A couple weeks ago I was asked whether it was safe for a patient with an abdominal aortic aneurysm (AAA) to have pulmonary function testing. My first thought was that it was probably unsafe but after a moment or two of thought I realized that I hadn’t reviewed the subject for a long time. When I checked the 2005 ATS/ERS general testing guidelines (there are no contraindications in the 2005 spirometry guidelines) I found that AAA wasn’t mentioned at all. In fact, the only absolute contraindication mentioned was that patients with a recent myocardial infarction (<1 month) should not be tested. Some relative contraindications were mentioned:

  • chest or abdominal pain
  • oral or facial pain
  • stress incontinence
  • dementia or confusional state

and activities that should be avoided prior to testing include:

  • smoking within 1 hour of testing
  • consuming alcohol within 4 hours of testing
  • performing vigorous exercise within 30 minutes of testing
  • wearing clothing that restricts the chest or abdomen
  • eating a large meal with 2 hours of testing

but these were factors where test results were likely to be suboptimal and not actually contraindications.

This got me curious since I thought that pulmonary function testing was contraindicated for more conditions than just an MI. I reviewed the 1994 and and then the 1987 ATS statements on spirometry but again found no mention of contraindications. Ditto on the 1993 ERS statement on spirometry and lung volumes. Finally, in the 1996 AARC clinical guidelines for spirometry I found a much longer list of contraindications:

  • hemoptysis of unknown origin
  • pneumothorax
  • recent mycardial infarction
  • recent pulmonary embolus
  • thoracic, abdominal or cerebral aneuysms
  • recent eye surgery
  • presence of an acute disease process that might interfere with test performance (e.g. nausea, vomiting)
  • recent surgery of thorax or abdomen

So where did the AARC’s list of contraindications come from? And why is there such a discrepancy between the ATS/ERS and the AARC guidelines?

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The effects of anemia on exercise

Last week I was reviewing the exercise test results from a patient that appeared to have a relatively straightforward cardiovascular limitation when I noticed the patient also had severe anemia (Hgb = 7.1). Once that fact came up it was no longer clear the patient actually had a cardiac limitation at all.

First the results:

Rest: %Predicted: AT: %Predicted: Max: %Predicted:
VO2 (LPM): 0.33 13% 0.73 28% 1.45 56%
VO2 (ml/kg/min): 5.0 11.0 21.6
VCO2 (LPM) 0.26 0.63 1.81
RER: 0.73 0.83 1.24
SaO2: 98% 97% 97%
PetCO2: 35.2 38.6 31.8
Ve/VO2: 34 26 43
Ve/VCO2: 47 31 35
Ve (LPM): 11.6 8% 19.2 13% 62.9 44%
Vt (L): 0.78 1.29 2.19
RR: 15 15 29
HR (BPM): 61 35% 92 52% 152 85%
BP (mmHg): 92/62 102/64
O2 Pulse (ml/beat): 5.8 39% 8.2 55% 9.8 66%

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What does an inverse I:E Ratio during exercise mean?

Inspiration and expiration usually take different lengths of time, with inspiration almost always being shorter than exhalation. This is due to both to the physiology of breathing and to the pathophysiology of disease processes. During incremental exercise testing there are usually patterns to the way that inspiratory and expiratory times change and these are occasionally diagnostic.

When I started in this field the relationship between inspiratory and expiratory time was usually expressed as the I:E ratio, which was most often written as something like 1:1.2. One of my medical directors pointed out to me that when talking about I:E ratio it was difficult to determine what you meant if you said it was increasing or decreasing. For this reason I started reporting the I:E ratio as the E/I ratio so that instead of 1:1.2 it’s just 1.2.

Somewhere along the way however, for exercise testing at least, the most common way of expressing the I:E ratio seems to have morphed primarily into Ti/TTot (which is the Inspiratory Time/Total Inspiratory and Expiratory Time ratio), less commonly as Ti/Te and almost never as I:E. Even so, I still prefer the E/I ratio approach, partly because I’m used to it but mostly because it emphasizes the expiratory time component. For example:

Ti/TTot: Ti/Te: E/I:
0.50 1.00 1.0
0.48 0.91 1.1
0.45 0.83 1.2
0.43 0.77 1.3
0.42 0.71 1.4
0.40 0.66 1.5
0.38 0.63 1.6
0.37 0.59 1.7
0.36 0.56 1.8
0.34 0.53 1.9
0.33 0.50 2.0

Anyway, at rest most subjects breathe with an E/I ratio somewhere between 1.2 and 1.5 (Ti/TTot 0.45 – 0.40). During exercise the E/I ratio usually decreases more or less steadily and usually reaches 1.0 (Ti/TTot 0.50) at or near peak exercise. When a subject has airway obstruction the E/I ratio often doesn’t decrease and in those with severe airway obstruction it often increases instead. E/I ratios above 2.0 aren’t all that uncommon in subjects with COPD. Occasionally a subject with normal baseline spirometry (i.e. a normal FEV1/FVC ratio) has an elevated and/or increasing E/I ratio throughout testing and this is a clue that they probably have some degree of airway obstruction that’s not otherwise evident, and possibly even EIA if it increases at peak exercise.

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Why DIY CPET reports?

When I first started performing CPETs in the 1970’s a patient’s exhaled gas was collected at intervals during the test in Douglas bags and I had a worksheet that I’d use to record the patient’s respiratory rate, heart rate and SaO2. After the test was over I’d analyze the gas concentrations with a mass spectrometer and the gas volumes with a 300 liter Tissot spirometer and then use the results from these to hand calculate VO2, VCO2, Rq, tidal volume and minute volume. These results were then passed on to the lab’s medical director who’d use them when dictating a report.

Around 1990 the PFT lab I was in at the time acquired a metabolic cart for CPET testing. This both decreased the amount of work I had to do to perform a CPET and significantly increased the amount of information we got from a test. The reporting software that came with the metabolic cart however, was very simplistic and neither the lab’s medical director or I felt it met our needs so I created a word processing template, manually transcribed the results from the CPET system printouts and used it to report results.

Twenty five years and 3 metabolic carts later I’m still using a word processing template to report CPET results.


Well, first the reporting software is still simplistic and using it we still can’t get a report that we think meets our needs (and it’s also not easy to create and modify reports which is a chronic complaint I have about all PFT lab software I’ve ever worked with). Second, there are some values that we think are important that the CPET system’s reporting software does not calculate and there is no easy way to get it on a report as part of the tabular results. Finally, and most importantly, I need to check the results for accuracy.

You’d think that after all these years that you wouldn’t need to check PFT and CPET reports for mathematical errors but unfortunately that’s not true. For example, these results are taken from a recent CPET:

Time: VO2 (LPM): VCO2 (LPM): Reported Rq: “Real” Rq:
Baseline: 0.296 0.220 0.74 0.74
00:30 0.302 0.214 0.77 0.71
01:00 0.363 0.277 0.77 0.76
01:30 0.395 0.306 0.78 0.77
02:00 0.424 0.353 0.99 0.83
02:30 0.459 0.403 0.92 0.88
03:00 0.675 0.594 0.89 0.88
03:30 0.618 0.584 0.94 0.94
04:00 0.836 0.822 1.00 0.98

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When hypoventilation is the primary CPET limitation

Hypoventilation is defined as ventilation below that which is needed to maintain adequate gas exchange. It can be a feature in lung diseases as diverse as chronic bronchitis and pulmonary fibrosis but determining whether it is present of not is often complicated by defects in gas exchange. When desaturation occurs during a CPET (i.e. a significant decrease in SaO2 below 95%) this is a strong indication that the primary exercise limitation is pulmonary in nature and from that point the maximum minute ventilation and the Ve-VCO2 slope can show whether the limitation is ventilatory or instead due to a gas exchange defect. But in this circumstance what what does it mean when both the maximum minute ventilation and Ve-VCO2 slope are normal?

Recently a CPET came across my desk for an individual with chronic SOB. The individual recently had a full panel of pulmonary function tests:

Observed: %Predicted:
FVC (L): 1.73 62%
FEV1 (L): 1.39 66%
FEV1/FVC: 80 106%
TLC (L): 2.99 62%
DLCO (ml/min/mmHg): 14.66 84%
DL/VA: 5.45 124%
MIP (cm H2O): 11.5 18%
MEP(cm H2O): 21.3 24%

The reduced TLC showed a mild restrictive defect. At the same time the relatively normal DLCO indicates that the restriction is probably not due to interstitial lung disease and more likely either a chest wall or a neuromuscular disorder, both of which can prevent the thorax from expanding completely but where the lung tissue remains normal. The reduced MIP and MEP tends to suggest that a neuromuscular disorder is the more likely of the two.

I take this with a grain of salt however, and that is because this individual never had pulmonary function tests before and for this reason there is no way to know what their baseline DLCO was prior to the restriction. At the same time far too many individuals perform the MIP/MEP test poorly and low results are not definitive, and in this case in particular the results are so low the individual should have been in the ER, not the PFT Lab.

The CPET results were somewhat complicated, in that a close inspection showed both pulmonary and cardiovascular limitations.
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Exercise and the IC, EELV and Vt/IC ratio

Determining whether a subject has a ventilatory limitation to exercise used to be fairly simple since it was based solely on the maximum minute ventilation (Ve) as a percent of predicted. There has been some mild controversy about how the predicted maximum ventilation is derived (FEV1 x 35, FEV1 x 40 or measured MVV) but these don’t affect the overall approach. Several decades ago however, it was realized that subjects with COPD tended to hyperinflate when their ventilation increased and that this hyperinflation could act to limit their maximum ventilation at levels below that predicted by minute ventilation alone.

The fact that FRC could change during exercise was hypothesized by numerous investigators but the ability to measure FRC under these conditions is technically difficult and this led to somewhat contradictory results. About 25 years ago it was realized that it wasn’t necessary to measure FRC, just the change in FRC and that this could be done with an Inspiratory Capacity (IC) measurement.

The maximum ventilatory capacity for any given individual is generally limited by their maximum flow-volume loop envelope. When a person with normal lungs exercises both their tidal volume and their inspiratory and expiratory flow rates increase.



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Hyperoxic CPETs

In patients with lung disease the use of supplemental oxygen during exercise increases oxygen consumption, endurance time and maximum workload, and decreases the sensation of dyspnea without increasing minute ventilation and maximum heart rate. My lab is occasionally asked to perform a CPET with an elevated FIO2 (hyperoxic CPET). We are capable of doing this but I’ve always had reservations, partly about the logistics involved in performing the CPET but more importantly with the interpretation of the results.

First, although it is certainly possible to perform some kinds of exercise test while the patient gets oxygen via a nasal cannula or mask, adding oxygen during a CPET requires that the patient breathes a hyperoxic gas mixture through their mouthpiece. Most commonly this is done by adding a two-way valve to the test system that is in turn attached to a reservoir bag which is filled from an oxygen blender.


Although functional, this adds extra dead-space and the valves add extra resistance, both of which increases the patient’s work of breathing. From a practical standpoint it also adds a fair amount of extra weight to the breathing manifold, often more than is comfortable for the patient. This means that some method for supporting the manifold must also put in place. About 25 years ago I performed CPETs using a treadmill that had a support arm and at that time the approach recommended by the equipment manufacturer was to suspend the breathing manifold using rubber tubing. This worked in that it supported the weight of the breathing manifold, but it didn’t do anything about its mass or inertia and when a patient transitioned from a walk to a jog, the mouthpiece manifold would bang against the patient’s teeth and mouth.

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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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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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Diagnosing Mitochondrial Myopathies

I’ve been reviewing my CPET textbooks trying to get a better idea of how to differentiate between different cardiovascular limitations. The other day I ran across an article on a related subject and thought it might be instructive.

The hallmark of cardiovascular limitations is the inability to deliver enough oxygenated blood to the exercising muscles. Another limitation that has similarities to this (and one that is infrequently diagnosed) is the inability of the exercising muscle to utilize the oxygen delivered to it. The best examples of this type of exercise limitation are mitochondrial myopathies (MM).

The mitochondria are the primary source of the ATP used by exercising muscle. There are several conditions that can cause the number of mitochondria to be reduced and there is wide variety of mitochondrial genetic defects. Mitochondria have their own genes and these can have both inherited or acquired genetic defects which can cause anything from mild to severe decreases in the ability to produce ATP. Mitochondria require oxygen to produce ATP so when the number of mitochondria are reduced or their ability to produce ATP is reduced the rate at which oxygen is consumed by an exercising muscle is also reduced.

A relatively common complaint of individuals with MM is dyspnea and exercise intolerance. One study found that 8.5% of all the patients referred to a dyspnea clinic had a mitochondrial myopathy of one kind or another. A definitive diagnosis requires a muscle biopsy but because the symptoms are often non-specific and a biopsy is an invasive procedure, it is usually not performed unless there more significant evidence suggesting a MM.

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