Welcome to the session cardiopulmonary exercise testing CPAP case studies part one. We're going to look at FITNORMAL and COPD. My name is Darcy Marcinak. It would help if you're able to review cardiopulmonary exercise testing parts one and two in preparation for this session. We're going to use a case study approach as a platform for practical clinical interpretation to look at characteristic responses, in this case, for FITNORMAL and patient with COPD. This is my conflict of interest disclosure. So we'll look at some numbers, some data, and then we're going to look at some graphs and relationships. So this is a FIT, 51-year-old female with normal pulmonary function studies who underwent maximal study, I've gone at the bottom here, 20 watts per minute on a bicycle ergometer, incremental study, inspiring room error. And we have various data points at rest, at end exercise, and then percent predicted. So this person, this female achieved 178 watts, which is 131% of predicted, that's very good. Peak VO2, 2.71 liters per minute, 147% of predicted, that's also very good. The anaerobic threshold was not reduced, normal would be greater than 0.75, here we are 1.59 liters per minute. At the end of exercise, had only used 72% of predicted maximal ventilation with a breathing reserve of 36 liters. And the ventilatory equivalent for CO2, the VECO2 at the anaerobic threshold was 29, so it was normal, normal being 34 and below, less than 35. Did not desaturate. Achieved predicted maximal heart rate at 180 beats per minute, which is just 102% of predicted. And at the end of exercise, reported modified Borg score, score of 3 for shortness of breath, excuse me, and 5 for leg fatigue, and no abnormalities on the ECG. So let's look at some of the graphs. This is VO2, predicted maximal VO2, and on the x-axis we have work rate and predicted maximal work rate. This is a straight line that goes from VO2 at rest to the intersect of predicted maximal VO2 and work rate. And this is exactly online, and in fact it goes above and beyond, even achieving a little bit of a plateau at the end. We're going to talk a little bit about that later. When we look at VCO2 versus VO2, this is the line of identity. Again, expected response, but it goes, you know, far high and far right, consistent with the excellent performance. And you can see where the change in slope occurs, which would infer anaerobic threshold. If we look at the heart rate, maximal predicted heart rate, with the VO2, predicted maximal VO2, and on the right side in red we have the O2 pulse. Remember that is the VO2 divided by heart rate. So as long as O2 content remains constant, using the Fick equation, that would correlate with stroke volume. So here we have heart rate increase a little bit down and to the right, but it keeps on going up, and it correlates with increased performance, a high peak VO2, okay, and achieved the predicted maximal heart rate. And that's partnered with a very good O2 pulse response that is also plateauing near the end. No abnormalities here. Similarly, on the right graph, when we look at the VO2 in red, and the VEVCO2 in blue, these are normal responses at the NIDRR. As mentioned, it's about 29, and we're, the lowest part of the blue curve, the VEVCO2, where red starts to increase, is also an indication of the anaerobic threshold. Minute ventilation, with predicted maximal ventilation here by this dashed line, FE1 times 37. A slope of the relationship between VE versus VCO2, this line is 35, making it a normal response with abundant ventilatory reserve at end exercise. Didn't come close to predicted maximal ventilation. And on the right, we have the hay plot, the modified hay plot, HEY, with tidal volume, vital capacity, which would represent the biggest VT1 could do. Minute ventilation on the x-axis. Oh, I'll just go back. Minute ventilation on the x-axis, with predicted maximal as assessed by the FE1 times 37, and then respiratory frequency in red. So, we have a good tidal volume response with an appropriate respiratory frequency, such as minute ventilation is over 90 litres at the end of exercise, and still have reserve. So, it's another way to look at that. Here, we have non-invasive estimate of dead space, which falls appropriately during exercise. We have a normal kind of an inverse U, or a hump here, with the end tidal CO2, goes up a bit, still in the mid-30s, and then falls at the end of exercise. And no significant arterial oxygen desaturation, starting from 100 and goes to about 97 here at the end of exercise. So, so far, so good, but very good performance. And then, when we look at the flow volume curve, the grey represents maximal expiratory and inspiratory curve. We have tidal breathing at rest in the middle of exercise in green, and then the dashed red line is at the end of exercise. So, a few things here. First of all, a little bit of flow limitation, but nothing out of the ordinary, and it did not lead to an increase in end-expired lung volume. In fact, end-expired lung volume at the end of exercise is less than it was at rest. That's a normal response. And there's still quite a bit of inspiratory reserve volume, the difference between the red and grey, and lots of area, both expiratory and inspiratory, to increase ventilation. So, no significant abnormalities here. So, this is a good example. The measurements are normal and consistent, including the VO2 plateau that we'll look at on the next slide. But higher than predicted work and aerobic capacity, that is never bad. That is associated with fitness training, so it's all good. In fact, in the very, very fit, more than this person with, you know, a VO2 slash kilogram within the 60s or 70s, and remember, Olympic athletes might go into the 80s and such, you may see evidence of ventilatory constraint, more flow limitation, encroachment of ventilation on the ventilatory capacity, and a reduced breathing reserve. We didn't see that here, but you might be able to see that. Even with desaturation, more so in females or the very fit aging, because in order to get to those degrees of fitness and excellence in cardiovascular performance, you'd encroach upon the respiratory reserve. So, as long as it's associated with very high performance, that's okay. So, determining early or mild impairment in these settings can be challenging because normal is super normal. So, serial studies can sometimes be meaningful and informative. And here, I just wanted to highlight where you see that flattening of that relationship between VO2 and work rate, the VO2 plateau, which probably is the truest indication of peak performance. Okay, so that's a fit, normal 51-year-old female. Let's move now to a 64-year-old male with moderate COPD. The FEV1 is 1.53 liters, 54% of predicted. So, the exercise was undertaken on a cycloergometer, and the patient achieved a maximal work rate of 90 watts, which is 62% of predicted, so that's impaired. Peak VO2, 1.22 liters, 66% of predicted, that's also impaired. But the annual threshold was normal, 57%, and anything above 40 would be normal. Most of the time, it's around 50 or 55. But ventilation at the end of exercise was 55.1 liters, which is 103% of predicted. So, they achieved their predicted maximal ventilation. So, it's very different than the prior study and what happens in normal, such that the breathing reserve was in fact negative or essentially zero. Did not desaturate, maximal heart rate was not achieved, 85% of predicted, and one could postulate, we'll look at the results, but the reason the maximal heart rate wasn't achieved was because they ran out of room to breathe. And the modified Borg score for shortness of breath at the end of exercise was six, four for leg fatigue, and they reported they just can't breathe anymore, they stopped because of their breathing. So, here we have the same relationships, but in a different setting, moderate COPD. So, first of all, the peak VO2 is not achieved, neither is a predicted maximal work rate. If we look on the right, again, you can see sort of a change in slope around here, which would indicate the annual threshold was normal. Maximal heart rate in blue was not achieved, and whenever you see these sort of increases in things, you'd have to, we always have to be on the lookout for arrhythmias and things like that. And in fact, sometimes it's just an artifact of poor pickup and so forth, but throughout these studies, safety is very important, looking at ST, T wave changes, any evidence of ischemia, and certainly arrhythmias. And then also the O2 pulse in this case, it's a little bit on the low side, but again, this is a sub, it's an absolute value of about eight, probably seven or eight, but this is a cardiovascular submaximal finding in the setting of ventilatory limitations, so you have to be careful not to over-interpret. And then when we look at the ventilatory thresholds, the ventilatory equivalent for oxygen, VE, VO2, and the ventilatory equivalent for CO2, the VE, VCO2 in red, these are abnormal. These are above 40 or at 40, so they're elevated. We have an increased ventilatory response. And in fact, typically we sent to see a U, but they don't keep going here. And I think because we know that this person ran out of room, they just couldn't breathe anymore. And there are multiple reasons why someone has elevated ventilatory equivalence or an increased ventilatory response. So increased dead space ventilation, likely the cause here. Hypoxemia, well, this person did not desaturate. Early anaerobic threshold, not the case here. And then it can be primary in hyperventilation syndromes and things. So in this case, it's probably associated with increased dead space ventilation attributable to the moderate COPD. And when we look at the ventilation over VCO2 relationship, you can see they came or even exceeded their FE1 times 35. Now, whether we use the FE1 times 35 or 37 or 40, they still came close. And the curve is shifted up and to the right. It is consistent with an increased ventilatory response. When we look at the breathing pattern response, VT is a little bit blunted. It goes from just shy of a liter to about 1.5, 1.5 liters, and respiratory frequency is above 30 at the end of exercise, but they just ran out of room. Dead space ventilation falls during exercise, but this is a 0.3, 0.4, 0.5. So it is elevated, in fact. Now, this is non-invasive estimates, so there's limitations, but it still is elevated. And the end tidal CO2 here is relatively low at the beginning of exercise, commonly seen because of hyperventilation, the testing, people watching and mouthpiece and such, but it increases a little bit during exercise. And then finally, if we look at oxygen saturation, it goes from about 97 to 94 here, so no significant arterial oxygen desaturation. And the flow volume curve, very characteristic for COPD. So you have an abnormal resting curve. This is at maximal expiratory and inspiratory curve at rest. Tidal breathing while on the mouthpiece here in blue, so their flow limited at rest. And then at the end of exercise in red, you can see they're encroaching even on their maximal inspiratory and maximal expiratory for significant proportion of their tidal breathing, VT. And the expired lung volume increases from rest from blue to red, and this is almost probably 600, 700 mils, so that's abnormal. That's indicative of dynamic hyperinflation. Inspiratory reserve volume is only a few hundred mils, so every breath is if it's the biggest breath they can take, and they're flow limited, so they have a number of abnormalities of flow volume curve consistent characteristic of COPD. So in COPD, it's characterized by impaired work and aerobic performance depending upon the magnitude of the abnormalities, reduced breathing reserve, ventilatory inefficiency, as characterized by elevated ventilatory equivalence, and depending upon the severity, abnormal gas exchange. In this case, there was no desaturation, but as the disease progresses, desaturation can be seen. And importantly, the flow volume curves typically demonstrate characteristic dynamic hyperinflation with an increase in expired lung volume as ours did. Minimal inspiratory reserve volume with reduced inspiratory lung volume, EILV, as our patient did, and expiratory flow limitation also as our patient did. In the clinical setting, these findings often coexist with deconditioning, and deconditioning can be dominant. So many patients, in fact, most patients with COPD typically don't stop because of their lung disease, but because of the avoidance and the conditioning that happens with avoiding exercise and symptoms of shortness of breath, such that peripheral muscle deconditioning becomes dominant. So that often is a finding. The importance of that is that it's amenable to pulmonary rehab rather than bronchodilator therapy or supplemental oxygen, although we often stack and complement each other in terms of our overall management. That's the end of the presentation. Thank you.

case studies

fit female

normal ranges

COPD

exercise test

Chronic Obstructive Pulmonary Disease