Treadmill protocols

Since I started performing exercise tests I’ve used both treadmills and bicycle ergometers. There are a several reasons that make ergometers somewhat better for exercise testing than treadmills. Most importantly the reduced noise and physical motion makes it easier to get blood pressure measurements and better quality ECG’s. In addition the workload can be set fairly precisely and they are safer for patients. Treadmills do have some advantages however, since patients are usually able to achieve a higher maximum oxygen consumption (~10%) and for many individuals walking is more natural than riding a bicycle.

When I’ve used a treadmill for exercise testing I’ve always used one version or another of the Bruce protocol. This choice was made by my medical directors but it has always seemed to get patients to their maximum exercise capacity within a reasonable period of time and it seemed to provide reasonable workloads for patients over a broad range of physical abilities. About a dozen years ago (the last time my PFT lab was moved) we no longer had room for a treadmill and replaced it with an ergometer. Since then, I haven’t thought much about treadmills and treadmill protocols.

Recently I was talking with a physician who is going to be performing exercise research with a treadmill. When he showed me the treadmill protocol he was planning on using I thought that the initial speed (3.3 MPH) was too high. Since his study population is going to consist of obese, deconditioned asthmatics, I suggested that for patient safety that it would be better to start at a lower speed and elevation. He asked if I could suggest a different treadmill protocol but I had to reply that all I had ever used was the Bruce protocol.

This brought up an interesting question however, and that is whether there is any such thing as an optimal treadmill protocol. To answer this question I undertook a broad survey of treadmill protocols and have to say that the answer is probably no. Strictly speaking, each treadmill protocol is intended for a specific range of physical effort and the selection of any one protocol has to be based on the expectations and limitations of a patient’s physical abilities.

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Static reports, dynamic world

Reports are how patient test results are distributed. Paper versions have become less common because reports are now stored electronically in hospital information systems. Even if the way in which a report’s image is now stored, retrieved and distributed has changed, reports are still generated by our lab’s software systems and the ways in which this is done have not changed in any significant way for quite a while.

Reports are the public face of any pulmonary function lab and they should be designed to be readable and pertinent. It is critically important for any lab to create and manage reports correctly. So why does our lab software make it so hard to do this?

Over the last several months I’ve had the opportunity to compare the reporting systems of the three largest manufacturers of pulmonary function equipment in the US. There are differences of course between each reporting system since each has its own approach towards formatting, editing and printing reports. What they all share however, is a similar underlying model for reports that I call static report pages.

What I mean by static is that the report elements and their position on a report page are determined and fixed in place when the report is formatted. When the report is printed, regardless of whether the results are present or not, the report page does not change. This means that if you format a report to contain spirometry, lung volumes and DLCO, and the only test you perform is spirometry, when you print the report the sections for lung volumes and DLCO will contain no results but they will still appear.

The number of tests that need to be placed on a report will vary from lab to lab depending on what equipment they are equipped with. For example, these tests are available on one manufacturer or another’s test systems:


Lung Volumes – Plethysmography

Lung Volumes – N2 Washout

Lung Volumes – Helium Dilution

Diffusing Capacity







There are probably other tests as well but even if there aren’t, there are other report elements such as demographics, text notes, flow-volume loops, trends etc. that also need to be managed.

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Transgender PFTs

I was reviewing PFT reports today and noticed that a patient appeared to have had the wrong gender entered in their demographic information. Specifically, the patient had an unambiguously masculine name but had been entered as female. Just to be sure I checked the patient’s on-line medical record and there he was listed as male. I had noticed from the trend report that the patient had been in the PFT lab numerous times. Since the basic patient demographics (name, date of birth, height, gender, etc.) are automatically forwarded into a new demographics record when a new PFT lab visit is created it struck me as odd that after all this time we had somehow managed to make a mistake with something as basic as gender. For this reason I thought it would be a good idea to see how far back this problem existed and started going back through the patient’s PFT records. About four visits ago the patient’s name suddenly changed to one that was unambiguously feminine.

I was immediately concerned that two different patient’s records had somehow gotten merged. The last time this happened was over 20 years ago and was due to an entry error in the patient ID that was further compounded by how the lab’s software handled new demographic records at the time. Merged records is therefore a symptom of a serious database problem but when I compared the date of birth of the two patients, I was immediately able to see that they were the same. Since this is incredibly unlikely my thought then was that the patient may have had a gender reassignment. When I went back to the patient’s online medical record and searched more carefully, I was able to find that this had occurred over a year ago. This is not the first time we’ve had a transgender patient and so it is an issue we’ve learned how to handle.

So what effect does gender reassignment have on an individual’s pulmonary function test results?

None whatsoever. Gender reassignment by itself does not affect FVC, FEV1, TLC or DLCO. What it does affect is how we interpret the test results and it can also cause some interesting data management problems that are worth noting.

All pulmonary function reference equations differentiate between genders. Although the differences between races and ethnicities is somewhat open to question, there is little doubt about the differences between genders. When individuals with the same height are compared, females universally have lower flow rates, volumes, respiratory muscle strength, gas exchange and oxygen consumption than males. Because lung function is determined during an individual’s childhood and adolescent developmental periods, gender reassignment does not affect lung function and when it is assessed this has to be done using reference equations that are appropriate to an individual’s original gender.

Depending on which way a gender reassignment occurs, results that would be considered normal for a female would likely look reduced for a male, and results that would be considered reduced for a male would likely look normal for a female. The selected gender will therefore make a difference about what an individual’s PFT results look like to a reviewer.

The patient whose gender raised this issue has relatively severe lung disease and is probably not the best example for this, but its what’s in front of me right now.

Female: Observed: %Predicted: Predicted:
FVC: 1.37 42% 3.25
FEV1: 0.92 36% 2.54
FEV1/FVC: 67 84% 80
TLC: 2.69 54% 4.93
RV: 1.34 79% 1.69
DLCO: 14.90 78% 19.12

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How does a CPET show a Cardiac Limitation?

Recently a patient was referred to my lab for a CPET by his oncologist. The patient had been complaining of excessive shortness of breath particularly when climbing only a few stairs. The patient recently had a full PFT panel (spirometry, lung volumes, DLCO) and the results had showed mild restriction with a mild gas exchange defect. The patient’s shortness of breath symptoms were far more severe than could be explained by his PFTs however, so he had been referred to Cardiology and had an ECG stress test. The stress test results were normal so Cardiology told the oncologist that the patient’s problems were probably not cardiac.

Because the patient’s PFT results were reduced the patient’s oncologist consulted with a couple of our pulmonary physicians and they suggested a CPET. When I reviewed the patient’s CPET results despite a mildly reduced TLC and DLCO it was quite clear the patient’s primary limitation was in fact cardiac. Why was there such a discrepancy between Cardiology’s ECG stress test and our CPET? The simple answer is that a CPET measures oxygen consumption and a routine ECG stress test does not.

Strictly speaking, during a progressive exercise test any individual with normal heart and lungs usually reaches a cardiac limit before they reach any kind of a pulmonary limit and this is normal. A fit, athletic individual usually has a higher than normal stroke volume (and cardiac output) while a somebody that is out-of-shape has a reduced stroke volume (and cardiac output). This is one of the key differences between being conditioned and being de-conditioned.

So what are the hallmarks of an abnormal cardiac limitation?

There are, of course, many different types of cardiac disease but the common factor (at least in terms of a CPET) is an abnormal decrease in cardiac output. Cardiac output cannot be measured during exercise without specialized equipment or indwelling catheters but there is an intimate connection between cardiac output and VO2 as shown by the Fick equation:


Note: CaO2 and CvO2 refer to the oxygen content (in vol%) of arterial and venous blood respectively. I’ve frequently seen CaO2 and CvO2 described as the concentration of oxygen in the blood but although this may be semantically correct I feel it is imprecise because it is easily confused with the partial pressure of oxygen or oxygen saturation when it is actually a function of both of these properties:


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