EEG. • Second round is for scoring respiratory events: by studying airflow. SPO2. During this round. as the final report and ultimately the final diagnosis are largely based on the various scores. HI. The scorer should identify movements that meet the criteria for PLMs and identify those associated with arousals.10e. SLEEP ARCHITECTURE Definitions • Time in bed (TIB) is the monitoring period (from lights-out to lights-on). arousals. and snoring. This confusion can be avoided by a proper history taking and a proper biocalibration. Apneas and hypopneas become easily identified if tracings are compressed so that the computer screen accommodates three epochs at a time (90 s). . Different approaches for scoring may be followed by which the scorer goes through the study several rounds. to underestimation of REM sleep. APPROACH TO PSG SCORING Scoring PSG is the most important part of PSG interpretation. EOG. PLM-I and PLM-AI can then be determined. • Third round is for scoring leg movements: by studying the leg EMG. V-sum. AI. The following is a suggested approach: • First round is for scoring sleep stages. chest and abdominal movements. if unnoticed. and chin EMG.
Figure 10. summarizing the normal sleep architecture in a young adult. • Sleep efficiency (SE) is TST/TIB ratio represented as a percentage. • Sleep onset latency (SOL or sleep latency) is the number of minutes from lights-out to the first epoch of sleep.11. It is typically reduced in patients with narcolepsy. • Wake after sleep onset (WASO) is the minutes of wakefulness after initial sleep onset and before the final awakening.. sleep fragmentation) and results in daytime hypersomnolence (e. Increased WASO indicates poor sleep efficiency (i.g. . 109 • Total sleep time (TST) is the total minutes of sleep (stages 1–4 and REM). • REM latency is the number of minutes from sleep onset (not from lights-out) to the first epoch of REM sleep. • Sleep architecture is the division of TST among the different sleep stages where sleep stages are represented as percentages of TST (or SPT). circadian rhythm disorder. 111 but can be reduced also in OSA. endogenous depression.110.e.11. FIGURE 10.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 241 • Movement time refers to epochs in which sleep stage is indeterminate due to movement artifacts. A histogram.112 and withdrawal from REM-suppressing drugs. • REM density is the average number of eye movements (REMs) per unit time.83.. Prolonged sleep latency (sleep-onset insomnia) may be seen in patients with depression. • Sleep period time (SPT) is TST + WASO [also called total sleep period (TSP)]. • Hypnogram or histogram109 is a graphic representation of sleep architecture. sleep-maintenance insomnia).
see Table 10. On the other hand. see Table 10. elder.11. The REM density also increases as sleep progresses. Age has little influence on REM sleep. Sleep architecture in the young.178 Normally. Figure 10.2. The NREM sleep predominates the first-half of the night while REM sleep predominates the second. and gets shorter as sleep progresses. Figure 10.2. which takes place just before the final awakening.113 • Because of this composition.11. – Skeletal muscle hypotonia: develops during REM sleep to prevent the acting out of dreams. have little stage 3 sleep and their deep sleep is mainly of stage 4. Patients with REM behavior disorder have abnormalities of this protective mechanism and they may have violent behavior.242 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Normal Sleep Architecture • The proportions of sleep stages vary with age and sex. and OSA Normal sleep (% SPT) Age 20 Wake Stage Stage Stage Stage 1 2 3 and 4 REM 1 5 45 21 28 Age 60 8 10 57 2 23 OSA (% SPT) 10 25 55 0 10 . Young people. • During REM sleep. • The first cycle of deep sleep starts quickly after sleep onset and is the longest. sleep stage 2 is the longest in all age groups and in both sexes representing up to 50% of SPT. TABLE 10. several unique physiologic changes take place in the body: – Most dreams (including nightmares) take place during REM sleep. parasomnias of deep sleep (such as somnambulism) usually occur during the early hours of sleep while parasomnias of REM sleep (nightmares) are more common in the early morning hours.2. REM sleep occurs every 90–120 min with the first cycle being the shortest and starts late (REM latency of 70–120 min) and the last cycle is the longest. however. Sleep stages 1 and 2 and WASO normally increase with age while deep sleep (stages 3 and 4) decreases with age and becomes predominantly composed of stage 3 sleep. • The human sleep is normally composed of 3–5 cycles of NREM sleep interrupted by 3–5 cycles of REM sleep.
number of central.118 Final PSG Report Components of the Final Report • The final report summarizes the findings of PSG after scoring and can be presented in both numerical and graphic forms. and AHI. and mixed events. that is when phasic REM is most pronounced. number of REM periods. – SPO2 summary: showing the different levels of SPO2 during stage W. and REM sleep.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 243 – Hypotonia of upper airway muscles: results in upper airway obstruction during REM in vulnerable patients leading to OSA.**** Additionally. 116 Patients with underlying lung disorders experience the most severe O2 desaturation during the early morning hours. This form includes a hypnogram **** Diaphragm becomes the only active inspiratory muscle during phasic REM. – Nocturnal penile tumescence takes place during REM sleep. A sleep stage summary is presented in the form of WASO and the different sleep stages which are expressed as percentages of TST or SPT.114 – Ventilatory irregularity: takes place during the phasic REM sleep (REM with eye movements) and results in a reduction in tidal volume (VT).115. – Apnea and hypopnea analyses that present AI. SOL. there is reduced ventilatory response to hypoxemia and hyprecapnia during REM sleep. HI. This is why obstructive apneas take place preferentially during REM. SE. and REM latency. NREM. All of the ventilatory muscles except the diaphragm become inactive in REM and hence the hypoventilation and arterial oxygen desaturation. – PLM summary: including PLM index and PLM-AI. • The graphic form is usually composed of five sections with the time represented on the X-axis. number of events associated with arousals and number of events in relation to position (supine and nonsupine). obstructive. number of events during REM and NREM sleep. The numerical form contains the following: – Sleep architecture: includes TSP.117 – Thermoregulatory mechanisms are almost totally shut down during REM sleep. . SPT.
SPO2 tracing. Figure 10. The presence of a hypnogram allows identifying events in relation to sleep stages.†††† – Examine the respiratory events during sleep: ■ AHI – to score degree of sleep apnea if present. – Identify the indication for PSG.12. Check number of events in relation to the following: (a) REM (in OSA. – Go through the patient’s complaints. and REM [to make sure that the patient had a period of sleep long enough to make a diagnosis (including enough REM)]. FIGURE 10. It is hard to pinpoint a minimum duration of sleep sufficient enough to make a confident diagnosis from a PSG. Notice that most respiratory events and desaturations occur during REM sleep and while the patient is supine. – Examine sleep architecture and sleep stages by checking SE. Interpretation of the Final Report • The following is a suggested approach: – Identify the patient’s demographics.244 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE combined with respiratory events’ summary. We suggest a minimum duration (TST) of 3 h with at least 10% of REM sleep. body position and PLMs.12. TST. The final report summarized in this graphic form. events are more likely to be in supine position) (c) Identify if events are predominantly obstructive (OSA) or central (CSA). and current medications. †††† . past history. events are more common during REM) (b) Position (in OSA.
• The procedure is similar to the diagnostic PSG except that the patient uses C-PAP machine during the study. Auto C-PAP Titration • An auto C-PAP (smart) machine is capable of automatically changing C-PAP pressure according to patient needs. – Examine ECG monitoring comments (made by the scorer) to report any arrhythmias associated with respiratory events. daytime sleepiness. The PAP . a high index (>5/h) is suggestive of PLMD (PLM-AI of >25/h is consistent with the diagnosis of PLMD). C-PAP titration PSG is commonly done to detect the appropriate C-PAP pressure.e. the patient’s sleep is interrupted as he/she is awakened for application of C-PAP. Additionally.. therefore. An elevated PLM index with a normal PLM-AI is suggestive of PLM of sleep.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 245 Study the AI and HI in a similar way as AHI. ■ ■ Other Forms of Overnight Sleep Studies C-PAP Titration PSG • After prescription of C-PAP in patients with confirmed OSA. it may influence accuracy of PSG as the duration and quality of the diagnostic PSG are reduced. • A follow-up study may be performed to assess the adequacy of the initially selected pressure particularly with return of symptoms of OSA (i. Split Night PSG • The night is divided into two parts: a diagnostic PSG is done in the first part and a C-PAP titration PSG is done in the second part. The pressure should be adequate to resolve sleep apnea including the respiratory events taking place during REM sleep in the supine position. Finally. the time reserved for C-PAP titration may be insufficient for adequate results. Different C-PAP pressures are applied throughout the night and the pressure that best controls the respiratory events is then selected as the appropriate pressure for the patient. which is not associated with sleep fragmentation and. Although less costly. – Examine PLM-AI. Study SPO2 that is best made by looking at the graphic tracing. snoring and daytime sleepiness).
. • These studies can be attended (by a technician) or unattended. e. This is not a limited channel study and has to be done under supervision in a sleep laboratory. or respiratory movement and airflow). ECG or heart rate. • Overnight oximetry is usually done in the home ‡‡‡‡ as it is simple and can easily be set up by the patient. EOG. Interpretation of type 3 and 4 studies should be done with caution as they cannot score sleep. or can be of limited duration (<6 h). including ventilation or airflow (at least two channels of respiratory movement.246 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE data are recoded throughout the night and can be downloaded to a computer. airflow. sleep studies are categorized into four types: – Type 1: it is the standard PSG with a minimum of 12 channels.g. – Type 4: most monitors of this type measure a single parameter or two parameters. and SPO2.120 and readily available as a portable test. respiratory effort. – Type 3: minimum of four channels. as described earlier. Limited Channel Sleep Studies (Portable Monitoring Devices)119 • Sleep studies can be done with fewer channels than the standard PSG. including EEG. It is considered a type 4 sleep study because it monitors two variables: SPO2 and heart rate. – Type 2: minimum of seven channels.119 OVERNIGHT OXIMETRY Introduction • Overnight oximetry is a widely used tool for diagnostic and screening purposes for sleep apnea. Certain guidelines are currently available to guide the use of these limited sleep studies. and SPO2. The pressure that the auto C-PAP machine delivered the most during the night is the pressure that is most likely optimal for the patient. At the same time. The data are ‡‡‡‡ Overnight oximetry is done sometimes for inpatients if admitted for unrelated issues and are found incidentally to have OSA clinically. chin EMG. which is the most popular type 4 method. For the sake of classification. It is simple. inexpensive.. heart rate or ECG. making these studies less expensive and more portable (can be done in the home). these studies are less informative but they can still be useful with appropriate patient selection. overnight oximetry. full night or split-night.
Figure 10. the lowest. data are plotted as saturation and heart rate vs. which may suggest that the patient was in REM sleep during that event. – Numerically.121–125 Other numerical data include the highest. (b) A compressed (4 h) tracing of the same overnight oximetry shown in (a) showing the typical appearance of SPO2 and heart rate in a positive test.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 247 recorded in a recording card and the results can be downloaded and analyzed electronically. Notice the significant desaturations accompanied by significant variation in heart rate.13. a b FIGURE 10. which is defined as the number of desaturation events per hour. and the mean SPO2 and heart rate. Notice the significant desaturations that reached critical levels (<50%) at 4:30 AM. (a) A 1-h tracing of an overnight oximetry for a patient with severe OSA (ODI: 63/h). time. the single most important figure is the oxygen desaturation index (ODI). The results are usually presented as numerical and graphic forms. – Graphically. A desaturation event in a respiratory sleep disorder is defined as a reduction in SPO2 by ≥ 4% from baseline.13. .
121. 137 – Central apneas. which. This phenomenon is responsible for the saw-tooth waveform pattern of SPO2 if plotted against time. use 5 or 10 events/h as the threshold and all of these values are supported by evidence.). by arousal). 124–127 ODI cutoff point for the diagnosis of OSA is not well defined.137 With permission.§§§§ the interpreter is more confident to consider a study positive. which is due to circulatory and instrumental delay (Modified from Netzer et al. Generally. Figure 10.127. with an ODI of ≥15/h.14.g.248 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE Interpretation • Oxygen desaturation index (ODI): – Is normally less than five events per hour. produce more symmetrical waveform as the breathing FIGURE 10. as it has to be combined with graphic changes. 134 ODI alone is not sufficient to make a useful conclusion from an overnight oximetric study.. §§§§ . 138 This wave pattern combined with a high ODI (>15/h) is considered diagnostic in the presence of the appropriate clinical scenario.128–132 Some laboratories. increases the sensitivity but may not significantly change the specificity if compared to an ODI of 15.135. SPO2 drops gradually during an obstructive event but returns rapidly to the baseline when the obstructive event is terminated (e. however.137.14. 124–127. if used.121. Notice the slow desaturation and the rapid resaturation. Notice also that there is a delay in the nadir saturation in relation to airflow. especially when part of Cheyne-Stokes respiration. 136 • Graphically: – In OSA. An ODI of 10 is widely used as the cutoff point. The characteristic saw-tooth pattern of SPO2 in OSA. 133.
15. The heart rate rapidly increases when an obstructive event is terminated.139. 140 – The heart rate response typically shows reflex bradycardias that develop during obstructive events (apneas or hypopneas) in relation to the nadir negative intrathoracic pressure.137 – The overlap syndrome¶¶¶¶ may be differentiated from OSA by the duration of the desaturations. in patients with AHI of ≥ 25 events/h. Figure 10. but these values decreased to 75% and 86%.141–149 . In CSA (Cheyne-Stokes respiration). respectively.128–133. Figure 10.137 ¶¶¶¶ The overlap syndrome refers to the coexistence of OSA and COPD. respectively.127 It is often difficult to differentiate central from obstructive events with oximetry. being much longer in the overlap syndrome. The sensitivity and specificity of overnight oximetry is 100% and 95%.127 This indicates that oximetry is an effective tool for screening patients with moderate-to-severe OSA. Other studies showed similar sensitivities and specificities. 138 Central apneas may produce the saw-tooth pattern as well. Reliability of Overnight Oximetry • Overnight oximetry is most useful when the clinical index of suspicion for OSA is high. these patients will often require full diagnostic PSG. pattern here is more regular (crescendo–decrescendo pattern) compared to that of OSA.16 presents a reasonable approach to properly utilize overnight oximerty. SPO2 produces more regular and symmetrical waveform due to the regular crescendo–decrescendo pattern of respiration (Modified from Netzer et al.137 With permission. especially if not associated with Cheyne-Stokes respiration. Central apneas are not generally associated with this pattern of heart rate response.13.).15.137. .DIAGNOSTIC TESTS FOR SLEEP DISORDERS 249 FIGURE 10. in patients with AHI of ≥15 events/h. • On the other hand. overnight oximetry has less diagnostic value in patients with mild OSA.125 Figure 10.
151 if utilized appropriately. 125. FRC (O2 reserve) is preserved and O2 consumption is reduced compared with obese patients.**** ASSESSMENT OF DAYTIME SLEEPINESS# Multiple Sleep Latency Test Preparation • Multiple sleep latency test (MSLT) is useful to assess conditions with excessive somnolence. # Tests used to assess daytime sleepiness are done during the day as opposed to PSG that is done at night to assess sleep efficiency.250 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE FIGURE 10. particularly narcolepsy. The following are important points in preparation for MSLT: – MSLT should be preceded by a PSG (usually done on the night that precedes the day of the test) to exclude conditions **** False negative oximetries occur mostly in nonobese patients or in those with short duration apneas. overnight oximetry can be a useful diagnostic test. The aim of this test is to measure the tendency to fall asleep during the day by measuring the sleep and the REM latencies.).16. In the case of thin patients. It is also a very cost-effective test120. Approach to patients with strong clinical suspicion for OSA using overnight oximetry as an initial diagnostic study (Modified from Netzer et al. 150. • In conclusion. .137 With permission. which are abnormally short in narcolepsy.
– Avoidance of alcohol and caffeine on the day of the test is required. A sleep Drugs that affect sleep latency include sedatives. PSG can detect PLMD. – Fails to reach REM sleep in 15 min after 1st epoch of sleep.152–156 – Medications that are known to affect sleep or REM latency††††† should be stopped (if possible) at least 2 weeks prior to MSLT. and quiet room with appropriate temperature. The patient is then allowed to nap 4–5 times throughout the day. with CPAP). Interpretation • The normal mean sleep latency during MSLT is 10–20 min. mainly OSA.5–3 h after a normal PSG. drugs that affect REM latency include tricyclic antidepressants. MSLT results are influenced by the chronic or acute usage or acute withdrawal of these drugs. selective serotonin reuptake inhibitors (SSRIs).157–159 ††††† . A PSG is also useful to ensure that the patient slept adequately the night before. 2 h apart and 1. which may have the same effect on MSLT as OSA. monoamine oxidase inhibitors. hypnotics. Therefore.g. antihistamines and stimulants. – Achieved one epoch of unequivocal REM sleep. and chin EMG for sleep staging. The patient should dress in comfortable street clothes and the test should be performed in a comfortable.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 251 (e.. Acute withdrawal from high doses of caffeine is prohibited. Urine drug screening may be needed in suspected cases.160–167 which decreases with any dyssomnia. • Naps are terminated if patient: – Fails to initiate sleep in 20 min. Recordings should be monitored closely by an experienced technologist.g. A repeat PSG while on CPAP prior to the MSLT is important to ensure that OSA is well controlled before testing. Procedure • MSLT requires only the monitoring of EEG. OSA) that may affect sleep architecture and may cause REM-sleep fragmentation resulting in increased REM score in the MSLT. – A 1–2-week sleep diary is important to document the sleep pattern as MSLT results may be affected by lack of adequate sleep in any of the preceding seven nights. the presence of OSA makes the interpretation of the MSLT difficult indicating that sleep apnea should be properly treated first (e. lithium. and amphetamines. dark. EOG. • The patient is given 20 min to fall asleep after lights-out and once asleep an additional 15 min to reach REM sleep..
Scoring 3–6/24 is considered normal. SSRI]. MWT latency increases significantly when these conditions are treated. • Unlike MSLT. This test is then repeated 4–5 times throughout the day. • Short sleep latency during the night is considered normal. 161. 166 Sleep-onset REM is seen in 10–15% of patients with narcolepsy173 but may indicate chronic sleep disturbance174 or coexistence of OSA and narcolepsy. tricyclic antidepressants (TCA). and chin EMG for detection of sleep. 155. 169 A sleep latency of 5–10 min is a diagnostic gray area170 but may be considered mild sleepiness. being shortest near noon or early afternoon (third or fourth nap) and longest during the late afternoon (fifth nap). not alertness. 168. EOG.153. patients here are encouraged to resist sleep for 40 min while seated upright in a bed in a dark. or acute withdrawal of REM-suppressing drugs [e. Table 10. quiet room..252 PULMONARY FUNCTION TESTS IN CLINICAL PRACTICE latency of <5 min is pathological160 and associated with impaired functional performance.162 • Scoring 0–1 REM periods per five naps is seen in normal individuals but two or more REM periods are diagnostic for narcolepsy. It represents an eight-statement questionnaire that aims at the detection of the degree of the daytime sleepiness over the last month. During the day. 176 MSLT should be repeated after the coexisting condition is properly treated. sleep latency varies.3.171. Subjective Tests Epworth Sleepiness Scale177 • Is the most popular subjective method of assessing daytime sleepiness.‡‡‡‡‡.172 . • The normal MWT latency is 19 min. psychological disorders. It is primarily designed as a measure of safety in occupations dependent on alertness although this test measures wakefulness. Maintenance of Wakefulness Test • Maintenance of wakefulness test (MWT) is used to test the ability to stay awake during the day. The test is terminated if sleep is detected or after 40 min if patient remains awake. Li.g. • Patients undergoing this test should provide a 1–2 weeks sleep diary and should be off medications or beverages that influence sleep. The patient is monitored by EEG.165. Scoring 7–9 indicates mild daytime sleepiness and ‡‡‡‡‡ ≥ 2 REM/4 or 5 naps may be seen in patients with OSA.175. which is reduced in case of dyssomnias including OSA and narcolepsy.
sleep onset appears imminent. Epworth sleepiness scale In the last 30 days.DIAGNOSTIC TESTS FOR SLEEP DISORDERS 253 TABLE 10. Relaxed. responsive. Sitting & reading ( ) Watching TV ( ) Sitting inactive in a public place ( ) As a passenger in a car for an hour without a break ( ) Lying down to rest in the afternoon ( ) Sitting and talking to someone ( ) Sitting quietly after lunch with no alcohol ( ) In a car while stopped for a few minutes in traffic ( ) Total score out of 24: ( ) TABLE 10. 7. 8. woozy. Foggy. Sleepy. beginning to lose track. Almost in reverie. Situations: 1. 3. alert. 2.4. 5. 3. 2. 4. high chance of dozing. vital. scoring ≥10/24 indicates moderate to severe sleepiness. difficulty in staying awake. 5. 7. Even if you have not done some of these things recently try to work out how they would have affected you. Feeling active. cannot stay awake.4. A little foggy. 6. Scoring 24/24 indicates an extraordinary sleepiness while scoring 0/24 suggests a hyperarousable or insomniac patient. 6. .3. Scoring 1–2 is considered normal and the more you score. Table 10. 0 1 2 3 = = = = would never doze. prefer to lie down. moderate chance of dozing. 1. Stanford Sleepiness Scale179 • Represents a series of statements to the subject who is required to check the one statement that most accurately describes the current state of sleepiness. It is less widely used as it is less specific and relates only to the state of the patient at the time the test is filled. wide awake. slight chance of dozing. able to concentrate. how likely are you to doze off or fall asleep in the following situations (in contrast to feeling just tired)? This refers to your usual way of life in recent times. awake but not fully alert. the more sleepy you are. Stanford sleepiness scale Circle the one number that best describes your level of alertness or sleepiness right now. Functioning at a high level but not at peak. let down. 4.
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Appendix 1: Abbreviations PFT ALS ARDS ATS BD BHT BMI CHF CLdyn CLstat CO CO2 COPD CVA dl DLCO ERS ERV FEF FET FEV1 FEV6 FIF FIVC FRC FV curve FV loop FVC Amyotrophic lateral sclerosis Acute respiratory distress syndrome American Thoracic Society Bronchodilator(s) Breath-hold time Body mass index Congestive heart failure Dynamic compliance Static compliance Carbon monoxide Carbon dioxide Chronic obstructive pulmonary disease Cerebrovascular accident Deciliter Diffusing capacity of carbon monoxide European Respiratory Society Expiratory reserve volume Forced expiratory flow Forced expiratory time Forced expiratory volume in the 1st second Forced expiratory volume in 6 s Forced inspiratory flow Forced inspiratory vital capacity Functional residual capacity Flow volume curve Flow volume loop Forced vital capacity .
266 GAW g H2O He Hgb IC ILD IPF IRV IVC APPENDIX 1: ABBREVIATIONS Airway conductance Gram Water Helium Hemoglobin Inspiratory capacity Interstitial lung disease Idiopathic pulmonary fibrosis Inspiratory reserve volume Inspiratory vital capacity Metered dose inhaler Milligram Maximal expiratory pressure Myocardial infarction Maximal inspiratory pressure Maximal med-expiratory flow Millisecond Musculoskeletal disease Maximal voluntary ventilation Nitrogen Neuromuscular disease Oxygen Obstructive sleep apnea Atmospheric pressure or barometric pressure Diaphragmatic pressure Peak expiratory flow Esophageal pressure Pulmonary function test Peak inspiratory flow Partial pressure of inspired oxygen Nasal pressure Gastric pressure Airway resistance Residual volume Specific airway conductance Shortness of breath Specific airway resistance Slow vital capacity Thoracic gas volume Total lung capacity MDI mg MEP MI MIP MMEF ms MSD MVV N2 NMD O2 OSA Patm. PB Pdi PEF Pes PFT PIF PIO2 Pnas Pga RAW RV SGAW SOB SRAW SVC TGV (VTG) TLC .
APPENDIX 1: ABBREVIATIONS 267 VA VC VTG VT VT curve % pred. ABG ABG AG AGMA AV malf. BE Cl COPD FIO2 H [H+] HCl HCO3+ [HCO3+] ILD K kPa Na+ NAG NAGMA NaHCO3 NH4+ NH4Cl O2 P(A-a)O2 PaCO2 PACO2 PaO2 PAO2 PatmO2 PH2O PIO2 + − Alveolar volume Vital capacity (TGV) Thoracic gas volume Tidal volume Volume time curve Percent predicted Arterial blood gas Anion gap Anion gap metabolic acidosis Arteriovenous malformation Base excess Chloride Chronic obstructive pulmonary disease Fractional inspired oxygen Proton Hydrogen ion concentration Hydrochloric acid Bicarbonate Bicarbonate concentration Interstitial lung disease Constant Kilopascal Sodium Nonanion gap Nonanion gap metabolic acidosis Sodium bicarbonate Ammonium Ammonium chloride Oxygen Alveolar arterial oxygen gradient Partial pressure of arterial carbon dioxide Partial pressure of alveolar carbon dioxide Partial pressure of arterial oxygen Partial pressure of alveolar oxygen Partial pressure of atmospheric oxygen Partial pressure of water vapor Partial pressure of inspired oxygen .
268 RA RQ RTA SaO2 TPN APPENDIX 1: ABBREVIATIONS Room air Respiratory quotient Renal tubular acidosis Arterial oxygen saturation Total parenteral nutrition Ventilation perfusion mismatch Delta gap VQ mismatch ΔG Exercise test 12MWT 6MWD 6MWT AT BP C. CaO2 CF CHF – Cv O2 DVT ECG Ft HR LVF MI PE PETCO2 PETO2 RR SPO2 SV – SvO2 VA VD VD/VT 12-min walk test 6-min walk distance 6-min walk test Anaerobic threshold Blood pressure Cardiac output Arterial oxygen content Cystic fibrosis Congestive heart failure Mixed venous oxygen content Deep venous thrombosis Electrocardiogram Foot (Feet) Heart rate Left ventricular failure Myocardial infarction Pulmonary embolism End-tidal carbon dioxide tension End-tidal oxygen tension Respiratory rate Arterial Oxygen saturation with pulse oximetry Stroke volume Mixed venous oxygen saturation Alveolar volume Dead space volume Dead space fraction .O.
APPENDIX 1: ABBREVIATIONS 269 VA VCO2 VD V D/V E VE VO2 Alveolar ventilation per minute Carbon dioxide production per minute Dead space ventilation per minute Dead space fraction Minute ventilation Oxygen consumption per minute Diagnostic tests for sleep disorders AHI AI COPD CPAP CSA ECG EEG EMG EOG GERD HI Hz LOC MSLT MWT NREM ODI OSA OSAH PLM-AI PLMD PLM-I PSG REM RERA RLS ROC SE SEM SOL Apnea hypopnea index Apnea index Chronic obstructive pulmonary disease Continuous positive airway pressure Central sleep apnea Electrocardiography Electroencephalography Electromyography Electrooculography Gastroesophageal reflux disease Hyponea index Hertz Left outer canthus Multiple sleep latency test Maintenance of wakefulness test Nonrapid eye movement Oxygen desaturation index Obstructive sleep apnea Obstructive sleep apnea/hypopnea Periodic limb movement arousal index Periodic limb movement disorder Periodic limb movement index Polysomnography Rapid eye movement Respiratory effort-related arousal Restless leg syndrome Right outer canthus Sleep efficiency Slow rolling eye movement Sleep onset latency .
270 SPO2 SPT SSRI SVT TIB TST UARS VT VT WASO APPENDIX 1: ABBREVIATIONS Oxygen saturation by pulse oximetry Sleep period time Selective serotonin reuptake inhibitors Supraventricular tachycardia Time in bed Total sleep time Upper airway resistance syndrome Tidal volume Ventricular tachycardia Wake after sleep onset .
but can be as low as 55% >0. >30% drop suggests diaphragmatic paralysis PFT Absolute Figures (for an Average Young Adult Male.Appendix 2: Normal Values PFT Normal Values (ATS) – Apply Mainly to Young and Middle Ages FVC FEV1 FEV1/FVC ratio FEF25–75 FEF25–75/FVC ratio TLC FRC RV DLCO MEP MIP Supine FVC 80–120 (% Pred.66 (more accurate) 80–120 75–120 75–120 80–120 >90 cmH2O <−70 cmH2O Within 10% of the sitting value.) 80–120 80–120 >65% pred. restrictive. or mixed. Listed in a Decreasing Order) TLC FVC FEV1 FRC ERV RV DLCO 6L 5L 4L 3L 1–2 L 1–2 L 25 ml/min/mmHg PFT Grading of Severity of Obstructive and Restrictive Disorders (A) Grading of severity of any spirometric abnormality based on FEV1: • After determining the pattern to be obstructive. FEV1 is used to grade severity: .
preferred) Mild Moderate Severe TLC > 70 (% pred.) 60–69 50–59 35–49 <35 ABG NORMAL VALUES pH PaCO2 PaO2 HCO3 BE SaO2 AG P(A–a)O2 7.45 35–45 mmHg >80 mmHg 21–26 mmol/L (consider it 24) 0 to −2 mmol/L >95% 10 ± 4 <15 (increases with age) .272 APPENDIX 2: NORMAL VALUES Mild Moderate Moderately severe Severe Very severe FEV1 > 70 (% pred.) 60–69 50–59 35–49 <35 (B) Traditional method of grading the severity of obstructive and restrictive disorders: • Obstructive disorder (based on FEV1) – ratio < 0.) 60–69 <60 • Restrictive disorder (based on FVC.35–7. in case no lung volume study is available) Mild Moderate Moderately severe Severe Very severe FVC > 70 (% pred.7 May be a physiologic variant Mild Moderate Moderately severe Severe Very severe FEV1 = 100 (% pred.) 70–100 60–69 50–59 35–49 <35 • Restrictive disorder (based on TLC.
APPENDIX 2: NORMAL VALUES 273 EXERCISE TEST NORMAL VALUES VO2max AT BP O2 pulse HR max HR reserve RQ (at peak exercise) RR max Ventilatory reserve Breathing reserve VE/VCO2 (at AT) VE/VO2 (at AT) VD/VT (at peak exercise) 83% >40% of predicted Vo2max <220/90 >80% predicted (220 − age) ± 15 beats or >90% of that predicted for age 0 ± 15 beats or <15 beats/min £1 <60 breaths/min >11 L/min <85% <34 <31 0.2–0.3 .
20.10 7.8 = 80 nmol/L. • When pH is outside that range (this can be applied within that range too): – pH of 7.8. – Then increasing or decreasing pH by 0. acidosis decreases pH and increases [H+]).30–7. – So if pH is 7.84 = 40.00 7.8 × 0. – If pH is 6. • If you do not want to bother yourself with these boring calculations.8) = 156.15 7.25 7. then [H+] = 100/(0.35 7. – If pH is 7.5 CONVERTING PH TO [H+]: • When pH is within 7.Appendix 3: Conversions TO CONVERT FROM KILOPASCAL TO MMHG: Multiply by 7.20 7. then [H+] = 100 × 0.8 = 64 nmol/l.8 × 0. – So if pH is 7. – Then every increase or decrease of pH by 0.80.55 7.45 7.40. the following table can be of help: pH 7. – If pH is 7. then [H+] will equal 100 × 0.00 ↔ [H+] = 100 nmol/L.05 7.30 [H+] 100 89 79 71 63 56 50 pH 7.35.50 7.50 – pH of 7.40 7. for instance.60 7.01 is equivalent to decreasing or increasing [H+] by 1 nmol/L (remember that [H+] changes in the opposite direction of pH. then [H+] will equal 40 + 5 = 45 nmol/L.10 is equivalent to multiplying or dividing [H+] by 0.65 [H+] 45 40 35 32 28 25 22 .10. then [H+] will equal 100 × 0.40 ↔ [H+] = 40 nmol/L.
276 APPENDIX 3: CONVERSIONS ESTIMATING FIO2 WHEN USING SUPPLEMENTAL O2 The information provided in this section is acquired from “American Heart Association. 2001” and represents just a rough estimation of the FIO2. • Breathing through nasal cannula: Consider FIO2 at RA (20%). • Breathing through a face mask with O2reservoir (nonrebreather mask): each liter of O2 (starting from 6 l) corresponds to 10% increment in FIO2 (starting from 60%). then each liter of O2 corresponds to 4% increment in FIO2 over the 20%: – 1L 24% – 2L 28% – 3L 32% – 4L 36% – 5L 40% – 6L 44% • Breathing through a face mask: 6–10 l of O2 increases FIO2 to ~60%. Advanced Cardiac Life Support (ACLS) provider manual. – 6L 60% – 7L 70% – 8L 80% – 9L 90% – 10–15 L ~100% • Breathing through a venturi mask: gives a more accurate estimation of FIO2 (amount of FIO2 delivered is written on the mask itself). .
See also Human sleep. 222. See Apnea hypopnea index AI. See also Pulmonary function tests (PFT). See Anaerobic threshold ATPS. See Anion gap AGMA. 145–146 Acidemia. See also Spirometry acceptable trials of. 166 methods to identify. 165 Anion gap. 231 Arterial blood gases. 25. 137 Apnea. 231–232. definition of. See also Respiratory events Apnea hypopnea index. 60 DLCO adjustement for. 133 Acute respiratory acidosis. 142–143 respiratory alkalosis. 18–20 reproducibility criteria. 10–14 PFT reference values. 134 respiratory acidosis. 86–87 Airway resistance. definition of. characteristics of. See also Respiratory events Airway conductance. 145. 136 effect of albumine level on. 232–234. 246 277 . 176 Alveolar volume. 145–147. 236.Index A Abdominal movements. 232. 139–141 normal values. in sleep disorder. definition of. See Arterial blood gases Abnormal lung volumes. 142. wave patterns ALS. See Ambient temperature pressure standard ATS guidelines. 14–18 Auditory monitoring. See Anion gap metabolic acidosis AHI. 143–145 values. characteristics of. See Amyotrophic lateral sclerosis Alveolar–arterial gradient. 133 Alkalosis. techniques in. 234 Apnea index. causes of. 133 Alpha waves. 272 AT. 23 Acid-base nomogram. See Apnea index Airflow measurement. See also Respiratory events ABG. 150–155 henderson equation in. causes of. 86–87 Albumine level. definition of. See also Anion gap Alkalemia. 63 measurement of. 234 Arousal index. 147–148 Alveolar gas equation. 82 Anaerobic threshold definition of. 143. 8 Amyotrophic lateral sclerosis. 136–139 metabolic alkalosis. 49–50 Abnormal spirometric components. 133 Acidosis. 134–135 metabolic acidosis. in clinical practice case studies for. See also Respiratory acidosis Acute respiratory alkalosis. 145 Anion gap metabolic acidosis. 62 Ambient temperature pressure standard. See also Polysomnography Auto C-PAP titration. See also Respiratory alkalosis AG. 167–170 Anemia disease patients and VO2. definition of.
76 technique in. 165 and VO2. 166 Cardiopulmonary exercise test equipment used in. See also Human sleep. 165–166 VO2 relationship. 218 Chest movements. relationship of. definition of. See also Respiratory events Chin electromyography. 170–171 Body box. for expiratory muscle strength. 162 O2 uptake. See Body plethysmography Body plethysmography. 40–43. 185 Cardiac output factors determining. in clinical practice indications and contraindications for. 220 role of. wave patterns BHT.278 INDEX B Base excess (BE). See also Respiratory acidosis Chronic respiratory alkalosis. 133 Beta waves characteristics. 45–47. See Continuous positive airway pressure C-PAP titration PSG. 163–165 role of. 160–161 techniques in. See also Lung volumes Body temperature pressure standard. 162. 226 scoring sleep on. 166–170 BP response. See Chin electromyography Chronic obstructive pulmonary disease. 162–163 Cardiovascular monitors. 245 CPET. 165 Carboxy-Hgb (CO-Hgb). 75 interpretation for. See also Respiratory system. See Chronic obstructive pulmonary disease Cough gastric pressure. 22. 162 BP response. 142. See Cardiopulmonary exercise test . 179–182 (see also Exercise testing) Central sleep apnea syndrome. See also Respiratory alkalosis Chronotropic disorders patients and VO2. See also Cardiopulmonary exercise test Cardiovascular system assessment of AT. 165 and exercise testing. 8 Borg scale importance of. 144. See also Pulmonary function tests (PFT). assessment of Bronchial challenge tests. See Body temperature pressure standard C Carbon dioxide production per minute. 73–75 Bronchial response to allergen. 85 Cough Pga. 159 role in CPET. 3 Chronic respiratory acidosis. See Blood pressure response Breath-hold time. 218. 220 COPD. 85 CPAP. 61 Breathing reserve. See Breath-hold time Blood pressure response. See also Spirometry BTPS. 227–229 Chin EMG. 165 Continuous positive airway pressure. phases of. See Cough gastric pressure Cough test. 222. 170–171 exercise parameters. 64 Cardiac disease patients and VO2. 232. adjustment to. 165 pattern in. 172. 72 Bronchodilator response study.
See also Cardiopulmonary exercise test D Daytime sleepiness. 236 artifact. 22 Exercise oximetry. in clinical practice epworth sleepiness scale. 227–229 wave patterns in. See also Daytime sleepiness. 217 E 10–20 EEG electrode placement system. 51. 220 role of. 6–8. See also Spirometry Expiratory reserve volume. See Lung diffusing capacity for carbon monoxide Dynamic hyperinflation COPD and. 220 electrodes. 255 stanford sleepiness scale. wave patterns Diaphragmatic function. 161 6MWT. See Expiratory reserve volume European Respiratory Society. 183–186 maximal effort. 174 Dyssomnias. 174–175 Delta waves characteristics. 179–182 exercise capacity. 222. 38 F FET. 221 scoring sleep on. 176–178 respiratory system. 93–97 for restrictive disorders. 11 for lung volumes measurement. 163 Expiratory flow–volume curve. 255–256 MSLT. 224 waves. 227–229 Epworth sleepiness scale. 178 gas-exchange response. 225–226 scoring sleep on. See Forced expiratory time FEV1. 164–165 Flow–volume curve. 157–159 normal values of. 181–183 limitations of. See also Cardiopulmonary exercise test ERS. definition of. 162. 176 termination of. 220 in arrhythmias detection. 253–255 MWT. See also Pulmonary function tests (PFT). assessment of Ergometer. See also Human sleep. 47–49 for obstructive disorders.INDEX 279 CSA. concepts of. 186–208 interpretation cardiovascular system. estimation of. characteristics of. 2 Fick equation O2 pulse and. 8. 273 pulse oximetry and. assessment of. 222–225 Electroocculography (EOG). ratio of. 5 . 255–256. 221–222 in PSG. 27–31 F1O2. See Central sleep apnea syndrome Cycle ergometer. in clinical practice case studies for. 227 role of. assessment of. 173 definition of. 84 DLCO. See Forced expiratory volume in the 1st second FEV1 and FVC. 159 Exercise testing. 162. See European Respiratory Society ERV. 166 and VO2. 236 (see also Polysomnography) Electroencephalography (EEG). 223 Electrocardiography (ECG). 222 recording and scoring. 24–27 in PFT interpretation. 256 Dead space fraction. See also Pulmonary function tests (PFT). 276 Forced expiratory time.
See Gastroesophageal reflux disease H Heart disease and heart rate (HR). 60 IPF. 162. assessment methods.280 INDEX Forced expiratory volume in the 1st second. See Leg electromyography Lung compliance (CL) technique. 87 Forced vital capacity (FVC). 220 GAW. 176 Gas-exchange response and exercise testing. 65–66 measurement methods of. definition of. 43 FV curve. 203 ILD. 233–234. See Inspiratory capacity IC/ERV ratio. See Interstitial lung disorders Inert gas dilution techniques. 1. 37. 225 Leg electromyography. 49–50 and flow-volume curve. See also Exercise testing Gastroesophageal reflux disease. 38–39 clinical significance of. 1–2 Functional residual capacity (FRC). See Idiopathic pulmonary fibrosis K Kilopascal to mmhg. See also Lung volumes Inspiratory capacity. 222–225 Hyperchloremic metabolic acidosis. 87 Lung diffusing capacity for carbon monoxide. 45–47 . types of I IC. in clinical practice components of. in clinical practice adjustments for. 150. 164–165 Henderson equation. 179–180 HR reserve. 242 wave patterns. 59–60. 8. See Expiratory flow–volume curve. 40–43. 39 Inspiratory vital capacity (IVC). correlation of. 2 Forced oscillation technique. 234–236 Leg EMG. See Hypopnea index HR and O2 pulse vs. 61–62 Lung volumes. VO2 curves. 53. 165 Human sleep NREM cycles. 61 Instantaneous forced expiratory flow. 134–135. 39 Inspiratory reserve volume (IRV). 183–186. 3 Interstitial lung disorders. 234 Hypoxemia. definition of. usage of. conversion of. 43–45. See Nonanion gap (NAG) Hyponea. 47–49 measurement of static body plethysmography technique. mechanisms of. 1–2. See also Arterial blood gases HI. 50–51 nitrogen washout method. 63–64 causes of abnormal. See also Respiratory failure. 148–149 Hypoxemic respiratory failure characteristics. 23. See also Cardiopulmonary exercise test Gas exchange. Flow–volume curve G Gas analyzers. See Anaerobic threshold Left outer canthus (LOC). See also Pulmonary function tests (PFT). 54 Idiopathic pulmonary fibrosis. See Airway conductance GERD. See also Pulmonary function tests (PFT). See also Respiratory events Hypopnea index. 275 L Lactate threshold.
25 causes of. 164–165 Oxygen desaturation index. 21 Obstructive sleep apnea (OSA). 53. See Maximum midexpiratory flow Motor neuron disease. See Maximal inspiratory pressure MMEF. See 6-min walk distance MWT. See also Pulmonary function tests (PFT). usage of. 25 MVV. of phrenic nerve. 217–218 ODI. 51–55 M Magnetic stimulation. Maximum voluntary ventilation 6MWD. 24–27 and PFT. 221 O Obstructive disorders. 43–45 types of. 85–86 MDI. See Forced oscillation technique Overnight oximtery. 171 Maximum mid-expiratory flow. See also Arterial blood gases Metabolic alkalosis. 251–253 role of. 137. VO2 curve. See also Spirometry Maximal inspiratory pressure. 158 6-min walk test. See Musculoskeletal disorders Multiple sleep latency test (MSLT). 255 Maximal expiratory pressure. See Maximal expiratory pressure Metabolic acidosis. 217–218 Obstructive sleep apnea hypopnea (OSAH). 253–255 Musculoskeletal disorders. See also Lung volumes Nonanion gap (NAG). 37–39 usefulness of. 53. 271–272 severity grading. 247 . 172–174 vs. 71 Minute ventilation. 166 concepts of. 136 Nonanion gap metabolic acidosis (NAGMA). See Amyotrophic lateral sclerosis MSD. 3 Maximum voluntary ventilation. See also Arterial blood gases Metered dose inhaler. 54–55 FV and VT curves. See Metered dose inhaler MEP. See Oxygen desaturation index Oscillometry. 246–247 Overnight sleep. See Maximal voluntary ventilation. 165 concepts of. See 6-min walk test N Neuromuscular disorders (NMD). 184 6-min walk distance. in bronchial challenge. 136–139. 138 Nonrapid eye movement (NREM). 51–52. 81–83 Maximal voluntary ventilation. 245–246 Oxygen consumption per minute and cardiac output components. See also Spirometry definition. 81–82 Maximal respiratory pressures.INDEX 281 nitrogen washout and inert gas dilution techniques. 22 Methacholine. lung volumes measurement. 139–141. 3 diagnosis. 43. 157–159 MIP. See Maintenance of wakefulness test 6MWT. 81–82 Maximal flow–volume loop. 84 Maintenance of wakefulness test. 82 Nitrogen washout method. 8. 163–164 factors determining. 247–251 reliability of. in clinical practice analysis of.
125–126 case study XIII. See Provocative concentration PD. 243–245 role of. 128–130 case study XV. 91–92 approach to spirometry. 126–128 case study XIV. 232 Polysomnography. 107. 157–159 normal values of. 110–112 case study III. lung volumes and DLCO measurements. 75 interpretation for. 185–186 Pulmonary function studies. role of. 150–155 Henderson equation. 142–143 respiratory alkalosis. 112–113 case study IV. combination of. 273 pulse oximetry and. 163 interpretation of. 97–98 clinical history. 163–165. 119–120 case study X. 219 artifacts. and technician comments in. 107–110 case study II. 87 maximum voluntary ventilation. 272 bronchial challenge tests. interpretation of. methods in. 117–119 case study VIII. 72 Provocative dose. 115–116 case study VI. 76 technique in. See Polysomnography Pulmonary disease. 71 indications and contraindications for. See also Cardiopulmonary exercise test P Parasomnias. characteristics of. 108 approach for. 234 H to H+. 86–87 lung compliance and forced oscillation technique. 235 Pneumotachography. 217 PC. See also Pulmonary function tests (PFT). 275 p PLM arousal index. 116–117 case study VII. pattern in. 136–139 metabolic alkalosis. 161 6MWT. 130–132 exercise testing case studies for. in clinical practice arterial blood gases. 92–93 lung volume and gas tranfer study. 99–100 spirometry. 73–75 case study I. 155 Provocative concentration. 186–208 interpretation. 3 Peak inspiratory flow (PIF). 180 Oxygen uptake. 176 termination of. 227 report of. 72 PSG. conversion of. 113–114 case study IX. 236–238 channels. See Provocative dose Peak expiratory flow (PEF). 166 heart disease and. 221. 23 Periodic limb movement (PLM). 85–86 Pulmonary function tests (PFT). in clinical practice airway resistance and conductance.282 INDEX Oxygen pulse concept of. 220–221 scoring. 227 recording and scoring. 176–186 limitations of. 134–135 metabolic acidosis. 100–104 . 134 respiratory acidosis. 120–121 case study V. 123–125 case study XII. 143–145 values. patient’s demographics. 236 and EEG recording. 139–141 normal values. 234–236 Periodic limb movement disorder (PLMD). 150 case studies for. 238–239 Posthypercapnic metabolic alkalosis. 219. 121–123 case study XI.
31–35 usage of. 81–83 sniff tests for. measurement of body plethysmography technique. 176 Pulse oximetry. 217–220 periodic limb movement of. 63–64 causes of abnormal. 27–31 severity grading in. 86–87 lung compliance and forced oscillation technique. 61–62 normal values for. 22–24 curves of. 1 static lung volumes. 40–43. See also Arterial blood gases Respiratory disturbance index. 87 maximum voluntary ventilation. 143–145. 5–8 obstructive disorders. 240 rule for scoring sleep. 239–243 assessment of daytime. See Airway resistance Renal tubular acidosis. 18–20 respiratory muscle function cough test and supine spirometry for. 45–47 components of. 107. 24–27 restrictive disorders. 59–60 adjustments for. 217 stages. 65–66 measurement methods of. 253–256 disordered breathing. PFT patterns of. 227–229 spirometry ATS guidelines. 51–55 values of. 108 obstructive and restrictive disorders. 8–10 upper airway obstruction. 85 maximal respiratory pressures. 37 Respiratory acidosis. 221. and arousal of. 49–50 flow-volume curve for. 220 and O2 saturation measurement. PFT pattern of. 271–272 pulmonary function studies airway resistance and conductance. 83–84 transcutaneous electrical phrenic nerve stimulation. overnight oximetry. 220–221 related disorders. 139 RER. 84–85 sleep apnea. 221 latency. 246–253 architecture. 162 (see also Cardiopulmonary exercise test) in exercise testing. wakefulness. 234–236 polysomnography in study of. See Respiratory exchange ratio RERA. 47–49 nitrogen washout and inert gas dilution techniques. See Respiratory effortrelated arousal Residual volume. See also Arterial blood gases Respiratory alkalosis. 20–21 technique of. PFT patterns of. 229–230 sleep and physiologic changes.INDEX 283 volume-time and flowvolume curve approach to. 10–20 bronchodilator response study and components of. 43–45 usefulness of. 85–86 reference values for. 93–97 lung diffusing capacity for carbon monoxide. 142–143. 7. 232 (see also Respiratory events) R Rapid eye movement (REM). 242 RAW. 234 . 271 Pulse oximeter in CPET. 53.
83 Sniff tests. 219–220. 232 scoring. 226 Slow vital capacity. 27–31 and PFT. 165–166 Respiratory failure. 11–13 Sniff esophageal pressure test (sniff Pes test). EOG and chin EMG. 271–272 severity grading in. See Residual volume S Scoring sleep on EEG. wakefulness. See Restless leg syndrome ROC. 223 stages. See also Pulmonary function tests (PFT). in clinical practice apnea. 182–183 monitors. 84 SOL. 217–220 Respiratory system assessment of. 221. 232 pulse oximetry. in clinical practice . 85 maximal respiratory pressures. See Right outer canthus RQ. 227–229 study types. 150 Respiratory muscle function. 239 Sleep onset latency. See also Pulmonary function tests (PFT). 217 spindles. respiratory muscle function. 52–55 features of. 239–243 assessment of daytime. 24 flow–volume curve for. 83–84 Sniff transdiaphragmatic pressure test (sniff Pdi test). See Volume–time curve Spirometry. 246 Sleep efficiency. 83–84 transcutaneous electrical phrenic nerve stimulation. 81–83 sniff tests for. 234–236 polysomnography in study of. See Renal tubular acidosis RV. 162 (see also Cardiopulmonary exercise test) Restless leg syndrome. See Sleep efficiency SEM. 246–253 architecture. 84 Sniff nasal pressure test (sniff Pnas test). in clinical practice cough test and supine spirometry. 165 Respiratory rate. See Slow rolling eye movements Single breath technique. 61. 1 Smooth flow–volume (FV) curve. See also Pulmonary function tests (PFT). 220–221 related disorders. See also Spirometry causes of. 62 Sleep. 25–26 definition of. See Respiratory quotient RR. 21 Right outer canthus. 3 diagnosis. 234 Restrictive disorders. 239 Slow rolling eye movements. 232–234 Respiratory exchange ratio. 227–229 rules for. definition of. 84–85 Respiratory quotient. 171–172 and exercise testing. 253–256 disordered breathing. 217–220 periodic limb movement of. lung volumes measurement in. overnight oximetry. types of. See Respiratory rate RTA. 225 RLS. See Sleep onset latency Spirogram. 229–230 SE. 239 Sleep period time. 234 Respiratory events airflow. 166 Respiratory sleep disorders. 231–232 chest and abdominal movements. and arousal of.284 INDEX Respiratory effort-related arousal.
179 Supine spirometry. See Oxygen consumption per minute Volume–time curve. types of Ventilatory reserve. 84 SV. 14–18 bronchodilator response study and components of. 239 Total lung capacity (TLC). 60 Total sleep time (TST). 234 Urine net charge (UNC). 84–85. 171 Visual monitoring. 39 Time in bed (TIB). 1 Split night PSG. 39 Thromboendartrectomy. definition of.INDEX 285 ATS guidelines acceptable trials of. See Minute ventilation Ventilatory failure. See also Polysomnography Vital capacity. in sleep disorder. See Slow vital capacity VO2. assessment of Stroke volume. 37 estimation. 22 obstructive disorders. 18–20 reproducibility criteria. 7. characteristics of. 256. See Volume–time curve VTG. 8–10 usage of. 10–14 PFT reference values. See Tidal volume VT curve. 33–35 variable extrathoracic obstruction. See Slow vital capacity T Theta waves characteristics. in clinical practice U Upper airway obstruction (UARS). 236. See Pulse oximetry SPT. 31–35 curves of expiratory flow–volume curve. 93 VT. See Carbon dioxide production per minute VE. 6–8 maximal flow–volume loop. alveolar volume in. 20–21 technique of. 5. 85 Supramaximal stimulation. 239 Total thoracic compliance. assessment of. 27–31 upper airway obstruction. 31–33 Upper airway resistance syndrome. See also Spirometry for obstructive disorders. 8 volume–time curve. 245–246 SpO2. 87 Transcutaneous electrical phrenic nerve stimulation. See Alveolar volume VCO2. 22–24 common disorders patterns. 24–27 in PFT interpretation. 222. 31 variable intrathoracic obstruction. See also Pulmonary function tests (PFT). See Thoracic gas volume W Wake after sleep onset (WASO). 11. 160 . 150. 220. See Stroke volume SVC. 192 Tidal volume. See also Daytime sleepiness. See also Respiratory failure. 24–27 restrictive disorders. See Sleep period time Stanford sleepiness scale. See also Human sleep. 138 V VA. wave patterns Thoracic gas volume (TGV). for respiratory muscle function study. 5 severity grading of pulmonary disorders. 239 Wassermann’s gears and body organ system. See also Spirometry fixed upper airway obstruction.
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