Top 10 spirometry errors and mistakes

A couple of days ago my medical director and I had a short discussion about teaching pulmonary fellows to read PFTs and agreed that in order to be good at interpreting PFTs it isn’t the basic algorithms that are hard, it’s gaining an understanding of test quality and testing problems. My medical director then suggested this topic. At first I wasn’t sure I could find 10 errors but after spending a couple hours digging through my teaching files I managed to come up with just a few more than that. So strictly speaking it’s not a top 10 list but I kept the title because I liked it.

Spirometry errors and mistakes seem to fall into four categories: demographics, reference equations, testing and interpretation.


Normal values are based on an individual’s age, height and gender. When this information is entered incorrectly the normal reference values will also be incorrect. These errors often go uncaught because whoever reviews and interprets reports usually isn’t the same person who sees the patient and performs the tests. This type of error often doesn’t get corrected until the results are uploaded into a hospital information system or the patient returns for a second (or third or fourth) visit.

1. Wrong gender.

Pulmonary function reference equations are gender specific and for individuals with the same age and height, men will have a larger FVC and FEV1 than women do. When a patient’s demographics information is manually entered into a PFT system it’s always possible for somebody to enter the wrong gender. When this happens the predicted values will be either over- or under-estimated. This happens in my lab at least a half a dozen times a year and it’s why when I review reports I try to check the patient’s gender right after reading their name.

This is also a problem area for individuals who have gone through gender reassignment (transsexuals). An individual’s physiologic/developmental gender needs to be used to generate predicted values but this may be at odds with their gender recorded in a hospital’s information system. Some PFT lab systems populate their demographics information from their hospital’s information system when an order is received and it may or may not be possible to alter gender once this has happened. In other cases, an individual’s demographics may be cross-referenced when PFT results are uploaded into hospital information system and may throw an error if the wrong gender is present.

2. Wrong height

All lung volumes and capacities scale with height. Like any other manual entry height can be mis-entered and the most common error I’ve seen is for somebody to enter 60 inches when they meant 6 feet 0 inches.

Height can also be mis-measured if the patient isn’t asked to remove their shoes or to stand straight, or if the patient is asked for their height and it isn’t even measured. An error of an inch or two probably won’t make a big difference in a patient’s predicted values (particularly given the discrepancies between different reference equations) but for somebody who’s on the edge of normal and abnormal it can make a significant difference in how a report is interpreted.

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Which DLCO should be reported?

I like to think my lab is better than most but every so often something comes along that makes me realize I’m probably only fooling my self.

Earlier this week I was reviewing the DLCO test data for a patient with interstitial lung disease. At first glance the spirometry and DLCO results pretty much matched the diagnosis and I had already seen they weren’t significantly different from the last visit. The technician had written “fair DLCO reproducibility” which was reason enough to review the test data but I’ve actually been making a point of taking a careful look at all DLCO tests, not just the questionable ones, for the last couple of weeks. I took one look at the test data, put my head in my hands, and counted to ten before continuing.

Reported: %Predicted: Test #1: Test #2: Test #3:
DLCO: 13.22 66% 10.08 92.17 16.36
Vinsp (L): 2.17 2.20 2.15
VA (L): 3.45 66% 2.89 2.93 4.02
DL/VA: 3.78 91% 3.49 31.5 4.07
CH4: 60.84 60.94 43.15
CO: 34.46 0.51 23.13

Even though the averaged DLCO results were similar to the last visit, the two tests they were averaged from were quite different. Reproducibility was not fair, it was poor. But far more than that, something was seriously wrong with the second test and the technician hadn’t told anybody that they’d had problems with the test system. {SIGH}. It’s awful hard to fix a problem when you don’t even know there is one in the first place.

I usually review reports in the morning the day after the tests have been performed, so the patient was long gone by the time I saw the results. This left me with a problem that I’m sure we’ve all had at one time or another and that was whether any of the DLCO results were reportable.
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When is a change in FVC significant?

Most of the COPD patients that are seen in my lab tend to have little change in their FEV1 from visit to visit but their FVC often changes significantly. A change in FVC is usually related to how long a patient is able to exhale and this in turn is usually related to how well they are feeling at the time. This would seem to imply that a significant change in FVC, particularly for a patient with COPD, is, if not clinically significant, at least clinically important even when the FEV1 hasn’t changed.

The problem with this is that expiratory time can be affected by things other than how the patient is feeling. Dyspnea and fatigue, of course. As importantly some technicians are better at motivating patients than other technicians so it can also be related to which technician is performing their tests. Even when the same technician is involved however, there is no guarantee that the level of motivation or a patient’s response to that motivation will be the same.

So how do you know if a change in FVC clinically significant or not?

Recently a spirometry report from a patient with very severe COPD came across my desk. When comparing the results to those of the last visit I could see that there had been a small (but not significant) increase in FEV1 but at the same time there had been a large (and significant) increase in FVC.

Visit 1: Observed: %Predicted:
FVC (L): 1.28 36%
FEV1(L): 0.53 19%
FEV1/FVC: 41 53%
Visit 2: Observed: %Predicted:
FVC (L): 1.93 55%
FEV1(L): 0.60 22%
FEV1/FVC: 31 40%

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Six-Minute Walk with Helium-Oxygen

We recently performed a 6-minute walk test with helium-oxygen (heliox) for a patient of one of the physicians that specializes in airway stenting. His reasons for the test weren’t particularly clear (and he hasn’t bothered to try to clarify them with me) but most probably it has to do with differentiating between central and peripheral airway obstruction. Interestingly, he predicted the patient would have a significant improvement in 6-minute walk distance and instead there was little difference between the heliox 6MWT and one performed with 3 LPM supplemental O2.

6MWT: SaO2: Distance:
80% Helium – 20% O2, by mask 95% 440 meters
3 LPM O2, by nasal cannula 98% 457 meters

Helium is an inert, insoluble, low mass gas and both its therapeutic use and its use in physiological measurements has to do with it’s low density (and the fact that it’s highly insoluble, but that’s for purposes different than those discussed here).

  Density (g/m3)
He 0.179
N2 1.251
O2 1.429
Air (78% N2, 21% O2) 1.293
Heliox (80% He, 20% O2) 0.429

A typical way to assess its effect is by comparing air and heliox flow-volume loops:


Interestingly, despite an apparent increase in flow rates there is usually no significant difference in FEV1 (one study showed a range of +2% to +7% in a group of over 1500 subjects). The most common heliox FVL measurements are the change in expiratory flow at 50% of the FVC (ΔMEF@50%) and the Volume of Isoflow (which is the point at which the air and heliox expiratory flows become equivalent). Many of the earlier studies with heliox also measured ∆MEF@75% and ∆FEF25-75, and a tiny handful of studies (particularly given the technical difficulties) have measured ∆RAW and ∆sGAW.
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Ventilatory response to hypoxia and hyperoxia

While reading a recently published article I found they had performed response to hypoxia and hyperoxia testing as part of the study. At one time or another in the past I’ve read about response to hypoxia testing but I’d never heard about hyperoxia testing before. I had some difficulty understanding their interpretation of the study’s results and for this reason I’ve spent some time reading up on the subject. I’m not sure this helped because there appears to be a lack of consensus not in only how to perform these tests but also in how they are interpreted, except perhaps in the most simplistic sense. Hypoxia and hyperoxia testing has been performed primarily to gain a deeper understanding of the way in which the peripheral (carotid) and central chemoreceptors function. There are a variety of sensor-feedback network models and results are often presented in terms of one model or another and this makes comparing results from different studies difficult. Interpretation and comparison is further complicated by the fact that results depend not only on the length of time that hypoxia or hyperoxia is maintained but whether the subject was exposed to hypoxia, hyperoxia or hypercapnia previously.

The ventilatory response to hypoxia tends to have three phases. First, once a subject begins breathing a hypoxic gas mixture within several seconds there is a rapid increase in minute ventilation known as the Acute Hypoxic Ventilatory Response (AHVR). Second, after several minutes there is a decrease in ventilation and this is usually called the Hypoxic Ventilatory Depression (HVD). Third, there is a progressive rise in ventilation after several hours which is related to acclimatization to altitude. It is the first phase, AHVR, that is most commonly measured during a hypoxic ventilatory response test. The actual length of time that is spent in any of these phases is widely variable between individuals and there is also a relatively large day-to-day variability within the same individual.
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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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Asleep at the wheel

During this last week I was contacted by two different individuals who were asking for help in understanding their PFT results. In both cases they had a markedly elevated TLC and the interpretation included the notation that they had gas trapping and hyperinflation. Even though the amount of information they provided was minimal I am extremely skeptical that the TLC measurements were correct.

Gas trapping usually only occurs with severe airway obstruction. Hyperinflation, which at minimum consists of a chronically elevated FRC and RV, usually only occurs after prolonged gas trapping. An elevated TLC usually occurs only with prolonged hyperinflation and given the improvements in the care and treatment of COPD I’ve seen over the last several decades, has become relatively uncommon.

But one individual had perfectly normal spirometry:

FVC: 107%
FEV1: 112%
FEV1/FVC: 105%
TLC: 143%

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Does the FEV1/SVC ratio over-diagnose airway obstruction?

A low FEV1/VC ratio is the primary indication for airway obstruction.


From ATS/ERS Interpretive Strategies for Lung Function tests, page 956.

The ATS/ERS statement on interpretation says

The VC, FEV1, FEV1/VC ratio and TLC are the basic parameters used to properly interpret lung function (fig. 2). Although FVC is often used in place of VC, it is preferable to use the largest available VC, whether obtained on inspiration (IVC), slow expiration (SVC) or forced expiration (i.e. FVC).”

I understand and in general agree with the idea of using the largest VC regardless of where it comes from and this is because the FVC is often underestimated for any number of good (and not so good) reasons. When this happens the FEV1/FVC ratio will be overestimated and airway obstruction will be under-diagnosed. However the ATS/ERS statement is also grounded in the notion that all vital capacities (FVC, SVC, IVC) are the same and this isn’t necessarily true. The problem comes from the fact that the predicted values and lower limit of normal (LLN) for the FEV1/VC ratio always come from reference equations for FEV1/FVC ratios. Because the SVC (and IVC) are usually larger than the FVC this means there is at least the potential for airway obstruction to be over-diagnosed.

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When flow-volume loops get kinky

One of the more recognizable flow-volume loop contours is the one associated with severe airway obstruction. Specifically, this type of loop shows an abrupt decrease in flow rate following the peak flow with a more gradual decrease in flow rates during the remainder of the exhalation.


This abrupt decrease in flow rates was first described on a volume-time curve and the inflection point was called a “kink” but this point also corresponds with the inflection point on the flow-volume loop. This feature has also been called a “notch” or a “spike” but a number of researchers have called this the Airway Collapse pattern (AC) and it is more formally defined as a sharp decrease in flow rate from peak flow to a discontinuity point at less than 50% of the peak flow and occurring within the first 25% of the exhaled vital capacity.

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What’s a normal Flow-volume Loop?

Dozens of articles have been written about the correlation between different abnormal flow-volume loop contours and pulmonary disorders. In contrast very little has ever been written about what constitutes a normal flow-volume loop and what this looks like has been primarily anecdotal.

Interestingly, the ATS/ERS standard for spirometry includes an example of a “normal” flow-volume loop but its source and what makes it normal is not explained.


From the ATS/ERS standard on spirometry, page 327.

One feature that is commonly seen as a feature of normal flow-volume loops has been variously called a ‘shoulder’ or ‘knee’.


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