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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.

	Rest:	%Predicted:	AT:	%Predicted:	Maximum:	%Predicted:
VO2 (LPM):	0.26	24%	0.49	44%	0.54	48%
VCO2 (LPM):	0.21		0.43		0.65
RER:	0.84		0.87		1.27
SpO2 (%)	97%		94%		92%
PetCO2 (mm Hg):	41.2		46.5		53.4
Ve/VCO2:	49		39		30
Ve (LPM):	9.7	16%	15.7	28%	18.2	31%
Vt (L):	0.37		0.46		0.48
RR (f):	27		36		39
Heart Rate (BPM:	72	48%	86	58%	89	60%
BP (mm Hg)	156/78		162/82		170/84
O2 Pulse (ml/beat)	3.6	48%	6.0	79%	6.2	80%

In addition, the chronotropic index was 0.68 (normal 0.80 to 1.30), the Ve-VCO2 slope from rest to AT was 14.5 and the Ve-VCO2 slope from rest to peak exercise was 16.4. Although the maximum minute ventilation and maximum heart rate are well below their ULN of 85% of predicted, the RER of 1.27 at peak exercise indicates that there was an adequate exercise test effort.

That there is a cardiovascular limitation is indicated first by the reduced VO2 at anaerobic threshold. The LLN for this individual based on their age and gender was 54% so the observed value of 44% is well below normal. This shows that there was an oxygen delivery problem and this is usually related to a decrease in cardiac output. In addition, the chronotropic index is also reduced and since the individual is taking metoprolol, a beta blocker, this is not a major surprise. Together these factors could indicate that the individual’s primary exercise limitation was cardiovascular but the reduced SaO2 at maximum exercise indicates that the primary limitation has to be pulmonary.

But even though the individual has a restrictive ventilatory defect the maximum minute ventilation is well below the ULN of 85% so there was a large ventilatory reserve at peak exercise. Moreover, the ULN for the Ve-VCO2 slope from rest to AT is 34 and for the Ve-VCO2 slope from rest to peak exercise it is 40. The respective Ve-VCO2 slope values of 14.5 and 16.4 are well below this ULN and this (as well as the normal DLCO) is a strong indication that gas exchange was normal. So why is did this individual desaturate?

There are two strong clues. First, PetCO2 was elevated, both somewhat at rest and most distinctly at peak exercise. A normal resting PetCO2 is usually between 30 and 35 and at peak exercise between 35 and 45.

Note: A maximum PetCO2 above 40 is usually seen only in subjects with above average fitness and usually only at higher levels of exercise. PetCO2 can become elevated because an increased cardiac output decreases pulmonary capillary transit time and end-expiratory alveolar air therefore begins to reflect the venous PCO2. In these instances however, even though the PetCO2 is elevated, arterial PCO2 is usually normal and less than PetCO2.

In this case a resting PetCO2 of 41 is a touch high but not necessarily abnormal, but the pattern during exercise was. A normal PetCO2 pattern is a peak near AT (usually slightly after) and then a decline thereafter. For this individual however, PetCO2 actually increased throughout exercise. In addition the maximum PetCO2 of 53.4 is well above any normal.

Second, the Ve-VCO2 slopes, although technically within normal limits, are actually much too low. A normal Ve-VCO2 slope from rest to AT should have been around 29 for this individual.

Note: Ve/VCO2 is the relationship between minute ventilation and CO2 production at any one instant whereas the Ve-VCO2 slope is the relationship between the change in minute ventilation and the change in CO2 production over time. Traditionally the Ve/VCO2 at AT has been used to assess ventilatory efficiency and in this case the Ve/VCO2 of 39 at AT is elevated (ULN is 35). However, it has been pointed out that AT is where the nadir of Ve/VO2 occurs, not Ve/VCO2, and that because the AT is in this sense an arbitrary point at which to assess Ve/VCO2 the lowest observed Ve/VCO2 is a better indicator of of ventilatory efficiency. The lowest observed Ve/VCO2 for this individual is 30 and WNL.

In addition, it has been shown that the Ve/VCO2 at AT is a function of the Ve-VCO2 slope from rest to AT and it’s offset (i.e. , what Ve would be if VCO2 was zero). The offset of the Ve-VCO2 is different between individuals and disease states for reasons that remain unclear. Because of all this, and given that the Ve-VCO2 slope is generated from a relatively large number of data points, it’s my opinion that the Ve-VCO2 slope from rest to AT is a more reliable indicator of ventilatory efficiency than Ve/VCO2.

The Ve-VCO2 slopes of 14.5 and 16.4 are abnormally low and indicate little change in minute ventilation when compared to the change in VCO2 and given the large ventilatory reserves at peak exercise there is no apparent reason for this.

Finally, in addition there is one minor additional point and that is that there was only a small increase in tidal volume during exercise. Tidal volume normally doubles or triples during exercise and a low increase in tidal volume along with all the other factors:

• Mild restriction with a relatively preserved DLCO
• Reduced MIP and MEP
• Elevated PetCO2
• Reduced Ve-VCO2 slope
• Elevated ventilatory reserve

is a strong suggestion that the individual in question is hypoventilating due to respiratory muscle weakness. Their exercise limitation may be exacerbated by their chronotropic incompetence, but the primary limitation is still hypoventilation. There are a variety of possible causes for this weakness but the individual was referred to my lab by a physician outside the hospital network and for this reason there is no history available for review (and unfortunately any follow up will probably also occur outside the hospital network so I may never find out what the cause was).

It is moderately unusual to find hypoventilation by itself, without any gas exchange defect, as a primary exercise limitation. Hypoventilation can be a factor in both COPD and interstitial diseases, but in these cases there is usually a mix of both ventilatory and gas exchange limitations. The primary difference between those cases and the present one, and which showed a lack of underlying lung disease, was the Ve-VCO2 slope and PetCO2. Given that there was no ventilatory or gas exchange limitations, the only reasonable cause can be hypoventilation.

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

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:

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

And the other only had mild airway obstruction:

	%Pred:
FVC:	107%
FEV1:	96%
FEV1/FVC:	89%
TLC:	178%

The individuals did not say what method was used to measure their lung volumes and since they contacted me anonymously I am not able to find this out. In a sense it doesn’t matter however, since no matter what technique was used (helium dilution, N2 washout or plethysmography) the most common testing errors lead to an overestimation of RV, FRC and TLC.

I also don’t know whether the tests were performed at a hospital-based PFT lab or one that was based in a physician’s office. Office-based PFT labs used to be rare but particularly in group pulmonology practices they have become more commonplace. A number of readers have complained that they’ve seen Medical Assistants being trained to perform spirometry, lung volumes and DLCO’s in group practice PFT labs, even in states that have legislation or regulations that require a CRT, RRT, CPFT or RPFT to perform pulmonary function testing. Although this practice is likely unethical both in the sense that it is skirting the law and more so since it is using poorly educated and trained staff to perform complex testing, it usually goes unnoticed because there is no regulatory body overseeing testing in private offices.

I would hope that trained and licensed staff would have some qualms about reporting elevated TLC’s, particularly when spirometry was normal or almost normal, but to be honest I see too many technicians who believe that whatever the computer tells them must be so and fail to look at the big picture.

Regardless of who is performing the tests, the real problem (and the responsibility) lies with the interpreting physician. Gas trapping and hyperinflation with essentially normal spirometry? Really? The kindest thing I can say about this is that the interpreting physician was asleep at the wheel. If I was feeling less kind I’d have to say they’re either woefully ignorant about testing issues, or worse, they are willfully ignoring poor quality tests.

Having said that, testing errors are rarely front and center when PFT interpretation is being taught, and I’ve seen this even with the pulmonary physicians and fellows I’ve worked with. I understand that it is important to teach the basic algorithms for interpretation when starting out and that it does take time to get these down pat. At some point though, there also needs to be a firm understanding of testing errors and what they look like, and this seems to be the part that is most often neglected.

When I started working in a pulmonary function lab in the early 1970’s pulmonary fellows were expected to spend a couple weeks actually performing tests and calculating the results from the traces on kymograph paper. That stopped after I’d been in the lab only a couple of years and was never re-started. I believe the main reason for this is that since that time pulmonary medicine has expanded into the intensive care unit and sleep medicine and pulmonary fellows don’t have the time to “waste” on pulmonary function testing. Of course I think this is shortsighted and wrong but then again I don’t have any say about what’s in the pulmonary fellowship program.

In these two instances the interpretation of gas trapping and hyperinflation is most likely wrong. For the patients this probably means extra tests, doctor visits and maybe even medications that they don’t need and I have to wonder how long, if ever, it will take for this misapprehension to be corrected. The problem likely started with the inadequate training of whoever performed the tests in the first place, and I say this whether they were technicians or MA’s, but the final nail was placed by the interpreting physician and for that reason this is where the primary responsibility for the error lies.

GIGO. Quis custodiet ipsos custodes?

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

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

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.

An FVC maneuver is designed to measure the maximum expiratory flow rates, in particular the FEV1 and the PEF. It has long been recognized that the effort involved in the FVC maneuver can cause early airway closure, even in individuals with normal lungs, and that for this reason the vital capacity can be underestimated due to gas trapping. This effect is usually magnified with increasing age and in individuals with obstructive lung disease. Moreover, it is universally acknowledged that the FVC maneuver can be a stressful maneuver for many patients and there are a number of good reasons why an expiration should be terminated before the maximum possible vital capacity has been exhaled.

An SVC maneuver is designed to measure the lung volume subdivisions, Inspiratory Capacity (IC) and Expiratory Reserve Volume (ERV), and to maximize the measured volume of the vital capacity. Due to the more relaxed nature of the SVC maneuver there is significantly less airway closure and for this reason the SVC volume is usually larger than the FVC, even in individuals with normal lungs.

There are very few studies that have derived reference equations for FVC, SVC and FEV1 from the same population., but those from Marsh et al make the differences between FVC and SVC relatively clear.

Because the SVC is usually larger than the FVC, the FEV1/SVC ratio will usually be lower than the FEV1/FVC ratio. Although Marsh et al derived a reference equation specifically for the FEV1/FVC ratio they did not do the same for the FEV1/SVC ratio. For this reason, I’ve calculated a predicted FEV1/FVC ratio from the individual reference equations for FVC and FEV1, and then a predicted FEV1/SVC ratio from the individual reference for SVC and FEV1 (this may well be mis-using the reference equations but I’m trying to show comparable values). For an LLN I’ve used the LLN from the NHANES III reference equations, which is approximately 89%.

What this shows is that a normal FEV1/SVC ratio is lower than the FEV1/FVC ratio for all ages and that the difference increases with increasing age. This also means that a spirometry effort with a normal FEV1/FVC ratio will sometimes be considered abnormal when an SVC is used to calculate the FEV1/VC ratio.

Is this really a problem?

On the one hand, I’d say that the FVC is often underestimated and that the SVC is probably a better indication of a patient’s VC than the FVC. On the other hand I’ve seen FVC efforts with a normal FEV1/FVC ratio that met (or exceeded) all ATS/ERS criteria for test quality but where the SVC was sufficiently larger than the FVC that the FEV1/SVC ratio showed mild airway obstruction.

Since the ATS/ERS statement on interpretation does not acknowledge that there is any difference between an FVC and an SVC there are no particular guidelines for assessing whether or not a reduced FEV1/SVC by itself is a reliable indicator of airway obstruction. In fact, since this topic does not appear in any literature searches and none of the textbooks I have discuss it (other than to say to follow the ATS/ERS guidelines) there does not appear to be any guidelines on this issue whatsoever.

I think this has to be decided on a case-by-case basis and that this issue rests first and foremost on the quality of the FVC measurement. Whenever there is any reason to believe the FVC may be underestimated, and this can be the case even when the ATS/ERS criteria are met, then there is no reason not to the believe what the FEV1/SVC ratio is saying. For all other cases, particularly when it is only the FEV1/SVC ratio that is below the LLN, this leaves any diagnosis of airway obstruction in a somewhat gray area.

Any certainty that a reduced FEV1/SVC ratio indicates airway obstruction is present has to depend at least in part on how far it is below the FEV1/FVC LLN. A good question however, is how far below it needs to be. Since the discrepancy between FVC and SVC increases with age, I would be more likely to believe that a reduced FEV1/SVC ratio indicates airway obstruction in a young individual than in one that was elderly. The reference equations from Marsh et al indicate that the FEV1/SVC LLN is approximately 2 percentage points below the FEV1/FVC LLN at age 20 and approximately 8 percentage points at age 80. Marsh et al is only a single study however, and to be honest it was chosen as an example because it showed a reasonably clear difference between FVC and SVC at all ages. Another study (Gutierrez et al) also has reference equations for FVC, SVC and FEV1 derived from the same population but shows a much smaller difference in FVC, SVC, FEV1/FVC and FEV1/SVC over the same age range.

Note: On a related issue, it’s one thing to knowingly compare the FEV1/FVC and FEV1/SVC ratios, but I’ve seen lab software that automatically substituted the SVC for the FVC (and vice versa) without any indication this has happened (i.e. the report still said FVC, FEV1/FVC and SVC despite them having been interchanged). I don’t necessarily have a problem with software automatically substituting an SVC for an FVC (although I do with vice versa) but I’d want to know this had happened.

We seem to have an interesting blind spot about the FVC and the SVC being the same when it is easy to demonstrate that they are not. When it comes to routine clinical spirometry however, the FVC is frequently underestimated and an SVC (or an IVC) is likely a better indication of a patient’s VC. The problem is that in these cases we are assessing the presence of airway obstruction using the FEV1/SVC ratio but with reference equations and LLN’s for the FEV1/FVC ratio. The number of individual’s that are mis-diagnosed by a reduced FEV1/SVC ratio is probably small, but it more likely occurs in the elderly than in the young, and since it has never been studied the false-positive rate is unknown.

In a sense, the crux of the matter is that the FEV1/FVC ratio depends on both the FEV1 and FVC. Even when the ATS/ERS criteria are met we can’t ever be 100% certain we’ve measured a patient’s maximum VC (and this is one of the arguments in favor of the FEV6 and FEV1/FEV6 ratio). At best we can only approximate it. Given that the FEV1/VC ratio depends on one measurement that requires maximum expiratory flow (FEV1) and one that requires maximum volume (VC), it would seem that the maneuvers needed to achieve these values should probably be different. Until such time as the standards for routine spirometry change to include separate FEV1 and VC maneuvers however, and that the reference equations reflect this, the best we can do is to keep the differences between FVC and SVC in mind when reviewing test results.

References:

Brusasco V, Crapo R, Viegi G. ATS/ERS task force: Standardisation of lung function testing. Interpretive strategies for lung function tests. Eur Respir J 2005; 26: 946-968.

Gutierrez C, et al. Reference values of pulmonary function tests for Canadian caucasians. Can Respir J 2004; 6: 414-424.

Marsh S, Aldington S, Williams M, Weatherall M, Shirtcliffe P, McNaughton A, Pritchard A, Beaseley R. Complete reference ranges for pulmonary function tests from a single New Zealand population. New Zealand Med J 2006; 119: N1244.

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

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.

Although the AC pattern is associated with severe decreases in FEV1 and the FEV1/FVC ratio, its presence cannot be predicted by either the FEV1 or FEV1/FVC ratio. For example, compared to the above example the following loop actually has a slightly lower FEV1 and FEV1/FVC ratio:

The AC pattern is a consequence of a loss of elastic recoil in the lung and dynamic airway compression during a forced exhalation. More specifically numerous researchers have shown that the AC pattern is closely associated with emphysema. When groups of individuals with similar FEV1’s and FEV1/FVC ratios those with the AC pattern were more likely to have more gas trapping and hyperinflation, a higher airway resistance and to have a lower DLCO than those with a more curvilinear exhalation.

A recent study used a computer algorithm to place a pair of regression lines on flow-volume loops. Best fit was determined by mean square error and the angle between the two lines was measured. This angle was called the angle of collapse and using this approach, a lower angle implies a sharper “kink”.

When they compared FEV1, FEV1/FVC ratio, DLCO and the presence (defined as an area of hypovascular low attenuation) and amount of emphysema (defined as the percent of voxels with an X-ray attenuation value below -950 HU) from CT scans they found that angles of collapse below 131º had a positive predictive factor of 95.5% for the presence of emphysema. As importantly they also found that there was a direct correlation with the angle of collapse and the severity of emphysema. Individuals with lower angles of collapse uniformly had lower FEV1’s, lower FEV1/FVC ratios, lower DLCO’s and a greater amount of emphysema as assessed by their CT scan. They also found that lower angles of collapse had a higher predictive value for emphysema than did a low DLCO or a low FEV1/FVC ratio.

Although it has been hypothesized that decreased elasticity is a major factor in the presence of the AC pattern there has been somewhat equivocal evidence to support this. Of the two studies that looked at compliance, one showed no statistical difference in compliance in patients with and without the AC pattern. The second study showed significantly lower elasticity in patients with the AC pattern when compared to those with a curvilinear patter. There was however, a notable difference between the two studies. In particular the first study looked at individuals with similarly reduced FEV1’s and FEV1/FVC ratios whereas the second study only considered the presence or absence of the AC pattern and in addition the authors of the second study criticized (mildly) the statistical methods of the first study. This is not to say that individuals with the AC pattern don’t have decreased elasticity just that it may not be the sole factor for the development of the AC pattern.

Patients that have an AC pattern on their flow-volume loop rarely, if ever, revert to a more curvilinear flow-volume loop contour. The persistence of the AC pattern implies that the physiological changes that cause it to occur are likely irreversible. Having said that, at least one study showed that an individual with a curvilinear flow-volume loop shifted to an AC pattern during a methacholine challenge and reverted to curvilinear afterwards.

The formal definition of the AC pattern includes a decrease in flow to less than 50% of the PEF. Although this is reasonable as a working definition, it is somewhat arbitrary. There are a number of patients whose flow-volume loop shows a “kink” but at flow-rates above 50% of the PEF. For example, this patient had a mild OVD (the FEV1/FVC ratio was 81% of predicted and FEV1 83% of predicted):

So an interesting question, and one that does not seem to have been studied, is whether this small kink is an early sign of emphysema, a possible sign of a loss of elasticity or whether it just a normal variant in mild airway obstruction. I will mention that this patient had signs of gas trapping (elevated FRC, RV and RV/TLC ratio) despite having only mild airway obstruction but as a sample of one, it is hardly indicative of broader patterns.

A reduced FEV1 and FEV1/FVC ratio indicates the presence of airway obstruction, and the degree by which they are reduced correlates with the severity of the airway obstruction. The FEV1 and FEV1/FVC ratio alone however, cannot differentiate between asthma, chronic bronchitis and emphysema. The AC pattern is easily recognizable and appears to be highly specific to emphysema. Importantly, there is a good correlation between the “kinkiness” of a flow-volume loop and the severity of the emphysema. Although measuring the angle of collapse appears to be a way to quantify “kinkiness” (and would allow for an automated interpretation in office spirometers) I am concerned that it attempts to match straight lines to what are, in reality, curves. Having said that, compared to other approaches to the graphical analysis of flow-volume loops it appears to be a better way to describe the AC pattern (although I’m somewhat doubtful that it’s a relevant approach to analyzing curvilinear flow-volume loops without an inflection point).

Note: While researching flow-volume loops I’ve found that there is a marked lack of consensus in the words used to describe them. Our eyes may be good at recognizing contours but our ability to describe and communicate what we see is somewhat limited. Are these flow-volume loops kinky, do they have a notch, is it a sharp inflection point, is it a spike or are they AC patterns? Are more curvilinear flow-volume loops curved, scooped, coved or concave (or depending on how you look at it, convex)? Are loops from individuals without airway obstruction flat, convex or is normal sufficient, and is that a shoulder or a knee? Maybe it’s not important since we do understand these terms reasonably well but it does seem to me that this is one area we should be able to be more precise.

References:

Campbell AH, Faulks LW. Determinants of expiratory airflow obstruction in patients with chronic airways obstruction. Thorax 1973; 28(1): 48-54.

Healy F, Wilson AF, Fairshter RD. Physiologic correlates of airway collapse in chronic airflow obstruction. Chest 1984; 85(4): 476-481.

Jayamanne DS, Epstein H, Goldring RM. Flow-volume curve contour in COPD: correlation with pulmonary mechanics. Chest 1980; 77(6): 749-757.

Saltzman HP, Ciulla EM, Kuperman AS. The spirographic “kink”. A sign of emphysema. Chest 1976; 69(1): 51-55.

Topalovic M et al. Computer quantification of airway collapse on forced expiration to predict the presence of emphysema. Respiratory Research 2013; 14: 131

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

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.

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

The cause of the ‘shoulder’ is unknown but has been speculated to be due to flow limitation in the trachea. If this is true then a ‘shoulder’ is actually a sign of a limitation in peak flow rather than as a prolongation of peak flow.

A recent article used results from a large population study to explore this particular flow-volume loop feature and were able to show that in general it was associated with normal or above normal FEV1/FVC ratios. They also showed it was more common in younger individuals than older, and more common in females than in males.

So, a ‘shoulder’ is associated with normal spirometry but if FEV1 and the FEV1/FVC ratio are to be used as the way to determine normalacy, because this specific contour does not occur in all individuals with normal spirometry it cannot be considered to be the only ‘normal’ contour. For example, this loop comes from a relatively young female:

	Observed:	%Predicted:
FVC:	4.81	109%
FEV1:	3.95	109%
FEV1/FVC:	82	101%
PEF:	13.07	147%

Flow-volume loops associated with airway obstruction have a concave expiratory contour are usually described with some degree of ‘scooping’ or ‘coving’. Despite the ‘scooping’ in this loop, the results are actually normal, so this contour’s association with airway obstruction is not a given. For reasons of accuracy therefore, instead of describing a flow-volume loop as ‘normal’ it would be better to describe its contour objectively.

During an exhalation the force that can be applied by the respiratory muscles and the lung’s elastic recoil are greatest near TLC. These combined forces decrease as lung volume decreases towards RV. Airway resistance on the other hand, is lowest at TLC and increases as the airways are compressed when lung volume decreases towards RV. Along with gas density these two factors are primarily responsible for the shape of the maximal flow-volume loop but the exact physiology of how they relate to the various distinctive contours of flow-volume loops is often unclear.

Even so, flow-volume loop contours can be exceptionally useful in the interpretation of spirometry results. If the reason for some contours is not as well understood as it should be at least their associations with specific lung disorders is often well characterized. One problem with this is that although certain lung disorders usually occur with a specific flow-volume loop contour, specific flow-volume loop contours do not only occur with specific lung disorders.

So, are there ‘normal’ flow-volume loops? Yes, but they can be concave, convex or flat. Instead of using ‘normal’ as a way of describing a flow-volume loop it’s probably better to use the more objective and descriptive terms “shoulder”, “scooping” or “flat”.

References:

Brusasco V, Crapo R, Viegi G. ATS/ERS Task Force: Standardisation of lung function testing. Standardisation of spirometry. Eur Respir J 2005; 26: 319-338.

Shin HH, Sears MR, Hancox RJ. Prevalence and correlates of a ‘knee’ pattern on the maximal flow-volume loop in young adults. Respirology 2014; 19: 1052-1058

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

Recently my lab has had some turnover with a couple of older staff leaving and new staff coming on board. While reviewing reports I’ve found a number of instances where the incorrect FVC and FEV1 were reported. Taking these as “teachable moments” I’ve been annoying the staff with emails whenever I find something notably wrong. I had thought that our rules for selecting the best FVC and FEV1 were fairly straightforward but given the number of corrections I’ve made lately it seemed like it would be a good idea to revisit our policy on this subject.

The process I’ve used for selecting the best FVC and FEV1 has evolved over the years. Initially I was told to select the single spirometry effort that had the largest combined FVC and FEV1. Later on test quality became a factor (not that is wasn’t in the beginning but there aren’t a lot of quality indicators for a pen trace on kymograph paper). How to juggle the different quality rules wasn’t altogether clear however (they seemed to change a bit with whichever physician was reviewing PFTs at the time), and I was still supposed to somehow select just a single spirometry effort.

Most recently this was simplified by only having to select the largest FVC (regardless of test quality) from any spirometry effort and then the largest FEV1 as long as it came from a spirometry effort with good quality. This is pretty much in accord with the ATS/ERS spirometry standards but with one important difference, and that is that we use use Peak Expiratory Flow (PEF) as an indicator of test quality.

Strictly speaking the ATS/ERS standards state that

“The largest FVC and the largest FEV1 (BTPS) should be recorded after examining the data from all of the usable curves, even if they do not come from the same curve.”

There are, of course, a number of quality indicators for spirometry efforts that are used to indicate whether a curve is “usable”. These include things like back-extrapolation, expiratory time, terminal expiratory flow rate and repeatability but the one thing they do not include is PEF.

Despite not being within the ATS/ERS standards the reason that we use PEF in the selection process is found in the phrase “maximal forced effort” that is part of the ATS/ERS definition for FVC and FEV1. It has long been recognized (certainly since the early 1980’s and most likely earlier) that the FVC and FEV1 from a submaximal spirometry effort were often higher than the FVC and FEV1 from a maximal effort. So, is the largest FEV1 correct (as long as it meets the basic ATS/ERS criteria) or should it be the FEV1 from the effort with the highest PEF?

These two efforts from the same patient testing session highlight this dilemma. Both meet the ATS/ERS criteria for the start of the test which is what primarily applies to FEV1 (and PEF).

	Blue:	Red:
FVC (L):	2.72	3.06
FEV1 (L):	1.73	1.99
PEF (L/sec):	6.28	3.82

When transpulmonary pressure is measured (not exactly the same thing as alveolar pressure but close enough) during a forced exhalation, overall expiratory effort is related to the area under the curve of pressure versus volume. Some investigators have shown that the spirometry efforts with the highest PEF had the highest transpulmonary pressure-volume areas. Moreover, during a forced exhalation it takes about 250 milliseconds for the respiratory muscles to achieve maximal expiratory pressure. Peak flow therefore occurs while respiratory force is increasing and is largely dependent on patient effort. For these reasons PEF is a good index of expiratory effort.

Expiratory airflow is a function of driving (alveolar) pressure and the resistance to that flow, but only up to a point. Researchers have found that above a critical driving pressure expiratory flow rates either fail to increase or can actually decrease. This effect is usually called negative effort dependence (although a couple of researchers called it inverse effort dependence instead).

Part of the reason why an increased expiratory effort (and increased alveolar pressure) causes a decrease in expiratory flow has to do with thoracic gas compression. In order to generate a driving pressure the lung (thorax) has to be compressed and according to Boyle’s Law, this pressure is directly related to the amount of compression. A higher alveolar pressure therefore means more thoracic compression. More thoracic compression in turn means that the lung is actually at a lower volume than is apparent from the measured exhaled volume and therefore at a higher level of airway resistance and lower expiratory flow rates.

Negative effort dependence is usually more noticeable in subjects with airway obstruction and in general the worse the airway obstruction, the worse the negative effort dependence. The reason for this is mostly related to the equal pressure point. Since airways are elastic, they will be compressed when the pressure in the lung tissue surrounding them is higher than the pressure inside of them. This is the equal pressure point. Since airway elasticity depends to a large extent on the elasticity of the supporting lung tissue when that tissue loses elasticity due to disease processes, the amount of pressure necessary to collapse airways decreases as well. This is the reason why the maximum expiratory flow rate during quiet tidal breathing can be higher than the maximal expiratory flow rate at the same lung volume during a spirometry effort in individuals with COPD and also why a submaximal effort can produce a higher FEV1.

A number of studies have confirmed that PEF is related to effort and that FEV1 tends to be lower when taken from spirometry efforts with the highest PEF. Although at least one study showed these differences to be statistically significant, a couple other studies have shown the difference is marginal and not significant. Moreover is has been shown that FEV1 tends to correlate better with FVC than with PEF and that when FVC is factored in, there is no significant difference in the FEV1 from spirometry efforts with the largest PEF and those with a lower PEF. For these reasons selecting an FEV1 solely because that spirometry effort has the highest PEF doesn’t necessarily make sense.

Having said that, it remains reasonably clear that tests with a maximal or near maximal PEF are more likely to be maximal efforts. Because by definition FEV1 (and FVC) are supposed to be maximal, PEF should play some role in selecting which spirometry effort the FEV1 is taken from. If this is done however, when the largest FEV1 is in a spirometry effort with a PEF below the patient’s maximal PEF, how far below the maximal PEF is acceptable?

The ATS/ERS spirometry standards aren’t particularly helpful about this since PEF is discussed mostly as a stand-alone procedure and does not discuss the PEF obtained during spirometry except to define it in terms of the flow-volume loop. Moreover, acceptable ATS/ERS repeatability for PEF is an absolute value (0.67 L/sec or 40 LPM) without regard to patient gender, age or height. More pertinently a study on the reproducibility of peak flow showed that +/- 5% could be obtained in the majority of subjects however that study used peak flow meters and was not concerned about selecting FEV1.

When using PEF as part of the FEV1 selection or comparison process the closest to any kind of consensus is that a couple of researchers have used 90% of the maximal PEF as a cutoff. Although arbitrary, a 10% window seems like a reasonable starting point and for this reason my lab’s policy (written about 10 years ago) for selecting spirometry efforts states:

“Selection of a test should not be made solely on the basis of the best peak flow, but the selected test should be within 10% of the best peak flow out of all of the tests performed.”

The original problem I had noted while reviewing reports was that FEV1 is too often being selected simply from the effort with the highest PEF and that higher FEV1’s from efforts with similar PEF’s (well within 10% of the best PEF) were being ignored. This is mostly an education issue and I will continue to pester our staff until it goes away.

A variety of methods for choosing the “best” FVC and FEV1 have been proposed at one time or another. These include:

• The spirometry effort with the highest combined FVC + FEV1.
• Averaging the FVC and FEV1 from three acceptable efforts.
• Averaging the FVC and FEV1 from two efforts with the highest FVC + FEV1.
• The highest FVC and FEV1 regardless of which effort they came from.

The reason for some of these proposals has more to do with session to session repeatability than with whatever constitutes the “best” FEV1 and FVC. Even so, all of these methods has been studied and all show a reasonable level of intersession repeatability (although it should be no surprise that averaged results showed the highest reproducibility). There seems to be no reason therefore, not to attempt to define the “best” FEV1 as long as it is used consistently.

The ATS/ERS statement on spirometry does not include PEF as component in the FEV1 selection process and I think this is a mistake. Within limits PEF appears to be a reasonable way to assess how maximal or submaximal a spirometry effort may be. Choosing the largest FEV1 from a spirometry effort with a PEF within 10% of the highest observed PEF is admittedly somewhat arbitrary but it is an approach that will likely exclude submaximal spirometry efforts and prevent them from being reported.

References:

Aggarwal AN, Gupta D, Jindal SK. The relationship between FEV1 and Peak Expiratory Flow in patients with airway obstruction is poor. Chest 2006; 130(5): 1454-1461.

Brusasco V, Crapo R, Viegi G. Series ATS/ERS Task force: Standardisation of lung function testing. Standardisation of spirometry. Eur Respir J 2005; 26: 319-338.

Coates AL, Desmond KJ, Demizio D, Allen PD. Sources of variation in FEV1. Am J Respir Crit Care Med 1994; 149(2): 439-443.

Hegewald MJ, Lefor MJ, Jensen RL, Crapo RO, Kritchevsky SB, Haggerty CL, Bauer DC, Satterfield S, Harris T. Peak expiratory flow is not a quality indicator for spirometry. Peak expiratory flow variability and FEV1 are poorly correlated in an elderly population. Chest 2007; 131(5): 1494-1499.

Holcroft CA, Eisen EA, Sama SR, Wegman DH. Measurement characteristics of peak expiratory flow. Chest 2003; 124(2): 501-510.

Koyama H, Nishimura K, Ikeda A, Tsukino M, Izumi T. A comparison of different methods of spirometric measurement selection. Respiratory Medicine 1998; 92: 498-504.

Krowka MJ, Enright PL, Rodarte JR, Hyatt RE. Effect of effort on measurement of forced expiratory volume in one seconds. Am Rev Respir Dis 1987; 136: 829-833.

Nathan SP, Lebowitz MD, Knudsen RJ. Spirometric testing. Number of tests required and selection of data. Chest 1979; 76(4): 384-388

Park SS. Effect of effort versus volume on forced expiratory flow measurement. Am Rev Respir Dis 1988; 138(4): 1002-1005

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

Recently a report came across my desk from a patient being seen in the Tracheomalacia Clinic. The clinic is jointly operated by Cardio-Thoracic Surgery and Interventional Pulmonology and among other things they stent airways. The patient had been stented several months ago and this was a follow-up visit. Given this I expected to see an improvement in spirometry, which had happened (not a given, BTW, some people’s airways do not tolerate stenting), but what I didn’t expect to see was a significant improvement in lung volumes and DLCO.

When I took a close look at the results however, it wasn’t clear to me that there really had been a change. Here’s the results from several months ago:

	Observed:	%Predicted:	Predicted:
FVC:	1.19	50%	2.38
FEV1:	0.64	35%	1.79
FEV1/FVC:	53	71%	76
TLC:	3.21	76%	4.22
FRC:	2.34	96%	2.43
RV:	2.11	113%	1.85
RV/TLC:	66	150%	44
SVC:	1.15	48%	2.37
IC:	0.87	48%	1.80
ERV:	0.25	41%	0.58
DLCO:	6.59	38%	16.18
VA:	1.78	43%	4.12
IVC:	1.04

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And here’s the most recent results (the slight change in predicted values is because the patient had a birthday in-between tests):

	Observed:	%Predicted:	Predicted:
FVC:	1.83	78%	2.35
FEV1:	1.00	57%	1.76
FEV1/FVC:	55	72%	76
TLC:	3.80	90%	4.21
FRC:	2.48	102%	2.43
RV:	1.99	106%	1.85
RV/TLC:	52	118%	44
SVC:	1.82	78%	2.35
IC:	1.33	75%	1.78
ERV:	0.49	87%	0.57
DLCO:	13.08	81%	16.06
VA:	3.15	77%	4.10
IVC:	1.79

Although the change in DLCO is impressive (+6.50 ml/min/mmHg, +99%), the baseline DLCO was actually a very marginal test. The inspired volume was only a bit over a liter (and also somewhat less than the FVC), and this is barely enough for an adequate washout and alveolar sample. More importantly the patient’s severe airway obstruction (the FEV1 was 35% of predicted) likely meant there was poor gas mixing inside their lung. This is evident from the fact that the VA is only 55% of the TLC.

The most recent test however, had an inspired volume (IVC) that was 72% higher (1.78 L vs 1.04 L) and a VA that was 77% higher (3.15 L vs 1.78 L). Since calculated DLCO scales linearly with VA (assuming that the exhaled CO and tracer gas concentrations remain the same) if the baseline DLCO had the same VA as the most recent DLCO then the DLCO would have been 11.68 ml/min/mmHg and that’s within the same ballpark as the most recent DLCO.

Even after correcting for VA I wouldn’t necessarily expect the two DLCO tests to be the same and this is because the inhaled DLCO gas mixture is not distributed homogeneously throughout the lung. In particular the low IVC in the baseline test means that only some compartments of the lung actually received the DLCO gas mixture at that time. Even so, the corrected baseline DLCO and the most recent DLCO are close enough that I have to think that despite the apparent improvement there has actually been little change in the patient’s DLCO.

The improvement in TLC isn’t as impressive (+0.69 L, +22%) but the baseline test shows an apparent restrictive defect while the most recent results are normal. There was, however, very little change in FRC (2.34 vs 2.48) and all lung volume tests (and that includes helium dilution, nitrogen washout and plethysmography) start by measuring FRC. TLC and RV are then derived from FRC using the Inspiratory Capacity (IC) and Expiratory Reserve Volume (ERV) from the Slow Vital Capacity (SVC) maneuver.

In general you might expect that when a patient becomes less obstructed that this would improve their ability to exhale more. Assuming that the FRC remains the same they would therefore have a larger ERV. That is true to some extent here since ERV does improve, but the IC improved even more and you’d expect this mostly if the FRC changed as well. Since it hadn’t this got me curious (well, more curious than I was already) so I took a look at the raw data for the baseline lung volumes (performed by plethysmography). When I did I saw that the patient had made a single acceptable effort out of six tries and the reported lung volumes were from that single effort. When I looked at the raw data for the more recent lung volumes (also plethysmography) I saw the patient had made three acceptable efforts out of four tries and that the reported lung volumes were an average of these three efforts.

FRC often changes a bit from test to test. Since the IC and ERV also change along with it (assuming you have good quality SVC efforts) this is unimportant since TLC and RV will tend to remain the same. In this case however, a single FRC measurement was being compared to an average of three measurements. IC measurements are usually the most reliable part of an SVC maneuver since a maximal inhalation is easier than is a maximal exhalation. Given the fact that the baseline FRC came from a single measurement and that the patient had been having problems performing the test in the first place, I am willing to assume that the baseline FRC was underestimated and that the improvement in TLC comes from both an increase in test quality and an increase in IC.

Post-stent the patient had a significant improvement in spirometry, but also appeared to have notable improvements in lung volumes and DLCO. I am fairly certain however, that the lung volumes and DLCO improved not because of the stent or any underlying improvement in lung function, but because of an improvement in vital capacity and test quality.

This is a reminder that not all increases or decreases in pulmonary function test results from visit to visit are real. Small changes in test quality can cause large changes in test results. I’d could say that it’s also a reminder that test quality matters but we already know that and the problem is that all too often we have to make do with whatever we’re able to get from our patients. The key however, is that anybody reviewing tests needs to understand the effect that factors like the IVC has on DLCO and the IC has on TLC and to be willing to look at more than just what’s on the surface of the report.

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

Everyone uses the FEV1/FVC ratio as the primary factor in determining the presence or absence of airway obstruction but there are differences of opinion about what value of FEV1/FVC should be used for this purpose. Currently there are two main schools of thought; those that advocate the use the GOLD fixed 70% ratio and those that instead advocate the use the lower limit of normal (LLN) for the FEV1/FVC ratio.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has stated that a post-bronchodilator FEV1/FVC ratio less than 70% should be used to indicate the presence of airway obstruction and this is applied to individuals of all ages, genders, heights and ethnicities. The official GOLD protocol was first released in the early 2000’s and was initially (although not currently) seconded by both the ATS and ERS. The choice of 70% is partly happenstance since it was one of two fixed FEV1/FVC ratio thresholds in common use at the time (the other was 75%) and partly arbitrary (after all why not 69% or 71% or ??).

The limitations of using a fixed 70% ratio were recognized relatively early. In particular it has long been noted that the FEV1/FVC ratio declines normally with increasing age and is also inversely proportional to height. For these reasons the 70% threshold tends to over-diagnose COPD in the tall and elderly and under-diagnose airway obstruction in the short and young. Opponents of the GOLD protocol say that the age-adjusted (and sometimes height-adjusted) LLN for the FEV1/FVC ratio overcomes these obstacles.

Proponents of the GOLD protocol acknowledge the limitation of the 70% ratio when it is applied to individuals of different ages but state that the use of a simple ratio that is easy to remember means that more individuals are assessed for COPD than would be otherwise. They point to other physiological threshold values (such as for blood pressure or blood sugar levels) that are also understood to have limitations, yet remain in widespread use. They also state that it makes it easier to compare results and prevalence statistics from different studies. In addition at least two studies have shown that there is a higher mortality of all individuals with an FEV1/FVC ratio below 70% regardless of whether or not they were below the FEV1/FVC LLN. Another study noted that in a large study population individuals with an FEV1/FVC ratio below 70% but above the LLN had a greater degree of emphysema and more gas trapping (as measured by CT scan), and more follow-up exacerbations than those below the LLN but above the 70% threshold.

Since many of the LLN versus GOLD arguments are based on statistics it would be useful to look at the predicted FEV1/FVC ratios in order to get a sense of how much under- and over-estimation occurs with the 70% ratio. For this reason I graphed the predicted FEV1/FVC ratio from 54 different reference equations for both genders and a variety of ethnicities. Since a number of PFT textbooks have stated that the FEV1/FVC ratio is relatively well preserved across different populations what I initially expected to see was a clustering of the predicted values. What I saw instead was an exceptionally broad spread of values.

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Looking closely I am unable to see any particular relationship between ethnicity or geographical location and the FEV1/FVC ratio. This fact is highlighted by the slope (rate of decline) of the FEV1/FVC ratios with age.

Many of the studies that were the source of these reference equations did not include an LLN specifically for the FEV1/FVC ratio. For this reason I used 90% of predicted as a conservative substitute (this decision is based on the NHANESIII FEV1/FVC ratio LLN that is approximately 89%-90% of the predicted across the range of ages for all ethnicities).

When this is done, the limitation of the 70% ratio in relation to increased age becomes more obvious, particularly since the average of all LLN’s (for males) reaches 70% at age 65. This means that approximately half of the reference equation LLN’s show a decrease below 70% before that age, and some as young as age 33. Theoretically at least, using the GOLD criteria by age 65 up to half of the world population could have spirometry that was potentially within normal limits but would be considered to have COPD.

At first glance this is a strong argument in favor of the use of the LLN to determine the presence of airway obstruction, and in general I would agree. However, what it also makes quite clear is that the LLN is highly dependent on which reference equation is chosen and this to some extent bolsters the pro-GOLD argument about its simplicity.

I was surprised at the wide range of values from the different reference equations particularly since the FEV1/FVC ratio is often considered to be a highly conserved value between ethnicities (and notably within the NHANESIII and GLI studies there is little difference between Blacks, Hispanics, Caucasians and Asians). The reasons for this wide range of results are unclear and may be related to differences in the size or makeup of the different study populations, differences in statistical analysis and/or differences in the spirometry equipment. It should also be noted that the criteria used to assess test quality and the acceptability of spirometry results are based on the individual characteristics of the FVC and FEV1, not on the FEV1/FVC ratio.

The ATS/ERS statement on interpretation recommends the use of the largest vital capacity, regardless of source, when calculating the FEV1/FVC ratio. The effect that this has on the prevalence of airway obstruction by either the LLN or 70% threshold does not appear to have been explored, however. Using the reference equations from Gutierrez et al (chosen because the same population was used to derive reference equations for both spirometry and lung volumes) it appears that the FEV1/SVC ratio is lower than the FEV1/FVC ratio at all ages and that the difference between the two increases as age increases.

Although I fully understand and agree with the point of using the SVC when it is larger than the FVC, this makes it clear that the LLN for the FEV1/FVC ratio does not apply to the FEV1/SVC ratio.

Conversely, the FEV1/FEV6 has less variability than the FEV1/FVC ratio and for this reason has been suggested as a more reliable substitute. FEV6 however, can also be reduced when obstruction is present and for this reason the decrease in the FEV1/FEV6 ratio may not be a reliable indicator of the severity of obstruction.

The GOLD criteria were developed primarily to diagnose the presence of COPD. One of the hallmarks of COPD is that it is only minimally responsive to short-acting bronchodilators. For this reason at least some of the confusion surrounding the GOLD 70% threshold lies in the fact that it should only be applied to the post-bronchodilator FEV1/FVC ratio. It has been shown that the number of individuals considered to have airway obstruction using the GOLD criteria increases by up to 30 percent when only the pre-bronchodilator FEV1/FVC ratio is considered. This doesn’t necessarily make the 70% threshold more correct but it also shouldn’t be applied as a general rule to all spirometry either.

One criticism that I’d level at a number of the papers advocating the use of the LLN over the GOLD 70% threshold is that the authors often begin by defining airway obstruction as an FEV1/FVC ratio below the LLN and then proceed to critique the 70% threshold for mis-categorizing individuals. I don’t necessarily disagree with the underlying premise but this approach is a little specious since at least one study has indicated that the use of the LLN alone tends to under-diagnose COPD. Other studies have indicated that the addition of a reduced FEV1 (either below 80% of predicted or the LLN) and an elevated RV/TLC ratio are needed in addition to an FEV1/FVC below the LLN in order to improve specificity.

There is some evidence that individuals with an FEV1/FVC ratio below 70% tend to have more significant lung disease and a higher mortality. Numerous studies however, have shown that the GOLD threshold overestimates airway obstruction in the elderly and the tall and underestimates it in the young and the short. The predicted FEV1/FVC ratio LLN’s largely agree with this finding. I think that the greatest fault of the GOLD 70% threshold is that for too many individuals it confuses the normal changes that occur as part of aging with a disease process. Since an incorrect diagnosis of COPD can lead to inappropriate care plans, testing and medications for a patient, this alone probably outweighs any advantages the 70% threshold may have.

The preponderance of evidence is in favor of the FEV1/FVC ratio LLN. Moreover it is applicable to all forms of airway obstruction which includes pre-bronchodilator spirometry and this generally makes it more useful than the 70% threshold, particularly for the young. The LLN approach is not without its own problems, however, and any diagnosis of COPD should be multifactorial and rely on more than just the FEV1/FVC ratio. In addition more than one study has noted that which patients are considered to have airway obstruction was dependent on which set of reference equations were used for analysis and as can be seen the differences between reference equations, even within the same ethnicities, can be quite large.

Part of the problem with either approach is that most patients being screened for COPD are often performing spirometry for the first time in their lives. Without any knowledge of an individual’s baseline results the quality of any diagnosis is necissarily going to be limited. A simple answer to this is that spirometry, like blood pressure, needs to become a more commonly performed test, most particularly for patients that for whatever reason (smoking, work exposure, elevated air pollution, genes) have a higher level of risk.

The broad spread in the FEV1/FVC ratio reference equations is a problem for both the 70% threshold and the LLN. For the 70% threshold it puts into question both whether the FEV1/FVC ratio is actually preserved across different population and moreover whether 70% itself is correct. For the LLN, it may well be true that the LLN is more statistically correct, but the selection of the most appropriate reference equations for any one individual remains problematic.

FEV1/FVC Ratio Reference Equations, Study characteristics:

	Ethnicity:	#Female:	Female Ages:	#Male:	Male Ages:
[A]	Saudi	292	18-65	175	18-65
[B]	Ethiopian Jewish	45	25-70	47	25-70
[C]	Hispanic	143	20-80	116	25-75
[D]	Asian Indian	137	20-80	226	16-80
[E]	Iranian	1110	21-80	1302	21-80
[F]	White	327	20-79	300	20-79
[G]	White	927	21-80	476	21-80
[G]	Black	772	21-80	422	21-80
[G]	Hispanic	872	21-80	506	21-80
[H]	Chinese	595	18-80	494	18-80
[I]	Northern Indian	540	15-74	422	15-74
[J]	White	1129	27-82	1106	27-82
[K]	White	176	20-69	86	25-70
[L]	White	7009	18-80	4565	18-80
[M]	Chinese	0		440	18-80
[N]	American Indian	253	45-74	190	45-74
[O]	White	102	18-70	110	18-70
[P]	Black	117	18-47	143	18-47
[Q]	White	471	20-84	517	20-84
[R]	White	97	Not stated	102	Not stated
[S]	Korean	694	20+	926	20+
[T]	White	270	25 to >75	373	20 to >75
[U]	Iranian	255	17-82	295	17-82
[V]	Filipino	153	16-68	130	17-78
[W]	White	96	18 to >70	83	18 to >70
[X]	Malaysian	614	20-69	1385	20-69
[Y]	Jewish-Ashkenazi	663	20-74	1154	21-79
[Y]	Jewish-Sephardic	547	20-69	786	21-84

FEV1/FVC Ratio Reference Equations, Direct

Male:		FEV1/FVC Ratio:
[A]	Saudi	(-0.068*Height)-(0.095*Age)+98.41
[C]	Hispanic	86.5881-(0.116*Age)
[E]	Iranian	(-0.0978*Height)-(0.104*Age)+107.21
[F]	White	109.396-(0.113*Height)-(0.21*Age)
[G]	White	88.066-(0.2066*Age)
[G]	Black	89.239-(0.1828*Age)
[G]	Hispanic	90.024-(0.2248*Age)
[I]	Northern Indian	103-(0.35*Age)+(0.002*Age^2)-(0.07*Height)
[L]	White	EXP(6.291-(0.341*LN(Height))-(0.00441*Age)+(0.000026*Age^2))
[M]	Chinese	112.75058-(0.25439*Age)-(0.1181*Height)
[N]	American Indian	(-0.328*Age)+94.789
[O]	White	108.1-(0.24*Age)-(10.6*(Height/100))
[T]	White	(-0.175*Height)-(0.197*Age)+120.3
[W]	White	(-21.476*(Height/100))-(0.242*Age)+126.252
[Y]	Jewish-Ashkenazi	111.77-(0.123*Age)-(14.295*(Height/100))
[Y]	Jewish-Sephardic	99.09-(0.123*Age)-(6.57*(Height/100))

Female:		FEV1/FVC Ratio:
[A]	Saudi	(-0.072*Height)-(0.142*Age)+100.67
[C]	Hispanic	91.7259-(0.1862*Age)
[E]	Iranian	(-0.133248*Height)-(0.084349*Age)+112.1081
[F]	White	104.509-(0.089*Height)-(0.182*Age)
[G]	White	90.809-(0.2186*Age)
[G]	Black	91.229-(0.2039*Age)
[G]	Hispanic	92.36-(0.2248*Age)
[I]	Northern Indian	111-(0.36*Age)+(0.003*Age^2)-(0.1*Height)
[L]	White	EXP(5.637-(0.219*LN(Height))-(0.00249*Age)+(0.000004*Age^2))
[N]	American Indian	(-0.1967*Age)+89.565
[O]	White	108.1-(0.24*Age)-(10.6*(Height/100))
[T]	White	(-0.14*Height)-(0.158*Age)+111.5
[W]	White	(-0.172*Age)+88.134
[Y]	Jewish-Ashkenazi	111.77-(0.123*Age)-(14.295*(Height/100))
[Y]	Jewish-Sephardic	99.09-(0.123*Age)-(6.57*(Height/100))

FEV1/FVC Ratio Reference Equations, Indirect

Male:		FEV1:	FVC:
[B]	Ethiopian Jewish	(2.26*(Height/100))-(0.0221*Age)-0.0593	(3.994*(Height/100)-(0.0234*Age)-2.507))
[D]	Asian Indian	-1.936+(0.035*Height)-(0.026*Age)	-2.754+(0.043*Height)+(-0.024*Age))
[H]	Chinese	-2.404-(0.0254*Age)+(0.03978*Height)	-4.424-(0.0193*Age)+(0.05434*Height))
[J]	White	-4.261-(0.0296*Age)+(5.465*(Height/100))	-6.142-(0.0281*Age)+(7*(Height/100)))
[K]	White	-6.5147+(0.0665*Height)-(0.0292*Age)	-8.7818+(0.0844*Height)-(0.0298*Age))
[P]	Black	-3.6679-(0.0331*Age)+(0.0501*Height)	-6.839-(0.0195*Age)+(0.0695*Height))
[Q]	White	(0.092*(Height/2.54))-(0.032*Age)-1.26	(0.148*(Height/2.54))-(0.025*Age)-4.241)
[R]	White	(0.092*(Height/2.54))-(0.032*Age)-1.26	(0.138*(Height/2.54))-(0.027*Age)-3.445)
[S]	Korean	(0.04578*Height)-(0.0002484*Age^2)-3.4132	(0.05292*Height)+(0.010947*80)-(0.00008633*Age^2)-4.8434)
[U]	Iranian	(0.043822*Height)-(0.028801*Age)-2.425	(0.062271*Height)-(0.027131*Age)-5.086)
[V]	Filipino	-3.2068+(0.0436*Height)-(0.0205*Age)	-4.4496+(0.0526*Height)-(0.0099*Age))
[X]	Malaysian	(0.0353*Height)-(0.0315*Age)-1.78	(0.0407*Height)-(0.0296*Age)-2.343)

Female:		FEV1:	FVC:
[D]	Asian Indian	-0.401+(0.021*Height)-(0.021*Age)	-0.842+(0.027*Height)-(0.02*Age))
[H]	Chinese	-1.272-(0.0199*Age)+(0.02825*Height)	-2.697-(0.0149*Age)+(0.03894*Height))
[J]	White	-1.747-(0.0263*Age)+(3.619*(Height/100)	-4.04-(0.0259*Age)+(5.364*(Height/100)))
[K]	White	-1.405+(0.0309*Height)-(0.0201*Age)	-2.9001+(0.0427*Height)-(0.0174*Age))
[P]	Black	-1.6158-(0.0178*Age)+(0.0298*Height)	((-2.9208-(0.0122*Age)+(0.0407*Height))))*100
[Q]	White	(0.089*(Height/2.54))-(0.025*Age)-1.932	-3.335+(0.049*Height)-(0.024*Age))*100
[R]	White	(0.085*(Height/2.54))-(0.025*Age)-1.692	(0.114*(Height/2.54))-(0.024*Age)-2.795)
[S]	Korean	(0.03558*Height)-(0.000192*Age^2)-2.4114	(0.03951*Height)+(0.006892*65)-(0.00012728*Age^2)-3.0006)
[U]	Iranian	(0.039489*Height)-(0.023593*Age)-2.498	(0.046167*Height)-(0.022557*Age)-3.274)
[V]	Filipino	-1.0375+(0.0256*Height)-(0.0187*Age)	-1.4297+(0.0302*Height)-(0.0159*Age))
[X]	Malaysian	(0.0294*Height)-(0.0238*Age)-1.609	(0.0312*Height)-(0.022*Age)-1.64)

References:

Aggarwal AN, Gupta DG, Agarwal R, Jindal SK. Comparison of the lower confidence limit to the fixed-percentage method for assessing airway obstruction in routine clinical practice. Resp Care 2011; 56; 56(11): 1778-1774.

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PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

This relatively odd DLCO testing error came across my desk today. Although it’s fairly unusual it brings up some interesting points about how the Breath-Holding Time (BHT) is determined and what effect it has on DLCO.

Specifically, at the beginning of the DLCO test the patient took a partial breath in, then exhaled, then took a complete breath in. The patient performed the DLCO test three times and did exactly the same thing each time despite being coached by the technician to only take a single breath in. I’m sure this says something about human nature but I’m not exactly sure what.

Anyway, our test systems uses the Jones-Meade approach to measuring breath-holding time (the ATS/ERS recommendation). The J-M algorithm starts the measurement of BHT when the inhalation has reached 1/3 of the inspiratory time. In this case the computer detected the beginning of the first inspiration and detected when the patient had reached the end of inspiration (which is standardized at the point at which 90% of the final inhaled volume has been reached), but it ignored what happened in the middle. For this reason, the software set the beginning of the breath-holding time before the “real” inhalation.

Although the patient did inhale a small amount of the DLCO test gas at the beginning, they immediately exhaled it so it is hard to count the first inhalation as the real start of the test. If the second inhalation is back-extrapolated, a new start of the BHT can be determined. When this is done, the BHT decreases from 10.52 seconds to 9.25 seconds.

To re-calculate the DLCO:

since only the BHT changed the right-hand side of the equation can be ignored. With the original BHT, the left side of the equation calculates as 0.383. When the new BHT is substituted it calculates as 0.436, an increase of 13.8%. The calculated DLCO then increases from 15.14 ml/min/mmHg (60% of predicted) to 17.22 ml/min/mmHg (68% of predicted). By my lab’s criteria this changes the DLCO from mildly to moderately reduced to just mildly reduced but realistically doesn’t otherwise change the overall interpretation.

When patients perform a single-breath DLCO test they do not instantaneously inhale the test gas mixture nor do they exhale it instantaneously. It takes a certain amount of time to do both. Diffusion actually begins once the inspired gas passes a patient’s anatomical deadspace but does not reach it’s maximum rate until near full inhalation. Although the rate of diffusion decreases during exhalation, it nevertheless continues throughout exhalation, or at least until the alveolar sample is taken. The DLCO calculation however does not take inspiratory time or expiratory time into consideration.

The Jones-Meade algorithm attempts to take what occurs physiologically during inhalation and exhalation into consideration by starting to measure the breath-holding time once 1/3 of the inspiratory time has occurred and ends half-way through the alveolar sampling period. The algorithm assumes that the patient inhales and exhales as quickly as possible. When a prolonged inspiration or expiration occurs it’s possible that the measured BHT will not accurately reflect the period during which diffusion occurred.

Patients don’t usually have a problem with the inhalation phase of the DLCO test (other than not exhaling to RV first or not inhaling to TLC). For whatever reason this patient had a false start every time they started to inhale. This caused the breath-holding time to be overestimated which in turn caused the calculated DLCO to be underestimated. Although in this case it did not really change the overall interpretation the discrepancy in DLCO would become important when results are trended.

References:

Brusasco V, Crapo R, Viegi G. ATS/ERS Task Force: Standardisation of pulmonary function testing. Standardisation of the single-breath determination of carbon monoxide uptake in the lung. Eur Respir J 2005; 26(4): 720-735.

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

This idea originates, as far as I know, from Michael Sims, president and CEO of NspireHealth. I got it second hand and suspect that it is a small part of a larger presentation but this one point is worth discussing by itself. Specifically, we call the places we work “Pulmonary Function Laboratories” and this is at best an outdated and somewhat obscure term that doesn’t do much to make it clear what we do.

What’s wrong with calling it a Pulmonary Function Lab?

Well “Pulmonary” is okay since it’s a rather dignified and erudite term for the part of the body we’re primarily concerned with. “Function” however, is a somewhat vague or ambiguous term. The dictionary definition (or at least one of them since the other is mathematical) is “an activity or purpose natural to or intended for a person or thing”. That sort of applies to what we do but not with any particular precision or clarity.

I think that it’s the words “Lab” or “Laboratory” are the biggest problem since they conjure up images of Bunsen burners, test tubes and white-coated scientists engaged in research (the buzzing electrical arcs climbing up Jacobs’ Ladders and cries of “it’s alive!” are optional). The dictionary definition is “a room or building equipped for scientific experiments, research, or teaching, or for the manufacture of drugs or chemicals.” Not particularly specific to what we do and not necessarily a place you’d want to have any tests performed.

Michael Sim’s suggestion was that we re-brand our place of work by calling it “Pulmonary Diagnostic Services” instead. This is an unambiguous title that clearly identifies what we do. More than that, it gives us an opportunity to re-imagine and re-define exactly what it is we do.

So, exactly what is it we do?

Well, pulmonary function tests, what else? End of story, right?

No, not really. Our purpose is the diagnostic testing and monitoring of lung disorders. That may sound like the same thing but it’s a matter of focus. It still means doing pulmonary function tests (and no matter what, we’ll be calling them that for a long time), but only as a means to an end, not as an end in itself. Once you start thinking of our purpose in these terms the priorities become clearer.

Most importantly I think this means that we need to be open to performing any tests that can improve the diagnostic process no matter what they are. As an example, when spirometry is ordered what is most often performed is a Forced Vital Capacity. That’s fairly adequate for detecting expiratory airway obstruction, but spirometry can also consist of:

• Upright and supine spirometry to detect diaphragmatic weakness.
• A Slow Vital Capacity in order to acquire the largest VC for the FEV1/VC ratio.
• A Slow Vital Capacity to measure IC and ERV.
• A Forced Inspiratory Vital Capacity to detect inspiratory airway obstruction.

And how often are these performed? We need to work smarter and use all the tools in our toolbox. I’ve known technicians that dug in their heels and resisted doing anything that wasn’t considered traditional pulmonary function testing. The time for this kind of thinking is long past even assuming it was ever correct in the first place.

Accurate diagnostics cannot be based on incomplete information. This means, at least as far as I’m concerned, that technicians should have the ability to perform additional tests for a given patient based on findings as they occur. Why should a patient have to wait a couple of weeks for a PFT report to be read only to find they need to come back for more tests? A patient’s wheeze can lead to an order for just spirometry but what happens when the results clearly indicate that a restrictive disorder is far more likely instead? Either written orders need to be more open-ended or there needs to be mechanisms for a technician to quickly get additional orders.

Monitoring patients is just as important and accuracy in this means managing test equipment so that tests remain accurate and repeatable over long periods of time. It means managing patient test data also over long periods of time so that it can be quickly retrieved and compared. It also means reporting results and trends in a clear and unambiguous manner.

Re-defining our purpose will not work unless as technicians step up to the plate as well. It’s not enough to be knowledgeable about the mechanics of performing tests, we also need to understand the diagnostic purposes of the tests, the implications of the test results and to be careful and diligent when performing tests. To some extent continuing education should be a department-level responsibility as well as a responsibility of the medical director, but in the end it’s really our responsibility.

Finally I’m going to say that if you work in Pulmonary Diagnostic Services, it’s time you had your CPFT or RPFT certification and this needs to be a requirement, not an option.

We’ve all seen the upward creep in job titles. Sanitation Engineer for janitor. Media Distribution Agent for paperboy. Field Nourishment Consultant for waitress (a real job title!). Twenty years or so ago I scoffed somewhat when they renamed the hospital’s housekeeping department as “Environmental Services”. A funny thing happened along the way however, because the people in that department started becoming truly concerned about the patient’s environment and not just about mopping floors and emptying wastebaskets. As importantly they also started to have a real say in how rooms were laid out, how they were equipped and how to keep them safe for patients.

Our places of work have been called Pulmonary Function Laboratories probably since the 1960’s. That title may have made sense at one time because in the beginning at least, pulmonary function testing was still somewhat experimental and somewhat like research. That’s no longer the case and how we, and the patients and physicians we serve, perceive our profession are influenced by the words we use to label it. Pulmonary Diagnostic Services is a far better description of our purpose and re-branding ourselves this way will affect how we and everyone else will think of it.

It may only be a matter of perception but wouldn’t you suspect that our chances of getting our staffing and equipment requests approved are measurably better if we make them as Pulmonary Diagnostic Services instead of the Pulmonary Function Lab?

In a real sense, there is nothing in being Pulmonary Diagnostic Services that we don’t already know and shouldn’t already be doing. I’m not going to say that re-branding will fix our problems but it’s at least a positive step towards re-prioritizing, re-imagining, re-defining and hopefully at least, re-invigorating our field.

PFT Blog by Richard Johnston is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License