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Various fields of application

Pro Oxycon Pro
CPET of the highest quality

Oxycon Mobile
A milestone in CPET

Vmax und Cardiosoft
CPET made by SensorMedics, ECG made by Marquette Hellige

Special Edition: Cardiopulmonary Exercise Testing
Information, Diagnostics, Essays

1st edition, April 2002


History, approaches and applications

Table of Contents Essay
Exercise Testing: The "How" and the "Why" Author: Prof. Brian J. Whipp Ph.D., D.Sc. .............................. 3

Fields of Application
CPET - Various Fields of Application Indications and relevance of CPET .......................................... 8

Oxycon Pro CPET of the Highest Quality .................................................. 10

Dear readers, It has always been the wish of mankind to go to the limits of our capacities. Even the ancient Greeks used to send messages through couriers who were able to run hundreds of miles in a couple of days. If the first marathon runner in history had had our knowledge and had been trained according to current standards, he would not have collapsed of exhaustion after having been informed of the first Athenian victory over the Persian troops in 490 b.c. However, despite our medical findings, cardiopulmonary exercise testing is still a fascinating subject for physicians and researchers of various medical fields. This first special VIASYS info edition is especially aimed at clinicians who wish to be informed about reasons, indications and interpretation of cardiopulmonary exercise testing and who are interested in their collegues' research findings. Apart from its application in athletic performance, cardiopulmonary exercise testing can be used in various medical fields (an overview of which is provided on page 8). Until now, exercise testing has only been practiced by experts. Today we see an increasing interest from healthcare providers. We hope to inform you with interesting literature suitable to support you in your daily work. If you are interested in learning more about cardiopulmonary exercise testing - please read through our brochure or simply refer to the literature references on page 31. Sincerely Yours,

Practical Guidelines
CPET- Practical Guideline Author: Wolfgang Mitlehner, M.D. ........................................ 12

Vmax and Cardiosoft CPET made by SensorMedics, ECG made by Marquette Hellige ........................................... 20 Oxycon Mobile ....................................................................... 23

Clinical Relevance of CPET Author: Prof. Karl-Heinz R¸hle, M.D. .................................. 24

Evaluation and Interpretation of a cardiopulmonary exercise test Author: Hermann Eschenbacher, Ph.D. ................................. 26

The Last Page
Literature references, Training courses, seminars .................. 31

Paul ter Grote
Managing Director of Erich JAEGER GmbH, a subsidiary of VIASYS Healthcare


VIASYS info Special Edition CPET, April 2002


Testing: Exercise Testing: The "How" and the "Why"

Brian J. Whipp, Ph.D., D.Sc. Centre for Exercise Science and Medicine, University of Glasgow, Glasgow, UK
1. Aims To address the role of exercise testing in elucidating the causes of exercise intolerance, with particular reference to pulmonary disease. To discuss the value of clinical exercise testing, in: a) establishing the limits of system function b) defining the effective operating range c) identifying potential causes of exercise intolerance d) evaluating the normalcy of the response with regard to a reference population e) establishing the normalcy of response with regard to other physiological functions f) providing a frame of reference for change with respect to therapeutic interventions or training, and g) as a means of "triggering" an abnormality. To emphasise the importance of domains of exercise intensity and identifying the determinants of an "appropriate" ventilatory response, including considerations of: a) to what extent are the "requirements" met? b) what is the "cost" of meeting these requirements? c) to what extent is the system "constrained" or "limited"? and d) how "intensely" is the response perceived? To establish the physiological basis of the profiles of cardiopulmonary system responses to incremental exercise performed to the limit of tolerance. To recognise when the value of a particular variable or its response profile reflects an abnormality of system(s) functioning, both with respect to (a) the work rate itself or to other related variables and (b) consideration of responses that are often misrepresented as reflecting systems behaviour. Introduction 2. Introduction The tolerable range of work rates in patients with lung disease is constrained by a combination of factors, chief of which are: a) impaired pulmonary-mechanical and gas exchange function which increases the demand for airflow and ventilation; b) limitations in response capabilities, either of airflow generation or of lung distension; c) increased physiological costs of meeting the ventilatory responses, in terms of respiratory muscle work, blood flow and O2 consumption; d) predisposition to 'shortness of breath' or 'dyspnoea' as a consequence of the high fraction of the achievable ventilation demanded by the work rate, commonly exacerbated by arterial hypoxaemia; and e) the often-marked reduction in the range of spontaneously-selected daily activities, which results from the dyspnoea, and further reduces the state of physical training. Strategies designed to increase exercise tolerance in such patients should therefore attempt both to increase (where possible) the ventilatory limits, reduce the demand for ventilation and reduce the intensity of, or attempt to desensitize the subject to, the consequent dyspnoea. In order to meet the increased demands for pulmonary gas exchange during exercise, the lungs must replenish the O2 extracted from the alveoli by the increased flow of more desaturated mixed venous blood. This preserves alveolar, and hence arterial, O2 partial pressure. The lungs must also provide to the alveoli diluting quantities of CO2-free (atmospheric) air at rates commensurate with the increased delivery rate of CO2 in the mixed venous blood. This maintains alveolar, and hence arterial, PCO 2 . However, the metabolic (chiefly lactic) acidosis of highintensity exercise requires that alveolar and arterial PCO 2 be reduced to provide a component of respiratory compensation which constrains the fall of arterial pH. The pulmonary system is therefore confronted by different demands for blood-gas and acid-base regulation during exercise. There are competing ventilatory demands for alveolar PO2 and PCO2 regulation when the respiratory exchange ratio differs from unity, and also for arterial PCO2 and pH regulation when the exercise results in a metabolic acidosis. In patients with lung disease, this process is further complicated by pulmonary gas exchange inefficiencies which result in often-marked differences between alveolar (either ëidealí or ërealí) and arterial gas partial pressures. Consequently, the impaired pulmonary gas exchange in patients with chronic lung disease further increases the ventilatory demand during exercise; the impaired pulmonary mechanics, however, constrains or even limits the ability to meet the demands.

VIASYS info Special Edition CPET, April 2002


"The challenge is to select exercise testing procedures that optimize the stress profile..."
Exercise 3. Exercise Testing The principle that underlies strategies of clinical exercise testing is that system failure typically occurs while the system is under stress. The challenge is to select exercise testing procedures that optimize the stress profile. A major objective of exercise testing, therefore, is to observe the patient and make measurements of ventilation and gas exchange to distinguish among the pathophysiological mechanisms causing dyspnoea and exercise intolerance. A wide variety of tests are available, each being more or less suitable as a stressor of a particular component of the patientís pathophysiology. However, the appropriateness of the integrated systemic responses is best studied (at least, for the initial exercise evaluation) by means of an incremental test, as this provides a smooth gradational stress which spans the entire tolerance range. Exercise Exercise 4. Exercise Tolerance and Exercise Intensity While the tolerable duration of a given work rate is known to depend upon the intensity of the exercise being performed, there is to date no generally-agreed scheme for characterizing work intensity. Two widely-used procedures fail to meet the demands of critical scrutiny in this regard: the "met" increment and the "percentage" of the maximal O2 uptake (V'O2max). The onset of the metabolic (lactic) acidaemia of exercise (i.e. the lactate threshold ATL) does not occur at a common "met" increment in different individuals. Consequently, different subjects at the same "met" level can have markedly different degrees of metabolic acidaemia. Similarly, while in normal individuals ATL occurs at approximately 50% of V'O2 max, the distribution is very large, with the normal range extending from 35% to at least 80%. Consequently, if the exercise intensity is assigned to a particular percentage of V'O2 max (e.g. 70%), then one subject could be exercising at a sub-ATL) work rate and be "comfortable" whereas another could exhaust at V'O2 max. Often, however, patients may not be able to attain a V'O2 max in the conventional sense (or the investigator may not wish to stress them to these levels) because of limitation by some system-related perception (e.g. angina, dyspnoea, claudicating pain). However, as ATL estimation does not require such efforts, it therefore provides: a) an index of the functional status of the respiratory-circulatory-metabolic integration that allows exercise to be sustained aerobically; b) an index of sustainability for a particular task; c) a frame of reference for optimizing training protocols; d) an index of the efficacy of physical training, rehabilitation and drug interventions; and e) an essential component of decision-making strategies for elucidating the dominant system(s) responsible for exertional dyspnoea and exercise intolerance. acidaemia can be used as a defensible index of exercise intensity. That is, three intensity domains may usefully be identified: a) moderate - work rates below ATL, with no increase in arterial blood [lactate] or [H+] and steady states of ventilation and pulmonary gas exchange being achievable; b) heavy - that range of work rates above ATL, for which [lactate] and [H+] are elevated, and can achieve a steady state; and c) severe - even higher work rates, for which [lactate] and [H+] increase inexorably throughout the test, and steady states of ventilation and gas exchange are not achieved, V'O2 being set on a trajectory to V'O2 max. 5. Test Design The appropriateness of the integrated systemic responses to the tolerable range of work rates are best studied utilizing incremental exercise testing, as this allows: a) determination of whether the pattern of response of particular variables is normal with respect to other variables or to work rate; b) the establishment of a subjectís limiting or maximum attainable value for physiological variables of interest; and c) the establishment of exercise intensity domains, such as the transition between moderate and heavy intensity exercise. It does this by providing a progressive, gradational stress that spans the tolerable work rate range. This minimizes or obviates the effects of sudden and large increments (that would be less well tolerated by many patients). Although exercise testing should ideally be task-specific, laboratory exercise testing is usually confined to treadmill and cycleergometer exercise. Regular and accurate calibration is important. The motor-driven treadmill imposes progressively increasing stress through various combinations of speed and grade incrementation. An advantage of the treadmill over the cycle ergometer is the recruitment of a larger muscle mass which causes more marked system stress, with V'O2max being some 5-10% higher than for the cycle ergometer. A major disadvantage of the treadmill is the difficulty of accurately quantifying the power. This reflects the difficulty of providing a metabolic equivalent of the grade and speed profile, coupled with individual variations in body weight, walking efficiency, pacing strategy and the contribution from holding on to the treadmill handrails. These factors can substantially

"There is no generally-agreed upon prointensity..." cedure for normalizing work intensity..."

Therefore ATL has proven to be a useful index of the onset of an exercise-induced metabolic acidaemia. One can forego the necessity for serial blood sampling and even, in many cases, enhance the discriminability of ATL by utilizing a particular cluster of ventilatory and pulmonary gas-exchange, which provides noninvasive estimation of ATL. ATL discriminability, however, under "complicating" conditions such as chronic hyperventilation syndromes, progressive exercise-induced hypoxaemia, or impaired peripheral chemosensitivity with an associated high airway resistance, for example, remain to be established. Although there is no generally-agreed upon procedure for normalizing work intensity, most would concede that moderate exercise may be sustained for long periods but heavy or severe exercise may not. The measured or appropriately-estimated degree of metabolic

"AT "ATL has proven to be a useful index of the onset of an exercise-induced metabolic acidaemia..."


VIASYS info Special Edition CPET, April 2002

modify the metabolic rate up to an unpredictable degree. discriminate threshold behavior. More rapid rates of change impose greater strength demands, and introduce complexities of threshold discrimination resulting from transients of CO2 stores wash-in. A range of protocols are available for treadmill testing. However, the recommendation is for tests that increment the work rate at constant rate, with small increments providing the best discrimination. It is preferable to employ increments in treadmill grade at a constant speed. After an incremental test has been performed, there are circumstances in which the investigator may wish to conduct constantload testing in order to gain additional information about system response kinetics in different intensity domains. Such additional tests should, of course, be performed on separate occasions. 6. Formatting the Outputs Having performed such a test appropriately, the investigator then needs to format the results in a manner that optimizes the ability to discriminate essential response features; i.e. to establish "interpretive clusters" of the variables of interest. The challenge in assessing the normalcy, or otherwise, of the system responses to the exercise is to select the appropriate response variables that are themselves reflective of the particular system(s) behavior and to display their profiles of response either as a function of work rate or within the context of the response of a related physiological variables. That is, what the response of a particular variable means and, often as importantly, what it does not mean. 7. Useful Noninvasive Responses relationship VO2-WR relationship In response to a constant work rate challenge, V'O2 increases exponentially to attain a steady state (over the work rate range for which steady states are attainable). The magnitude of the steady-state increase in V'O2 as function of the work rate increment (i.e.DV'O2/ DWR) is considered to be the functional system "gain" (functional is used here as purists insist that gain has no units). This gain is functionally the inverse of the work efficiency, the difference being that in the efficiency computation DV'O2 is transformed into its energy equivalent by taking into account the substrate mixture undergoing oxidation, i.e. the gain is higher for fatty acid oxidation than for carbohydrate whereas the actual work efficiency is not different.

"Electronically-braked cycle ergometry with a reasonable constant pedaling frequency is recommended..."
The cycle ergometer has several advantages: lower cost, less space, less prone to movement artifacts, and more accurate quantification of power. A variable contribution to the oxygen cost of cycling at unloaded pedaling; i.e. largely a function of the weight of the legs. However, if the pedaling cadence remains essentially constant throughout the test, this amount becomes a constant for all work rates and therefore does not influence the oxygen cost associated with a particular work-rate increment. Electrically-braked cycle ergometers are becoming increasingly popular, although the older friction- braked versions are adequate (recalling, of course, that the power depends on the pedaling rate). The electrically-braked models have the considerable advantage that power is independent of pedaling frequency, typically over quite a wide range, and that work rate control can be implemented remotely by a computer. Technological advances have made it possible for sufficient density of data for rigorous response-profile discrimination to be acquired in a test lasting less than 20 min. Such a test should include the following phases: a) rest b) at least 3 min. of unloaded exercise c) incremental exercise (~10-12 min), and d) a recovery period Electronically-braked cycle ergometry with a reasonably constant pedaling frequency (e.g. 60 rpm) is recommended. Essentially similar results are obtained when work rate is either increased continuously (ramp test) or by a uniform small amount at regular short intervals (e.g. one-minute incremental test) until the patient can no longer sustain the work rate (e.g. he/she cannot cycle > 40 rpm) or is not able to continue safely. The increment size should be set according to the physical capabilities of the subject, to ensure an incremental phase of ~10-12 min; this corresponds to an incrementation rate of ~10 to 20 W/min for a healthy sedentary subject, but as little as 5 W/min in a patient. However, further modifications to the protocol design of the protocol may be necessary if, for example, the subject is severely debilitated or is highly fit. Slower rates of change, in addition to inducing boredom and seat discomfort, also reduce the ability to

"For incremental exercise tests of the ramp type, a constant rate of change of WR replaces the constant absolute WR as the challenge..."
For incremental exercise tests of the ramp type, a constant rate of change of WR replaces the constant absolute WR as the challenge. Consequently, this yields a constant rate of change of (i.e. linear with respect to time and therefore WR) after a small lagphase which reflects the system response kinetics. The O2 gain has been shown (at least in healthy subjects) not to differ from that of the steady-state response (normally 9-11 ml/ min/Watt). The value of V'O2 at any work rate on a ramp test is therefore lower than that for the steady state at that work rate, although its rate of change is normally the same. The incremental gain is therefore often used as an index of the work efficiency. However, in many patients with cardiopulmonary diseases, this incremental gain can be very low (e.g. 8 ml/min/Watt or less). This may be interpreted in one of two ways: (a) The intramuscular energy transduction mechanisms linking ATP production to oxygen utilization have become Ñhyperefficientì (an unlikely scenario) or (b) that unlike healthy subjects, the time constant of response is not a constant irrespective of WR but rather may lengthen as WR increases. Remarkably, to date, the criteria that justify the incremental gain as being reflective of the steady-state gain have never been established, except in healthy subjects. The highest value achieved with good subject effort is termed the "PeakV'O 2 (VO2peak). In those instances in which V'O2 does not continue to increase with further increases in WR (i.e. a plateauing results) yields what is termed the maximal V'O2 (V'O2max). Plateaux of V'O2, however, seem not to be common, such that without evidence from other tests that the highest attained meets the original criterion for V'O2 max, the value should be reported as V'O2 peak. It is important to recognise, however, that while V'O2 max is not different with different ramp slopes the maximum work rate attained is progressively greater the faster the ramp.

"... the pattern of the VCO2-VO2 relationship is highly dependent upon the rate at which the WR is incremented..."

VIASYS info Special Edition CPET, April 2002


VCO2-VO2 relationship The profile of pulmonary CO 2 output (V'CO2) as a function of V'O2 during incremental exercise is dependent upon two factors: the substrate mixture undergoing oxidation (i.e. the RQ effect) and the CO2 storage into from muscle and blood (i.e. the factor that causes RER to differ from RQ). Consequently, the pattern of the VCO2-VO2relationship is highly dependent upon the rate at which the WR is incremented. The typical pattern, however, is one in which the V'CO2 response initially lags that of V'O2 early in the transient and then increases often as a linear function of V'O2. The slope of the relationship (DV'CO2/DV'O2) in this region has been termed S1, with a value typically close to unity in subjects on typical western diet - but can be greater than 1, even without hyperventilation! The slope of the V'CO2-V'O2 relationship increases at a particular V'O2 as the aerobically produced CO 2 released from bicarbonate buffering of protons associated with lactate accumulation. The slope in this higher WR region has been termed S2, and as the amount of CO2 released in the proton buffering process is a function not of the magnitude of [bicarbonate] decrease but its rate of decrease, this slope is highly dependent on the WR incrementation rate. Furthermore, at slow WR incrementation rates, additional CO2 from compensatory hyperventilation supplements the V'CO2 in the S2 range; this is not the case for rapid incrementation rates, for reasons not fully understood. Maximum RER, being so dependent on the ramp slope is consequently not a good index of subject "effort". The S1-S2 transition reflects a metabolic rate above which CO2 is released from the body that does not originate in either aerobic metabolism or hyperventilation. And as bicarbonate is clearly the origin of this extra CO2, and the [bicarbonate] change is a close proportional function of the increase in muscle [lactate], this is considered to be a valid noninvasive index of the lactate (or anaerobic) threshold. When the V-slope plot may not be partitioned into two defensibly-linear segments the unit tangent to the curve may be used as a second order estimate of the lactate threshold. V'E-V'CO2 relationship and ventilatory equivalents The ventilatory (V'E) response to exercise as a function of V'CO2 is fundamentally related to the regulation of arterial PCO2 (PaCO2) and pH. For alveolar ventilation (V'E) the relationship is: V'A= 863 x VCO2 /PaCO2 Consequently, to regulate PaCO2, V'A must change as an appropriate linear function of V'CO2. However, with respect to total ventilation (i.e. V'E) the relationship is complicated by the ventilation of the physiological dead space or by the dead space fraction of the breath (VD/VT) such that: V'E= 863 x VCO2 /[PaCO2 (1 - VD/VT)] High values of V'E/V'CO2 therefore reflect either a low PaCO2, high VD/VT or both. Naturally, if one is known or may be plausibly assumed, then the high V'E/V'CO2 may be interpreted in terms of the other. It should be noted, however, that a high VD/ VT does not necessarily reflect abnormal pulmonary function, as it is highly dependent on the pattern of breathing: rapid, shallow breathing, for example, yields a high VD/VT even in subjects with normal pulmonary function. V'E has been widely demonstrated to change as a linear function of over a wide range of WRs, i.e.: V'E = mV'CO2 + c Different investigators use different aspects of these latter equations to characterise the ventilatory response: a) the ratio V'E/ V'CO2 and b) DV'E/DV'CO2 (i.e. m). Clearly, V'E/V'CO2 is important, as it is influenced only by VD/VT and PaCO2. Note that in cases in which PaCO2 is constant, VE/ V'CO2 falls in exact proportion to that of VD/ VT. Interestingly, the constant m can be defined as: m =V'E /V'CO2 - c/V'CO2 That is, m may be considered to be the asymptote of the decliningV'E/V'CO2-profile; not necessarily its lowest value achieved during the test. Alternatively, V'E/V'CO2 may be considered to decline during exercise as a result of the positive intercept c. For rapidincremental tests, interestingly, the linearity of the V'E-V'CO2 relationship is maintained beyond the lactate threshold; i.e. V'E changes in proportion to the total CO2 load, with no evidence of PaCO2 being reduced to provide respiratory compensation (isocapnic buffering). The respiratory compensation begins at higher WR, when both V'E/V'CO2 and m begin to increase.

"End-tidal gas tensions are easy to measudifficult re and extremely difficult to interpret..."
As V'E is so closely linked to V'CO2 and as V'CO2 varies markedly with the WR incrementation rate, V'E does not change in a usefully-constant relationship to V'O2, and hence is rarely used in this context. The ratio V'E/ V'O2 however, is used as an index of the additional ventilatory drive that attends the accelerated CO2 output at work rates above the lactate threshold. Having declined throughout the moderate work-rate range, V'E/VO2 begins to increase reflective of increased V'CO2, and when coupled with V'E/VO2 not increasing (i.e. isocapnic buffering) provides good support that the increased ventilatory drive is not consequent to hyperventilation in which case both V'E/V'O2 and V'E/VCO2 and the slope of the V'CO2- V'O2 relationship increases. End-tidal gas tensions End-tidal gas tensions, i.e. the values determined at the end of an exhalation, are easy to measure and extremely difficult to interpret. During exhalation, alveolar PCO 2 (PACO2) continues to increase at a rate that is dependent on the mixed venous PCO2 value and to a level that depends on the duration of the exhalation; The end-tidal value being greater than the mean alveolar and arterial value, as work rate increases in normal subjects is therefore entirely to be expected. The end-tidal to mean alveolar PCO2 difference continues to increase as WR and therefore increases, but can then stabilise at WRs at which tidal volume ceases to continue to increase with respect to V'CO2, and breathing frequency therefore accelerates, progressively to shorten expiratory duration. PETCO2 may therefore be considered to be the peak of the oscillation of PACO2 during the breathing cycle. In the "ideal" lung, "arterial" blood will also manifest such an oscillation, but this oscillation is not measured: what is measured is the mean of this oscillation in PaCO2, as blood is sampled over several respiratory cycles. Mean PaCO2, however, differs from mean PACO2 as a result of ventilation-toperfusion inhomogeneities and/or right-toleft shunt - leading to P ET CO 2 being commonly less than PaCO2 in patients with COPD for example. Consequently, PETCO2 equal to or less than mean PaCO2 during exercise is reflective of abnormal gas exchange.

"...a high VD/V T does not necessarily reflect abnormal pulmonary function, as it is highly dependent on the pattern of breathing..."


VIASYS info Special Edition CPET, April 2002

"In the "ideal" lung, arterial blood will also manifest such an oscillation, but this oscillation is not measured..."
End-tidal PCO2 should therefore not be used to represent arterial PCO2 in computing VD/ VT. Doing so overestimates VD/VT in normal subjects (tending to make abnormal what is normal) and underestimates it in patients with lung disease (tending to make normal what is abnormal). Algorithms for estimating PaCO2 from PETCO2 are poor in normal subjects and do not work in subjects with lung disease. Consequently, the profile of PETCO2 with increasing WR is normally such that it increases progressively up to the lactate threshold, then stabilizes in the region of isocapnic buffering, and subsequently decreases as frank compensatory hyperventilation is manifest. In contrast, end-tidal PO2 (PETO2) progressively decreases up to the lactate threshold, after which it increases systematically, accelerating further with the onset of compensatory hyperventilation. VO2 heart rate relationship and oxygen pulse The oxygen pulse, or the stroke extraction of oxygen (V'O2/HR) bears a similar relationship to the V'O2/HR-slope as the ventilatory equivalent for CO2 does with the V'E/V'CO2Slope. That is, heart rate changes effectively linearly as a function of V'O2 with a slope that is an inverse function a physical fitness. It is instructive to consider the axes differently however: that is, plotted as function of heart rate. This relationship has a negative intercept on axis. Consequently, the oxygen pulse, which by definition is the absolute VO2to heart rate ratio increases hyperbolically as work rate increases. But the oxygen pulse is of interest in an additional sense: it is numerically equivalent to the product of stroke volume and the arterio-venous oxygen content difference. It is important to point out, however, that it should not be considered a function of either of these variables - only the product. Consequently, only if it is possible to make a reasonable assumption regarding the change (or not) in either of the two defining variables may one interpret the non-invasive O2 pulse profile to reflect that of the alternative variable. This, of course, would be both more difficult to determine directly and would require an invasive procedure. If the O2 pulse fails to increase with increasing work rates, then the product of the variables is constant. But this may be because each is constant or one is increasing while the other decreases. Flatness in the O2 pulse profile should be considered with care, however, as subjects who are normal but unfit have a shallow slope of V'O2 plotted as a function of heart rate and hence the curvature of the O2 pulse profile will be shallow appearing to be flat when in fact it is not. For the O2 pulse to be flat there must be a change in the slope such that heart rate accelerates relative to such that over this region the slope extrapolates back to the origin of the plot. When this does occur continued increase in is heart rate dependent. considered to represent the subjectís breathing reserve (BR). The breathing reserve can be zero (or even less than zero, for example, in a subject who bronchodilates during exercise) either as a result of the MVV being low, as in patients with lung disease, or in normal but highly fit subjects who can achieve high rates of metabolic rate and hence of ventilation. Similarly if the maximum expiratory airflow produced with a maximum expiratory effort is considered to reflect the greatest possible flow at a particular lung volume (this of course is not necessarily the case in subjects with obstructive lung disease) then failure to achieve these flows on a breath during exercise is reflective of flow reserve. Similarly, a tidal volume that encroaches upon the inspiratory capacity is reflective of lack of volume reserve. Whether a subject has significant heart rate reserve at maximum exercise is usually judged in the light of the expected maximum value for a subject of that age - unfortunately, the variability of this expected age-dependent maximum heart rate is very wide.

"...the oxygen pulse, which by definition is the absolute VO2 heart rate ratio, increases hyperbolically as work rate increases..."
8. Values attained at the limits of tolerance When a subject has ostensibly exercised to the limit of tolerance it is useful to discern whether certain features of the systems that contribute to the energy exchange have reached their limit. Naturally to make this judgement it is necessary to have an index of what that limit is. For example, if the MVV determined at rest is considered to be the maximum ventilation attainable then the difference between this and the value actually attained at the end of exercise can be
References References

1. Gallagher, C. Exercise and chronic obstructive pulmonary disease. Med. Clinics N. Am. 74:619Gallagher, 641, 1990. 2. Hadebank, D., Reindl, I., Vietzke G., et al. Ventilatory efficiency and exercise tolerance in 101 health volunteers. Eur J Appl Physiol 77:421-426, 1998. 3. Johnson, B.D., Badr, M.S., Dempsey, J.A. Impact of the aging pulmonary system on the reBadr, Dempsey, sponse to exercise. Clin Chest Med 15:229-246, 1994. 4. Jones, N.L. Exercise testing in pulmonary evaluation: Rationale, methods, and the normal respiratory response to exercise. New Engl. J. Med. 293:541-544, 1975. 5. Neder, J.A., L.E. Nery, C. Peres, and B.J. Whipp. Reference values for dynamic responses to Neder, Nery Peres, incremental cycle ergometry in males and females aged 20 to 80. Am. J. Respir. Crit. Care Med. 164:1481-1486, 2001. 6. Roca, J., Whipp, B.J. (eds): Clinical Exercise Testing. European Respiratory Monograph vol 2, No 6. Sheffield: European Respiratory Journals, 1997. 7. Rowell, L.B., Shepherd, J.T. (eds). Handbook of Physiology, Sect 12, Exercise: Regulation J.T. and Integration of Multiple Systems. New York: Oxford Univ Press, 1996. 8. Wagner, P.D. Determinants of maximal oxygen transport and utilization. Ann Rev Physiol 58:21agner, P.D. 50, 1996. 9. Wasserman, K., Hansen, J.E., Sue, D.Y., Casaburi, R, Whipp, B.J. Principles of exercise D.Y., testing and interpretation. Philadelphia, Lippincott, Williams & Wilkins, 1999. 10. Weisman, M., Zeballos, R.J. Clinics in Chest Medicine. Saunders, 1994.

"Subjects who are normal but unfit have a shallow slope of V'O2 plotted as a function of heart rate..."

VIASYS info Special Edition CPET, April 2002



Various CPET - Various Fields of Application
Indication and relevance of cardiopulmonary exercise testing
Definition: Cardiopulmonary exercise testing is defined as the continuous measurement of respiratory gases during exercise.
Introduction Introduction CPET is a diagnostic procedure that analyzes the response and cooperation of the heart, circulation, respiration and metabolism during continuously increasing muscular strain. In this way, maximum exercise capacity and the endurance capacity threshold can be detected. These parameters are of special importance in the fields of: Pulmonology Cardiology Sports medicine Occupational medicine Intensive care Rehabilitation If exercise capacity is limited, the characteristic patterns of the parameters provide important information about which organs are affected by the impairment. As testing sytems become more and more user-friendly, the interest in comprehensive cardiopulmonary exercise testing is continuously increasing. Due to the variety of parameters provided, the fields of application are widely distributed. If an organ or an organic system is impaired, the subjects' ability to adjust to increasing strain is impaired. recorded Four basic parameters will be recorded breathing with the help of a breathing mask and electrodes: ECG electrodes: Minute ventilation Oxygen uptake Carbon dioxide output Heart rate (stress ECG) Prior to CPET the following should be completed: Patient history ECG at rest Pulmonary function test Work, sitting Driving a car Driving a truck Work, standing Walking (4.5 km/h) Crane operating Cleaning the floor Light warehouse work Painting, wall paper hanging Bricklaying, carpentry Working with Jack hammer Steel worker

Estimated oxygen uptake during different activities and occupations: [ml/kg/min] 4,25 4,25 5,30 8,75 10,50 8,75 9,45 10,50 14,00 14,00 - 21,00 21,00 27,00

During cardiopulmonary exercise testing the subject is placed either on an ergometric bicycle or treadmill where load can be continuously increased. The complex requirements of cardiopulmonary exercise testing are met by ramp protocols. During this type of test, strain is increased in small increments. The duration of the test should be between 8 to 12 minutes. For a complete analysis of respiratory function, the flow-volume curve should be recorded at rest, prior to exercise and during submaximal and maximal exercise. The same applies to blood gas values and P(A-a)O2. To clarify special questions concerning gas exchange (for example diffusion disorders), a constant workload test below anaerobic threshold including blood gas analysis may be performed. Exercise should be symptom-optimized, whereby the usual termination criteria for exercise tests have to be observed.


VIASYS info Special Edition CPET, April 2002

Obstructive and restrictive ventilatory disorders Interstitial disorders Pulmonary hypertension Diffusion and distribution disorders Flow disorders Stress dyspnea of unknown cause Suspected limited exercise capacity due to circulatory or pulmonary disorders Suspected exercise-induced asthma Trend control in presence of respiratory and pulmonary diseases Risk estimation for lung transplant patients

Coronary heart disease Cardiomyopathy Valvular heart disease Congenital cardiac defects Risk estimation for heart transplant patients Cardiac insufficiency

Occupational Medicine
Determination of occupational exercise tolerance Determining the degree of disability or work limitation/inability Fitness checkups (high altitude, air travel, tropical climate, diving)

Sports Medicine
Measurement of physical performance for effective training adjustment Quantification of an increase in performance

Intensive Care
Risk assessment prior to surgery Nutrition control (adjusting parenteral nutrition of intensive care patients)

To optimize rehabilitative measures Applications of CPET During CPET the following paramters can recorded: be recorded: Maximum oxygen uptake (peak VO2) Oxygen uptake at anaerobic threshold (VO2AT) Oxygen pulse (O2 Pulse) Breathing equivalents (EQO2, EQCO2) Dead space ventilation (VD/VT) Aerobic capacity (dVO2/dWR) Alveolar-arterial oygen pressure difference (P(A-a)O2) Respiratory exchange ratio (RER) Work rate (watts) Heart rate reserve (HRR) Breathing reserve (BR) Curve analysis In addition to the assessment of the achieved maximum values, the curve trends of the individual parameters have to be assessed over the entire exercise test. Modern CPET systems with breath by breath analysis (such as the Jaeger Oxycon series) allow for a high resolution of the individual parameters. On the basis of the nine panel graph, deviations of the expected curve trend can be easily assessed. Depending on the limiting clinical picture, typical changes are to be expected. On-line recording of the flow-volume curves during exercise is also very helpful. By superimposing the maximal envelope and the current flow curve, the impairment is revealed in the form of a volume or flow limitation. To assess and document rehabilitative and therapeutic progress

Documentation Comprehensive and reproducible documentation of the exercise test is indispensable. Test type and load protocol, as well as an assessment of the achieved capacity according to clinical criteria, should be documented independently of the achieved measured values. At the end of the test the subject should be interviewed on the basis of the Borg scale. This simplifies interpretation of examination results, especially if measured values suddenly differ greatly.

Fig. right: Intrabreath

Fig. left: 9-panel graph

VIASYS info Special Edition CPET, April 2002



Pro Oxycon Pro - CPET of the Highest Quality
A modern diagnostic system must not only be technically convincing, it must above all, be tailored to the routine clinical needs. Therefore, we made Oxycon Pro even faster, more precise and above all, even more economic. For your daily routine you need a practical tool which is suitable for its tasks. After all, you prefer to give attention to your patients and not to your equipment. That is why Jaeger developed the Oxycon Pro.

Oxycon is your expert system if you need a favorably priced CPET system including ECG recording at rest and during exercise. Oxycon Pro is the perfect solution for routine cardiopulmonary exercise testing. The small handy unit combines everything required for routine examinations and offers unparalleled ease of operation. And as costs are an important factor in modern day medicine, Oxycon Pro is favorably priced and meets the highest quality standards. The modular concept provides sufficient possibilities for upgrades or subsequent expansion, whenever required or your investment policies allow it. The heart of the Oxycon Pro is its precise and reliable ergospirometry measurement program. Ergospirometry and related parameters can either be measured "Breath by Breath", "Intrabreath" or via the mixing chamber. User-specific work load protocols for exercise on bicycle or treadmill guide you through the test. The screen display is clearly structured. Preset and logically arranged graphs and groups of graphs show the status of the current workload phase with predicted/actual value comparison. Oxycon Pro precisely analyzes, differentiates and quantifies the functional cooperation of heart, lungs, circulation and metabolism. Oxycon Pro is a secure investment for physicians working in the fields of cardiology, occupational medicine, pediatrics, pulmonology and intensive care. It is the ideal system for the secure assessment of physical performance.

Integrated PC-based ECG: All data at a glance: A notable feature of Oxycon Pro is the exceptional stability of the stress ECG baseline traces. 12-channel ST monitoring is based on a 10-second-interval. A clearly structured ST graph displays the ST changes in different color. In addition, automatic arrythmia detection is provided.

Fig. above: 12-channel ECG including ergospirometry data


VIASYS info Special Edition CPET, April 2002


Oxycon Pro
O2/CO2-analyzer Digital volume sensor (TripleV) Pentium PC Ink-jet printer Trolley

Oxycon Pro

Ergospirometry data during testing - clear and easy

Pro: The advantages of Oxycon Pro: Windows-based user interface Automatic calibration programs Fast and highly precise gas analyzers Precise, low-resistance volume sensor, no flow limitation in the physiological range Standard measurement programs: Spirometry/Flow-Volume Breath by Breath, Intrabreath (partial Flow-Volume loop) Indirect calorimetry Integrated, optional paper-free 12 channel ECG Interpretation program ÑIntelliSupportì Informative, detailed reports All components available from JAEGER Modular concept Interfaces for stress-testing devices and other systems, for example, external ECG Data management for practice administration systems and for hospital networks
Oxycon Pro on trolley

Standard programs: Patient data Automatic volume calibration Volume calibration via manual cal. pump Automatic gas analyzer calibration Ambient conditions Spirometry/Flow-Volume Off-line blood gases/lactate Breath by Breath Intrabreath Mixing chamber High/Low FiO2 Indirect calorimetry - Hood - Ventilator - Hood with high FiO2 - Hood for children Cardiac output Compliance during exercise P0.1 during exercise Resting and stress ECG Screen and printer report Interpretation program: IntelliSupport Generation programs: ReportDesigner Layout editor Profile editor Parameter text editor LaguageMaker User predicted values Predicted value generation Other programs: Data base Load control Connection to practice/hospital EDP syst. ECG suction device Pulse oximeter Standard Option

VIASYS info Special Edition CPET, April 2002


Practical Guideline

Testing Cardiopulmonary Exercise Testing
Author: W. Mitlehner M.D. Authorized translation from German

Exercise testing and ECG recording have been known for about 60 years (1, 2) and have meanwhile been standardized. The goal of this routine test is to detect coronary heart disease. More than 70 years ago, A.V. Hill was the first researcher to examine gas exchange and acid-base-metabolism during exercise while studying muscular physiology (3). During the 1940's, a precise method for testing gas exchange (oxygen uptake and carbon dioxide release) was established for the first time by P.F. Scholander (4). During the 1950's, cardiopulmonary exercise testing had been applied in clinical examinations of patients with cardiac diseases (5, 6). A non-invasive stress testing procedure was hence established that allowed recording of cardio-circulatory and ventilatory, as well as "peripheral" parameters during exercise in addition to electrocardiographic changes. However, a great deal of experimental methods were required making the procedure not clinically feasible. It were Issekutz and Rohdahl, (7) as well as Wasserman et al., (8) who finally developed a method to reliably record oxygen uptake (V'O2) and carbon dioxide release (V'CO2) with the help of fast gas analyzers on a breath-by-breath basis.

Introduction Introduction to CPET Computer technology and advancement of the methods introduced more than 20 years ago have made it possible to easily perform reliable exercise tests, especially in the field of cardiology and pneumolgy. The increasing interest in this procedure caused us to compile a practical and comprehensible introduction to CPET in healthy subjects and patients with lung disease. Literature references can be found at the end of this brochure.

product as well as pyruvate and lactate as an anaerobic intermediate product. Thanks to cardiopulmonary exercise testing, it is possible to quantify a subject's oxygen uptake (VíO2) and carbon dioxide release (VíCO2) and can indirectly observe vesicular breathing in humans and consequently cellular respiration.

As we will later see, the test results are highly reproducible. Consequently, this method is especially suited: 1. to determine the severity of a perforperforrespect repr epromance limitation with respect to reproducibility (for approaches in cardiology, pulmonology and assessments) 2. to define the effect of therapeutic intereffect interventions in the presence of exercise limitation 3. to provide support in differential diagsupport differ ferential nosis regarding the cause of exercise limitation (cardiac, pulmonary or peripheral). Indications for peforming cardiopulmonaexercise (Tab. ry exercise testing (Tab. 1) Sports medicine As cardiopulmonary exercise testing measures a subject's exercise capacity, it is often used to examine healthy subjects in the field of sports medicine. In contrast to the stress ECG, which is somewhat simpler, cardiopulmonary exercise testing allows for the objective and non-invasive measurement of a subject's cardiorespiratory performance and of an athlete's anaerobic threshold. The results provide important information for training purposes. This method has been applied for years (9) and is a routine measurement in sports medicine (10).

Cardiopulmonary exercise testing can be defined as "performance testing on the basis of cardiac, circulatory and ventilatory parameters" for non-invasive quantification of a subject's physical training limits. In addition to determining a subject's exercise capacity (e.g. sports medicine) the test goals are to record the cause of a possible performance impairment and to measure the effect of therapeutic interventions. Metabolic processes and life are only possible if energy is provided in the body cells. At rest, this process takes place in the muscle cells where primarily glucose undergoes aerobic metabolic processes in order to form phosphates that are rich in energy (ATP). During physical strain (under stress) ATP is first formed aerobically. If stress increases, ATP is increasingly produced anaerobically by glycolysis. This process, which is known as cellular respiration, requires oxygen and substrates that are rich in energy (primarily glucose) and forms carbon dioxide as a final

Due to adequate ventilation (VíE), the breathing mechanism allows for gas exchange (VíO2 and VíCO2) which provides the muscles with oxygen (DíO2) and assures that carbon dioxide be transported off (DíCO 2 ) bridged by the cardiovascular system (cardiac output). Coupling the processes of cellular respiration, the cardiovascular system and ventilation are regulated as required according to the blood- and tissue-homeostasis rules for pH, oxygen and carbon dioxide content by central and peripheral regulatory mechanisms. These control mechanisms are responsible for the interaction between these three systems so that the increasing metabolic requirements in the cells under stress can be met. Sufficient oxygen flow to the cells and blood gas homeostasis (pH) in increased carbon dioxide generation through physical activity are regulated as needed. If one of the systems is disturbed (peripheral, cardiovascular, pulmonary or central regulation), considerable changes occur which can be quantified during cardiopulmonary exercise testing.


VIASYS info Special Edition CPET, April 2002

Practical Guideline
Cardiology In order to test the cardiorespiratory function in patient groups with cardiac diseases, cardiopulmonary exercise testing is regarded to be the best suited test (11) and should be routinely performed in transplant patients (11) to determine the severity of the limitation and to give evidence of the failure of other therapeutic interventions. In patients with etiologically undefined stress dyspnea, the test is extremely useful for differentiating dyspnea with primarily pulmonary cause from dyspnea with primarily cardiac cause (12, 13, 14). Pulomonology In the presence of restrictive and obstructive ventilatory disorders and their different causes, cardiorespiratory exercise testing is suitable for characterizing the resulting causes, such as limitation of breathing mechanics, peripheral deconditioning, gas exchange disorders and stress hypoxaemia. Similarily, it is possible to objectively quantify the effect of pharmocologic interventions in both groups of patients as well as the suitability of oxygen application (15, 16). Last but not least, exercise testing is useful in selecting patients for lung transplantation and post-surgical rehabilitation (17). the patient exercise to a maximum?") and an objective measurement of his/her exercise capacity as well as the causes of a possible limitation. For both cardiological and pneumological assessments specific scales are provided classifying the degree of limitation which are based on cardiopulmonary exercise testing (21, 22). Rare approaches Cardiopulmonary exercise testing has been used to assess muscular diseases, neuromuscular diseases and hemoglobinopathy. The rank of CPET, here, is not clearly defined.

Performance testing

Sports medicine, Disability evaluations, Cardiology Pneumology

A A A C A A A A A A A A B C A B Table 1: Indications for CPET

Muscular and Neuromuscular Diseases Training recommendations Undefined dyspnea Transplantation Therapeutical intervention Rehabilitation Cardiology, Pneumology Disability Assessments Cardiology, Pneumology CMP, Cardiac Valve Defects, Oxygen Therapy, Interstitial Pulmonary Disease, Rehabilitation Resection of lung tissue Coronary heart disease CHD - ischemic left ventr. insuff. Pulmonary vascular disease Pneumology Cardiology Cardiology Cardiology, Pneumology

Value: A = highly informative B = informative C = less informative

Cardiac patients with therapeutic interventions, the effect of which can be proved by an increased performance, should always be examined with the help of cardiopulmonary exercise testing in order to get an objective assessment (e.g. therapeutic interventions in the presence of cardiomoyopathy, mitral valve defects, pre and post heart transplantations). In the field of rehabilitation of patients with cardiac diseases, the test is suitable for defining an adequate training program and objectively assessing the effects of training (11). Generally, the test can be used for routine testing in cardiology, when performance capability is to be tested (11).

In pre-surgical examinations (resection of lung tissue) exercise testing is suitable for excluding post-surgical complications (18, 19). Cardiology and Pulmonology Exercise testing allows the observation of cardiopulmonary interaction and is therefore indispensable in defining the dominant cause of undefined stress dyspnea (20, 11). Disability evaluations For disability evaluation, cardiopulmonary exercise testing is of great importance. In contrast to simple stress testing and "Oxyergometry" cardiopulmonary exercise testing provides both a score of the test quality (did

In a nutshell, we can say that cardiopulmonary exercise testing can be used in many internal medical fields. Among many known methods, CPET is the most comprehensive and most informative non-invasive method and is likely to become the standard method of routine exercise testing in the field of internal medicine.

"The physiological processes during exercise are quite complex and of intercharacter..." disciplinary character..."

VIASYS info Special Edition CPET, April 2002


Practical Guideline
Physiological Basics The physiological processes during exercise are quite complex and of interdisciplinary character and can only be summarized in a very simplistic form. The author explicitly refers to the respective literature (e.g. 12, 23 - 25, 31). Physical exercise is physical work (= Power x Distance = 1 kp x m). This work is measured in terms of performance quantities (Performance = Work/Time unit = 1 kpm/ min). Physiological performance is traditionally given in watts (1 watt = 6,12 kpm/min). For muscle contraction during exercise, additional energy above basal metabolic rate must be provided by the metabolism. The increased metabolic requirements are met by increased fat or carbohydrate oxidation (cellular respiration). The energy released by combustion can be defined in terms of kilocalories (oxidation of 1 g fatty acid = 9 kcal; oxidation of 1 g carbohydrate = 4 kcal). The increased oxygen demands during work are met by external respiration (gas exchange) and by the cardiovascular system (oxygen transportation). In the case of pure carbohydrate combustion, the physiological demands for oxygen can be calculated as follows: one liter O2 is required for generating 5,1 kcal (4,6 kcal in case of fatty acid oxidation). Consequently, 1 l oxygen can produce an average of 5 kcal. The carbon dioxide and bicarbonate (CO2, HCO3), which is simultaneously released during substrate combustion, considerably influence the pH value of the blood and are released into the environment via the cardiovascular system (carbon dioxide transport) and via external respiration (gas exchange). The physiological demands, i.e. maintenance of a sufficient oxygenation of the tissue as well as a physiologically tolerable pH value in the blood serum are met by a precise humoral and neuromechanical regulation mechanism. This sets the varying parameters (respiration, circulation, metabolism) by homeostasis as required at rest and during exercise. Cellular respiration and muscular bioenergetics Muscle contraction and its power are based on the interaction of the contractile proteins actin and myosin. This energy-consuming process is made possible by hydrolytic separation of phosphate from ATP molecules. Fig. 1 Type I fibers are especially rich in oxidative enzymes, whereas type IIb fibers contain mainly glycolytic enzymes. Under incremental exercise, recruitment of the fibers takes place as follows: S fibers with exercise onset, next cascade-like FR and FI and finally FF. ATP consumption is regenerated by four physiological mechanisms: aerobic respiratory chain phosphorylation anaerobic glycolysis creatine kinasis adenylate kinasis On the basis of their myofibrillar ATPase activity, the voluntary muscles can be diffevoluntary rentiated histochemically in different metabolic and functional fiber portions: Type I, IIa, II b and IIx fibers. Depending on their contractional and fatigueinduced behaviour, muscle fibers and related motoneurons can be physiologically differentiated in S (= slow-fatigue-resistant), FR (= fast-fatigue-resistant), FI = (fast-fatigueintermediate) and FF (= fast fatigable) motor units. These motor units are closely related to histochemical classification: the aerobic type I fibers are slow and fatigue-resistant (S), whereas the anaerobic type IIb fibers are fast fatigable (FF). Types IIa and IIx are of intermediate character.


Fig. 2


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Practical Guideline
The load-dependent recruitment of different types of fibers and consequent different metabolic pathways (type I fibers type IIb At a load range, which physiologically is between 40% and 65% of the individually achievable maximal O2 uptake (VíO2 max.), course of the VíCO2 and VíO2 slope until AT was reached and beyond AT followed the course of the VíCO2 curve, changes again and may show a steeper slope than VíCO2. This is called the "Respiratory Compensation Point" and shows that tissue acidosis is increasing (as a result of muscle fatigue). The anaerobic threshold and the "Respiratory Compensation Point" can also be calculated on the basis of the respiratory equivalents of O2 (EQO2 = VíE/VíO2) and CO2 (EQCO2 = VíE/VíCO2). Please refer to Fig. 4. A permanent increase of EQO2 during exercise reflects the anaerobic threshold, whereas the rise in EQCO2 beyond AT reflects the "Respiratory Compensation Point" (Fig. 4). The neural and humoral regulation mechanisms, which influence the ventilatory adjustment to ventilation, are very complex and yet not completely known. They cannot be discussed in the frame of this essay (also compare 25). Fig. 3 fibers) are an explanation for the predominant aerobic processes during onset of incremental exercise as compared to the predominant anaerobic processes (type IIb fibers - FF fibers) at the end of exercise. These mainly work glycolytically and under increased lactate production, but each having a higher contractility (FR FI FF fibers). At rest and with the onset of exercise, muscular energy (ATP) is yielded from glucose and fat under aerobic conditions. With increasing work rate and on the basis of a continuoulsy increasing O2 demand a relative O2-deficiency occurs in the tissue in addition to ATP regeneration giving rise to an increase in anaerobic processes (involving the already mentioned fiber types FR, FI, FF), which form less ATP, but more lactate and H+ions as well as CO2. Under the anaerobic conditions of muscular metabolism, CO2 forming is four times higher giving rise to an increasing acidosis. Simultaneously, increasing lactate production during anaerobic glycolysis and increasing tissue acidosis result in an unproportional rise in ventilation or ventilatory demand (anaerobic threshold) during exercise (Fig. 1, 2, 3). With steadily increasing exercise, muscle fibers are increasingly recruited and blood supply and consequently O2 supply to the muscles continuously increase. Simultaneously, CO2 production in the muscles rises as a linear function. CO2 production has a greater slope than O2consumption as aerobic processes of energy production are increased due to recruitment of IIa and IIb fibers. Consequently, the production of lactate and H-ions rises and CO2 even rises by four times the normal amount. In order to counteract the resulting tissue acidosis, ventilation is stimulated unproportionally to the previously increased O2 demand via chemoreceptors. During exercise, this gives rise to an unproportional increase of ventilation (VíE/VíO2) in the presence of an increasing respiratory exchange rate (RER = VíCO2/VíO2). This ventilatory adjustment to anaerobic metabolic conditions, i.e. the unproportional rise of the ventilatory equivalent for oxygen (VíE/VíO2) under exercise is termed as "anaerobic threshold" (ATan). The simultaneous unproportionate CO2 production and release (VíCO2) can be illustrated by the steeper slope of the VíCO2 curve as compared to the VíO2 curve under increasing load. In this way, the anaerobic threshold (ATan) can be constructed geometrically from the curve trends of VíO2 and VíCO2. This threshold is at 40 - 60% of VíO2 max. Consequently, RER, which under exercise decreased to values < 0.8, will again increase. When exercise is continued, H-ions are increasingly produced beyond aerobic threshold, which give rise to a further central stimulation of ventilation exceeding the already high VíCO2-dependent increase. Here, at approximately 70 - 90% of VíO2 max, the slope of the VíE-curve, which followed the Respiratory mechanics during exercise Effective ventilation (VíE in l/min) is determined by tidal breathing (VT in ml) and breathing frequency (BF in breaths/min). During exercise both parameters will increase in healthy subjects. At a low work rate, VT rises first (up to approximately 50% of VC). Next, VT and BF will increase similarly. At approximately 70 - 80% of VíO2 max BF can generally only be increased. The dominant increase of VT during the onset of exercise is a result of a continuous decline in the endexpiratory reserve volume and an increase in the endinspiratory pulmonary volume. Especially the endexpiratory decline in pulmonary volume during exercise optimizes the power/length ratio of the respiratory muscles (26). At higher work rates, the increase in breathing frequency is characterized by a declined expiration time (t E) and an increased inspiration time (t I), i.e. ( ti / t TOT > 0.4 - 0.55) (25). The breathing frequencies achieved during exercise are between 50 - 60/min (23). In healthy subjects, the airway resistance changes during exercise as a result of bronchodilation, which can be due to a decline in vagal stimulation (27), an increase in sympathic afference or a release of NO (28). Despite bronchodilation, the increase in VT during exercise gives rise to an increase in respiratory work as elastic respiratory work increases (thoracic expansion, expansion of the lung tissue). Additional factors for an increase in resistance at rising VT are the increasing flow turbulances as well as dynamic airway compression, which also occurs in healthy subjects.

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Practical Guideline
An increased ventilation during exercise gives rise to an increased O2 demand of the respiratory muscles (VíO2 resp.). At rest and with moderate work rate, the share of VíO2 resp. of total VíO2 is reported to be approximately 5% (29, 30). In healthy athletes, this share can increase to 7% up to a maximum of 15 - 20% of VíO2. During expiration the mixed expiratory CO2 pressure (PECO2) and the endexpiratory CO2 pressure (PET-CO2) can be measured. Analogous measurements are responsible for the expiratory/inspiratory O2. The PECO2 is defined by a gas mixture, which is determined by dead space (anatomical and physiological dead space) and alveolar ventilation. The parts of the lung with different VíA/Q relation are responsible for the composition of the gas mixture. It should, however, be noted that with capillary PaO2 measurement, the arterial PaO2 values are not always correct (32). Additionally, it should be pointed out that the precision of blood gas analyzers can vary (33), so that only changes of values > 5 mmHg should be considered. Yet, despite these technical measurement problems, certain deviations from the initial PaO2 under load (up to < 70 mmHg) are experienced while testing healthy patients (older patients, competitive athletes) under physiological conditions. Both alveolar and arterial O2 pressures will discretely change during exercise (Fig. 5). Furthermore, alveolar-arterial pressure difference rises. At rest, the value is approximately 8 mmHg (30) and can amount up to 40 mmHg in top athletes (31). The cause for the increase of this difference is thought to be a limitation of O2 diffusion and an increase in V'A/Q mismatch (31). Cardiovascular response Systemic oxygen transportation to the working muscles depends on the blood supply of the tissue (Cardiac Output) and on the oxygen contents of the arterial blood (= arterial O2 pressure + contents of hemoglobin + O2 to hemoglobin affinity). The increased oxygen transportation during exercise is primarily achieved by increasing cardiac output. With increasing work rate, oxygen uptake and cardiac output will increase in a linear relation (Fig. 6). These parameters rise until an individual maximum value is reached. This point is referred to as maximum oxygen uptake (VíO2 max) and forms an individual plateau value that cannot be exceeded. Consequently, VíO2 max is a stable and reproducible individual physiologic variable in humans. Age and body position (lying, upright position) will change the increase in cardiac output in relation to exercise (slope and absolute values) due to the different cardiac pumping behavior. Cardiac output can be increased dependent of work rate by increasing both heart rate and stroke volume. Depending on the individual training condition, the stroke volume in well-trained subjects is first increased from approx. 60 to 200 ml (30), followed by an increase in heart rate. On the contrary, in untrained subjects cardiac output is increased via an increase in heart rate. The poorer the subject's training condition is, the faster heart rate increases. On the other hand, a person's physical training will increase stroke volume and reduce heart frequency (Fig. 6)

Breathing reserve (BR) is defined to be the difference between maximum voluntary ventilation (MVV) and maximum ventilation during exercise (VíE max): BR = MVV - VíEmax. Healthy subjects terminate the test with a peak ventilation not exceeding 50 - 70% of MVV. This is due to the fact that VT normally reaches only approximately 50 - 60% of VC during exercise (31). Similarily, the maximum breathing frequencies achievable at rest cannot be reached during exercise. Consequently, these persons have a breathing reserve. However, top athletes utilize their breathing frequency up to their breathing mechanism limit.

Therefore, the relation between arterial blood gases and composition of mixed expiratory gas concentrations are an index for the effectivity of gas exchange. Physiological dead space (VD/VT) is calculated as follows:
VD/VT = (PaCO2 - PECO2)/PaCO2

As physiological dead space is an important variable for gas exchange, a change in its share can considerably contribute to the adjustment to the higher ventilatory demand during exercise.

Fig.4 Gas exchange At rest, dead space ventilation (VD/VT) is > 30% and considerably declines in healthy subjects (far below 20%). If, during dead space ventilation measurement, PETCO2 is measured instead of PaCO2, dead space ventilation is overestimated in normal subjects and underestimated in patients with lung disease. That's why many evaluation programs allow the entry of the arterial PaCO2 as a correction factor for dead space calculation.

Alveolar ventilation (VíA) and perialveolaracinic perfusion (Q) are the determinants of gas exchange.
The balance between VíA and Q (VíA/Q) defines the effectivity of gas exchange of a certain alveolar region in the lung. Under certain conditions (physiological rest) there are regions of different VíA/Q sections, e.g. in dependant parts of the lung, perfusion is higher than ventilation. Consequently, alveolar O2 pressure (PAO2) is lower and CO2 pressure (PACO2) is higher than in regions of lower perfusion as compared to ventilation.

Oxygen saturation which during exercise is mainly measured as PaO2, is kept in the range of the values measured at rest in healthy subjects.


VIASYS info Special Edition CPET, April 2002

Practical Guideline
Exercise Protocols
Bruce Protocol Balke Protocol Naughton 4 steps /3 minutes (1.7 mph and 10% slope up to 4.2 mph and 16 % slope) Constant speed and increase of slope by 1%/min. 15 test steps of 3 minutes each, starting at 3.2, km/h with 3.5% slope/3 min. respectively and increase in speed by 1.6 km/h every 6 min.

Bicycle ergometer
Incremental exercise test Ramp 60 RPM; increase 5 - 25 W/min.; planned test duration 6-12 min Test termination: exhaustion or termination criteria Continuously increasing exercise; increase at a one-second interval

Stress testing methods stress Standardized stress tests can be performed with the help of: - bicycle ergometers - treadmill ergometers - hand-cranked ergometers Each of these methods has certain benefits. The decision as to which method is used depends on the space available and on the amount of patients to be tested. The test results and predicted values are to be stated dependent on the applied testing method. It should however, be noted that with treadmill tests V'O2 max is about 7% - 10% higher than with bicycle tests. Whereby ventilatory and lactate parameters will be higher with bicycle tests than with treadmill tests (34, 35, 36). The test results are, furthermore, considerably influenced by the selected load protocol. Basically, we can differentiate between constant and constantly-increasing work load types. Differ ferent exercise Different modalities of constant exercise tests have been developed: - Maximum work load for a constant time. - Constant work load with a duration of 6 min. - Intermittent constant work load with a duration of 6 min. with an increase in work load between two tests, whereby the pause between the tests is between 15 min. and 24 hours. Constantly increasing work loads can be realized in one test aiming at stressing the patient to a maximum.

Fig. 5 An acute increase of haematocrit with heavy work load is possible in healthy subjects; however, this is not an important factor regarding improvement of oxygen transportation while exercising (30). In top athletes, however, training gives rise to an increase in blood volume and consequently in oxygen transport capacity and thus becomes relevant for an increase in exercise capacity. Assuming that one of the variables (e.g. SV) remains constant during exercise, oxygen pulse is a function of the other respectively. During exercise, arterial-venous O2 difference remains constant as long as oxygen utilization and consequently arterial-venous O2 difference increases at the end of exercise. From now on oxygen pulse can be regarded to be an indicator for the increase in stroke volume.

Oxygen pulse (VíO2/HR) is a variable that can be determined by cardiopulmonary exercise testing and can be deduced from the product of stroke volume and the difference of arterial and central-venous oxygen contents i.e. VíO2/HR = SV x (CaO2 - CvO2).

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Practical Guideline
be planned in a way that the subject/patient is stressed to a maximum, provided that no submaximal exercise (50 - 85% of pred) is to be achieved for clinical reasons. Goals The predicted exercise capacity can be estimated as follows (38): pred Watts pred = Body weight (kg) x 3(Male) Body weight(kg) x 2,5(Female),


Athlete Fig. 6

Today, constantly increasing exercise tests (maximum or submaximum stress) are mainly performed for practical reasons. The previously described constant exercise tests have mainly been developed on the basis of scientific approaches, such as the determination of VíO2 max or ventilatory kinetics. It should, however, be pointed out that V'O2 max can only be precisely determined on the basis of an intermittent constant exercise test. With constantly increasing exercise, on the other hand, that means without steady state conditions, it is possible to achieve a peak work load allowing to measure "VíO2 peak". It is an individual peak value that is recorded with the latter method, but not a plateau value as demanded for VíO2 max (37). It should be noted that the applied predicted values have to be obtained with the same testing method as applied during recording. In Western Europe bicycle ergometry is mainly used. Work load steps of three or more minutes steady state, that have been used a few years ago, are not required. Steady state cannot be achieved with maximum work load (38).

Today, mainly steps of 2 (-1) minutes are possible for technological reasons, however, with simultaneous right-ventricular catheterization different steps are required. The total duration of work load should be approx. 10 minutes and should not exceed 15 minutes. A duration of < 7 minutes can lead to erroneous results (39). Depending on the subject's or patient's condition, the examination should

minus 10% per age decade > 30 years, respectively (38). During bicycle ergometry 60 (70) RPM should be used. The slope of the exercise increase depends on the planned exercise duration. However, the absolute increase/min. between 20 and 50 watts will not influence the results during ramp testing with healthy subjects (40,41). In conclusion, we can say that symptom-limited exercise tests should meet the following demands: planned test period of 10 minutes, predicted work load according to calculation given above, slope increase of work load/minute according to these two parameters. The initial work load should depend on the estimated individual fitness. Measurements should be taken at rest for a period of at least 5 minutes before and after the exercise (36).

Fig. 7


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Practical Guideline
1. 2. 3. 4. 5. 6. 7. 8. 9 Goldhammer, S., Scherf, D.: Elektrokardiographische Untersuchungen bei Kranken mit Angina pectoris. Z.klin. Med. 122 (1932), 134 f. Goldhammer, Dietrich, S., Schwiegk, H.: Angina pectoris und Anoxie des Herzmuskels, Z. klin. Med. 125(1933), 195 f. A.V., Hill, A.V., Long, C.N.H., Lupton, H. : Muscular exercise, lactic acid and supply und utilisation of oxygen. 1. Proc. Roy. Soc. London, Ser. B. 96 ( 1924), 438 - 475. Scholander, K.F. Scholander, K.F., Analyser for accurate estimating of respiratory gases in one-half cubic centimeter samples. J. Biol. Chem. 167 ( 1947), 235 - 259). Huckabee,W.E. .E., Huckabee,W.E. J. Clin. Invest., 37 (1958), 1577 - 1592, 1593 - 1602: The role of anaerobic metabolism in the performance of mild muscular work. I. relationship to oxygen consumption and cardiac output, and the effect of congestive heart failure. II. the effect of asymptomatic heart disease. aylor, Taylor, H.L., Buskirk, E., Henschel, A. , J. appl. Physiol. 8 (1955), 73 ff: Maximal oxygen intake as an objective measure of cardio-respiratory performance. K., Issekutz, B., Rohdahl, K. J.appl. Physiol., 16 (1961), 606 - 610: Respiratory quotient during exercise. Beaver, .L., Wasserman, K., Whipp, B.J., Koyal, S.N., Beaver, W.L. J. appl. Physiol, 35 (1973), 236 - 243 : Anaerobic threshold and respiratory gas exchange during exercise. aylor, H.L. Taylor, E. Buskirk, A. Henschel J. Appl. Phys. 8, (1955), 73 - 80: Maximal oxygen intake as an objective measure of cardio-respiratory performance.

Mellerowicz,H owicz,H.Urban u. Schwarzenberg, M¸nchen, 1979: Ergometrie. 10. Mellerowicz,H al., 11. Gibbons, R. et al. JACC 30 ( 1997), 260 - 315: ACC/AHA Guidelines for exercise testing. A report of the american college of cardiology/american heart association task force on practice guidelines (committee on exercise testing). DY., BJ.: 12. Wasserman, K., Hansen, JE., Sue, DY., Whipp, BJ. Principles of exercise testing and interpretation. Philadelphia: Lea and Febiger, 1987. Eschenbacher, A., 13. Eschenbacher, W., Mannina, A. Chest 97 (1990), 263 - 267: An algorithm for the interpretation of cardiopulmonary exercise tests. 14. Mc Connel, TR., Laubach CA., Clark BA., J Cardiopulmon Rehabil, 15 (1995), 257 - 261: Value of gas exchange analysis in heart disease. Mitlehner,W Kerb,W. ,W., 15. Mitlehner,W., Kerb,W Respiration, 61 (1994), 255 - 266: Exercise hypoxemia and the effects of increased inspiratory oxygen concentration in severe chronic obstructive pulmonary disease. al. 16. Harris-Eze, AO., et al Am. J Respir. Crit Care Med. 150 (1994), 1616 - 1622: Oxygen improves maximal exercise performance in interstitial lung disease. Iademarco E.P, 17. Howard, DK., Iademarco EJ., Trulock E.P, Clinics in chest medicine 15 (1994), 405 - 420: The role of cardiopulmonary exercise testing in lung and heart - lung transplantation. Brenoe, B.N.; 18. Larsen,R., Svendsen, UG., Milman, N., Brenoe, J., Petersen, B.N. Eur. Resp. J.,10 (1997), 1559-1565: Exercise testing in the preoperative evaluation of patients with bronchogenic carcinoma. Bolliger, al., 19. Bolliger, CT et al Am J Respir Crit Care Med 151 (1995), 1472 - 1480: Exercise capacity as a predictor of postoperative complications in lung resection candidates. Mahler, Horowitz, MB., 20. Mahler, DA., Horowitz, MB. Clinics in chest medicine 15 (1994), 259 - 270: Clinical evaluation of exertional dyspnea. Marx, H.: 21. Marx, H.H., Klepzig, H. Medizinische Begutachtung innerer Krankheiten. Thieme Verlag, Stuttgart, 7∞, 1997. 22. American thorax society: Evaluation of impairment/disability secondary to respiratory disorders. Am Rev Respir. Dis, 133 (1986), 1205 ff. N.L.: 23. Jones, N.L. Clinical exercise testing. W.B. Saunders, 3∞, 1988. 24. Whipp, B.J., Clinics in chest medicine, 15 (1994), 173 - 192: The bioenergetic and gas exchange basis of exercise testing.. C., 25. Johnson, B D., Beck, K C Allergic and respiratory disease in sports medicine, 11 (1997), 1 - 34: Respiratory system responses to dynamic exercise. Dempsey, 26. Dempsey, JA, Hanson PG, Henderson, , KS, Schweiz. Z. Sportmedizin (1992), 40, 55 - 64: Demand vs. capacity in healthy pulmonary system. arren TJH, 27. Warren JG, Jennings SJ, Clark TJH Clin. Sci. (1984), 66, 79 - 85: Effect of adrenergic and vagal blockade on the normal human airway response to exercise. PM. 28. Morrison KJ, Gao Y, Vanhoutte PM Am J Phys.(1990), 258, L 254 - L 262: Epithelial modulation of airway smooth muscle. Aaron JA, 29. Aaron EA, Johnson BD, Seow CK, Dempsey JA J Appl Physiol. (1992), 72, 1810 - 1817: Oxygen cost of exercise hyperpnea: measurement. 30. Murray J F: The normal lung.2∞, W.B. Saunders, 1986. 31. Whipp, BJ, Wagner PD, Agusti A: in European respiratory monograph (1997), 2,6, 3-31: Response to exercise in healthy subjects. Sauty, Uldry L-F, Leuenberger, P, J-W, 32. Sauty, A, Uldry, C, Debetaz L-F, Leuenberger, P, Fitting, J-W, Eur. Respir. J. (1996), 9, 186 - 189: Differences in PO2 and PCO2 between arterial and arterialized earlobe samples. Macgregor egor, RL, 33. Scuderi, Ph E, Macgregor, DA, Bowton, DL, Harris, LC, Anderson, R, James, RL Am Rev. Resp. Dis. (1993), 147, 1354 - 1359: Performance characteristics and interanalyser variability of PO2 measurements using tonometered human blood. 34. Shepard, RJ, Int Z. angew. Physiol. (1966), 23, 219 - 230: The relative merits of the step test, bicycle ergometer and treadmill in the assesment of cardio-respiratory fitness. RJ, 35. Shepard, RJ Standard tests of aerobic power. In Shepard RJ, : Frontiers of fitness, Charles E. Thomas, Springfield, 1971. 36. Hansen, JE, Am Rev Resp. Dis. (1984), 129 Suppl. S 25 - S27: Exercise instruments, schemes and protocols for evaluating the dyspneic patient. aylor, 37. Taylor, HL, Buskirk E., Henschel A, J appl. Physiol. (1955), 8, 73 - 80: Maximal oxygen uptake as an objective measure of cardio-respiratory performance. 38. H. Lˆllgen. Kardiopulmonale Funktionsdiagnostik, Editio CIBA , Ciba - Geigy, Wehr, 2∞, 1992. Buchf¸hrer DY, BJ: 39. Buchf¸hrer MJ, Hansen JE, Robinson TE, Sue DY, Wasserman K, Whipp BJ Am Rev Respir Dis (1982), 125, Suppl., 259: Optimizing the work rate protocol for clinical exercise tests. orres F, 40. Whipp BJ, Davies JA, Torres F, Wasserman , J Appl Physiol (1981), 50, 217 - 221: A test to determine parameters of aerobic function during exercise. 41. Davies JA, Whipp BJ, Lamarra N, Huntsman DJ, Frank MH, Wasserman K, Med Sci Sports (1982), 14, 339 - 343: Effect of ramp slope on measurement of aerobic parameters from the ramp exercise test. Reindell: 42. H. Roskamm, H. Reindell Herzkrankheiten, Springer Verlag, Berlin. 1982.

Wolfgang Mitlehner, M.D. Internist Pulmonary and Bronchial Diseases, Allergology Specializing in Pulmonology and Oncology Turmstr. 21, Haus K D-10559 Berlin +49 (0)30 3918747 +49 (0)30 39903889 eMail: wolfgang-mitlehner@t-online.de www.dr-mitlehner.de

VIASYS info Special Edition CPET, April 2002



Vmax and Cardiosoft
CPET by SensorMedics, ECG by Marquette Hellige.

Are you looking for a sophisticated, high-end cardiopulmonary exercise testing system and don't want to go without a high-quality ECG system? SensorMedics provides a perfect solution and combines two leading products in one system.
Thanks to the close cooperation with Marquette-Hellige, SensorMedics successfully combined Vmax and Cardiosoft in one system. Five different screen displays, that can be selected during the test allow you to decide whether you want to view CPET or ECG data only or whether you want to combine all data on one screen. Of course, patient data doesn't have to be entered twice; a special program does that for you automatically. It is also possible to record an individual stress ECG or, optionally, an individual ECG at rest. SensorMedics Vmax product series Vmax is a versatile cardiopulmonary exercise testing system which meets the demands of doctors whether they be in hospital or private practice. Whether you need a system for routine testing or research, for adults or children, for patients or athletes - Vmax can always be tailored to your needs. Vmax is an open system that allows you to record important parameters such as O2 uptake, CO2 output, RER, ventilation (V'E), O2 pulse etc. on a breath by breath basis. The results can be displayed on-line in numeric and graphic form. The test can be performed via mouthpiece or mask. The lightweight mass flow sensor is insensitve to moisture and always provides highly-precise ventilatory data due to its small dead space. With Vmax, you define the product. You might even design your own configuration, for example with indirect calorimetry, diffusion measurements (even during exercise), cardiac output, P0.1, bodyplethysmography etc. Vmax, of course, provides a program for pulmonary function analysis. You can easily measure the flow-volume loop at rest and during exercise and display both loops in one screen for diagnosis of a ventilatory impairment.

Above: CPET including Vmax Right: Vmax CPET including Hellige ECG

All data at a glance: Stress ECG with CPET results


VIASYS info Special Edition CPET, April 2002



Cardiopulmonary Exercise Testing

Indirect Calorimetry

Last but not least, Vmax makes it possible to perform a bronchial challenge testing with the flow-volume loop. SensorMedics has always attached great importance to absolute precision. The analyzers can be checked during automatic 2-point calibration. The same applies to volume calibration. A further unique feature is the builtin quality control for correct measurement performance. If required, the system indicates accuracy and reproducibility of the flowvolume loop. The fast and precise analyzers meet the highest standards and, unlike other types of analyzers, don't have to be exchanged at regular intervals. The help program is a real trendsetter that explains and illustrates every measurement and setting with the assistance of animated pictures. The tutor on CD-ROM, which is included, provides valuable information regarding measurement technology and parameters.

Marquette-Hellige*1-ECG The Hellige ECG is a first-class 12-channel PC-ECG and consists of Corina amplifier and Cardiosoft software. Thanks to clinical verification, the algorithms for ECG analysis of Marquette-Hellige are the most precise and reliable algorithms in the world. You can either use adhesive electrodes or the KISS suction electrodes. During stress ECG recording, a real-time arrythmia analysis and a 12channel on-line ST analysis is performed. The Hellige Cardiosoft program automatically controls the ergometer, as well as the blood pressure measurement so that you can concentrate on your patient. Optionally, the 12-channel ECG can be continuously saved. ECG at rest including dimensioning and interpretation is also available as an option.

The advantages at a glance:
Powerful analyzers Flow-volume loop during exercise Report Maker Predicted Value Maker Tutor Arrhythmia detection CPET stand-alone

Items included: Computer, color ink-jet printer and monitor on an ergonomic trolley Vmax analyzer and test module Vmax software "Vision" Comprehensive help program Vmax "Tutor" Amplifier "Corina" made by Marquette-Hellige Software "Cardiosoft" made by Marquette-Hellige KISS suction electrodes or leads for adhesive electrodes Integrated isolating transformer Calibration pump Accessories kit

Above F/V loop during exercise Left: Spirometry measurement


a GE Medical Systems company Vmax CPET and Hellige ECG

VIASYS info Special Edition CPET, April 2002


Diagnostics All features at a glance:
Maintenance-free O2/CO2 analyzer Ambient module for temperature and pressure Mass flow sensor Breath by breath Mixing chamber Powerful PC Color ink-jet printer Mobile cart Volume calibration program Automatic gas calibration Patient data base Spirometry/flow volume program CPET program Entry of blood gas analysis values including markers Capnogram display Off-line entry of blood pressure, SaO2 User-specific graphics design User-specific parameter tables Flow-volume loop during exercise Automatic AT calculation Manual AT calculation Automatic VO2 peak calculation Manual VO2 peak calculation Warning if limit value is exceeded Screen and printer reports User-specific design of assessments Predicted value editor Work load control Measurement with elevated/lowered FIO2 Indirect calorimetry - with hood - for ventilated patients - hood with elevated FiO2 - hood for children Cardiac output Single breath diffusion measurement Intrabreath diffusion measurement Diffusion during exercise Membrane measurement FRC measurement N2 washout O2 single breath for closing volume Bodyplethysmography P0.1/Pmax Compliance Provocation Pulse oximeter Calibration and test gas Pressure reducer Network Lung function interpretation program 3-channel ECG
Standard Option

Hellige-ECG Cardiosoft
Amplifier module "Corina" Software "Cardiosoft" Adhesive electrodes or KISS suction unit Interface to SensorMedics Vmax Data base 12-channel ergometry program On-line arrhythmia detection Warning in case of critical arrhythmias On-line-ST analysis Trend graphs Single electrode control HR alarm, acoustically and optically Anti-drift system 35 Hz and 50 Hz filter Automatic zeroing Display as on recording paper Exercise control On-line storage of entire ECG ECG at rest Interpretation of ECG at rest Arrhythmia marking and classification



Cardiopulmonary exercise testing and ECG perfectly combined in one unit.
VIASYS info Special Edition CPET, April 2002



Oxycon Mobile
A milestone in CPET
Execellent diagnostic possibilities are achieved by traditional stress testing equipment like treadmill and bicycle ergometer. Up until now this equipment has been limited to indoor usage. Now we have the Oxycon Mobile.

Oxycon Mobile offers on-the-spot measurements of all relevant CPET parameters. The small sophisticated unit is attached to a comfortable belt system. This is slipped over the test subject's shoulder. The test can be performed via a breathing mask and the subject is not impeded by tubes and cables. The recorded data is telemetrically transferred to the PC or saved on a small chip card. After being transferred, the data is analyzed using the powerful Oxycon Software by Jaeger. Oxycon Mobile records all key parameters such as: Ventilation V'E VO2, VCO2 Anaerobic threshold RER HR EQO2, EQCO2 Main features: Telemetric data transfer Portable, lightweight unit attached to a belt system, which is slipped over the shoulders. Complete CPET test including flowvolume loop, heart rate, ECG, anaerobic threshold etc. Long-range telemetry for real-time data monitoring Applicable to a wide range of test subjects from seriously ill patients to elite athletes Powerful evaluation software with report generator

Fields of application: Pulmonology, cardiology, intensive care Suspected stress-induced asthma Monitoring of patients with heart diseases Monitoring of parenteral fed patients Rehabilitation Therapy monitoring Occupational medicine Determination of occupational exercise tolerance Determination of degree of handicap Sports medicine Optimizing of training

Fig. left: Belt system Display of anaerobic threshold

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Clinical Importance of CPET
Author: Prof. Karl-Heinz R¸hle, M.D.

In regards to exercise tolerance, cardiopulmonary exercise testing is an excellent tool for diagnosis and therapy. However, the values obtained at rest during cardiopulmonary function diagnostics are often not enough to establish a proper therapy. The results of cardiopulmonary exercise testing can be interpreted on the basis of the nine-panel graph which gives a clearly structured overview of exercise capacity, cardiac parameters, pulmonary performance values and gas exchange parameters.
cardiopulmonary exercise Indications for cardiopulmonary exercise testing
A. Disability assessment Maximum exercise capacity Factors of exercise limitation Risk/prognosis B. Risk/prognosis Risk assessment prior to pulmonary resection (pneumonectomy, lobectomy) Risk assessment prior to heart transplantation C. Therapy assessment Training O2 therapy Drug therapy A. Disability assessment Maximum exercise capacity With good patient effort, definition of maximum oxygen uptake is the best method to define a subject's physical exercise capacity. Indication that the subject has reached his/ her maximum exercise capacity is the plateau-formation of the continuously measured V'O2 in the ramp protocol, despite increasing work load. This value is referred to as V'O2 max. If V'O2 rises only slightly, one can be sure that the patient is stressed to a maximum and consequently a cardiopulmonary limitation is present. This is of special importance for disability assessments. If no plateau is reached, we talk about Peak V'O2 (or V'O2 peak). In fact, this is the highest V'O2 achieved during the test. Here, it is not possible to decide whether patient effort was good or not. In this context, it is helpful to consider base excess (BE). If this value falls below -6 up to -9 mmol/l in healthy subjects, it can be assumed that the subject has been stressed to a maximum. Especially in the presence of pulmonary diseases maximum exercise capacity cannot be exactly predicted on the basis of functional parameters measured at rest. It is therefore indispensable for disability assessments to describe the impairment caused by e.g. functional pulmonary or cardiac disorders during exercise, as well as the resulting reduced exercise capacity on the basis of V'O2 max. Functional impairments are highly relevant with regard to their effects on occupation and way of life. Disability In some occupations, people are exposed to short-termed maximum loads. By determining V'O2 peak, it can be decided whether the subject can meet this requirement during specific conditions (disability for a certain occupation). The measurement of V'O2 peak provides important information about the endurance capacity. The demands of a normal 8-hour working day should be considerably below the endurance limit. If an exact description of the working place including the average oxygen uptake during work or power in watts is available, disability can be better assessed by determining maximum oxygen uptake with regard to the possible performance. Factors of exercise limitation Even with a great deal of expenditure cardiopulmonary exercise testing only allows to describe approximately 50% of the influencing factors. Other limiting factors, such as dyspnea or claudicating pain cannot be quantified objectively. A study with COPD patients showed that in 46% of all cases muscle exhaustion was the main cause for exercise cessation. Cessation due to dyspnea was only reported in 36 % of the cases. Patients with interstitial pulmonary fibrosis however ceased exercising due to dyspnea (62%) and muscle exhaustion (25%). To determine maximum oxygen uptake, the Borg scale is highly recommended. Dyspnea often rises linearly with increasing work load (V'O2,Watt or V'E/MVV); however, the work load dependant increase of dyspnea varies with the type of disease and can also be used to estimate the probable maximum exercise capacity during examination. An important aspect of cardiopulmonary exercise testing is that it allows to exclude a relevant cardiopulmonary impairment.


VIASYS info Special Edition CPET, April 2002

This is valid, whenever a patient complains about stress dyspnea, but nevertheless reaches his/her steady state/unsteady state exercise capacity according to the respective reference values. Consequently, exercise capacity is normal but the subjects are either not able to assess their condition or suffer from psychogenically induced dyspnea. With normal exercise capacity the patient can be reassured. Alternatively a psychotherapy or a drug therapy (sedatives, anxiolytics) can be prescribed. Additional examinations are often not required. Lack of training and reduced exercise capacity, for example in case of adipositas, cannot be differentiated from cardiac impairments. It should be generally noted that the results of the cardiopulmonary exercise test cannot be assigned to a specific clinical picture, but only provides important information for further diagnosis. Poorly trained subjects or patients with cardiac diseases have a similiar reduced maximal oxygen uptake, breathing reserve (MVV/V'E), oxygen pulse and low anaerobic threshold. Reduced load capacity, including the early onset of lactic acidosis, indicate a poor training condition. This information cannot be obtained by clinical data, body-plethysmography or blood gas analysis at rest. Risk/prognosis B. Risk/prognosis Risk assessment prior to pulmonary resection By quantifying the functional reserves, in the case of pulmonary resection it is possible to define which patients are at risk and consequently the pre/post-surgical mortality rate declines. An important goal is the pre-surgical determination of the risk for complications after a major surgery. Nowadays the most important information is retrieved out of the measured static and dynamic lung-volume before surgery, out of which the post-surgery values for FEV1 can be derived and estimated, even better in combination with a quantitative perfusion-scintigraphy. Due to the high discrimination, determination of maximum V'O2 for estimation of the surgical risk is favored. If V'O2max is less than 60% of the predicted value, the removal of more than one lung lobe is not recommended. If V'O2max is higher than 75% of the predicted value it can be assumed that no post-surgical complications will occur. Risk assessment for heart transplant patients Prognosis and clinical trend in the case of cardiac insufficiency can be examined on the basis of the patient's own account, according to NYHA classification or by objective testing procedures with the help of Wmax or V'O 2 peak. There is a good correlation between the measured V'O2 peak and the mortality in patients with heart failure according to NYHA III and IV. With a cutoff of V'O2max below 10 ml/kg/ min. mortality after one year is 77%. C. Therapy assessment Training One of the most important tasks of rehabilitation is the increase of exercise capacity by training the muscles of the upper and lower extremities. In the case of COPD, maximum exercise capacity is limited during exercise as the large and small airways will collapse. As the endexpiratory volume increases with increasing work load, the lungs are working in an unfavorable area of the pressure-volume-curve. Furthermore, there is fatigue of the peripheral muscles, increasing hypoxemia in the presence of severe obstruction, a reduction in cardiovascular capacity as well as the increased lactic acidosis in the presence of a reduced capacity of the peripheral muscles. In the case of COPD, cardiopulmonary exercise testing is important to control muscle training, i.e. when defining work load levels for training purposes. At the beginning of an exercise program the exercise intensity, at which an increase in exercise capacity under training is to be expected, has to be defined. However, there are still no standardized guidelines regarding duration, frequency and intensity of training. With the help of a ramp protocol, maximum exercise capacity, as well as a range for training can be defined on the basis of which the anaerobic threshold is determined. Some studies recommend a range from 50% of peak oxygen uptake to values below maximum oxygen uptake. Cardiopulmonary exercise testing allows to objectively quantify the success of training programs. Parameters to be measured are, among others, maximum oxygen uptake, lactate, minute volume, breathing frequency, V'CO 2 , ventilatory equivalents, heart rate,VD/VT and anaerobic threshold. These parameters can be determined best on the basis of a ramp protocol performed prior to and after training. O2 therapy To compensate hypoxemia and its effects on exercise capacity, it can be attempted to increase exercise capacity by O2 insufflation during exercise. Studies regarding O2 therapy in the presence of different pulmonary diseases are available for patients with COPD, interstitial fibrotic lung diseases and cystic fibrosis. Drug therapy Endurance capacity is a very sensitive and clinically relevant variable for evaluating drug effects, especially of fl-sympathicomimetics and anticholinergics. By measuring lung volumes such as FEV1, FVC and inspiratory capacity (IC), an improvement after administration of anticholinergics can be documented. Hyperinflation at rest, measured via IC, is a very good predictive parameter of V'O2 max. Dynamic hyperinflation and the simultaneous increase of the endexpiratory volume (EELV) during exercise and their reduction after administration of antiobstructive medication correlates best with the increase in endurance capacity.

Prof. Karl-Heinz R¸hle, M.D. Klinik Ambrock Ambrocker Weg 60 D-58091 Hagen +49 (0)2331 974 0 eMail: klinik-ambrock.pneumo@t-online.de

VIASYS info Special Edition CPET, April 2002



Evaluation and Interpretation
of a cardiopulmonary exercise test
Author: Hermann Eschenbacher, Ph.D.

Cardiopulmonary exercise testing is a comprehensive testing procedure suited for differential diagnosis and examines a subject's cardiopulmonary exercise capacity or limitation. In addition to cardiac parameters, (e.g. stress ECG) respiratory parameters are recorded at defined work rates. The test provides a variety of parameters which, as compared to the individual stress ECG, allow for a comprehensive assessment.
The goal of this essay is to explain an easy and understandable procedure that allows assessment of individual areas of exercise limitation in order to deduce clear results. There are a variety of proposals and flow charts in literature (e.g. Eschenbacher (1990), Roca (1997), Wasserman (1999), Schardt (1999)) describing certain methods, one of which is the evaluation on the basis of the nine-panel graph. This method has been recommended by Wasserman for years and has been proven to be well suited. Although recording of the dynamic flow-volume loop during exercise, which has become increasingly important during the past years, has not yet been considered. As seen in Fig. 1, the nine-panel graph can be divided into several areas (whereby the graphs are numbered from left to right): Graph 1, 4 and 7 Ventilation: Cardiopulmonary: Graph 2, 3 and 5 Graph 6, 9 and 4 Gas exchange: Graph 8 Metabolism: Anaerobic threshold: Anaerobic threshold: Graph 5, 6, 8 and 9 Recording of the flow-volume loop during exercise and comparing it with the maximal flow-volume loop provides additional information, mainly on ventilatory limitations (Fig. 2). Comments on the evaluation and interpretation of a cardiopulmonary exercise test with the help of these graphs, explained step by step, follow. As far as the sequence of the individual graphs is concerned, there are different views (e.g. Wasserman (1999), R¸hle (2001)) depending on where emphasis is placed. As far as I'm concerned, the procedure described below is the best suited. increase How does oxygen uptake increase during exercise exercise (Graph 3)? Linearity? In healthy subjects, oxygen uptake normally increases linearily with increasing work load and, according to Wasserman, can be estimated as follows:
V'O2 [ml/min] = 151 mL/min + 5.8*body weight[kg] load[Watt] + 10.5 * work load[Watt]1

Assessment of cardiac (cardiopulmonary) exercise monary) exercise capacity
exercise What is the subject's exercise capacity (Graph 3)? On the basis of the predicted values in Graph 3, it can be immediately recognized whether the subject has reached or even exceeded his/ her expected exercise capacity and oxygen uptake (as in Fig. 1: 194% pred). If reached, these values clearly show that none or at least no severe limitation or impairment is present. It should, however, be noted that oxygen uptake in obese subjects is higher than in persons of normal weight. This is due to the increased body mass and means that oxygen uptake, although reduced, can reach normal values if the overweight is not considered in the predicted values (see Fig. 3 => select correct predicted values!).

This linear relation is also valid for obese subjects (Fig. 3, left); however, oxygen uptake is parallel shifted upwards due to body weight. Flatening with increasing work rate? Each subject has an individual cardiovascular/cardiopulmonary limitation, which is reflected by a flatening in oxygen uptake despite increasing work load. However in normal subjects, this flatening is often not reached (xV'O2 peak), as this requires a lot of effort and healthy subjects are rarely willing to do so, so that this flatening is only reached with really limited patients or with top athletes who stress themselves to a maximum (Fig. 3 - right).










Fig. 1 (left): CPET test on the basis of the nine-panel graph. The graphs are numbered from left to right as follows: 1-3, 4-6 and 7-9. Fig. 2. (top): Left curve: Maximal and dynamic F/V loop of a subject with no limitation. Right curve: Obstruction. The graph shows that ventilatory limitation is reached (flows, tidal volume).


VIASYS info Special Edition CPET, April 2002

As long as the individual body cells are sufficiently supplied with oxygen, the increase is linear. As soon as the supply is no longer sufficient, the curve flattens. If limitation starts already below the predicted value, we can assume for sure that exercise capacity is limited. Limitation is the greater, when flatening starts earlier. Nevertheless, the body has to meet the increased demands, which means that energy has to be produced anaerobically. Due to the limited anaerobic capacity, the subject will soon stop exercising depending on his/her individual reserves. Slope of oxygen uptake? Another important aspect is the increase of oxygen uptake during exercise. The slope of V'O2 with increasing work load (= aerobic capacity, normally approx. 10.5 ml/watt1, see above) provides information on whether the peripheral muscle cells are sufficiently supplied with oxygen. If not, for example in the presence of peripheral stenosis or a left ventricular functional impairment, a lower slope can be observed (Fig. 3, center). To be able to assess this increase, it is recommended to simultaneously record work load in Graph 3 and to plot it in relation to V'O2 with a scale of 1:10 (an increase of 1 watt equals an 10 mL V'O2 increase), so that both slopes can be directly compared with each other (see Fig. 1, Graph 3: green and blue curve). Does heart rate rise continuously; what is maximum HR (Graph 2)? In healthy subjects, heart rate is expected to rise continuously and approximately linearly with work load. In healthy subjects and athletes a slight decline of the slope can often be observed at high work rate levels, whereas mainly patients with cardiac impairments often show an increase of the slope. Especially when testing patients with pacemakers, investigators should pay close attention to a continuous increase in heart rate. In order to assure that the subject is stressed to a maximum and is not limited by other symptoms (e.g. pulmonary limitation), maximum heart rate should almost reach the maximum predicted value (less than 10 beats). How does heart rate rise during exercise exercise (Graph 5)? Oxygen transport can be described on the basis of Fick's Principle:
VO 2 = HR * SV * (CaO2 - CvO2).

levels so that oxygen transport per beat can only be increased by oxygen extraction. Since this increase is soon limited, O2 pulse will reach a plateau as soon as maximal extraction is reached. A further increase in work rate will then consequently result in an overproportional increase in heart rate (see Fig. 4).

Increasing heart rate (HR), increasing stroke volume (SV), as well as the difference of oxygen content between arterial and mixed-venous blood, (CaO2-CvO2) contribute to increase V'O2. In general, all three parameters change with increasing work load whereby there will be an approximately linear relation between heart rate and oxygen uptake in healthy subjects. However, the lower the stroke volume (e.g. in unfit or obstructive subjects), the higher the basic heart rate has to be. If no further increase in stroke volume is possible, and if CaO2-CvO2 is already utilized, there is no choice but to increase heart rate in order to increase oxygen uptake. This is reflected by the overproportional increase in Fig. 4. How does oxygen pulse rise with increasing increasing work load (Graph 2)? On the basis of Fick's Principle oxygen pulse is obtained through division by heart rate:
O2 Pulse = V'O2/HR = SV * (CaO2 - CvO 2)

Assessment of ventilatory perforventilatory performance
F/V-loop Graph 1, 4, 7 as well as dyn. F/V-loop exercise Does ventilation rise during exercise (Graph 1)? Ventilation normally increases linearily until the anaerobic threshold is reached and rises overproportionally due to the increased amount of anaerobically produced CO2 during exercise provided that the breathing reserve is sufficient.
ventilatory increased Is the ventilatory demand increased (Graph 4)? Respiratory drive is mainly controlled by the CO2 that has been released. A healthy subject requires an increase in ventilation by about 20 to 25 L per additional liter of CO2. If dead space ventilation is increased and/or an impairment in gas exchange is present, ventilation must be increased so that the same amount of CO2 can be released. This graph is discussed in detail later in relation to the respiratory equivalents (Graph 6). Breathing breathing reserve Breathing pattern, breathing reserve (Graph 7)? Depending on the breathing frequency (BF) and tidal volume (VT) there are several possibilities to reach the same ventilation: For example: VE=50 L/min can be reached as follows: 50 breaths ‡ 1 L (lower isopleth) or 20 breaths ‡ 2.5 L (upper isopleth, see Fig. 1, Graph 7). Subjects with flow limitations will try to breathe as deeply and as slowly as possible, whereby the V'E curve will be plotted along the upper isopleth. A subject with ventilatory restriction, on the other hand, achieves maximum tidal volume quikkly due to his/her low VC and then ventilation can only be increased by increasing breathing frequency. Consequently, VT will soon reach a plateau, move towards the lower isopleth and probably intersect. Furthermore, the measured maximum voluntary ventilation (MVV) and inspiratory capacity (IC) can be plotted illustrating whether the subject has reached his/her maximum ventilation and consequently whether a ventilatory limitation is present.

Consequently, oxygen pulse measures the amount of oxygen that is transported by the blood per beat and therefore directly reflects cardiac function; if cardiac function is good, the amount of oxygen transported per beat is high. O2 pulse is continuously increasing during exercise (increase in SV and in CaO2CvO2). In unfit or, for example obstructive subjects, O2 pulse will continuously increase; however, the curve trend will be lower due to smaller stroke volume. If cardiac function is poor or bad, the stroke volume is already utilized at low work rate

Fig. 3. Oxygen uptake: Position, slope, linearity (modified accoding to Wasserman (1999)). See text for explanation.

VIASYS info Special Edition CPET, April 2002


Fig. 4. Increase in heart rate with oxygen uptake (Graph 5; for a better overview the 2. Y-axis has been left out). Left: Athlete (low HR, low slope); Center: untrained subject (increased heart rate but linear and normal slope, finally slightly flattened); Right: cardiac limitation (clear unproportional slope at the end of exercise). Breathing breathing reserve Breathing pattern, breathing reserve F/V-loop)? (Dynamic F/V-loop)? Thanks to modern digital technology it is, however, easier to record the dynamic flowvolume loop during exercise in addition to the maximum flow-volume curve at rest (see Fig. 2). This allows you to immediately determine whether a subject's ventilatory reserves are sufficient or whether his/her maximum possible flow and tidal volume have already been reached, i. e. whether he/she is already exhausted. The evaluation of dynamic flow-volume loops are discussed in detail by Schwarz in Fritsch (1999) and in the JAEGER info, Special Edition Ergospirometry (1999). In close vicinity to the anaerobic threshold, a healthy subject has a ventilatory demand of approximately 20 to 25 L for one liter of oxygen uptake or 25 to 30 L VE to release one liter of CO2. Both an increased dead space ventilation and an impaired gas exchange will result in an increased ventilation to assure an adequate gas exchange. Consequently, the respiratory equivalents are increased (also see Fig. 7, Graph 6). Diffusion impairment or increased dead Diffusion increased requir equired, space (if required, Graph 9)? There are different possibilities to differentiate between an increased dead space ventilation and an impaired gas exchange: Blood gases: PaO2, PaCO2 Dead space ventilation If blood gases are taken during exercise, the amount of dead space ventilation can be calculated according to the Bohr formula:
VD/VT = (PaCO2 ñ PECO2)/PaCO2 ñVDapp/VT4

ing exercise will result in an increased slope5. Consequently, evaluation of this slope has increasingly gained importance over the last few years, mainly with regard to the degree of severity of the impairment, as well as regarding the mortality (Johnson (2000), Kleber (2000), Meyer (2001)).

aerobic-anaDetermination of the aerobic-anaearobic (AT threshold) earobic transition (AT threshold)
Graph 5, 6, 8 (and 9):
What is the subject's endurance capability? In addition to other findings (is exercise capacity normal, at least up to AT? Is AT within the normal range? Are impairments occuring below AT?) this transition is of importance mainly for diagnosing exercise capacity in the field of endurance sports, as well as for disability assessments. Due to the additional anaerobically produced CO2, cardiopulmonary exercise testing allows reliable determination of anaerobic threshold by non-invasive methods on the basis of several recorded or computed parameters: AT-determination on the basis of RER (Graph 8): If the CO2 release exeeds the O2 uptake (i.e. no hyperventilation, CO2-rebreathing etc., i.e. RER > 1) during incremental exercise tests, the additional CO2 has to be produced anaerobically. However, not every subject is able to adjust his/her metabolism to combust 100% carbohydrates. Consequently, additional anaerobically produced energy has to be provided at, for example, RER = 0.9 (often reflected by the quick increase in RER, also see Fig. 6, bottom left). Therefore, AT determination via RER = 1 can only be regarded as a rough estimation and RER = 1 as the upper limit for AT. AT determination according to V-Slope (Graph 5, second Y-axis): At rest and at low work rate levels both carbohydrates (RER = 1.0) and fat (RER = 0.7) are combusted (mixed combustion) so that the ratio between oxygen uptake and carbondioxide release is approximately 0.85. This energy production is reflected by the first linear portion (also see Fig. 6, top left).

Assessment of a ventilationperfusion mismatch
Graph 6, 4 (and 9)
ventilatory increased Is the ventilatory demand increased (Graph 6 and 4)? In Graph 6, the two ventilatory equivalents for oxygen (EQO2 ª V'E/V'O2)2 and carbon dioxide (EQCO2 ª V'E/V'CO2)3 are displayed. Ventilation V'E is composed of alveolar ventilation V'A (here gas exchange takes place) and dead space ventilation V'D: V'E = V'A + V'D. During exercise onset, dead space ventilation is relatively high due to the low tidal volume but decreases with increasing tidal volume. This is also reflected by the trend in ventilatory equivalents: At the beginning, they are relatively high and decline with increasing tidal volume (due to reduced dead space ventilation and due to an improved gas exchange).

At maximum work load, this value is normally between 0.15 and 0.20, values higher than 0.30 indicate an increased dead space ventilation. -arterial differ ference Alveolar-ar Alveolar-arterial oxygen difference P(A-a)O2: A diffusion impairment can be best determined on the basis of P(A-a)O2 which is calculated from blood gases and CPET data:
P(A-a)O2 = FiO2 * (BP ñ 47) ñ PaCO2 * (FiO2 + (1-FiO2)/RER)

At rest, this value is normally between 10 to 15 mmHg; during exercise, this value is agedependent and is between 25 (subjects < 40 years) and 35 mmHg (> 50 years). If the blood gas values are plotted in Graph 9 together with the values for PETO2 and PETCO2, this information is immediately displayed on the screen. Slope and offset of ventilation (Graph 4)? As already mentioned, ventilation is composed of V'E = V'A + V'D. Normally, there is an increase in ventilation of aproximately 25 liters per liter CO2. An increased dead space ventilation will therefore mainly give rise to a parallel displacement, whereas a disturbed gas exchange dur-

Fig. 5: Oxygen pulse (modified acc. to Wasserman (1999))


VIASYS info Special Edition CPET, April 2002

With increasing exercise, the body tries to improve oxygen utilization so that fat combustion declines and combustion of carbohydrates increases. Consequently, RER increases from 0.85 towards 1.0. In other words, more CO2 is produced per oxygen portion. This adjustment is clearly reflected by the first break point. At a certain work rate level the additional oxygen amount is still not sufficient to produce the required amount of energy. Now the body activates its anaerobic reserves. Due to anaerobic metabolism, additional CO2 is released, whereby oxygen uptake is not increased proportionally. This results in a further increase in CO2 release as compared to oxygen uptake reflected at the second break point. AT determination on the basis of EQO2 (Graph 6): At rest and with the onset of exercise the subject breathes shallowly. Due to the anatomic dead space of 200 to 300 ml, a major part of the ventilation doesn't reach the alveoli resulting in relatively high breathing equivalents for both O2 and CO2 (also see Fig. 6, upper right corner). With increasing work load, tidal volume increases resulting in a decline in relative dead space ventilation. This is reflected by the fall of the ventilatory equivalents. At a certain tidal volume, which is defined by the subject's pulmonary function, the increase in ventilation can only be met by breathing frequency. This means that from this point on the ventilatory equivalents remain approximately constant. Normally CO2 is responsible for respiratory drive, the EQCO2 curve shows a constant trend after reaching AT, while the EQO2 curve rises due to increased ventilation. This rise has the same cause as the second break of the V-slope curve and can consequently be used to determine AT as well. The same applies to the FETO2 curve (PETO2 respectively) in Graph 9. This parameter will also rise at AT due to hyperventilation (with regard to oxygen - please refer to Fig. 6, bottom right). anaerobic threshold Evaluation of anaerobic threshold Before going into details, I would like to point out that it is often not easy or sometimes even impossible to determine anaerobic threshold. Often, subjects are not able to even reach the anaerobic threshold. Although we are talking about a threshold, we have to realize that in fact, it is a transition area. Consequently, if defined by different methods, the threshold is not always at the exactly same point depending on the method of evaluation. It is therefore recommended to simultaneously use all available methods and define the point which has the best possible match with all methods (Fig. 6). The anaerobic threshold considerably contributes to endurance capacity evaluation and according to Wasserman, should be approximately 60% of maximum predicted oxygen uptake. Unfortunately, this has not been accepted so far in different guidelines for assessment (Fritsch 1999). Instead, it is still referred to maximum oxygen uptake. However, this is only valid if both anaerobic thresholds are within the normal range and the subject has been stressed to a maximum.

As a summary of all the different parameters, graphs and trends discussed above, view the following example: Before treatment: Figure 7 shows the results of a patient with valvular heart defect, aortostenosis, pulmonary hypertension, as well as an exercise-induced pulmonary shunt.

Fig. 6. Anaerobic threshold acc. to various methods: Top left: V-slope (Graph 5 - right Y-axis), Top right: EQO2 (graph 6); Bottom left: RER (Graph 8); Bottom right: PETO2 (Graph 9).

Fig. 7. Example (prior to treatment); Details see text.

VIASYS info Special Edition CPET, April 2002


Literature: Literature: 1. Eschenbacher W. L., Mannina A.: An algorithm for the interpretation of cardiopulmonary exercise tests. Chest 97 (1990) . 263 - 267 Schwarz 2. Fritsch J., Schwarz S.: Ergospirometrie in der Begutachtung. Atemw Lungenkrkh 25 (1999) 117 - 137 Jaeger-Info: 3. Jaeger-Info: Schwarz S.: Ergspirometrie in der Begutachtung. Sonderausgabe Ergospirometrie, JAEGER (1999) 8-21

Fig. 8: Example (post treatment). Details see text. Assessment of cardiac (cardiopulmonary) performance Maximum oxygen uptake: approx. 1,286 mL Maximum V'O2 pred = 2,119 mL (approx. 61%) reduced Suspected pulmonary shunt and diffusion disorder b) Blood gases are not available but both Graph 4 (high slope) and Graph 6 (increased, rising during exercise) rather indicate a gas exchange disorder (pulmonary hypertension, pulmonary shunt). anaerobic threshold (AT) Definition of anaerobic threshold (AT) a) AT at approx. 993 mL b) AT at approx. 47 % of V'O2 pred siderably reduced After treatment: Although the subject was not stressed to a maximum, it is clearly shown after treatment (artificial valves and surgery of aortostenosis) that (Fig. 8): the lower limit of maximum oxygen uptake is reached (85% pred) oxygen pulse is within normal range (96% pred) heart rate increase is within normal range (only a small unproportional rise can be seen at the end) diffusion disorder is no longer present (EQO2 within normal range: approx. 22 at AT, even the slope in Graph 4 is low) AT is 1,495 mL and consequently within normal range. Last, but not least, I would like to point out that also the stress ECG, which is not discussed in this essay, may provide important information for evaluation and interpretation. con-

4. Johnson R. L.: Gas Exchange Efficiency in Congestive Heart Failure. Circulation 101 (2000) 2774 - 2776 5. Jones N. L.: Clinical Exercise Testing. Atemw Lungenkrkh 25 (1999) 117 -137 F. 6. Kleber F. X., Vietzke G., Wernecke K. D. et al.: Impairment of Ventilatory Efficiency in Heart Failure. Circulation 101 (2000) 2803 - 2809 F. 7. Meyer F. J., Borst M. M., Zugck C. et al.: Respiratory Muscle Dysfunction in Congestive Heart Failure. Circulation 103 (2001) 2153 - 2158 8. R¸hle K.-H.: Praxisleitfaden der Spiroergometrie. Kohlhammer (2001) 9. Roca J., Whipp B. J. Clinical Exercise Texting. ERS Monograph 6 (1997) F., 10. Schardt F., Bedel S.: Ergospirometrie in der arbeits- und sozialmedizinischen Begutachtung, Sonderausgabe Ergospirometrie, JAEGER (1999) 24-25 11. Wasserman K., Hansen J. E., Sue D. Y., Casaburi R., Whipp B. J.: Principles of Exercise Testing and Interpretation. Lippincott Williams & Wilkins, Philadelphia (1999)

a) V'O2: Linear, no flattening, normal slope yet no cardiac limitation b) HR: Linear increase, high HR reserve yet no cardiac limitation c) HR/V'O2: Slightly above normal, unproportional rise at the end slightly impaired cardiac function c) O2 pulse: Low, still increasing oxygen pulse yet no cardiac limitation but slightly impaired cardiac function Assessment of ventilatory performance a) V'E: Continuous increase in ventilation no ventilatory limitation b) V'E/V'CO2: Increased ventilation (both "offset" and slope) increased ventilatory demand VT/V'E: - Normal breathing pattern ventilatory limitation yet no

- Dynamic F/V not available but no graphical indication of any ventilatory limitation Assessment of a ventilation-perfusion-impairment a) Impairment (Graph 4 and Graph 6): the hardly declining ventilatory equivalents, which immediately rise after exercise onset are important.

Hermann Eschenbacher, Ph.D. Erich Jaeger GmbH Scientific Application and Training Center Leibnizstr. 7 D-97204 Hoechberg. +49 (0)931 4972-381, +49 (0)931 4972-319, eMail: he@jaeger-toennies.com

1 2 3 4 5

Wasserman proposes 10.3, literature gives values between 9.5 and 12; according to our experience, a value of 10.5 has proven to be suitable. The exact calculation also considers apparative dead space VDapp of mask or mouthpiece, as otherwise these parameters would depend on the equipment: EQO2 = VE/VO2 - VDapp*BF/VO2 see note 2: analoguous for EQCO2 Literature also supports estimation of dead space ventilation on the basis of FETCO2. However, this is not very precise, especially in patients with ventilation-perfusion disorders. This is the result of first model calculations I have perfomed; however, for manifestation, further examinations are required.


VIASYS info Special Edition CPET, April 2002

The Last Page
Exercise Interpretation: Principles of Exercise Testing & Interpretation: Including Pathophysiology and Clinical Applications von Karlman Wasserman (Editor), James E. Hansen, Darryl Y. Sue, Richard Casaburi und Brian J. Whipp ISBN 0683306464 The book is clearly structured and answers the question as to how and why cardiopulmonary exercise testing is to be performed. 83 cases are documented and discussed in detail. Interpretation is based on the nine-panel graph. Professor Wasserman's approach of the engaging gears illustrates the link between ventilation, circulation and muscle work. Exercise Clinical Exercise Testing von Norman L., MD Jones ISBN 072166511X The book provides a good survey of application, indications and contra-indications of exercise tests. According to the respective requirementes four steps of cardiopulmonary exercise testing are described. Recording of cardiac output according to the indirect Fick-method with CO2 is explained in detail. A discussion of sample cases perfectly completes the book. Exercise Clinical Exercise Testing von J. Roca, B.J. Whipp ISSN 1025-448x This describes factors limiting exercise tolerance in patients suffering from pulmonary diseases. It provides information on how to optimize a stress test, on interpretation of results and improvement of exercise intolerance. Exercise Prescription ACSMís ACSMís Guidelines for Exercise Testing and Prescription by American College of Sports Medicine von Larry Keenney, PHD FACSM, Reed H. Humphrey PHD FACSM, Cedric X. Bryant PHD FACSM ISBM 0683000233 New edition of a one-stop resource for the knowledge, skills and abilities needed for ACSM certifications and current clinical practices in sports medicine. It emphasizes the value and application of exercise testing and prescription in subjects with and without chronic disease. Expert insights cover a broad range of specialists including physiology, fitness, cardiology, pulmonary medicine, epidemiology, law, nursing, physician assisting and physical therapy. Exercise Prescription Manual of Clinical Exercise Testing, Prescription and Rehabilitation von Altug, Janet L. Hoffman, Jerome L. Martin (Herausgeber), Ziya Altug ISBN: 0838502415 This book provides the clinically relevant components of exercise testing, prescription and rehabilitation in an easy-to-read format. This format features tables, figures, lists and charts. The book is written primarily for physical therapists, occupational therapists, athletic trainers, exercise physiologists and physical educators specializing in sports medicine and/or work hardening (i.e. industrial rehabilitation). Cardiopulmonary Exercise Essentials of Cardiopulmonary Exercise Testing by Jonathan Myers ISBN: 0873226364 A practical guide to using gas exchange techniques in clinical and research settings, explaining exercise testing technology and its applications. After background material on exercise physiology and cardiopulmonary responses to exercise, coverage includes information on calibration procedures, instrumentation, interpretation of gas exchange data, and application of data to cardiovascular and pulmonary disorders. It lists normal values for exercise capacity, and gives instructions on specialized applications of invasive hemodynamic measurements.

CPET Seminars
Jaeger regularly offers CPET seminars intervals. For detailed information please refer to our website:

Seminars: Seminars: Cardiopulmonary Exercise Testing: - Introduction to CPET - Methods and Technologies - ECG at rest and during exercise - Practical measurements - Interpretation - Maintenance, cleaning and hygiene Interpretation of CPET: - Basics - Exercise profiles - CPET parameters - Assessment of measurements - Evaluation and interpretation - Case studies Training handouts: - 780525 Lung function - 780528 CPET - 780529 Lung function and CPET - 770708 CD

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Erich Jaeger GmbH Leibnizstr. 7 D-97204 Hoechberg +49 (0)931 4972-0 +49 (0)931 4972-46 Internet: www.jaeger-toennies.com www.viasys.tv

Hans-J¸rgen Peter, Walter Pittasch, Sabine Klier, Claudia Weberpals, Dr. Hermann Eschenbacher, Werner Steinh‰user, Carolina Neder Texts and graphics have been compiled very carefully. Jaeger does not assume liability for mistakes or consequential damage. Subject to technical alterations. Computer and software designations etc. mentioned in this publication are brand names and/or registered trademarks of the respective manufacturer. Circulation: 3000

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