Heart Rate and Electrocardiogram

Heart rate and rhythm should be monitored continuously using one or more modified chest leads. Standard precordial chest lead configurations (V₁–V₆) allow comparison with resting 12-lead tracings (Criteria for Acceptability 7-1). Twelve-lead monitoring during exercise is practical with electrocardiographs designed for exercise testing. These instruments incorporate filters (digital or analog) that eliminate movement artifact and provide ST-segment monitoring. Limb leads normally must be moved to the torso for ergometer or treadmill testing (modified leads). A resting ECG should be performed to record both the standard and modified leads. Single-lead monitoring allows only for gross arrhythmia detection and HR determination. It may not be adequate for testing patients with known or suspected cardiac disease.

The ECG monitor should allow the assessment of intervals and segments up to the patient’s maximal heart rate (HRmax). Computerized arrhythmia recording or manual “freeze-frame” storage allows the subsequent evaluation of conduction abnormalities while the testing protocol continues (Figure 7-4). Some digital ECG systems generate computerized “median” complexes averaged from a series of beats. These may be helpful in analyzing ST-segment depression. The “raw,” or nondigitized, ECG should also be available. Significant ST-segment changes should be easily identifiable from the tracing up to the predicted HRmax.

HR should be analyzed by visual inspection of the ECG, with manual measurement of the rate rather than by an automatic sensor. Most HR meters average RR intervals over multiple beats. Inaccurate HR measurements may occur with nodal or ventricular arrhythmias or because of motion artifact. Tall P or T waves may be falsely identified as R waves, causing automatic calculation of HR to be incorrect. Accurate measurement of HR is necessary to determine the patient’s maximal HR in comparison with the age-related predicted value.

Motion artifact is the most common cause of unacceptable ECG recordings during exercise. Allowing the patient to practice pedaling on the ergometer or walking on the treadmill permits adequacy of the ECG signal to be checked. Carefully applied electrodes, proper skin preparation, and secured lead wires greatly minimize movement artifact (see Criteria for Acceptability 7-1). Electrodes specifically designed for exercise testing are helpful. Most of these use extra adhesive to ensure electrical contact even when the patient begins perspiring. The skin sites should be carefully prepared. Removal of surface skin cells by gentle abrasion is recommended. Patients with excessive body hair may require shaving of the electrode site to ensure good electrical contact. Lead wires must be securely attached to the electrodes. Devices that limit the movement of the lead wires can greatly reduce motion artifact. Spare electrodes and lead wires should be available to avoid test interruption in the event of an electrode failure.

HR increases linearly with increasing workload, up to an age-related maximum. Several formulas are available for predicting HRmax. For most predicted HRmax values, a variability of ±10–15 beats/min exists in healthy adult patients. Two commonly used equations for predicting HRmax are as follows:

HRmax=220−Age(years) 1

1

HRmax=210−(0.65×Age[years]) 2

2

Equation 1 yields slightly higher predicted values in young adults. Equation 2 produces higher values in older adults. Other methods of predicting HRmax vary, depending on the type of exercise protocol used in deriving the regression data. Specific criteria for terminating an exercise test should include factors based on symptom limitation as well as HR and BP changes (see the section on safety).

HR increases almost linearly with increasing o₂. The increase in CO depends on both HR and stroke volume (SV) according to the following equation:

CO=HR×SV

Increases in stroke volume account for a smaller portion of the increase in CO, primarily at low and moderate workloads (Figure 7-5). While HR increases from 70 beats/min up to 200 beats/min in young healthy upright patients, SV increases from 80 mL to approximately 110 mL. At low workloads, increase in CO depends on the patient’s ability to increase both HR and SV. At high workloads, further increases in CO result almost entirely from the increase in HR.

Deconditioned patients usually have a limited SV. High HR values occur with moderate workloads in deconditioned individuals because it is the primary mechanism for increasing CO. Training (e.g., endurance or aerobic) typically improves SV response. This allows the same cardiac output to be achieved at a lower HR. Training usually results in a lower resting HR as well as a higher tolerable maximum workload. Except in highly trained patients, maximal exercise in healthy individuals is limited by the inability to further increase the CO. Reductions in SV are usually related to the preload or afterload of the left ventricle. Increased HR response, in relation to the workload, implies that SV is compromised.

Reduced HR response may occur in patients who have ischemic heart disease or complete heart block (Interpretive Strategies 7-1). Low HR is also common in patients who have been treated with drugs that block the effects of the sympathetic nervous system (β-blockers, calcium channel blockers). HR response may also be reduced if the autonomic nervous system is impaired or the heart is denervated, as occurs after cardiac transplantation (e.g., chronotropic insufficiency).

In patients who have heart disease (e.g., coronary artery disease, cardiomyopathy), increased HR is typically accompanied by ECG changes such as arrhythmias or ST-segment depression. Deconditioned patients without heart disease show a high HR at lower than maximal workloads but usually without ECG abnormalities. Horizontal or down-sloping ST-segment depression greater than 1 mm (from the resting baseline) for a duration of 0.08 seconds is usually considered evidence of ischemia. ST-segment depression at low workloads that increases with HR and continues into the post-exercise period is usually indicative of multivessel coronary artery disease. ST-segment depression accompanied by exertional hypotension or marked increase in diastolic pressure is usually associated with significant coronary disease. The predictive value of ST-segment changes during exercise must be related to the patient’s clinical history and risk factors for heart disease.

The most common arrhythmia that occurs during exercise testing is the premature ventricular contraction (PVC) (see Figure 7-4). Exercise-induced PVCs occurring at a rate of more than 10 per minute are often found in ischemic heart disease. Increased PVCs during exercise may also be seen in mitral valve prolapse. Coupled PVCs (couplets) often precede ventricular tachycardia or ventricular fibrillation. Occurrence of couplets or frequent PVCs may be an indication for terminating the exercise evaluation. Some patients with PVCs at rest or at low workloads may have these ectopic beats suppressed as exercise intensity increases. The most serious ventricular arrhythmias are sometimes seen in the immediate post-exercise phase.

Shortness of breath (SOB) brought on by exertion is perhaps the most widespread indication for cardiopulmonary exercise evaluation. The combination of cardiovascular parameters (e.g., HR, SV) with data obtained from the analysis of exhaled gas (i.e., o₂) permits the assessment of dyspnea on exertion. Table 7-5 generalizes some of the basic relationships between cardiovascular and pulmonary exercise responses. These relationships help delineate whether exertional dyspnea is a result of cardiac or pulmonary disease, or whether the patient is simply deconditioned. In some instances, poor effort may mimic exertional dyspnea. Comparison of data from cardiovascular and exhaled gas variables can confirm inadequate patient effort.

Table 7-5

Exercise Variables and Dyspnea*

	Cardiac	Ventilatory	Deconditioned	Poor Effort
o2max	Less than 80% of predicted	Less than 80% of predicted	Less than 80% of predicted	Less than 80% of predicted
Emax	Less than 70% of MVV	Greater than 90% of MVV; Emax less than 15 L	Less than 70% of MVV	Variable
Anaerobic threshold	Achieved at low o2	Usually not achieved	Achieved at low o2	Not achieved
HR	Greater than 85% of predicted	Less than 85% of predicted	Greater than 85% of predicted	Less than 85% of predicted
ECG/signs of ischemia	ST changes, arrhythmias, chest pain	Usually normal	Normal	Normal
Sao2	Greater than 90%	Often less than 90%, hypoxemia	Greater than 90%	Greater than 90%

MVV, Maximal voluntary ventilation; SaO₂, arterial oxygen saturation.

^*This table compares the usual findings for the exercise variables listed in subjects with dyspnea caused by cardiac disease, pulmonary disease, or deconditioning. Some subjects may have dyspnea because of a combination of causes. Poor effort during exercise may result from improper instruction, lack of understanding by the subject, or lack of motivation by the subject.

Blood Pressure

Systemic BP may be monitored intermittently with the standard cuff method. Automated noninvasive cuff devices for monitoring BP are also available. Although these methods work well at rest and at low workloads, they may be difficult to implement during high levels of exercise. However, recent advances in automated systems that pair sophisticated Korotkoff sound detection with QRS complex activation have improved the ability to measure exercise BP more accurately with these devices. BP sounds may be difficult to detect because of treadmill noise or patient movement. It is important to monitor the pattern of BP response at low and moderate workloads to establish that both systolic and diastolic pressures respond as anticipated.

Continuous monitoring of the BP may be accomplished by the connection of a pressure transducer to an indwelling arterial catheter (Figure 7-6). An indwelling line allows the continuous display and recording of systolic, diastolic, and mean arterial pressures. In addition, the catheter provides ready access for arterial blood sampling. Arterial catheterization may be easily accomplished using either the radial or the brachial site. The catheter must be adequately secured to prevent loss of patency during vigorous exercise. Insertion of arterial catheters presents some risk of blood splashing or spills. Adequate protection for the individual inserting the catheter, as well as for those withdrawing specimens, is essential. See Chapter 6 for specific recommendations regarding arterial sampling via catheters.

Systolic BP increases in healthy patients during exercise from 120 mm Hg up to approximately 200–250 mm Hg (see Figure 7-5). Diastolic pressure normally rises only slightly (10–15 mm Hg) or not at all. The mean arterial pressure rises from approximately 90 mm Hg to approximately 110 mm Hg, depending on the changes in systolic and diastolic pressures. The increase in systolic pressure is caused almost completely by increased CO and mostly by the SV. Even though CO may increase fivefold, (e.g., from 5–25 L/min), the systolic pressure only increases twofold. Systolic pressure only doubles because of the tremendous decrease in peripheral vascular resistance. Most of this decrease in resistance results from vasodilatation in exercising muscles. Increased systolic pressure (>250–300 mm Hg) should be considered an indication for terminating the exercise evaluation (Box 7-2). Similarly, if the systolic pressure fails to rise with increasing workload, the exercise test should be terminated and the patient’s condition stabilized. Variations in BP during exercise are often caused by the patient’s respiratory effort. Phasic changes with respiration are particularly common in patients who have large transpulmonary pressures because of lung disease (i.e., pulsus paradoxus). Differences of as much as 30 mm Hg between inspiration and expiration may be seen during the continuous monitoring of arterial pressure.

In maximal tests (e.g., the patient reaches HRmax), it may be impossible to obtain a reliable BP at peak exercise. Even with an arterial catheter, motion artifact may prevent recording of a usable tracing. Systolic pressure may transiently drop and diastolic pressure may drop to zero at the termination of exercise. To minimize the degree of hypotension resulting from abrupt cessation of heavy exercise, the patient should “cool down.” This is accomplished easily by having the patient continue exercising at a low work rate until BP and HR have stabilized at or slightly above baseline levels.

Safety

Safe and effective exercise testing for cardiopulmonary disorders requires careful pre-test evaluation to identify contraindications to the test procedure (Box 7-3). A preliminary workup should include a complete history and physical examination by the referring physician or the physician performing the stress test. Preliminary laboratory tests should include a 12-lead ECG, chest x-ray study, baseline pulmonary function studies before and after bronchodilator therapy, and routine laboratory examinations such as complete blood count and serum electrolytes.

The risks and benefits of the entire exercise procedure should be explained to the patient. Appropriate informed consent should be obtained. This includes an explanation of any alternative tests that might be done and what the consequences of not performing the stress test might be. A physician experienced in exercise testing should supervise the test. Tests may be performed by qualified practitioners on patients younger than 40 years with no known risk factors, provided a physician is immediately available. Criteria for terminating the exercise evaluation before the specified endpoint or symptom limitation occurs are listed in Box 7-2.

After termination of the exercise evaluation for whatever reason, the patient should be monitored until HR, BP, and ECG return to pre-test levels. ECG monitoring should continue for at least 5 minutes (as recommended by the American College of Sports Medicine). Tracings should be made at frequent intervals immediately after exercise.

Personnel conducting exercise tests should be trained in handling cardiovascular emergencies and all aspects of cardiopulmonary resuscitation (e.g., advanced cardiac life support [ACLS]). The laboratory should have available resuscitation equipment, including the following:

All emergency equipment should be checked daily or immediately before any cardiopulmonary exercise evaluation. Equipment such as defibrillators, laryngoscopes, and suction apparatus should be routinely evaluated for proper function according to institutional policies.

Equipment Selection and Calibration

The two common methods of exhaled gas analysis use either a mixing chamber (Figure 7-7) or computerized breath-by-breath measurements (Figure 7-8). Pneumotachometers are used in both mixing chamber and breath-by-breath systems and should be calibrated with a known volume (3-L syringe) or flow signal (Criteria for Acceptability 7-2). The flow sensor’s accuracy should comply with the criteria set by the American Thoracic Society and European Respiratory Society (ATS-ERS) for flow-measuring devices (e.g., ± 3.5% or 50 mL, whichever is greater and at three flow rates). Validation of a flow-measuring device can be performed by connecting it in series with a volume-based spirometer of known accuracy. Gas analyzers should also be calibrated and checked before each test procedure. Two-point calibration with gases that approximate the physiologic range to be tested provide the most appropriate means of ensuring accuracy. Three-point calibration is necessary to check the linearity of the analyzers. Table 7-6 lists some recommended gas concentrations for calibration of analyzers to be used for exercise tests.

If a gas collection valve (see Chapter 11) is used in the breathing circuit, it should have a low resistance (1–2 cm H₂O at 100 L/min) and a small dead space. In healthy adults, a valve dead space of 100 mL is acceptable. A valve with reduced dead space (25–50 mL) may be more appropriate for children or for patients who have dead space–producing disease or small tidal volumes. Some breath-by-breath systems can be programmed to reject small breaths (<100 mL). If this feature is used, the volume of rejected breaths should be matched to valve dead space. Breaths that do not clear valve dead space should be discarded. If valve dead space is too large for the patient, significant rebreathing may occur. In breath-by-breath exercise systems, this may show up as an expired CO₂ level that does not decrease to zero during inspiration. Many modern exercise systems have small flow sensors that do not require a valve system, so dead space and valve resistance become less critical.

If a mixing chamber is used, the patient should be allowed to breathe through the circuit with a noseclip in place long enough to wash out room air with expired gas. The exact washout volume, or time, depends on the volume of the mixing chamber. Breath-by-breath systems (see Figure 7-8) normally require minimal washout because fractional gas concentrations are sampled directly at the mouthpiece. If supplemental O₂ is breathed, the inspiratory portion of the breathing circuit as well as the patient’s lungs should be in equilibrium before gas sampling starts.

Depending on the protocol and equipment used, gas collection and analysis are performed over a specified interval during each exercise level. For steady-state protocols, gas collection is usually performed after 4–6 minutes at a constant workload. For incremental protocols, sampling may be averaged during the last minute of each stage. In breath-by-breath systems, sampling is done continuously, with data being displayed for each breath. Breath-by-breath data may also be averaged over several breaths.

In gas collection or mixing chamber systems, raw data collected includes the following:

These data can be recorded manually or by a multichannel recorder with appropriate analog signals. In most modern systems, the data are gathered into a computer by means of an analog-to-digital (A/D) converter (see Chapter 11). Computerized data reduction offers the advantage of immediate feedback for all measurements. Automated data collection also offers greater flexibility for using different exercise protocols (see Table 7-1). Breath-by-breath gas analysis requires that signals from the flow sensor be integrated with the gas analyzer signals for F_eo₂ and F_eco₂. The phase delay between volume and gas concentration signals must be considered (see Figure 7-8). This is done by measuring phase delay time (for each gas analyzer) during calibration. The phase delay is then stored, and subsequent measurements use this factor to align the volume and gas signals. Sampling flow or sample lines should not be altered after calibration because phase delay values may change. Water or particulate contamination of the gas analyzer sample line or damage to the sample line can also affect phase delay. Alterations of the phase delay can have a profound effect on the accuracy of the data (up to 30% error in the calculated o₂), especially at higher respiratory rates.

Minute Ventilation

Minute ventilation (_E) is the volume of gas expired per minute by the exercising patient, expressed in liters, BTPS. For an exercise system in which gas is collected, _E may be calculated as follows:

V⋅E=Volume expired×60Collection time(sec)×BTPS factor

Sample calculations and BTPS factors are on Evolve. Modern breath-by-breath systems measure the volume of each breath and continuously compute the minute ventilation.

Healthy adults at rest breathe 5–10 L/min. During exercise, this value may increase to more than 200 L/min in trained patients. It commonly exceeds 100 L/min in healthy adults (Figures 7-9 and 7-10). The increase in ventilation removes CO₂, the primary product of exercising muscles, as workload increases. Ventilation increases linearly with an increasing workload (i.e., o₂) at low and moderate levels of exercise. In healthy patients, this increase in ventilation during exercise follows the rise in co₂. Relating the _Emax to resting ventilatory function provides an index of ventilatory limitations to exercise. Maximal voluntary ventilation (MVV) (see Chapter 2) can be related to the _E achieved at the highest workload attained (_Emax). Ventilatory capacity (sometimes called ventilatory ceiling) is defined by the measured MVV or the FEV₁ (forced expiratory volume in 1 second) × 35 (some clinicians prefer FEV₁ × 40). The difference between _Emax and ventilatory capacity is often called the ventilatory (or breathing) reserve (Figure 7-11). Ventilatory reserve is calculated as follows:

Ventilatory reserve=[1−(VE·maxMVV)]×100

where:

_Emax = ventilation at highest exercise level reached, liters/minute

MVV= maximal voluntary ventilation, liters/minute

The ventilatory reserve is usually expressed as a percentage but can also be denoted as the actual difference. In healthy patients, the ventilatory reserve is typically 20%–40%. In patients with pulmonary disease, the reserve is less than 20% or the absolute difference between MVV and _Emax is less than 10–15 L. The latter relationship is important in individuals with a disease process that affects their ability to perform an MVV (i.e., those who have a low or abnormal MVV). In some cases, the abnormally low MVV can yield a _Emax/MVV ratio that is in the normal range, but the actual difference is reduced (see Table 7-5). A valid MVV maneuver is essential to compare exercise ventilation with MVV. Patients who have airway obstruction may actually achieve _E during exercise that equals or exceeds their ventilatory capacity. In both scenarios, exercise is limited by their inability to further increase ventilation and they are therefore identified as being “ventilatory limited.”

At high levels of ventilation in healthy patients (>120 L/min), increases in O₂ uptake gained by increased ventilation serve mainly to supply O₂ to the respiratory muscles. The same phenomenon may occur at much lower levels of ventilation in patients with severe lung disease because of the increased work of breathing. Because of the ventilatory reserve in healthy patients, exercise is seldom limited by ventilation. Maximal exercise is normally limited by inability to further increase cardiac output or inability to extract more O₂ at the tissue level in exercising muscles. Some highly trained athletes may achieve ventilatory limitation. Aerobic training can improve cardiovascular function so that ventilation, not cardiac output, limits maximal work.

Tidal Volume and Respiratory Rate

V_T during exercise may be calculated by dividing _E by f_b. Breath-by-breath systems record individual breaths and then report an average V_T over a short interval or after a fixed number of breaths have been analyzed. Observation of the breathing kinetics or breathing strategy of a patient during exercise can be an important adjunct in the interpretation of the exercise results. The normal response to exercise is to increase the V_T at low and moderate workloads. Increased V_T accounts for most of the rise in ventilation at these workloads; only a small amount results from increased f_b. This pattern continues until the V_T approaches approximately 50%–60% of vital capacity (VC). Further increases in total ventilation are accomplished by increasing f_b. These kinetic changes can be important in a patient complaining of shortness of breath (SOB) with normal lung function. A high-frequency, low–tidal volume breathing strategy will result in an increased V_D/V_T. More important, however, it may be the only physiologic reason for the patient’s perceived SOB. Likewise, a patient using a large V_T and low f_b may also complain of SOB without a physiologic abnormality.

In healthy individuals, the increase in V_T is accomplished both by using the inspiratory reserve volume (IRV) and by reducing the end-expiratory lung volume (EELV) (Figure 7-12, left panel). This allows efficient use of the respiratory muscles and chest wall pump. In patients with chronic airflow limitation, the inability to increase ventilation may be related to dynamic compression of the airways and dynamic hyperinflation (i.e., increased lung volume) that can occur during exertion. These patients have large resting lung volumes (hyperinflation). During exercise, EELV tends to increase even more as the patient attempts to optimize expiratory flow to meet ventilatory demand. The dynamic shift in lung volume places the respiratory muscles at an even greater disadvantage. The sensation of dyspnea increases tremendously, and the patient is unable to continue exercise. The consequence for these patients is an increase in the work of breathing from both flow limitation and breathing at higher lung volumes (see Figure 7-12, right panel). Patients who have airway obstruction may also be able to increase their _E but cannot attain predicted values

(Interpretive Strategies 7-1). If VC is markedly reduced by the obstructive process, there may be little reserve to accommodate an increased V_T. Obstructed patients who have a normal VC but increased resistance to flow may increase their V_T at a low f_b during exercise in an effort to minimize the work of breathing. This pattern continues until the V_T reaches a plateau, as described previously. Then the f_b must be augmented to further increase _E. Because of flow limitation, particularly during the expiratory phase, increases in f_b must be accomplished by shortening the inspiratory portion of each breath. Reduction of the inspiratory time in relation to the total breath time (T_I /T_tot) requires the inspiratory muscles to generate increasingly greater flows. The increased load placed on the muscles of inspiration typically results in dyspnea.

Unlike the pattern in obstruction, in restrictive disease V_T may remain relatively fixed. Increases in _E during exercise are accomplished primarily by increasing breathing frequency. It is usually more efficient for patients who have “stiff” lungs to move small tidal volumes at fast rates to increase ventilation. However, these tidal volumes may still comprise a relatively large portion of their vital capacity (60%–70%). Flow-volume (F-V) loop profiles may be close to normal, whereas the work of distending the lung is increased in restrictive patterns. The mechanism of increasing ventilation primarily by increasing respiratory rate places a load on the respiratory muscles. In combination with hypoxemia, this increased load often results in extreme SOB.

Flow-Volume Loop Analysis

Another method of determining the degree of ventilatory limitation is by monitoring F-V loop dynamics during exercise. Exercise tidal-volume loops may be plotted against the resting maximal F-V loop. This technique quantifies the amount of time the patient spends on the maximal flow-volume envelope and allows the clinician to identify the percent of flow limitation (Figure 7-13). This method may better define the increased work of breathing in individuals who do not reach a classic definition of ventilatory limitation but have a substantial component of flow limitation during exercise. Monitoring the tidal flow-volume loop during exercise can also show dynamic changes in the flow pattern. These changes can alert the clinician to intrathoracic, extrathoracic, or fixed-airway abnormalities that are demonstrated during exercise only. This technique may also be useful in monitoring breathing kinetics during exercise. As discussed previously, the normal method of increasing tidal volume during exercise is to use both inspiratory and expiratory reserve volumes. Patients with obstructive lung disease have to “move up” in their lung volumes (see Figure 7-12) to recruit tidal volume. In some cases, individuals with normal lung function can use an inappropriate breathing strategy by moving up in their lung volumes to recruit tidal volume without evidence of flow limitation. Using these inappropriate breathing strategies may cause a concomitant sensation of dyspnea. Some patients may breathe at low lung volumes, which approach residual volume. Breathing at these low lung volumes can cause flow limitation resulting from the position of tidal breathing along the absolute lung volume scale. This breathing strategy can elicit wheezing and SOB that can mimic asthma and has been coined a type of “pseudoasthma.” This phenomenon is often seen in morbidly obese subjects secondary to the weight on their thoracic cage that facilitates a reduction in their functional residual capacity (FRC).

Carbon Dioxide Production

Carbon dioxide production (co₂) is a direct reflection of metabolism. It is expressed in liters or milliliters per minute, STPD. co₂ may be calculated using the following equation:

V·ECO2=(FECO2−0.0003)  ×  V·E(STPD)

where:

F_Eco₂= fraction of CO₂ in expired gas

0.0003= fraction of CO₂ in room air (may vary)

_E(STPD) = calculated as in the equation for o₂

Pulmonary ventilation, consisting of alveolar ventilation (_A) and dead space ventilation (_D), may be related in terms of the co₂. The fraction of alveolar carbon dioxide (F_Aco₂) is directly proportional to co₂ and inversely proportional to _A. The concentration of CO₂ in the lung is determined by CO₂ production and the rate of removal from the lung by ventilation. This relationship may be expressed as follows:

FACO2=V·CO2V·A

co₂ in a healthy patient at rest is approximately 0.20 L/min (STPD). It may increase to more than 5 L/min (STPD) during maximal exercise in trained individuals. The adequacy of _A in response to the increase in co₂ is indicated by how well Paco₂ is maintained near normal levels. Alveolar ventilation keeps Paco₂ in equilibrium with alveolar gas at low and moderate workloads. At high workloads, _A increases dramatically to reduce Paco₂ when buffering of lactic acid takes place. At maximal workloads, even high levels of ventilation cannot keep pace with CO₂ produced metabolically and from lactate buffering. As a result, acidosis develops.

Respiratory Exchange Ratio

The respiratory exchange ratio (RER) is defined as the ratio of co₂ to o₂ at the mouth. RER is calculated by dividing co₂ by o₂; it is expressed as a fraction. In some circumstances, RER at rest is assumed to be equal to 0.8. For exercise evaluation or metabolic studies, however, the actual value is calculated. RER normally varies between 0.70 and 1.00 in resting patients, depending on the nutritional substrate being metabolized (see Chapter 10). RER reflects the respiratory quotient (RQ) at the cellular level only when the patient is in a true steady state. RER may differ significantly from RQ, depending on the patient’s ventilation.

RER typically increases from a resting level of between 0.75 and 0.85 as work increases. When anaerobic metabolism (see next paragraph) begins to produce CO₂ from the buffering of lactate, co₂ approaches o₂. As exercise continues, co₂ exceeds o₂ and the RER becomes greater than 1. RER is commonly elevated at rest because many patients hyperventilate during exhaled gas analysis before exercise begins (see Criteria for Acceptability 7-3). In steady-state exercise tests (i.e., 4–6 minutes at a constant workload), RER may equal RQ, and it then reflects the ratio of co₂/o₂ at the cellular level. Under steady-state conditions, co₂ reflects the CO₂ produced metabolically at the cellular level.

Anaerobic or Ventilatory Threshold

Measurement of and the analysis of exhaled gases during exercise allows a noninvasive estimate of the anaerobic threshold (AT). This threshold is also termed the ventilatory threshold when it is denoted by a change in ventilation and CO₂ production. The AT occurs when the energy demands of the exercising muscles exceed the body’s ability to produce energy by aerobic metabolism. The workload at which AT occurs is considered an index of fitness in healthy patients. The AT is also used to assess cardiac performance in patients with heart disease.

Historically, anaerobic metabolism was detected by noting an increase in the blood lactate level of an exercising patient. Analysis of _E and co₂ in relation to workload (o₂) can be used to detect the onset of anaerobic metabolism without drawing blood. This threshold is commonly referred to as the ventilatory threshold.

At low and moderate workloads, _E increases linearly with increases in co₂. When the body’s energy demands exceed the capacity of aerobic pathways, further increases in energy are produced anaerobically. The primary product of anaerobic metabolism is lactate. The increased lactic acid (from lactate) is buffered by HCO₃⁻, resulting in an increase in CO₂ in the blood. co₂ measured from exhaled gas increases because CO₂ is being produced by both the exercising muscles and the buffering of lactate. To maintain the pH near normal, _E increases to match the increased co₂. This pattern of increasing ventilation and CO₂ production can be detected when these parameters are plotted against o₂ (see Figure 7-9). Determination of the ventilatory-anaerobic threshold may be accomplished by visual inspection of an appropriate plot. Statistical analysis can also be used to determine the inflection point as displayed by the graph in Figure 7-14. Several different algorithms may be used to identify the AT. One of the most common techniques uses regression analysis to determine the “breakpoint” at which o₂ and co₂ change abruptly (V-slope method).

Noninvasive AT determination may be useful in assessing cardiovascular or pulmonary diseases (Interpretive Strategies 7-3). In healthy patients, AT occurs at 60%–70% of the o₂max. Patients who have cardiac disease often reach their AT at a lower workload (o₂). Early onset of anaerobic metabolism occurs when the demands of exercising muscles exceed the capacity of the heart to supply O₂. Occurrence of the anaerobic threshold at less than 40% of the o₂max is considered abnormally low. Patients who have a ventilatory limitation to exercise (i.e., pulmonary disease) may be unable to exercise at a high enough workload to reach their anaerobic threshold. In these patients, O₂ delivery is limited by the lungs, rather than by cardiac output or extraction by the exercising muscle.

Aerobic training improves cardiac performance, specifically the stroke volume (SV). Training allows more O₂ to be delivered to the tissues and increased utilization at the cellular level (e.g., more mitochondria), resulting in a delay in the AT until higher workloads are reached. Measurement of the AT is often used to select a training level (e.g., exercise prescription). Maximum training effects seem to occur when the patient exercises at a workload slightly below the AT. In sedentary patients, deconditioning may occur. Deconditioning is characterized by reduced SV and poor O₂ extraction by the muscles from lack of use. Deconditioning may be present when the AT occurs at a lower than expected workload and there is no evidence of cardiovascular disease.

The AT may also be determined by inspecting graphs of the ventilatory equivalents for O₂ and CO₂ (see the next section) plotted against workload (o₂). When _E/co₂ increases without an increase in _E/co₂, the AT has been reached. A similar pattern can be seen when the end-tidal O₂ and CO₂ gas tensions are plotted (see Figure 7-10). Sample calculations of _E, o₂, co₂, and RER, as used with one of the gas collection methods, are included on Evolve (http://evolve.elsevier.com/Mottram/Ruppel/).

Ventilatory Equivalent for Oxygen

Minute ventilation during exercise may be related to the work being performed (expressed as o₂). This ratio is termed the ventilatory equivalent for oxygen, or _E/o₂. It is calculated by dividing _E (BTPS) by o₂ (STPD) and expressing the ratio in liters of ventilation/liters of O₂ consumed per minute. The _E/o₂ is a measure of the efficiency of the ventilatory pump at various workloads.

During resting data collection in healthy patients, the ratio is in the range of 30 to 40 L depending on the degree of ventilation, including anticipatory hyperventilation. As the patient begins to exercise, this ratio decreases to about 25 ± 4 (see Figure 7-15). This initial kinetic change is assumed to be related to an improvement in /matching with increased cardiac output during exercise. At low and moderate workloads, ventilation increases linearly with increasing o₂ and co₂. The absolute level of ventilation depends on the response to CO₂, the adequacy of _A, and the V_D/V_T ratio. At workloads above 60%–75% of the o₂max, _E is more closely related to co₂. As ventilation increases to match the co₂ above the AT, the ventilatory equivalent for O₂ also increases.

Ventilation helps determine how much O₂ can be transported per minute. Therefore, it is often useful to evaluate the level of total ventilation required for a particular workload to assess the role of the lungs in exercise limitations. In some pulmonary disease patterns, the _E/o₂ may be close to normal at rest but increases with exercise out of proportion to increases in either o₂ or co₂. This usually occurs in individuals who have /abnormalities that worsen as cardiac output increases during exercise. Some patients who have pulmonary disease may have an elevated _E/o₂ at rest (i.e., greater than 40 L o₂) that decreases during exercise but does not return to the normal range. Many patients hyperventilate during the resting phase at the beginning of an exercise evaluation. The result is an increased _E/o₂ that usually returns to the normal range during exercise. This pre-test hyperventilation is usually denoted by an RER of greater than 1 that returns to a normal level when the patient begins to exercise.

Ventilatory Equivalent for Carbon Dioxide

The ventilatory equivalent for CO₂ (_E/co₂) is calculated in a manner similar to that used for the _E/o₂. Minute ventilation (BTPS) is divided by CO₂ production (STPD). The _E/co₂ mimics the initial _E/o₂ kinetic change, decreasing to a normal range of 25–35 L co₂. _E tends to match co₂ from low up to high workloads. Thus, the _E/co₂ remains constant in healthy patients until the highest workloads are reached. The _E/co₂ may be useful for estimating the maximum tolerable workload in patients who have moderate or severe ventilatory limitations. The ventilatory equivalents for O₂ and CO₂, measured with a breath-by-breath technique, may be useful in identifying the onset of the AT. Anaerobic metabolism is usually accompanied by a steady increase in the _E/o₂ while the _E/co₂ remains constant, or decreases slightly. The period in which _E/o₂ is increasing yet _E/co₂ is constant is called the isocapnic buffering zone (Figure 7-15). This zone indicates the onset of metabolic acidosis, where _E is no longer proportional to o₂ but is appropriate for co₂. Occurrence of this pattern coincides with the buffering of the lactate (AT). Eventually, the buffering system cannot keep pace with the metabolic acidemia, and the _E/co₂ increases as attempts to maintain pH. This same pattern may also be seen on a breath-by-breath display of Peto₂ and Petco₂ (see Figure 7-10). A markedly elevated _E/co₂ (>50) may also be observed in pulmonary hypertensive disease.

Oxygen Pulse

The efficiency of the circulatory pump may be related to the workload (i.e., o₂) during exercise by the O₂ pulse. O₂ pulse is defined as the volume of O₂ consumed per heartbeat and is derived from the Fick equation:

Cardiac output=V·o2CaO2−Cv¯O2

HR×SV=V·O2CaO2−Cv¯O2

V·O2HR(O2 pulse)=SV×(CaO2−Cv¯O2)

O₂ pulse is sometimes called the “poor man’s” estimate of stroke volume because of the relatively “consistent” change in the CaO₂-Cv_o₂ difference with exercise. The ratio is expressed as milliliters of O₂ per heartbeat. In healthy patients, O₂ pulse varies between 2.5 and 4.0 mL O₂/beats at rest. It increases to 10–15 mL O₂/beats during strenuous exercise.

In patients with cardiac disease, the O₂ pulse may be normal or even low at rest but does not increase to expected levels during exercise. This pattern is consistent with an inappropriately high HR for a particular level of work. Cardiac output normally increases linearly with increasing exercise (see Figure 7-5). A low O₂ pulse is consistent with an inability to increase the SV because of the relationship noted in the preceding paragraphs. O₂ pulse may even decrease in patients with poor left ventricular function. The pattern of low O₂ pulse with increasing work rate may be seen in patients with coronary artery disease or valvular insufficiency, but it is most pronounced in cardiomyopathy. Tachycardia or tachyarrhythmias tend to lower the O₂ pulse because of the abnormally elevated heart rate. Conversely, beta-blocking agents, which tend to reduce HR, may elevate the O₂ pulse.

O₂ pulse is often used as an index of fitness. At similar power outputs, a fit patient will have a higher O₂ pulse than one who is deconditioned. Fitness is generally accompanied by a lower HR, both at rest and at maximal workloads. Lower HR occurs because conditioning exercises (e.g., aerobic training) tend to increase SV. As a result, the heart beats less frequently but produces the same CO. Trained patients can thus achieve higher work rates before reaching their limiting cardiac frequency (i.e., attain a higher O₂ pulse).

Arterial Puncture

An alternate technique is to obtain a specimen by a simple arterial puncture at peak exercise. Use of a cycle ergometer for testing allows better stabilization of the radial or brachial artery sites. The site should be identified and the modified Allen’s test performed before beginning exercise. The sample should be obtained within 15 seconds of peak exercise. Blood gas tensions, particularly Pao₂, may change rapidly as blood recirculates. A serious disadvantage of the single puncture is that if the specimen cannot be obtained within 15 seconds, the procedure must be repeated. If any of the conditions listed in Box 7-4 are present, arterial catheterization should be considered.

Pulse Oximetry

Oxygen saturation during exercise may be monitored with a pulse oximeter (SpO₂) using the ear, finger, or forehead sites (see Chapter 11). Wherever the pulse oximeter is attached, the probe should be adequately secured. Motion artifact is a common problem, particularly with treadmill exercise.

An advantage of pulse oximetry is that it provides continuous measurements of saturation, compared with discrete measurements of arterial sampling. Continuous measurements can be helpful in evaluating patients who have pulmonary disease. These patients often display rapid changes in Pao₂ and SaO₂ during exercise. A decrease of 4%–5% in SaO₂ is indicative of exercise desaturation, even if some other factor (e.g., ventilation, arrhythmia) limits exercise.

Pulse oximetry may overestimate the true saturation if a significant concentration of carboxyhemoglobin (COHb) is present (Criteria for Acceptability 7-4). A low total Hb level (i.e., anemia) sometimes contributes to exercise limitation. This condition may not be detected by pulse oximetry alone. Inadequate perfusion at the site of the probe (e.g., ear or finger) may also cause erroneous readings (false positive) during exercise testing. Motion artifact, light scattering within the tissue at the probe site, and dark skin pigmentation may all cause discrepancies between Spo₂ and actual Sao₂ (see Chapter 6). A single arterial sample, preferably at peak exercise, may be used to correlate the Spo₂ reading with true saturation if the specimen is analyzed with a multiwavelength blood oximeter (see Chapter 11). If adequate correlation between Sao₂ and Spo₂ during exercise is established, further blood sampling may be unnecessary.

Arterial Oxygen Tension During Exercise

In healthy patients, Pao₂ remains relatively constant even at high workloads (Interpretive Strategies 7-4). Alveolar Po₂ increases at maximal exercise from the increased ventilation accompanying the increase in co₂. The alveolar-arterial (A-a) gradient (normally approximately 10 mm Hg) widens as a result of the increase in alveolar oxygen tension. The A-a gradient also increases somewhat because of a lower mixed venous O₂ content during exercise. The A-a gradient may increase to 20–30 mm Hg in healthy patients during heavy exercise because of these mechanisms.

A decrease in Pao₂ with increasing exercise can result from increased right-to-left shunting. Similarly, inequality of _A in relation to pulmonary capillary perfusion may result in a reduced Pao₂. Diffusion limitation at the alveolocapillary interface can also affect Pao₂. Because exercise reduces the mixed venous oxygen tension (Pv−o₂), a shunt or ventilation/perfusion inequality may result in a decrease in the Pao₂ or widening of the A-a gradient. This change in Pao₂ may occur without an absolute change in the magnitude of the shunt. Mixed venous blood with a lowered O₂ content (from extraction by the exercising muscles) passes through abnormal lung units and then mixes with normally arterialized blood.

In some patients who have decreased Pao₂ and increased P(a−a)o₂ at rest, oxygenation may improve with exercise. Increased cardiac output or redistribution of ventilation during exercise may actually cause an increase in Pao₂. Some improvement of Pao₂ may occur as a result of an increased Pao₂ caused by a reduction of Paco₂ at moderate to high work rates. Improved /relationships resulting directly from the changes in ventilation or cardiac output may also improve Pao₂. Because Pao₂ may either increase or decrease during exercise, measuring Pao₂ during exercise may be particularly valuable in patients with pulmonary disorders.

When Pao₂ decreases to less than 55 mm Hg or Sao₂ decreases to less than 85%, the exercise evaluation should be terminated. Patients with hypoxemia at rest or who desaturate at low work rates should be tested with supplemental O₂ (e.g., a nasal cannula) to determine an appropriate exercise O₂ prescription. Different flows of supplemental O₂ may be required at rest and for various levels of exertion. Correlation of Pao₂ while breathing supplemental O₂ at different exercise workloads allows precise titration of therapy to the patient’s needs. Measurement of o₂ while the patient breathes supplemental O₂ presents special problems. A closed system in which the patient breathes from a reservoir containing blended gas, typically F_Io₂ 0.30, is usually required.

Reported in some elite athletes at high levels of work (e.g., 400–500 watts or 9 mph/18% grade) is a widening of the A-a gradient with Pao₂ values falling into the range of 50–60 mm Hg. This phenomenon is thought to be related to the time constants of blood in the lung with very high cardiac outputs and high oxygen extraction at the cellular level.

Arterial Carbon Dioxide Tension During Exercise

In healthy patients, Paco₂ remains relatively constant at low and moderate work rates (Interpretive Strategy 7-10). _A increases to match the increase in co₂. End-tidal CO₂ increases at submaximal workloads, indicating that less ventilation is “wasted” (V_D/V_T decreases). At workloads in excess of 50%–60% of the o₂max, metabolic acidosis from anaerobic metabolism stimulates an increase in _E. This occurs in response to the augmented co₂ from the buffering of lactic acid as noted previously. Ventilation thus increases in excess of that required to keep Paco₂ constant. A progressive decrease in Paco₂ results, causing respiratory compensation for the acidosis associated with anaerobic metabolism (see Figures 7-9 and 7-10). Petco₂ decreases along with Paco₂ at high work rates.

Some individuals who have airway obstruction can increase _A to maintain a normal Paco₂ at low workloads. At higher workloads, however, they may be unable to reduce Paco₂ to compensate for the metabolic acidosis. In many patients with airway obstruction, maximal exercise is limited by lack of ventilatory reserve. These individuals typically do not reach the AT. Ventilatory limitation prevents them from attaining a workload high enough to induce anaerobic metabolism. In patients with severe airflow obstruction, _A may be unable to match any increment in co₂, resulting in hypercapnia and respiratory acidosis. Increased work of breathing and reduced sensitivity to CO₂, combined with the increased co₂ of exercise, allow Paco₂ to increase.

Acid-Base Status During Exercise

The pH, like Paco₂, is regulated by the _A at low work rates. _A increases in proportion to co₂ up to the ventilatory AT. At work rates above AT, proportional increases in ventilation maintain the pH at near-normal levels. Most of the buffering of lactic acid is provided by HCO₃⁻ and a decrease in Paco₂. At the highest work rates (above 80% of the o₂max), pH decreases despite hyperventilation because compensation for lactic acidosis becomes incomplete. In the presence of airway obstruction, ventilatory limitations may prevent compensation above the anaerobic threshold, with the development of significant respiratory acidosis. However, patients who have moderate or severe obstruction generally cannot exercise up to a level that elicits anaerobic metabolism. Increased Paco₂ (respiratory acidosis) may be the primary cause of acidosis in these patients.

Exercise Variables Calculated from Blood Gases

Arterial blood gases drawn during exercise allow several other parameters of gas exchange to be determined (Interpretive Strategies 7-4). These include physiologic dead space, alveolar ventilation, and the V_D/V_T ratio.

Calculation of V_D, _A, and V_D/V_T requires measurement of Paco₂. V_D may be calculated with the following equation:

VD=(VT×[1−FECO2×(PB−47)PaCO2])−VDsys

where:

V_T= tidal volume, liters (BTPS)

F_Eco₂= fraction of expired CO₂

P_B – 47= dry barometric pressure

Paco₂= arterial CO₂ tension

V_Dsys= dead space of one-way breathing valve, liters

When V_D has been determined, _A can be calculated with the following equation:

V·A=V·E−(fb×VD)

where:

_E= minute ventilation (BTPS)

f_b= respiratory rate (breaths/minute)

V_D= respiratory dead space (BTPS)

V_D/V_T ratio may be calculated as the quotient of the V_D (as just determined) and the V_T, averaged from the _E divided by f_b. Alternatively, V_D/V_T may be derived simply from the difference between arterial and mixed expired CO₂ at each exercise level:

VD/VT=(PaCO2−PE¯CO2)PaCO2

where:

PE¯CO2 = partial pressure of CO₂ in expired gas

Most breath-by-breath systems calculate V_D/V_T noninvasively by substituting end-tidal CO₂ for Paco₂. This method assumes that Petco₂ and Paco₂ are equal. This may not be the case at higher workloads and in patients who have pulmonary disease.

V_D, which is composed of anatomic and alveolar dead space, is the part of _E that does not participate in gas exchange. V_D/V_T expresses the relationship between “wasted” and tidal ventilation for the average breath. The healthy adult at rest has a _A of 4–7 L/min (BTPS) and a V_D/V_T ratio of approximately 0.20–0.35. The absolute volume of dead space increases during exercise in conjunction with increased _E. Because of increases in V_T and increased perfusion of well-ventilated lung units (e.g., at the apices), the V_D/V_T ratio decreases. This pattern is expected in healthy patients (see Figure 7-9). V_D/V_T increases with age, but the kinetic change with exercise remains the same. V_D/V_T may decrease in mild or moderate pulmonary disease states as well. In severe airway obstruction or in pulmonary vascular disease, V_D/V_T remains fixed or may even increase. An increase in V_D/V_T with exertion indicates ventilation increasing in excess of perfusion. This pattern is often associated with pulmonary hypertension. The vascular “space” is fixed in pulmonary hypertension; additional lung units cannot be recruited to handle the increased CO during exercise. V_D/V_T may also be elevated in individuals who use inappropriate breathing strategies. Small tidal volumes and high respiratory rates to recruit _E in an otherwise healthy patient can yield falsely high ratios. Coaching a patient to increase tidal volume and use a more normal breathing pattern can alleviate a falsely elevated V_D/V_T ratio.

During exercise in healthy patients, _A increases more than _E as V_D/V_T decreases. In patients whose V_D/V_T ratio remains fixed or increases, adequacy of _A must be assessed in terms of Paco₂ and not simply by the magnitude of _E.

Noninvasive Cardiac Output Techniques

The CO₂ rebreathing technique (also termed the indirect Fick method) uses the Fick equation for CO₂:

Q·T=V·CO2Cv¯CO2−CaCO2

where:

_T = CO, L/min co₂ = CO₂ production calculated from exhaled gases

Caco₂ = arterial CO₂ content, calculated from Paco₂

CV¯co₂ = mixed venous CO₂ content, calculated from alveolar Pco₂ after rebreathing to allow equilibrium of alveolar gas with mixed venous blood

The acetylene technique, also known as the soluble gas technique, can be performed with either closed-circuit or open-circuit methods. This method depends on the rate of uptake of a soluble gas (e.g., acetylene) that has a low diffusion coefficient. The rate of uptake is directly proportional to the pulmonary blood flow. As long as there is no intracardiac or pulmonary shunt, pulmonary blood flow equals cardiac output. Both of these breathing techniques correlate well with invasive techniques in healthy patients but have limited use in patients with maldistribution of ventilation.

Instrumentation with Doppler technology to estimate CO works on the principle of measuring flow with an ultrasound signal directed at the arch of the aorta. A measurement of the diameter of the aorta is also made with echocardiography. These two measurements allow for the determination of cardiac output (i.e., flow × cross-sectional area = total output). This method works well at rest and at low levels of exercise with a cycle ergometer, but motion artifact and increasing tidal volumes limit its usefulness at higher workloads.

Direct Fick Method

The direct Fick method is based on the measurement of O₂ consumption and arterial-venous content difference for O₂:

Q·T=V·O2C(a−V¯)O2  ×  100

where:

_T= CO, L/min

o₂= oxygen consumption, L/min (STPD)

C(a-v–)o₂= arterial-mixed venous O₂ content difference, mL/dL

100 = factor to correct C(a-V¯)o₂ to liters (content differences are normally reported in vol% or mL/dL)

o₂ is measured using one of the methods described previously. C(a-V¯)o₂ is obtained by measuring or calculating oxygen content in both arterial and mixed venous blood (see Chapter 6). Arterial and mixed venous blood specimens should be drawn simultaneously during the last 15–30 seconds of each exercise level. Oxygen consumption averaged over the same interval should be used for the calculation.

Thermodilution Method

Most pulmonary artery (Swan-Ganz) catheters include circuitry for the measurement of CO by thermodilution. A sensitive thermistor is placed near the tip of the catheter. A chilled saline solution (usually 10° C–20°C) is injected through a catheter port that is located in the right atrium. The thermistor senses the change in temperature as the solution is pumped through the right ventricle and into the pulmonary artery. The computer then integrates the change in temperature and the time required for the change to occur, and CO is calculated.

The thermodilution method is commonly used in critical care settings. It can also be used during exercise testing. Multiple measurements (two to four) should be made at each exercise level and the results averaged. Some automated systems allow other cardiopulmonary variables (e.g., ejection fraction) to be calculated as well.

Cardiac Output During Exercise

Cardiac output in healthy adults is approximately 4–6 L/min at rest. During exercise, it may increase to 25–35 L/min (Interpretive Strategies 7-5). CO is the product of HR and SV:

Q·T=HR×SV

where:

_T = CO, L/mL

HR= heart rate, beats/minute

SV= stroke volume, L/mL

In healthy upright adults, SV is approximately 70–100 mL at rest. SV may be slightly higher if the patient is supine or semirecumbent because of increased venous return from the lower extremities. SV increases to 100–140 mL with low or moderate exercise. HR increases almost linearly with increasing work rate as described earlier, so at low workloads an increase in CO is caused by a combination of HR and SV. At moderate and high workloads, further increases in CO result mainly from increased HR. Derivation of SV (dividing _T by HR) is useful for quantifying poor cardiac performance in patients with coronary artery disease, cardiomyopathy, or other diseases that affect myocardial contractility.

Patients who are able to reach their predicted o₂max and their predicted HRmax typically have normal CO and SV. A patient who has a reduced o₂max but achieves maximal predicted HR often has low CO because of low SV. Limited CO with increasing workload is often accompanied by early onset of anaerobic metabolism (anaerobic or ventilatory threshold). Reduced CO may be seen in both atrial and ventricular arrhythmias, valvular insufficiency, and cardiomyopathies.

In fit patients, SV is increased both at rest and during exercise. Endurance (aerobic) training normally results in increased SV. Other benefits of aerobic training include reductions in systolic BP and ventilation. Fit patients typically have a lower resting HR than their sedentary counterparts. Because HR (i.e., cardiac output) is the factor that limits exercise in most individuals, fit patients reach a higher o₂max. Depending on the frequency, intensity, and duration of training, fit individuals are able to maintain a higher level or work for longer periods because of improved CO.

Symptoms Scales

The measurement of RPE (or Borg scale) and other symptom scales can be essential for connecting subjective symptoms and the physiologic responses to exercise. Rating scales, when they are discordant, can assist the physician in counseling the patient. There are two versions of the RPE scale, often referred to as the Borg and modified-Borg scales (Table 7-7). These scales are usually printed on a card or poster that the patient can see or “point to” during exercise testing. The scales should be reviewed with the patient before exercise begins. This is particularly important if exhaled gas is being collected because the patient may have a mouthpiece or facial mask in place. The patient should be able to indicate his or her level of exertion even without vocalizing. General symptom (visual analog) scales can be adapted to any chief complaint the patient may be expressing by simply using a scale of 0–4 and grading intensity from “nothing at all” to “severe.” A patient complaining of lightheadedness or chest tightness can then alert the testing staff to his or her level of discomfort during the test using hand signals.

Table 7-8

Determining Maximal Effort

***	Heart rate:	> 85%–90% of predicted
***	End exercise:	50%–80% E of MVV or FEV1× 40; MVV −Emax ≤ 15L
**	SaO2	< 80%
*	Metabolic work:	RER >1.10 or lactate > 7 mmol/L
*	Clinical investigator:	Opinion of effort or early termination criteria met

Once a single criterion is met, test is graded a maximal effort.

^*= Weight of variable.

Quality of Test

General quality assurance and quality control of instrumentation is discussed in Chapter 11. However, the complexity of cardiopulmonary exercise testing warrants additional considerations, including a quality system approach to testing. The Clinical and Laboratory Standards Institute (CLSI): A Quality System Model for Laboratories, discussed in Chapter 12, incorporates the concept of the path of workflow process. This concept integrates pre-test, test, post-test, assessments of processes that can affect any section across the path of workflow. Pre-test processes include patient assessment, test request, patient preparation, and equipment preparation. Patient assessment, as it relates to cardiopulmonary exercise testing, might include a review of laboratory results, current medications affecting exercise performance (e.g., β-blockers, digitalis), or orthopedic issues that may affect ergometer selection. Test processes include, but are not limited to, making sure the subject understands the purpose of the test and the expected effort, testing staff are competent in identifying normal and abnormal responses to exercise, and appropriate response to patient conditions to maintain patient safety. In the post-test period, post-test assessments (i.e., post-FVCs, BP), selecting data for analysis, and the reporting process all need to be considered.

Additional quality processes specific to exercise testing systems include monitoring phase delay data, ergometer calibration, and biologic QC data. The importance of phase delay was previously discussed in the chapter. Cycle ergometer calibration can be specific to the device; however, many of the new electronic ergometers cannot be calibrated without expensive adjunct hardware. Treadmill outputs can be easily validated. Speed can be assessed by knowing the belt length and timing belt revolutions with a stopwatch. Grade can be verified by dividing the length of the treadmill by the height (Figure 7-16). The entire system can be monitored by performing biologic QC (BioQC). Several methods have been suggested; however, all include collecting steady-state data at rest and a predetermined submaximal workload(s). Determining an appropriate workload can be achieved by having the BioQC subject perform a maximal test, identify the anaerobic threshold, and select a workload below the AT. Another suggested method has the subject perform steady-state exercise (3-5 minutes at each stage) at two workloads 50 watts apart (example 25 and 75 watts). The expected oxygen consumption difference between the two workloads should be 500 mL because the normal o₂ to watt relationship is 10 mL/watt. Regardless of the method used, the data can be entered into a spreadsheet with the mean and two standard deviations calculated. The data can be monitored over time to identify “out of control” situations, which may not be recognized with a standard individual module (i.e., pneumotach and gas analyzer) calibration.

Interpretation Strategies

To interpret a study appropriately, the practitioner first needs to assess the degree of effort and determine whether the test is a maximal study (see Table 7-4). Once the test has been qualified as maximal or submaximal, an algorithmic approach to data review and interpretation is essential (see Interpretive Strategies 7-2, 7-3, 7-4, and 7-5).

The following scheme can assist in a stepwise approach to data analysis: