The CPET’s not over until it’s over

My guidelines for interpreting CPETs originally started as notes to myself about what needed to be on the report and what the normal values were. They grew into a more formal set of instructions that were given to the pulmonary fellows when they were reviewing CPETs. Lately I’ve been reviewing them and re-reading the source material in order to make sure what I had written was still correct and so I could add references.

I tend to focus on one aspect of testing at a time and noticed while reviewing material that the measurements made at peak exercise or anaerobic threshold are almost always considered to be the most important test values. This is true to an extent, but information gathered both before and after testing is also important. In particular, after exercise has ended, during the recovery period, there are several measurements that should be made routinely and are diagnostically significant.

Heart rate recovery (HRR)

When exercise ends, an individual’s heart rate should start decreasing from its peak value. The heart rate recovery (HRR) is the difference between the heart rate at peak exercise and at some interval, usually 1 minute, post-exercise. The rise in heart rate during exercise is due to a combination of parasympathetic withdrawal and sympathetic activation. Vagal reactivation is the principle determinant of heart rate recovery after exercise and a reduction in the heart rate recovery (HRR) indicates a decrease in vagal tone specifically, and parasympathetic tone generally.

In a study of several thousand people the median decrease in heart rate during the first minute following exercise was approximately 17 BPM (normal range 12 to 23 BPM). Numerous investigators have shown that a decrease in heart rate less than 12 BPM in the first minute is associated with an elevated risk of mortality. Individuals with an abnormal HRR have more adverse health risk profiles which includes heart and both obstructive and restrictive lung diseases. They were also more likely to reach a lower workload and had a lower maximum heart rate during exercise. Interestingly, more than one study has shown no significant difference angina, ST-segment depression, or in other abnormal ST-segment changes in patients with either a normal or a reduced HRR.

At least one study has indicated that the HRR less than 22 at two minutes may be a better predictor of mortality than the HRR at one minute, and that abnormal values made the presence of CAD probable but only a small number of studies have followed up on this observation.

The most recent AHA/EACPR CPET guidelines indicated that a HRR less than 12 should be considered abnormal. The increased risk in mortality has been variously shown to be 2 to 4 times higher in individuals with a low HRR than in those with a normal HRR. Some studies have indicated that mortality risk increases even more significantly at a HRR less then 8.

For obvious reasons HRR measurement requires accurately marking the end of exercise. Since the HRR has been studied in primarily in maximal CPETs, a submaximal test may also have a submaximal HRR.

Blood pressure recovery

Systolic blood pressure should reach a maximum at or near peak exercise. Although not as strong an indicator of mortality risk as HRR, a delayed decrease in blood pressure following exercise is a reasonably strong indicator of CAD and hypertension. Individuals with CAD usually have left ventricular dysfunction during exercise due to limited perfusion of the heart muscle. When exercise ends, myocardial oxygen demand decreases and ventricular function improves which causes systolic blood pressure to remain at elevated levels. When the systolic blood pressure (SBP) is measured 3 minutes following exercise and compared to peak systolic blood pressure, a ratio greater than 0.95 should be considered abnormal.

One study showed that an SBP measured 2 minutes post-exercise greater than 195 mm Hg was predictive of an increased risk for myocardial infarction. In a different study the same researchers showed that a ratio of the SBP measured 2 minutes post-exercise to the peak systolic blood greater than 0.95 showed an increased risk for stroke.

The comparison of post-exercise blood pressure depends on the accuracy of the peak exercise blood pressure measurement. Several studies have shown that exercise blood pressure measurements are can be inaccurate and that SBP can be mis-estimated by up to 40 mm Hg. This would appear to be particularly true during treadmill exercise and at high ergometer workloads. For these reasons the post-exercise SBP should be reported, but it should not be the sole parameter used to suggest the presence of cardiovascular disease.

O2 Pulse

It should not be overly surprising that individuals with a low cardiac output not only have difficulty in achieving a normal maximum VO2, but that the rate at which oxygen uptake decreases following exercise is reduced in comparison with normal individuals. These post-exercise differences are somewhat subtle however, and depend greatly on variables such test intensity and subject fitness and are therefore hard to quantify.

A more useful measurement is the O2 pulse at one minute post-exercise. O2 pulse is VO2 (in ml) divided by heart rate (BPM) and is an index of stroke volume. In normal individuals stroke volume decreases relatively rapidly following exercise. An increase in stroke volume is abnormal and tends to be seen in individuals with left ventricular failure and myocardial ischemia. This post-exercise increase in O2 pulse is thought to happen because left ventricular afterload decreases when blood pressure decreases following exercise which in turn improves left ventricular ejection and stroke volume. When this happens the O2 pulse at one minute following exercise will be higher than the O2 pulse at peak exercise.

FEV1

CPETs are often performed in order to assess an individual for exercise-induced bronchospasm (EIB). For this reason spirometry needs to be performed both pre- and post-exercise. There is, however, a lack of consensus regarding both the number and the timing of post-exercise spirometry efforts. Interestingly, the ATS/ACCP CPET guidelines are completely mute on the issue of post-exercise spirometry. The ATS clinical practice guidelines for EIB state that spirometry should be performed at 5, 10, 15 and 30 minutes. The AHA/EACPR CPET guidelines state the FEV1 and PEF should be measured at 1, 3, 5, 7, 10, 15 and 20 minutes post-exercise. The AHA CPET guidelines only state that FEV1 should be measured “periodically” post-exercise. Wasserman et al, states that spirometry should be performed at 3, 6, 10, 15 and 20 minutes post-exercise. Anderson et al, states that spirometry should be measured 5, 10, 15 and 30 minutes post-exercise. Madama states that spirometry should be performed every 5 minutes until FEV1 has returned to baseline or until 30 minutes have passed. Rundell et al, suggest 5, 10, 15 and 30 minutes post-exercise.

Since there are late as well as early responders for EIB, there does appear to be some value in performing spirometry out to 30 minutes. Measurements made earlier than 5 minutes post-exercise however, will likely interfere with post-exercise measurements of VO2, heart rate and blood pressure. For this reason, spirometry performed at 5, 10, 15 and 30 minutes following exercise appears to be the most reasonable approach.

Interestingly, the presence of asthma is usually based on a decrease in FEV1 following exercise but a small number of asthmatics actually increase their FEV1 instead. Normal individuals usually have an increase in FEV1 up to 5% or 7% following exercise. An increase greater than 20 percent however, is likely a sign of asthma.

Recommendations

There is clear evidence concerning the utility of the HRR and post-exercise O2 pulse. For this reason, gas exchange and heart rate measurements should continue for a minimum of 1 minute post-exercise and these values should be reported. Post-exercise blood pressure measurements should be performed for patient safety reasons regardless of the utility of comparing post-exercise SBP to peak SPB but there is no reason not to perform a BP measurement at 3 minutes post-exercise as opposed to a different time. When EIB is suspected, spirometry performed at 5, 10, 15 and 30 minutes post-exercise appears to have a good balance between the need for both early and late measurements. Improvements as well as decreases in FEV1 should be reported.

A CPET doesn’t end when the patient stops exercising. What happens during recovery is in many ways as important as what happened at anaerobic threshold and peak exercise. There are several measurements that should be made during the post-exercise period that are both informative and diagnostically significant, and should be a standard part of all CPET procedures.

Cardiopulmonary exercise testing is resource intensive. Not only does it require an investment in relatively expensive equipment, it requires an investment in patient, technician and physician time. It is therefore important to extract as much information as possible from every CPET. Some labs perform targeted testing, that is CPETs designed to evoke a particular set of results, but there really isn’t a lot of difference between a pre-op VO2 max CPET and a CPET to determine the presence of EIB. Not all CPET measurements will turn out to have been necessary after the fact, but determining which exercise limitations are actually present in a patient (particularly when expectations are to the contrary) is only possible when all possible measurements have been made and are available for review.

References:

Anderson SD, Pearlman DS, Rundell KW, Perry CP, Boushey H, Sorkness CA, Nichols S, Weiler JM. Reproducibility of the airway response to an exercise protocol standardized for intensity, duration and inspired air conditions, in subjects with symptoms suggestive of asthma. Respiratory Research 2010; 11:10

ATS/ACCP Statement on cardiopulmonary exercise testing. Am J Resp Crit Care Med 2003; 167: 211-277.

Chick TW, Cagle TG, Vegas FA, Poliner JK, Murata GH. Recovery of gas exchange variables and heart rate after maximal exercise in COPD. Chest 1990; 97: 276-279.

Cohen-Solal A, Laperche T, Morvan D, Geneves M, Caviezel B, Gourgon R. Prolonged kinetics of recovery of oxygen consumption in patients with chronic heart failure. Circulation 1995; 91: 2927-2932.

Cole CR, Blackstone EH, Pashkow FJ, Snader CE, Lauer MS. Heart-rate recovery immediately after exercise as a predictor of mortality. New Eng J Med 1999; 341: 1351-1357.

Gelb AF, Tashkin DP, Epstein JD, Gong H, Zamel N. Exercise-induced bronchodilation in asthma. Chest 1985; 87: 196-201.

Guzzi M, et al. EACPR/AHA Joint Scientific Statement. Clinical recommendations for cardiopulmonary exercise testing data assessment in specific patient populations. Eur Heart J 2012; 33: 2917-2927.

Koike A, Itoh H, Doi M, Taniguchi K, Marumo F, Umehara I, Hiroe M. Beat to beat evaluation of cardiac function during recovery from upright bicycle exercise in patients with coronary artery disease. Am Heart J 1990; 120: 316-323.

Laukkenen JA, Kurl S, Salonen R, Lakka TA, Rauramaa R, Salonen JT. The blood pressure response to exercise stress test and risk of stroke. Stroke 2001; 32: 2036-2041.

Laukkenen JA, Kurl S, Salonen R, Lakka TA, Rauramaa R, Salonen JT. Systolic blood pressure during recovery from exercise and the risk of acute myocardial infarction in middle-aged men. Hypertension 2004; 44: 820-825.

Lipinski MJ, Vetrovec GW, Froelicher VF. Importance of the first two minutes of heart rate recovery after exercise treadmill testing in predicting mortality and the presence of coronary artery disease in men. Am J Cardiol 2004; 93: 445-449.

Madama VC. Pulmonary function testing and cardiopulmonary stress testing. Published by Cengage Learning, 2007.

McHam SA, Marwick TH, Pashkiw FJ, Lauer MS. Delayed systolic blood pressure recovery after graded exercise. An independent correlate of angiographic coronary disease. J Am Coll Cardiol 1999; 34: 754-759.

Nishime EO, Cole CR, Blackstone EH, Pashkow FJ, Lauer MS. Heart rate recovery and treadmill exercise score as predictors of mortality in patients referred for exercise ECG. JAMA 2000; 284(11): 1392-1398.

Parsons JP, et al. An official American Thoracic Society Clinical Practice Guideline: Exercise-induced Bronchoconstriction. Am J Resp Crit Care Med 2013; 187(9): 1016-1027.

Rundell KW, Slee JB. Exercise and other indirect challenges to demonstrate asthma or exercise-induced bronchoconstriction. J Allergy Clin Immunol 2008; 122: 238-246.

Seshadri N, Gildea TR, McCarthy K, Pothier C, Kavuru MS, Lauer MS. Association of an abnormal exercise heart rate recovery with pulmonary function abnormalities. Chest 2004; 125: 1286-1291.

Sietsema KE, Ben-Dov I, Zhang YY, Sullivan C, Wasserman K. Dynamics of oxygen uptake for submaximal exercise and recovery in patients with chronic heart failure. Chest 1994; 105: 1693-1700.

Singh JP, Larson MG, Manolio TA, O’Donnell CJ, Lauer M, Evans JC, Levy D. Blood pressure response during treadmill testing as a risk factor in new-onset hypertension. Circulation 1999; 99: 1831-1836.

Wasserman K, Hansen JE, Sue DY, Stringer WW, Whipp BJ. Principles of exercise testing and interpretation, Fourth Edition. Lippincott, William and Wilkins, 2005.

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1 thought on “The CPET’s not over until it’s over

  1. Hi, interesting comments….the following reference addressed the specific issue you cogently raised (post-incremental CPET spirometry).

    Chest. 2005 Oct;128(4):2435-42.: Clinical role of rapid-incremental tests in the evaluation of exercise-induced bronchoconstriction. De Fuccio MB1, Nery LE, Malaguti C, Taguchi S, Dal Corso S, Neder JA.

    STUDY OBJECTIVE: To determine whether rapid-incremental work rate (IWR) testing would be as useful as standard high-intensity constant work rate (CWR) protocols in eliciting exercise-induced bronchoconstriction (EIB) in susceptible subjects.
    DESIGN AND SETTING: A cross-sectional study performed in a clinical laboratory of a tertiary, university-based center.
    SUBJECTS AND MEASUREMENTS: Fifty-eight subjects (32 males, age range, 9 to 45 years) with suspected EIB were submitted to CWR testing (American Thoracic Society/European Respiratory Society guidelines) and IWR testing on different days; 21 subjects repeated both tests within 4 weeks. Spirometric measurements were obtained 5, 10, 15, and 20 min after exercise; a FEV1 decline > 10% defined EIB.
    RESULTS:Twenty-seven subjects presented with EIB either after CWR or IWR testing; 21 subjects had EIB in response to both protocols (kappa = 0.78, excellent agreement; p < 0.001). Of the six subjects in whom discordant results were found, two had EIB only after IWR. Assuming CWR as the criterion test, IWR combined high positive and negative predictive values for EIB detection (91.3% and 88.6%, respectively). Tests reproducibility in eliciting EIB were similar (kappa = 0.80 and 0.72 for CWR and IWR, respectively; p 40% of maximum voluntary ventilation) ventilatory stresses did not differ between EIB-positive and EIB-negative subjects, independent of the test format. There were no significant between-test differences on FEV(1) decline in EIB-positive subjects (25.7 +/- 10.8% vs 23.7 +/- 10.0%, respectively; p > 0.05). Therefore, no correlation was found between exercise ventilatory response and the magnitude of EIB after either test (p > 0.05).
    CONCLUSIONS: Rapid-incremental protocols (8 to 12 min in duration) can be as useful as high-intensity CWR tests in diagnosing EIB in susceptible subjects. Postexercise spirometry should be performed after incremental cardiopulmonary exercise testing when EIB is clinically suspected.

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