Cardiopulmonary exercise testing (CPET) is a versatile tool that can be useful in patient management and clinical decision-making. Many physicians are unfamiliar with it, in part because historically it was cumbersome, done mostly in research or exercise physiology centers, and used mostly in assessing athletic fitness rather than pathologic conditions. In addition, medical schools provide little instruction about it, and hands-on use has typically been relegated to pulmonologists.
Improvements in hardware and software and ease of use have brought this test into the clinical arena to the point that clinicians should consider it earlier in the evaluation of appropriate patients. It now has a class I recommendation (ie, the test is indicated) from the American College of Cardiology and American Heart Association for evaluating exertional dyspnea of uncertain cause and for evaluating cardiac patients being considered for transplant.1 It also is a powerful prognosticator of outcomes in heart failure patients.
CARDIOPULMONARY EXERCISE TESTING MADE SIMPLE
CPET is the analysis of gas exchange during exercise. Modern systems measure, breath-by-breath, the volume of oxygen taken up (Vo2), and the volumes of carbon dioxide (Vco2) and air expired (Ve).
Testing can be done with nearly any kind of exercise (treadmill, cycle, arm ergometry), thus accommodating patient or provider preference. Most exercise protocols involve a gradual increase in work rather than increasing stages of work for smooth data collection, and graphical display for optimal test interpretation.
After undergoing baseline screening spirometry, the patient rides a stationary bicycle or walks on a treadmill while breathing through a nonrebreathing mask and wearing electrocardiographic leads, a blood pressure cuff, and a pulse oximeter. The test starts out easy and gets progressively harder until the patient fatigues, reaches his or her predicted peak Vo2, or, as in any stress test, experiences any other clinical indication for stopping, such as arrhythmias, hypotension, or symptoms (rare). We advise patients to wear comfortable workout clothes, and we ask them to try as hard as they can. The test takes about 10 to 15 minutes. Patients are instructed to take all of their usual medications, including beta-blockers, unless advised otherwise at the discretion of the supervising physician.
What the numbers mean
Table 1 lists common CPET variables; Table 2 lists common patterns of results and what they suggest. Other reviews further discuss disease-specific CPET patterns.2–5
Peak Vo2. As the level of work increases, the body needs more oxygen, and oxygen consumption (Vo2) increases in a linear fashion up to a peak value (Figure 1). Peak Vo2 is the central variable in CPET. Whereas elite athletes have high peak Vo2 values, patients with exercise impairment from any cause have lower values, and average adults typically have results in the middle. Peak Vo2 can be expressed in absolute terms as liters of oxygen per minute, in indexed terms as milliliters of oxygen per kilogram of body weight per minute, and as a percentage of the predicted value.
Ventilatory threshold. Before people reach their peak Vo2, they reach a point where the work demand on the muscles exceeds the oxygen that is being delivered to them, and their metabolism becomes more anaerobic. This point is called the anaerobic threshold, or more precisely the ventilatory threshold. In states of deconditioning or disease, this threshold is often lower than predicted. It can be detected either directly by measuring blood lactate levels or, more often, indirectly from the Vo2, Vco2, and Ve data (Figure 2).
Ve/Vco2 slope. As exercise impairment advances, ventilatory efficiency worsens. Put simply, the demands of exercise result in greater ventilatory effort at any given level of work. This is a consequence of ventilation-perfusion mismatching from a milieu of metabolic, ventilatory, and cardiac dysregulation that accompanies advanced cardiopulmonary or metabolic disease.6,7 The most validated CPET variable reflecting this is the minute ventilation-carbon dioxide relationship (Ve/Vco2 slope) (Figure 3).
Coupled with other common CPET variables and measures such as screening spirometry, electrocardiography, heart and respiratory rate responses, pulse oximetry, and blood pressure, the Ve/Vco2 allows for a detailed and integrated assessment of exercise performance.
USING CPET TO EVALUATE EXERTIONAL DYSPNEA
Shortness of breath, particularly with exertion, is a common reason patients are referred to internists, pulmonologists, and cardiologists. It is a nonspecific symptom for which a precise cause can be elusive. Possible causes range from physical deconditioning due to obesity to new or progressive cardiopulmonary or muscular disease.
If conventional initial studies such as standard exercise testing, echocardiography, or spirometry do not definitively identify the problem, CPET can help guide additional investigation or management. Any abnormal patterns seen, together with the patient’s clinical context and other test results, can give direction to additional evaluation.
Table 2 outlines various CPET patterns that can suggest clinically significant cardiac, pulmonary, or muscle disorders.8–13 Alternatively, normal responses reassure the patient and clinician, since they suggest the patient does not have clinically significant disease.
Case 1: Obesity and dyspnea
You evaluate a 53-year-old mildly obese man for dyspnea. Cardiology evaluation 1 year earlier included normal transthoracic and stress echocardiograms. He is referred for CPET.
His peak Vo2 is low in indexed terms (22.3 mL/kg/min; 74% of predicted) but 90% of predicted in absolute terms (2.8 L/min), reflecting the contribution of his obesity. His ventilatory threshold is near the lower end of normal (50% of peak Vo2), and all other findings are normal. You conclude his dyspnea is due to deconditioning and obesity.
Case 2: Diastolic dysfunction
You follow a normal-weight 65-year-old woman who has long-standing exertional dyspnea. Evaluation 1 year ago included an echocardiogram showing a normal left ventricular ejection fraction and grade II (moderate) diastolic dysfunction, a normal exercise stress test (details were not provided), normal pulmonary function testing, and high-resolution computed tomography of the chest. She too is referred for CPET.
The findings include mild sinus tachycardia at rest and low peak Vo2 (23.7 mL/kg/min; 69% of predicted). The Ve/Vco2 slope is substantially elevated at 43. Other measures of cardiopulmonary impairment and ventilatory inefficiency such as the end-tidal Pco2 response, oxygen uptake efficiency slope, and oxygen-pulse relationship (O2-pulse, a surrogate for stroke volume) are also abnormal. In clinical context this suggests diastolic dysfunction or unappreciated pulmonary hypertension. You refer her for right heart catheterization, which confirms findings consistent with diastolic dysfunction.