|Year : 2015 | Volume
| Issue : 2 | Page : 77-86
|Cardiopulmonary exercise testing in the assessment of exertional dyspnea
Debapriya Datta1, Edward Normandin2, Richard ZuWallack2
1 Department of Medicine, Division of Pulmonary-Critical Care Medicine, University of CT Health Center, Farmington, CT 06030, USA
2 Division of Pulmonary Medicine, St Francis Hospital and Medical Center, Hartford, CT 06105, USA
|Date of Submission||10-Jul-2014|
|Date of Acceptance||24-Aug-2014|
|Date of Web Publication||03-Mar-2015|
Division of Pulmonary- Critical Care Medicine, University of CT Health Center, 263 Farmington Avenue, Farmington, CT 06030
| Abstract|| |
Dyspnea on exertion is a commonly encountered problem in clinical practice. It is usually investigated by resting tests such as pulmonary function tests and echocardiogram, which may at times can be non-diagnostic. Cardiopulmonary exercise testing (CPET) measures physiologic parameters during exercise which can enable accurate identification of the cause of dyspnea. Though CPET has been around for decades and provides valuable and pertinent physiologic information on the integrated cardiopulmonary responses to exercise, it remains underutilized. The objective of this review is to provide a comprehensible overview of the underlying principles of exercise physiology, indications and contraindications of CPET, methodology and interpretative strategies involved and thereby increase the understanding of the insights that can be gained from the use of CPET.
Keywords: Anaerobic threshold, cardiopulmonary exercise test, carbon dioxide output, dyspnea, exercise limitation, oxygen uptake
|How to cite this article:|
Datta D, Normandin E, ZuWallack R. Cardiopulmonary exercise testing in the assessment of exertional dyspnea. Ann Thorac Med 2015;10:77-86
Exertional dyspnea is a common problem in patients with chronic lung diseases. This often leads to respiratory assessments such as spirometry, lung volume assessments, diffusing capacity, arterial blood gas determination, or cardiac assessments such as echocardiography. In essence, information from these tests which are performed in a resting state is used to assess a symptom which occurs with exertion. While this is often useful, exertional symptoms may correlate poorly with resting measurements.  Performing physiologic and subjective measurements during exercise often provides more relevant physiologic information and may give a more accurate estimate of functional capacity than testing done at rest in the laboratory. Furthermore, disease is often not confined to one organ system such as the lung, and testing the body's overall physiological response to exercise will provide useful data. This provides the general rationale for exercise testing in the evaluation of exertional dyspnea.
Categories of exercise testing
Several types of exercise tests are commonly performed in the clinical assessment of patients. These can be divided into field and laboratory tests. The former include the timed walk test (e.g., the 6 minute walk test)  and the incremental and endurance shuttle walk tests.  Besides giving an overall measurement of exercise capacity, these are easy to perform, are related to daily functional activities, and may even predict morbidity or mortality. They do not, however, provide much physiologic information on exercise limitation. Laboratory tests of exercise performance include the incremental and constant work rate cardiopulmonary exercise tests (CPET). Both provide a wealth of physiologic data. Incremental testing provides information on maximal responses and anaerobic threshold. Constant work rate testing, usually performed at a high fraction of maximal work rate is commonly performed before and after an intervention, such as bronchodilator therapy or exercise training.
Cardiopulmonary exercise testing (CPET)
CPET provides a comprehensive assessment of the exercise response, and reflects the influences (including interactions) of the cardiac, respiratory, musculoskeletal and hematological systems.  This testing provides data on respiratory gas exchange, including oxygen uptake (V O2 ), and carbon dioxide output (V CO2 ), tidal volume (VT) and minute ventilation (V E ), and other variables such as electrocardiographic, blood pressure and oxygen saturation. Testing can be done incrementally or at a constant work rate.
Integration of physiologic information allows for an analysis of the system as a whole,  while separate analyses help determine which system(s) limit exercise capacity or are related to exertional dyspnea. In general, CPET enables accurate determination of the physiologic reserves of the heart and lungs as well as functional capacity. [Table 1] lists many of the physiologic variables measured during CPET.
Though CPET has been around for decades and provides valuable and pertinent physiologic information on the integrated cardiopulmonary responses to exercise, it remains underutilized. The objective of this review is to provide a comprehensible overview of the underlying principles of exercise physiology, indications and contraindications of CPET, methodology and interpretative strategies involved and thereby increase the understanding of the insights that can be gained from the use of CPET.
| A brief review of exercise physiology|| |
A working knowledge of exercise physiology is essential to understand the various aspects of CPET. This is schematically illustrated in [Figure 1]. During exercise, to provide the energy required by the muscles, oxygen (O 2 ) is inhaled into the lungs, transported by the pulmonary vessels to the heart and delivered to the muscles by the arterial circulatory system. Q O2 is the O 2 utilized by the muscles and Q CO2 is the carbon dioxide (CO 2 ) produced by muscles with exercise which is then transported by the venous system to the heart and lungs and then exhaled. Analysis of the measured inspired and expired gases during exercise enables quantification of the oxygen consumed or oxygen uptake (V O2 ) and the CO 2 generated (V CO2 ). In steady state, Q O2 = V O2 and Q CO2 = V CO2 .
Increased O 2 utilization by the muscles is achieved by increased O 2 extraction from blood perfusing exercising muscles, increased O 2 delivery by dilatation of the arteries, increased cardiac output (by increasing stroke volume and heart rate) and increasing pulmonary blood flow by recruitment of the pulmonary vasculature. As exercise results in increased CO 2 production, it is exhaled by the lungs by an increase in ventilation by a rise in tidal volume (VT) and respiratory rate.
Energy required for exercise is derived from adenosine triphosphate (ATP) which is generated in the cells by 3 processes - aerobic oxidation of glycogen and fatty acids, anaerobic hydrolysis of phosphocreatinine and anaerobic metabolism of glycogen.  This is illustrated in [Figure 2]. In the early phase of exercise, local stores of muscle phosphocreatinine provide energy. Aerobic glycogen and fatty acid metabolism provide the major source of ATP and constitutes the only source during moderate intensity exercise. During heavy or sustained exercise, aerobic metabolism is unable to meet the demand; consequently, anaerobic generation of ATP occurs.
With aerobic metabolism, V O2 and V CO2 are generated in proportion to the amount of glycogen and fatty acid oxidized, with increase in V O2 normally being slightly greater than the increase in V CO2 . With anaerobic metabolism, lactic acid generated, is neutralized by bicarbonate (HCO 3 ), resulting in increased CO 2 production. Hence V CO2 rises more than VO 2 in anaerobic exercise. This further burdens the ventilatory system, which must eliminate this excess CO 2 .
The effects of increasing exercise intensity on ventilatory and gas exchange parameters are depicted in [Figure 3]. As work rate increases, V O2 , V CO2 and minute ventilation (V E ) increases linearly till anaerobic metabolism causes lactic acidosis.  Once lactic acidosis develops, HCO 3 buffers lactate and more CO 2 is generated (H + + HCO 3 - = H 2 CO 3 = H 2 O + CO 2 ). Consequently, rise in V CO2 is higher than rise in V O2 as more CO 2 is produced from HCO 3 buffering of lactic acid. V E rises at the same rate and in proportion to rise in V CO2 . Hence, V E /V CO2 and PET CO2 remain unchanged while PET O2 and V E /V O2 increases. With continued exercise, with worsening lactic acidosis, ventilation increases markedly to compensate for exercise-induced metabolic acidosis. The rise in V E is more than the rise in V CO2 . So V E /V CO2 increases while PET CO2 falls.
|Figure 3: Changes in physiological parameters with exercise (From Weisman: Clinics in Chest Medicine 2001, with permission.)|
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With increasing work, the point at which anaerobic metabolism begins is referred to as anaerobic threshold (AT).  At AT, V O2 does not decrease but V CO2 rises due to buffering of lactic acid generated by anaerobic metabolism. In incremental exercise testing, the AT is usually expressed as the V O2 at which this process begins. It can be measured directly by demonstrating an increase in lactate in arterial blood or indirectly through its effects on V O2 and V CO2 : Lactate entering the system is buffered by HCO 3 , resulting in an increase in the slope of V CO2 and resulting in increased VE. The indirect measurement of AT is commonly performed using the V-slope method [Figure 4], which determines when the V CO2−V O2 slope abruptly increases.
During exercise, heart rate, respiratory rate, VT and V E increase. V O2 and V CO2 rise steadily till anaerobic threshold is reached. With exercise, dead space (V D ) decreases due to increased pulmonary blood flow causing increased recruitment of pulmonary vessels. With increasing workload, V O2 peaks and remains constant, even though work intensity continues to increase. Maximal V O2 during exercise, which plateaus and remains constant, despite further increases in exercise intensity is V O2max . It serves as an indicator of exercise capacity. 
Indications for CPET
CPET is useful in determining the cause of exercise intolerance not diagnosed by history, physical examination, chest radiograph, PFTS and resting electrocardiogram and ECHO. Common indications for CPET are shown in [Table 2]. Absolute contraindications for CPET are shown in [Table 3]. Relative contraindications for CPET include uncontrolled hypertension ( SBP > 200, DBP > 120), moderate cardiac valvular stenosis, hypertrophic obstructive cardiomyopathy, high-grade AV block, significant pulmonary hypertension, advanced/complicated pregnancy, significant dyselectrolytemia and orthopedic or neurologic impediments to exercise.
| CPET Methodology || |
Cycle ergometer or treadmill?
Exercise testing in CPET is usually performed in the laboratory using a stationary cycle ergometer or a treadmill, although newer portable metabolic devices may permit exercise testing in non-traditional laboratory settings such as during activities of daily living.  Whether a cycle ergometer or a treadmill is used often depends more on the equipment in the particular laboratory and experience and preference of the testers than the specific clinical indication of the testing. Exercise testing on a cycle ergometer is less likely to be associated with falls. Many consider the electrically braked cycle ergometry the preferred method of testing since it produces less movement artifact, facilitates obtaining arterial blood specimen drawing, provides a smooth increase in load. In addition, it is less affected by weight and gait dynamics which allows for a more accurate estimate of the externally applied work. An important advantage of treadmill testing is that, unlike cycling, walking and running are familiar activities that are incorporated into many activities of daily living. V O2max in treadmill exercise testing is considerably more affected by body weight with treadmill testing than cycle ergometry. , Even if workload is estimated using weight, incline and speed, if the patient leans on the handrails this will introduce substantial error in this measurement.
Peak work rate, as expressed by V O2 , is about 5-10% higher with treadmill testing than cycle ergometry,  probably because more muscles are used. Exercise-induced hypoxemia in COPD patients appears to be more pronounced during treadmill testing than on the cycle ergometer.
Most CPET protocols generally fall into two broad categories:
These approaches provide different information and have different clinical indications. Incremental exercise testing involves gradually increasing work rate in a continuous or stepwise fashion over time. In cycle ergometer testing, work rate is usually increased by 5-25 watts each minute after a warm-up period of 1-3 minutes of unloaded pedaling. Exercise is usually continued to the point of symptom-limitation unless medical complications (such as chest pain, ECG changes, hemodynamic abnormalities, gait issues) develop. Criteria for terminating CPET  include:
- Incremental tests up to maximal exercise and
- Constant work rate test.
The pre-set rate increase in watts is determined by the exercise physiologist based on the physical state of the patient. In general, a test lasting 8-12 minutes is ideal.  This is long enough to provide useful physiologic information yet not so long as to be burdensome to the patient and staff. In severely limited patients, 5 minutes exercise time is reasonable. Incremental treadmill testing is similar in concept, but requires gradual increase in walking speed and incline. Incremental testing provides information on maximal exercise performance (such as peak VO 2 ) and potential mechanisms limiting that performance.
- Chest pain suggestive of angina,
- Ischemic EKG changes,
- Complex ectopy or 2 nd or 3 rd degree AV block,
- Drop in SBP > 20 mmHg from highest value during test,
- Uncontrolled hypertension (SBP > 250 mmHg; DBP > 120 mmHg),
- O 2 desaturation with O 2 saturation <80% or cyanosis and (viii) Dizziness or mental confusion or loss of coordination.
A typical protocol for constant work rate cycle ergometer testing is to begin with a 1 to 3 minute period of unloaded pedaling for warm-up, then increase workload abruptly to a high percentage (such as 75%) of that patient's maximal work rate. , Exercise is generally continued to a symptom-limited maximum. This approach, therefore, requires a prior incremental test to determine maximal work rate and a period of time (usually one or more days) to recover from the first test. The constant work test is useful for determining response to therapeutic interventions such as bronchodilators and pulmonary rehabilitation.
As stated earlier, an important advantage of CPET is that it not only determines maximal exercise performance, but also supplies important physiologic information during exercise. This may permit an analysis of physiologic derangement leading to exercise limitation and symptom-generation. The instruments used for measurement of physiologic variables during CPET are shown schematically in [Figure 5].  Stringent calibration of sensors to minimize errors is extremely important for quality control.
The primary physiologic measurements during CPET include the following physiologic information:
In selected cases, arterial blood is obtained during exercise testing to provide additional physiologic data. This may include
- Cardiac monitoring: Continuous heart rate, rhythm, and ECG changes
- Hemodynamic monitoring: Blood pressure at set intervals
- Breath-by-breath analysis of inspired and expired gas: V O2 , V CO2
- Pneumotachograph: Tidal volume, respiratory rate, V E , inspiratory capacity (IC)
- Pulse oximetry: Continuous measurement of oxygen saturation
- Symptom assessment: Periodic assessments of dyspnea and leg fatigue using a category (Borg) or analog (visual analog) scale.
Physiologic parameters derived from the above measured data also provide important information. These derived measurements include: Ve/VO 2 , Ve/VCO 2 , VO 2max , O 2 pulse (VO 2 /HR), Work efficiency (d VO 2 /d WR), Anaerobic threshold (AT), Respiratory quotient (R) (VCO 2 /VO 2 ), Dead space: (VD/VT), P( A-a ) O 2 , Heart Rate Reserve and Breathing Reserve.
- Arterial blood gas determinations
- Lactate levels
In addition to numeric data, composite graphic display of ventilatory and gas exchange parameters can be generated.  Computer analysis of physiologic data allows the generation of VO 2 and VCO 2 on a breath-by-breath basis. 
Physiologic variables measured during CPET
The following parameters are important in the interpretation of CPET and are discussed in more detail.
Oxygen uptake (V O2 ): ,,
This is calculated from the difference between the volume of O 2 in the inhaled and exhaled air during exercise per unit of time and in steady state is equal to metabolic O 2 consumption. The measurement of V O2 is based on the equation:
V O2 = VI × FIO 2 − VE × FEO 2 ,
where VI = Volume of inhaled air
VE = Volume of exhaled air
FIO 2 = Concentration of O 2 in the inhaled gases
FEO 2 = Concentration of O 2 in the exhaled gases
V O2 is determined by cellular O 2 demand and increases linearly as external work increases. In healthy subjects, a faster rate of increase in work results in a greater amount of work being achieved while peak VO 2 achieved is independent of the rate of increase in work.  The slope of the relationship between the increase in work versus the change in VO 2 determined during incremental CPET is unaffected by age, sex or height. A reduction in the value of this relationship is indicative of the abnormalities in O2 transport and utilization.
As work increases, V O2 increases until a point where it begins to plateau. This represents the highest attainable V O2 for a subject and is known as maximal V O2 or V O2max . It represents the maximal achievable level of oxidative metabolism involving large muscle groups. If a clear plateau is not obtained during CPET, the highest VO 2 attained is the V O2peak and can be used as a substitute for V O2max . V O2max (as well as V O2Peak ) serves as the index of aerobic exercise capacity. V O2max and V O2Peak should be expressed as an absolute value (in Liters/minute) as well as a percentage of predicted, referenced to body weight (in milliliters/kg/minute). A reduced V O2max or V O2Peak reflects reduced exercise capacity which may be due to cardiac, pulmonary, gas exchange, neuromuscular, muscular or effort limitation. However, in obesity, VO 2max and VO 2Peak are reduced in reference to body weight but the absolute value remains normal. 
Carbon dioxide output (VCO 2 )
This is calculated from the difference between the volume of CO 2 in the inhaled and exhaled air during exercise per unit of time and represents metabolic CO 2 output. The measurement of V CO2 is based on the equation:
V CO2 = VE × F ECO2 ,
where VE = Volume of exhaled air
FE CO2 = Concentration of O 2 in the exhaled gases
V CO2 is affected by the same factors as V O2 . However, it is more dependent on ventilation due to the increased solubility of CO 2 in the blood. Several variables in CPET including the RER/RQ, V D /V T and ventilatory equivalents are derived from V CO2 .
Respiratory exchange ratio (RER)
This is derived from the ratio of VCO 2 /VO 2 and corresponds to the gas exchange ratio. In steady state, it equals the Respiratory Quotient (RQ) which represents metabolism at the tissue level. Metabolism predominantly from carbohydrates results in an RQ of 1, while metabolism of protein results in an RQ of 0.8 and from fat, an RQ of 0.7. The production of lactic acid during exercise results in an RER greater than 1, since extra CO 2 is introduced into the system from bicarbonate buffering of the acid. Therefore an RER substantially greater than 1 at peak exercise is one marker of maximal effort. Hyperventilation may also cause an RER>1.
Anaerobic threshold (AT)
This represents the VO 2 at which anaerobic metabolism sets in during exercise. It can be expressed in L/min or as a percentage of the predicted value of V O2max . Direct measurement of AT requires continuous arterial sampling of lactate. However, it can be reasonably estimated from continuous physiologic data. In the modified V-slope method the AT is identified as that point where the slope of the relationship of V CO2 to V O2 changes. The abrupt increase in VCO 2 indicates an increase in the rate of CO 2 production from lactate buffering by bicarbonate.  In many cases the AT cannot be estimated from physiologic data. In other cases, exercise is limited before the AT is reached, such as in ventilatory-limited COPD patients. Its normal value is >40% of predicted V O2max .
Heart rate reserve (HRR)
It is the difference between maximum predicted heart rate and the observed maximum heart rate during CPET. Its normal value is <15. A high HRR may indicate a sub-maximal effort.
VO 2 -work rate relationship
The relationship between VO 2 and work rate at peak work rate is approximately 10 mL/min/watt. Values lower than this suggests abnormalities with oxygen delivery. It may be elevated in obesity.
O 2 pulse (VO 2 /HR)
This is determined by dividing VO 2 by HR and is expressed as mL/beat. A low O 2 pulse during exercise may indicate a reduced stroke volume or an abnormality in skeletal muscle O 2 extraction. A low HR during exercise, such as from beta-blocker medications, may elevate the O2 pulse by decreasing the denominator.
Maximal ventilation (V Emax )
Minute ventilation (V E ) is the volume of air exhaled from the lungs in 1 min. With exercise, V E increases due to increase in both tidal volume and respiratory frequency. The normal maximal value of respiratory frequency is less than 60 breaths per minute while the maximal VT is generally less than 60% of the vital capacity.  V Emax , the maximal ventilation achieved during exercise, reflects ventilatory demand.  Abnormalities in V Emax may indicate respiratory or neuromuscular limitation to exercise.
Ventilatory reserve (VR)
This reflects the difference between the measured or estimated maximal voluntary ventilation (MVV) and the V Emax . MVV is the volume of air that can be breathed per minute at rest with maximal effort. While the MVV can be determined in the lab, it can be reasonably estimated by multiplying the FEV1 by 35. VR is usually determined by the formula: VR= (V Emax /MVV) × 100. Normal values are ≥15% to ≤85%. VR is usually reduced in individuals with ventilatory limitation to exercise, such as patients with obstructive airways disease or interstitial lung disease.
Ventilatory equivalents for O 2 and CO 2 (V E / V O2 and V E /V CO2 )
The ventilatory equivalent for O 2 (V E / V O2 ) is the ratio of V E to V O2 , while the ventilatory equivalent for CO 2 (V E /V CO2 ) is the ratio of V E to V CO2 . With increasing exercise, V E /V O2 initially falls, reaches its nadir near the anaerobic threshold, and then rises. V E /V CO2 follows a similar trajectory, but rises after the rise in V E /V O2 , due to compensatory hyperventilation to counter metabolic acidosis. High values of V E /V CO2 are indicative of increased dead space during exercise. If the V E /V O2 and V E /V CO2 do not rise with maximal exercise that indicates high airway resistance or a general increase in pulmonary muscle load. Both increase with hyperventilation.
Dead space to tidal volume ratio (V D /V T )
The V D /V T reflects the adequacy or efficiency of gas exchange. With exercise, V D /V T decreases as tidal volume increase in response to increased metabolic demand and dead space ventilation remains relatively unchanged. An elevated V D /V T or absence of reduction in V D /V T with exercise suggests pulmonary vascular disease such as pulmonary hypertension.
Interpreting data from CPET
Exercise limitation during CPET is indicated by a reduced VO 2Peak . Exercise limitation could be secondary to cardiovascular, ventilatory, gas exchange, or neuromuscular limitation. In addition, physical deconditioning and poor effort are also considerations. Moreover, exercise limitation may result from several of the above limitations, although one factor is usually of more significance than the others.  Furthermore, overlap in response patterns to exercise may exist, sometimes making exact distinctions in mechanisms of exercise limitation problematical.
Before interpreting a CPET, it is essential to assess whether patient effort was adequate. Adequate effort is indicated by the following:
Other conditions, such as significant O 2 -desaturation, chest pain, lightheadedness, ECG abnormalities, orthopedic symptoms, or unexpected changes in blood pressure, may limit exercise before maximal effort is attained.
- Attaining maximal predicted heart rate,
- Attaining maximal predicted minute ventilation (VE ),
- RQ > 1.15, (iv) patient showing signs of exhaustion.
Certain physiologic patterns during exercise may indicate the cause of exercise limitation. The CPET pattern in some common disease states causing exercise limitation is as follows:
CPET pattern in cardiac disease
Exercise capacity is reduced as indicated by a reduced V O2max . Cardiovascular responses are abnormal- heart rate reserve is decreased or absent and O 2 pulse is reduced. Anaerobic threshold (AT) is early onset and less than 40% predicted V O2max . Ventilatory responses are normal, including normal Ventilatory Reserve (V Emax /MVV), normal maximal respiratory rate (<50/minute) and a normal paCO 2 . In cardiac disease, gas exchange maybe mildly abnormal, with a mildly reduced dead space (V D /V T ) at rest and a mildly increased ventilatory equivalents for O 2 and CO 2 (V E / V O2 and V E /V CO2 ) at AT.
The effect of exercise on physiologic parameters studied during CPET in a normal subject is shown in [Figure 6]. The changes in various physiologic parameters with exercise in heart disease (cardiac limitation to exercise) are depicted graphically in [Figure 7].
|Figure 6: Graphic display of response to exercise in a normal subject on cardiopulmonary exercise testing|
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|Figure 7: Graphic display of response to exercise in patient with lung disease on cardiopulmonary exercise testing (ventilatory limitation to exercise)|
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CPET pattern in lung disease
Exercise capacity (V O2max ) is reduced. Ventilatory responses are abnormal: Maximal voluntary ventilation (MVV) and Ventilatory Reserve (V Emax /MVV) are reduced; respiratory rate at maximal exercise is increased (>50/minute) and hypercapnia may be present. Cardiovascular responses are normal/borderline abnormal. Heart rate reserve may be increased or normal; O 2 pulse will be normal and AT may be normal or indeterminate. Mild gas exchange abnormalities may be present such as increased dead space (V D /V T ) at rest with < normal reduction with exercise and ventilatory equivalent for CO 2 and O 2 (V E /V CO2 and V E /V O2 ) may be mildly increased with reduced pO 2 or oxygen saturation with exercise. Individuals with ventilatory limitation to maximal exercise may have an increased heart rate reserve at peak exercise because ventilatory limitation may have occurred before cardiovascular limitation set in. The AT may be normal, reduced or indeterminate in individuals with ventilatory limitation. A decrease in end-tidal O 2 (PETO2) and CO 2 (PETO2) also indicates ventilatory limitation. The changes in various physiologic parameters with exercise in lung disease (ventilatory limitation to exercise) are depicted graphically in [Figure 8].
|Figure 8: Graphic display of response to exercise in patient with heart disease on cardiopulmonary exercise testing (cardiac limitation to exercise)|
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CPET pattern in pulmonary vascular disease
Exercise capacity is reduced, with a reduced V O2max . Cardiovascular responses are abnormal with low or absent heart rate reserve and low O 2 pulse. AT is early onset and reduced to <40% of predicted V O2max . Gas exchange is significantly abnormal with a moderate-to-severely increased dead space-to-tidal volume ratio (V D /V T ) at rest and no reduction in V D /V T with exercise. Ventilatory equivalent for O 2 and CO 2 (V E /V CO2 and V E /V O2 ) at AT is markedly increased with a low pO 2 /oxygen saturation and a markedly increased A-a gradient. In pulmonary vascular disease, ventilatory responses are normal with a low normal Ventilatory Reserve (V Emax /MVV), respiratory rate at maximal exercise <50/minute and a normal paCO 2 . The AT may or may not be reduced with gas exchange limitation. The changes in various physiologic parameters with exercise in pulmonary vascular disease (gas exchange limitation to exercise) are depicted graphically in [Figure 9]. 
|Figure 9: Graphic display of response to exercise in a patient with pulmonary hypertension on cardiopulmonary exercise testing (gas exchange limitation to exercise)|
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Otherwise healthy obese individuals have increased workload during exercise, but often their physiologic patterns are normal. The peak VO 2 in obesity is normal when expressed as L/min, but is low when expressed as ml/kg/min.  Exercise limitation due to physical deconditioning is characterized by reduced V O2max or V O2peak ; as such it may be difficult at times to differentiate from disease state limitations. Heart rate reserve may be reduced or absent. AT may be normal or reduced; O 2 pulse is reduced.  There is no evidence of ventilatory and gas exchange abnormalities. Suboptimal effort may be suspected by premature cessation of exercise, a reduced VO2peak , a normal or unattained AT, in conjunction with markedly increased heart rate reserve and ventilatory reserve and low RQ. The presence of irregular and erratic breathing patterns and respiratory rates unrelated to increase in work may be a clue to malingering.
| Conclusion|| |
The evaluation of exercise symptoms, such as exertional dyspnea, usually begins with tests done at rest, such as spirometry, echocardiography, or radiographic procedures. These assessments often provide useful information relating to the diagnosis of the limitation and its severity. CPET should be considered when there is some discord between the patient's symptoms or stated level of exercise limitation and the baseline diagnostic information. It makes sense to assess symptoms, limitation and physiologic responses during exercise rather than inferring these responses from tests done at rest. CPET adds complementary information to our usual diagnostic testing. The information obtained from CPET can alter the management of an individual patient by identifying the cause of exercise limitation. In some cases, exertional dyspnea may be related to obesity and deconditioning, which can be detected by CPET and help to provide reassurance to patients, as well as prevent further utilization of resources in further testing to determine cause of exercise intolerance.
| References|| |
Killian KJ, Leblanc P, Martin DH, Summers E, Jones NL, Campbell EJ. Exercise capacity and ventilatory, circulatory and symptom limitation in patients with chronic airflow limitation. Am Rev Respir Dis 1992;146:935-40.
ATS Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories. ATS statement: Guidelines for the six minute walk test. Am J Respir Crit Care Med 2002;166:111-7.
Singh SJ, Morgan MD, Scott S, Walters D, Hardman AE. Development of a shuttle walking test of disability in patients with chronic airways obstruction. Thorax 1992;47;1019-24.
Weisman IM, Zebellos RJ. An integrated approach to the interpretation of Cardiopulmonary exercise testing. Clin Chest Med 1994;15:421-45.
Sue DY, Wasserman K. Impact of integrative cardiopulmonary exercise testing on clinical decision-making. Chest 1991;99:981-92.
Mahler M. First-order kinetics of muscle oxygen consumption, and an equivalent proportionality between QO2 and phosphorylcreatinine level. Implications for the control of respiration. J Gen Physiol 1985;86:135-65.
Cassaburi R, Baristow TJ, Robinson T, Wasserman K. Influence of work rate on ventilatory and gas exchange kinetics. J Appl Physiol (1985) 1989;67:547-55.
Beaver WL, Wasserman K, Whipp BJ. A new method for detecting anerobic threshold by gas exchange. J Appl Physiol (1985) 1986;60:2020-7.
Taylor HL, Buskirk E, Hemschel A. Maximal oxygen intake as an objective measure of cardio-respiratory performance. J Appl Physiol 1955;8:73-80.
American Thoracic Society; American College of Chest Physicians. ATS/ACCP Statement on Cardiopulmonary Exercise Testing. Am J Respir Crit Care Med 2003;167:211-77.
ACC/AHA Guidelines for exercise testing. J Am Coll Cardiol 1993;30:260-311.
Stevens D, Elpein E, Sharma K, Szidon P, Ankin M, Kesten S. Comparison of hallway and treadmill 6 minute walk test. Am J Respir Crit Care Med 1999;160:1540-3.
McArdle WD, Katch FI, Pechar GS. Comparision of continuous and discontinuous treadmill and bicycle tests for maximal VO2. Med Sci Sports 1973;5:150-60.
Buchfuhrer MJ, Hansen JE, Robinson TE, Sue DY, Wasserman K, Whipp BJ. Optimizing the exercise protocol for cardiopulmonary assessment. J Appl Physiol Respir Environ Exerc Physiol 1983;55:1558-64.
Zaballos RJ, Weisman IM, Connery SM. Comparison of pulmonary gas exchange measurements between incremental and constant work exercise above anaerobic threshold. Chest 1998;113:602-11.
Beaver WL, Wasserman K, Whipp BJ. On-line computer analysis and breath-by-breath graphical display of exercise function tests. J Appl Physiol 1973;34:128-32.
Beaver WL, Lamarra N, Wasserman K. Breath-by-breath measurement of true alveolar gas exchange. J Appl Physiol Respir Environ Exerc Physiol 1981;51:1662-75.
Wagner PD. Determinants of maximal oxygen transport and utilization. Annu Rev Physiol 1996;58:21-50.
Debigare R, Maltais F, Mallet M, Casaburi R, LeBlanc P. Influence of work rate incremental rate on the exercise responses in patients with COPD. Med Sci Sports Exerc 2000;32:1365-8.
Zavala DC, Printen KJ. Basal and exercise tests on morbidly obese patients before and after gastric bypass. Surgery 1984;95:221-9.
Sue DY, Wasserman K, Moricca RB, Casaburi R. Metabolic acidosis during exercise in patients with COPD. Chest 1988;94:931-8.
Gallagher CG, Brown E, Younes M. Breathing pattern during maximal exercise and during submaximal exercise with hypercapnia. J Appl Physiol (1985) 1987;63:238-44.
Younes M, Kivinen G. Respiratory mechanics and breathing pattern during and following maximal exercise. J Appl Physiol Respir Environ Exerc Physiol 1984;57:1773-882.
Buskirk E, Taylor HL. Maximal oxygen intake and its relation to body composition, with special reference to chronic physical activity and obesity. J Appl Physiol 1957;11:72-8.
O'Donnell DE, Guenette JA, Maltais F, Webb KA. Decline of resting inspiratory capacity in COPD. Chest 2012;141:753-62.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
[Table 1], [Table 2], [Table 3]
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