Author: Richard Johnston

I have been taking a close look at the raw data from all lung volume tests lately in large part because N2 washouts are still relatively new to my PFT Lab and we’re continuing to learn from our mistakes. When I saw this N2 washout test I knew that there was something wrong with it. The patient had performed three N2 washout tests and the TLC, FRC and RV for this one test were significantly larger than for the other tests. The most common problem we’ve been having with N2 washouts has been with patient leaks during the washout period which almost always show up as an upwards drift in the tidal baseline. This test did not show any drift however, and it took me a little while before I could see what was wrong with it.

The N2 washout maneuver has the patient start by breathing tidally for a short period of time in order to determine where end-exhalation (FRC) is located. The patient then performs a slow vital capacity maneuver by steadily inhaling maximally to TLC and then exhaling maximally to RV. The technician then switches the patient into the washout breathing circuit at maximal exhalation and the patient resumes breathing tidally for the remainder of the test.

The key assumption in this procedure is that the patient is switched at their maximal exhalation and that all of the nitrogen that is subsequently washed out comes solely from the patient’s RV. TLC is then calculated by adding the SVC volume to the measured RV. FRC is calculated by adding ERV to RV.

In this case the patient paused during the maximal exhalation portion of the SVC and the technician switched them into the washout breathing circuit. The patient however, had not really reached RV and with the next breath actually exhaled past the point at which the switch-in occurred. The test system software then altered the volume position of RV according to this more maximal exhalation. When the test was completed the RV volume was then calculated from the amount of nitrogen that had been washed out, but this volume was actually the point where the patient was switched-in and not RV. RV was therefore overestimated and because of this, TLC and FRC were also overestimated.

This is not really a technician error or a patient error, but is instead a software error. The software assumes that switch-in occurs at RV but then allows RV to be determined from a maximal exhalation occurring at any point during the entire test. If RV can be set at any time during the test then there needs to be a distinction made between switch-in volume and RV just like the one between TGV and FRC in plethysmography.

This is a moderately unusual error because it required two different things to go wrong. First the patient did not exhale maximally and was switched-in to the washout circuit at a volume above RV. Second, and more importantly, they performed a maximal exhalation during the washout period when they should have been breathing tidally. Without this second part even though RV would have been overestimated, TLC and FRC would probably have been reasonably accurate.

I have notified the manufacturer and hopefully this will be fixed in the next software release we receive but until that time (and probably even after) I will continue to review the raw data for all lung volume tests and will be on the lookout for the next time it occurs. This problem may be specific to the brand of equipment we are using or may be to the version of software we are using but I would recommend that if you use N2 washout to measure lung volumes that you try this yourself to see if you get a similar error.

UPDATE (11/30/2012):  I have talked with the manufacturer and they claim that they do calculate the “switch-in” volume.  FRC is calculated from the initial exhalation to the “switch-in” volume and TLC and RV are then calculated from FRC, and not from presuming the “switch-in” volume is RV.  “Switch-in” volume is not reported and the way that lung volumes are calculated is not documented in their manual.  The overestimation of TLC may have been caused by patient leak or other problems.

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

The PFT Lab I am associated with has been making a point of having the technicians re-measure patient height with each visit. Part of the reason for this is that several years ago the medical assistants in the pulmonary outpatient clinic were tasked with obtaining patient heights, weights and blood pressures. For a period of time the technicians used these heights when entering the patient demographic information but it was soon noticed that patient heights often changed by several inches from visit to visit. For this reason we have asked the technicians to re-measure patient height instead.

One possible cause for the fluctuation in heights was that the medical assistants were measuring patient height using the height rod attached to the scale while also taking their weight. The PFT Lab has wall-mounted stadiometers in or near all of the lab’s testing rooms so that patient height can be taken with their back against the wall rather than free-standing.

Another reason to regularly re-measure patient height is that the lab’s population has a significant number of patients that have routinely been seen by the lab and the pulmonary physicians for years. The lab’s patient and results database now goes back over twenty years and patients that were seen 15 and 20 years ago have been referred again for pulmonary function testing and their height has changed in the meantime.

My feeling has been that it is important to base the patient’s predicted values on their current height, not on whatever their original height was. This is because the population studies that generate reference equations are based on the current height of their subjects, not their original height.

Recently I have seen several patients whose height was re-measured and are now one or two inches shorter than what was previously measured. This has caused enough of a shift in their predicted values that although their test results are essentially unchanged they are now within normal limits when before they were classified as obstructed or restricted. This makes it clear that accurate heights are essential to accurate interpretation of results.

Coincidentally or not I also recently ran across an article where the authors advocate the use of arm span over height when calculating predicted values for patients with COPD. Their contention is that because of disease processes and the effects of medications patients with COPD are more prone to an accelerated height loss and for this reason the severity of their lung disease is being underestimated. This is an interesting point and other investigators have noted that arm span most closely matches actual standing height when people are young adults and that as people age height is lost because of degenerative changes in the vertebrae and disks of the vertebral column but arm span tends to remain constant (although there are very few longitudinal studies so this is not as clear as it should be). For this reason the arm span to height ratio tends to increase with age. Other researchers have noted that an increased arm span/height ratio is associated with a reduced FVC and increased dyspnea as well as increasing age.

So arm span may very well be a more accurate representation of a patient’s original height but a reasonable response may be, so what? Since much of any individual’s height loss is from the vertebral column this has a direct effect on the volume of the thoracic cage and therefore the lungs. For this reason standing height may still be a better indicator of lung function than arm span and this is what the reference equations use. A counterpoint would be that arm span is and should be used to estimate height in patients with scoliosis or other skeletal deformities and that in these cases comparison of current results with what they “should” have been can be very informative.

I think the core question is that when we are calculating predicted values what are we trying to accomplish? For example, say that with MRI or other imaging of the thorax and airways it was possible to accurately determine what a patient’s actual lung volume and flow rates “should” be. If this was possible (and it already is to a reasonable extent with CAT scans), it would likely produce predicted values that were skewed to the patient’s disease process and a patient with advanced obstructive or restrictive lung disease could be “normal” when compared to what was “expected” for them. This would not be particularly informative so I think that the case for comparing patient test results with their theoretically normal values is fairly clear.

I am not convinced however, that arm span should routinely be used in place of standing height. There is a lot of variance in arm span/height ratios and I would like to see more research that categorizes and explains these differences. A much bigger and more important concern is a lack of standardization in how arm span is measured. There are stadiometers for measuring standing height but there is no equivalent for arm span and from personal experience I can say that a lot of inaccuracy is possible when using a tape measure.

I am also not convinced that using a patient’s original (greatest) height to calculate their predicted values is a correct approach but this is mostly because reference equations are created from their study population’s current height, not from any prior height. I can see that patient height loss is a factor that can affect lung function but I am not sure there is an organized approach for doing this.

I think there is enough evidence concerning the utility of arm span measurements that it may well be reasonable for a PFT Lab to add this as part of their routine practice. But regardless of whether standing height or arm span is used the first step has to be an accurate measurement.

References:

Aggarwal AN, Gupta D, Jindal SK. Interpreting spirometric data. Impact of substitution of arm span for standing height in adults from North India. Chest 1999; 115: 557-562.

Allen SC. The relation between height, armspan and forced expiratory volume in elderly women. Age & Ageing, 1989, 18: 113-+116.

Ansari K, Keaney N, Price M, Munby J, Kay A, Taylor I, King K. Precision in diagnosiing and classifying COPD: comparison of historical height with current height and arm span to predict FEV1. The Open Respiratory Medicine Journal 2012; 6:54-58.

Parker JM, Dillard TA, Phillips YY. Arm span-height relationships in patients referred for spirometry. Am J Respir Crit Care Med 1996; 154: 533-536

Tan MP, Wynn NN, Umerov M, Henderson A, Gillham A, Junejo S, Bansal SK. Arm span to height ration is related to severity of dyspnea, reduced spirometry volumes and right heart strain. Chest 2009; 135: 448-454.

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

The PFT Lab I am associated with performs cardiopulmonary exercise tests for pre-op cardiothoracic surgery patients with lung cancer. Surgeons have to make a decision to operate or not based at least in part on the amount of function they think will remain after a lung resection and this depends on which and how many lobes are involved. This calculation is done by taking a percentage based on the amount of lung tissue that will be lost which is weighted using ventilation-perfusion scan results off the baseline DLCO and vital capacity. When the result is inconclusive or there are other medical factors that can affect a patient’s prognosis the results from a CPET can help with the surgeon’s decision.

The criteria that has been most often cited as an indicator of acceptable surgical risk is a peak VO2 greater than 15 ml/kg/min. About ten years ago we encountered a patient with a significantly low body weight. His max VO2 was about 16 ml/kg/min which appeared to make him a good candidate for surgery but his actual maximum oxygen consumption in LPM was 45% of predicted. This discrepancy was due to the fact that his BMI was about 14. We re-calculated what his peak VO2 would have been if his body weight had been normal and that was less than 10 ml/kg/min. For this reason our recommendation at that time was that the patient was a poor candidate for surgery.Up until that time we had used a set of predicted peak VO2 equation that was based solely on height, age and sex. Our analysis of this patient’s results seemed inadequate so with a bit of research we found and decided to change to a set of predicted equations that incorporated body weight.

At that time we were aware of and were using the Ve/VCO2 at anaerobic threshold as part of the exercise interpretation process but we have since come to rely far more on the Ve-VCO2 slope. Because determining anaerobic threshold using ventilatory parameters is a “soft” measurement some investigators have recommended using the lowest observed Ve/VCO2 instead. From my point of view however, the Ve-VCO2 slope is measured from a series of data points rather than a single one and for this reason it is probably a more reliable measurement than Ve/VCO2 at AT.

I will mention in passing that the lowest Ve/VCO2 whether or not it occurs at AT is a function of the Ve-VCO2 slope and its intercept. Ve-VCO2 slope and Ve/VCO2 at AT have been investigated and reported many times but little has been reported about the Ve-VCO2 intercept and what, if anything, the intercept means is still unclear.

We recently had a similar low body weight patient for a pre-op CPET and I think our ability to analyze this patient’s results has improved. The patient had a diagnosis of lung cancer and COPD and had a BMI of 18.2. PFT data showed a FVC that was 60%VO2, FEV1 36% and DLCO 65% of predicted. CPET data showed a peak VO2 in LPM that was 52% of predicted, the peak VO2 in ml/kg/min was 16.2, peak Ve was 94% of predicted (FEV1x40), Ve/VCo2 at AT was 44, VO2 at AT was 45% of predicted in LPM and 14.0 ml/kg/min, Ve-VCO2 slope was 30.7 (intercept 9.9), the max heart rate was 101% of predicted and the SpO2 at peak exercise was 97%.

The maximum heart rate and peak minute ventilation shows the patient gave an excellent test effort. Overall the results indicate the patient had a primarily pulmonary mechanical limitation to exercise. Despite the low DLCO the lack of desaturation and normal Ve-VCO2 slope indicates that pulmonary vascular disease was not a primary limiting factor.

The literature concerning the effect of low body weight on exercise capacity is quite sparse. Interestingly, although there is an ERS statement on cardiopulmonary exercise testing it contains no recommendations about reference equations and does not discuss the effects of body weight on exercise results.

Patients with a low body weight are expected to have a lowered resting and peak oxygen consumption and this is due primarily to a loss of lean body mass (muscle), but because of their body weight this causes quite different expectations in max VO2 when expressed in LPM and when expressed in ml/kg/min.

A peak VO2 less than 15 ml/kg/min is not the only indicator of post-op complications and mortality and in this case in particular may not necessarily be the best one. An alternate criteria that we think is more widely pertinent than peak VO2 is a Ve-VCO2 slope greater than 34. A review of the literature shows that other possible negative pre-op criteria can include a peak VO2 (in LPM) less than 60% of predicted, a DLCO less than 60% of predicted and a VO2 at anaerobic threshold less than 11 ml/kg/min. Depending on what factors are emphasized there are different implications for this patient’s post-surgery prognosis.

Since the peak VO2 in ml/kg/min is likely overestimated in this patient I think its prognostic value is low and should be ignored. More pertinent is the fact that the peak VO2 was 52% of predicted and the reference equation used was specific for underweight individuals. On the other hand, the Ve-VCO2 slope and the percent predicted DLCO were above their cutoffs and these would tend to indicate a favorable prognosis. In addition the VO2 at AT was normal and there was no desaturation. Our final recommendation was that despite questions about the peak VO2 the normal Ve-VCO2 slope indicated the patient was likely a reasonable candidate for surgery.

When we originally encountered the problem of assessing the peak VO2 in ml/kg/min in a low body weight patient we interpreted the results by noting that the peak VO2 would have been markedly reduced if the patient’s body weight was normal which in retrospect was not the proper way to analyze the results. This time we had a better notion about what the patient’s predicted VO2 should be and as importantly we were able to use other criteria to help make an informed decision about the patient’s prognosis.

References:

Brutsche MH, Spiliopoulos A, Bolliger CT, Licker M, Frey JG, Tschopp JM. Exercise capacity and extent of resection as predictors of surgical risk in lung cancer. Eur Respir J 2000; 15: 828-832.

Corra U, Mezzani A, Bosimini E, Scapellator F, Imparato A, Giannuzzi P. Ventilatory response to exercise improves risk stratification in patients with chronic heart failure and intermediate functional capacity. Amer Heart J 2002; 143: 418-426.

Francis DP, Shamim W, Davies LC, Piepoli MF, Ponikowski P, Anker SD, Coats AJS. Cardiopulmonary exercise testing for prognosis in chronic heart failure: continuous and independent prognostic value for Ve/VCO2 slope and peak VO2. Eur Heart J 2000; 21: 154-161.

Horwich TB, Leifer ES, Brawner CA, Fitzgerald MB, Forarow GC. The relationship between body mass index and cardiopulmonary exercise testing in chronic systolic heart failure. Am Heart J 2009; 158(4-Suppl): S31-S36.

Morice RC, Peters EJ, Ryan MB, Putnam JB, Ali MK, Roth JA. Exercise testing in the evaluation of patients at high risk for complications from lung resection. Chest 1992; 101:356-361.

Palange P et al. ERS Task Force: Recommendations on the use of exercise testing in clinical practice. Eur Respir J 2007; 29: 185-209.

Salvadori A, Fanari P, Mazza P, Agosti R, Longhini E. Work capacity and cardiopulmonary adaptation of the obese subject during exercise testing. Chest 1992; 101:674-679.

Smith TB, Stonell C, Pukayastha S, Paraskevas P. Cardiopulmonary exercise testing as a risk assessment method in non cardio-pulmonary surgery: a systematic review. Anaesthesia 2009; 64: 883-893.

Tardie GB, Dorsey DA. Pre-opeartive cardiopulmonary exercise testing for a severely malnourished lung cancer resection surgery candidate. JEPonline 2005; 8:34-43.

Wang J, Olak J, Ferguson MK. Diffusing capacity predicts operative mortality but not long-term survival after resection for lung cancer. J Thorac Cardiovasc Surg 1999; 117: 581-587.

Wasserman K, Hansen JE, Sue DY, Stringer WW, Whipp BJ. Principles of Exercise Testing and Interpretation Including Pathophysiology and Clinical Applications Fourth Edition. Copyright 2005 by Lippincott Williams & Wilkins.

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

This PFT report came across my desk the other day. At first glance it looked wrong because when was the last time you saw a patient with a FRC that was 165% of predicted?

Lung volumes were done by plethysmography and I took a close look at the TGV loops (mouth pressure vs box volume) and they had excellent quality and reproducibility, about as good as you can ever expect. When I looked at the volume data however, it was apparent that the patient leaked during the panting maneuver while the shutter was closed.

As you can see there is a significant baseline shift before and after the shutter closed but this actually means it is the TLC that is underestimated not that the FRC is overestimated. In our plethysmograph system the FRC is determined from the tidal breathing before the shutter closes. When the shutter closes and the patient performs the panting maneuver TGV is measured. The system looks at where the shutter closed relative to the previously established end-of-exhalation baseline level and uses this to determine FRC. FRC is therefore based on what happened before the shutter closes not after.

After the shutter opens the patient returns to tidal breathing and then performs a slow vital capacity maneuver. ERV is measured from the original FRC level and the point of maximum exhalation from the SVC. RV is calculated from FRC minus ERV and TLC is calculated from SVC plus RV. In this case the baseline shifted downwards during the time the shutter was closed. This means that ERV is overestimated and therefore RV and TLC are underestimated.

I measured the baseline shift to be just about 0.48 liter. Add in the fact that the SVC is 0.52 liter less than the FVC this means the TLC is underestimated by at least 1.00 liter, so the “real” TLC is at least 6.12 liters or 142% of predicted. This makes about as much sense as the FRC of 165% of predicted.

In chronic, severe airway obstruction it is possible for patients to hyperinflate and over time develop barrel chests with an elevated TLC and FRC although even when this happens a TLC of 142% of predicted is on the high side. But this is with chronic, severe airway obstruction and as you can see the patient’s FEV1 is only moderately reduced. The patient also did not physically fit the picture of chronic emphysema nor did she fit it physiologically as the DLCO was 69% of predicted. Mild to moderate COPD maybe, but not chronic severe COPD.

I will mention in passing that a barrel chest is something you’re more likely to see in a textbook these days than in your PFT Lab. Severe emphysema used to be more common than it is now. Since the Surgeon General’s report in the 1960’s there are fewer smokers and COPD is recognized much sooner than it used to be. Improved medications and supplemental oxygen has made the barrel chest a much rarer creature than when I started doing pulmonary function testing forty years ago.

Do I believe the test results? Well, the TGV measurement and therefore the FRC measurement had excellent quality so they should be correct, but as a matter of fact, no, I don’t. It just doesn’t fit the picture presented by the patient herself. What I think is happening is that TGV itself is overestimated. Plethysmography used to be considered the gold standard for lung volume measurements, but it has come to be realized that TLC is usually overestimated when there is airway obstruction and the degree of overestimation tends to correlate with the degree of obstruction.

This is because a critical assumption that is made in plethysmographic lung volume measurements is that the airway pressure measured at the mouth is representative of the pressure inside the entire lung. This is a reasonable assumption in normal lungs but when airway obstruction and gas trapping is present this is no longer the case.

Could the leak while the shutter was closed cause an overestimation of TGV? All of the TGV loops were straight, narrow and without any inflections or curves. They were also highly reproducible so I have to say this is probably not the case.

Under normal circumstances I would say that the degree of obstruction indicated by a FEV1 of 68% of predicted might elevate the TGV a bit but not significantly. In this case however, there must be something about the quality of this patient’s airway obstruction that is leading to a marked overestimation of her lung volumes.

References:

O’Donnell CR, Bankier AA, Stiebellehner L, Reilly JJ, Brown R, Loring SH. Comparison of plethysmographic and helium dilution lung volumes: Which is best for COPD? Chest 2010; 137: 1108-1115.

Rodenstein DO, Stanescu DC, Francis C. Demonstration of failure of body plethysmography in airway obstruction. J Appl Physiol 1982; 52: 949-954.

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

The ATS/ERS have published standards for most Pulmonary Function tests. These standards include the criteria that are used for assessing test quality. What these standards don’t address however, is how poor a test’s quality can be yet still be acceptable for reporting.

We’ve all had patients that aren’t able to perform tests correctly. There can be many reasons why this happens. Lack of comprehension due to cultural or language barriers. Dementia. Extreme shortness of breath. Fatigue. Neuromuscular disease. Whatever the reason, you’ve done the tests with a patient and gotten the best you think you can get, how bad do they have to be before you don’t report them?It could be argued that any test results that do not meet ATS/ERS criteria should not be accepted or reported. If this was the case, however, many of our patients would never have any test results reported at all so there has to be some leeway. An opposing argument could be that any test result should be accepted because it at least shows the minimum a patient is capable of. But because poor quality results can imply the presence of a serious lung disease when it may not actually be present there has to be a point at which results should not be accepted.

I am sure we all overlook minor faults where tests don’t meet strict ATS/ERS criteria. Spirometry efforts that aren’t six seconds long. Diffusing capacity tests with a slightly low inspired volume. Lung volume tests where the SVC is lower than the FVC.

So where do we draw the line? At one extreme there is a monthly ALS clinic that usually sends over a half dozen patients in a single morning for spirometry (upright and supine) and MIPS/MEPS to the PFT Lab I am associated with. Once ALS starts to advance patients have a great deal of difficulty performing spirometry but as long as they are willing to try we will accept whatever they can do no matter how poor the quality is.

At the other extreme should be disability evaluations or their equivalent. I haven’t been involved in these for a while but at the first hospital I worked there were probably about a dozen a year. I think this is an area where any inability to meet strict criteria for both test quality and reproducibility should carefully documented and adhered to.

But in-between there is a lot of gray. In general I think that the guidelines should be to accept and report results when for physical or neurological reasons the result is the best the patient can do; when the error does not significantly alter the interpretation (i.e. still within normal limits); or when despite the error the results rule something out that is relevant to the patient.

For example a new patient with poor quality spirometry and the FEV1 or FVC is high enough (usually within normal limits) to rule out significant airway obstruction or restriction may be acceptable. For a returning patient when the FVC or FEV1 results are (significantly) better than they were at their last visit may also be a good reason for acceptance.

For the diffusing capacity test the most common error is probably a low inspired volume. VA is dependent both on inspired volume and how well the inhaled gas mixture is diluted in the lung. If the inspired volume is low but the VA is either near the TLC or within normal limits then the DLCO can probably be accepted.

I don’t think there is a lot of wiggle room for helium dilution or nitrogen washout lung volumes though. Most errors with these tests lead to an overestimation of FRC or RV and the degree of this overestimation is always unknown. On the other hand if the FRC or RV measurement is okay but the problem is the SVC component it may be worthwhile to report the results.

Testing system software can pinpoint many quality issues but I think it is a mistake to rely on it for anything more than simple checks. For this reason anybody that performs pulmonary function testing really needs to know the quality criteria for all tests they perform and should comment on test quality in the technician notes.

The policy in the PFT Lab I am associated with is that if it can’t be reported it can’t be billed. This is not an incentive to report bad results and is in fact a reason for the technicians to be cautious. They know that once a test has been billed it is very difficult to get it un-billed so they are more likely to bring questionable results to the lab manager or to the ordering physician’s attention before reporting them.

I don’t think that it is possible to come up with firm guidelines about when to accept low quality test results. Where the line is drawn for one patient is likely not going to be in the same location as it is for another patient. At some point questionable test results will have to be passed on to a reviewer. I think that feedback from the reviewer to the technician that performed the tests is important. The more a technician knows about test quality and when results should or should not be accepted the more likely they are to be able to improve test quality in the first place.

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

Pulmonary Function testing is almost unique among medical tests in that it requires maximum effort and cooperation from the patient for quality results. The better you are able to communicate with a patient the more likely you are to be able to get good quality test results. This is one of the more interesting and the more difficult parts of being a technician.

Performing tests means being a cheerleader to some extent and over the years I’ve seen a number of different approaches. At one extreme, which thankfully I haven’t seen for a while, is what I call the “Nazi” approach which is mostly yelling and telling the patient as condescendingly as possible that they aren’t doing the test right and to do it again. At the other extreme is the “Flower Child” who is chatty, sympathetic, cheerful and can never, ever bring themselves to tell the patient they are doing anything wrong.

Neither extreme can consistently get good quality tests out of patients because neither makes an effort to explain what the tests are for, how they need to be performed and most importantly, to lead and correct the patient in a way that makes sense to the patient. The three most important rules in patient communication is first to explain everything, second to keep explaining and finally to explain some more. I’ve always found that every bit of time I spent explaining what, how and why always saved double that when it came to performing the tests.

Yes, cheerleading is important. Patients often don’t know what they are capable of without encouragement. But pulmonary function testing shouldn’t be a yelling contest. The only patients I ever got a sore throat from were the ones that were hard of hearing. Effective communication is the key to testing not volume. Keep it simple. Keep it clear. Tell the patient what they did right and be specific about what they need to improve. Saying “you can do better” doesn’t tell the patient what they are doing right or what they are doing wrong. Instead say “I’d like you to try to blow a bit longer” or “I think you can blow a bit faster”.

Being good at communication though, means that you need to really understand what you are trying to explain so you can tailor your instructions to each patient and I think this is a critical point of failure for many technicians. You need a good understanding of physiology, anatomy, physics, and pulmonary testing to be able to adapt your explanations to the needs of the patient on the fly but too many technicians, even good ones, learn the minimum to get by with and then stop trying to learn any more.

I’ve probably been spoiled since I have worked at teaching hospitals and always had access to medical journals and textbooks throughout my career. There is no excuse nowadays though, because a number of journals (Chest, American Journal of Respiratory and Critical Care Medicine, Thorax, Journal of Applied Physiology etc.) allow free on-line access to articles a year or so after their publication date and there is also PubMed and Google Scholar for searches.

I have to be honest and say that I’ve never been able to come up with a reliable way to motivate staff to keep learning. I’ve tried regular weekly and monthly classes, I’ve tried a journal club, I’ve tried handing out photocopies of articles and book chapters with a quiz, I’ve tried passing out problematic patient reports and asking “what’s wrong with this PFT?”. About the only conclusion I’ve come to is that you can’t force-feed the desire for learning. What you can do as a manager however, is to make sure your lab has an adequate procedure manual that includes tips for patient communication, make sure that all new staff sign off on the procedures and then to monitor your staff and make sure they are at least trying to communicate effectively.

I believe that technicians should also be able to talk to their patients about test results. Patients have the right to know their results and who better to discuss them than the technician that did the tests? When I first started doing pulmonary function testing however, I was never allowed to discuss results with patients. I was told that whenever asked my answer was always to be “the doctor will discuss the results with you later”.

Part of the reason for this was based in reality. The testing equipment I used at that time was entirely manual and when I was done with a set of tests all I had was several feet of kymograph paper with spirometer tracings and the gas analyzer numbers I’d written down on a worksheet. With a ruler and a calculator a full battery of tests would usually take me about 20 minutes to calculate and then hand write a report (with two layers of carbon paper in order to make copies).

The other reason though, was that medicine was still very paternalistic in the 1970’s and patients weren’t supposed to know or understand what their test results were about. The physicians I worked with at that time expected that all patient information and test results would always go through them and nobody else.

Fortunately, the physicians at the hospital I’ve worked at for the last twenty years encouraged me and the other pulmonary technicians to discuss test results with the patients. I have always appreciated this but also realize that if the PFT Lab staff were going to do this that we had a responsibility to be careful about what we said and how we said it.

When you discuss test results with a patient it is essential to keep any discussion to just the results. You can tell a patient that a reduced FEV1 means they can’t blow their air out as fast as they should but you can’t tell them that means they have asthma or emphysema even when a patient asks specifically asks if that is the case. You can tell a patient that their results are lower or higher than they were before but you don’t say that means they’re getting better or getting worse.

Interacting with patients has always been one of the fun parts of the job for me. It can also be difficult because you need to deal with people that aren’t feeling well or are scared, depressed, anxious, short of breath, or are just, well, being people. Remember, though, it’s not about you and you shouldn’t take it personally, and if you don’t like people, why are you doing this job anyway? I hope that everybody has the time and takes the time to talk with their patients and explain, explain, explain!

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

One misconception about DLCO results that I’ve heard over and over is that DLCO/VA is DLCO “adjusted” for lung volume and that using it is a way of “normalizing” DLCO for lung volume. This is not true and the information that DL/VA can give you about a patient’s lung without also considering VA as well is very limited and can be misleading.

WARNING, MATH AHEAD!

The equation for calculating DLCO is: 

This may look daunting but it has all the components that go into the DLCO test:

• VA is lung volume in ml that was observed during the test
• BHT is the breath-holding time in seconds
• 60 is the number of seconds in a minute
• Pb is barometric pressure in mmHg
• PH2O is the partial pressure of water vapor in the lung (usually assumed to be 47)
• Fitrace is the inspired fractional concentration of tracer gas (helium or methane)
• FAtrace is the expired fractional concentration of tracer gas (helium or methane)
• FICO is the inspired fractional concentrations of carbon monoxide.
• FACO is the expired fractional concentrations of carbon monoxide.

This part of the equation:

is actually the Krogh factor, or K. This has been described as the flux of CO across the alveolar membrane or the rate constant for CO uptake but it is more accurate to think of it as the rate at which the concentration of CO decreases in the lung during breath-holding. A simpler way to write the equation is therefore:

When you divide DLCO by VA what you get is:

Since BHT (breath-holding time), Pb (barometric pressure) and PH2O (the partial pressure of water vapor) are fairly constant this value is therefore primarily proportional to the Krogh factor itself. For this reason DLCO/VA tends to be referred to as KCO.

Now, let’s look into what the Krogh constant describes. During breath-holding, CO does not disappear from the lung linearly but in an exponential decay curve. This is because as CO leaves the lung the driving pressure (partial pressure across the alveolar membrane) of CO decreases.

When you plot it on a logarithmic scale you get a straight line:

KCO normally increases as lung volume decreases below TLC for several reasons. Although there is a relationship between lung volume and alveolar surface area, surface area does not decrease at the same rate as lung volume. Next, the pulmonary capillary blood volume stays relatively constant as lung volume decreases. Finally (and this appears to be a somewhat overlooked factor) when lung volume is lower there are simply fewer carbon monoxide molecules present and the concentration drops faster. For these reasons the KCO at FRC tends to be more than 150% of what it is at TLC even though DLCO at FRC tends to be less than 80% of predicted.

Since KCO varies with lung volume, it is apparent it cannot be used to either “adjust” or “normalize” DLCO for lung volume. You cannot look at KCO in isolation, you must also look at VA and when you use lung volume to assess KCO you have essentially come full circle and are looking at DLCO once again.

KCO and VA are the major components of DLCO, however. When DLCO results are abnormal inspecting KCO and VA can help determine – within limits – the reasons for the reduction. A number of schemes for doing this have been proposed but once they get outside of simple relationships they tend to break down. For example a patient with interstitial disease will tend to have a decreased VA but a normal or decreased KCO. But since VA can be reduced because of maldistribution of the inhaled test gas mixture VA and KCO are often reduced in COPD as well. To use KCO and VA effectively you need to look outside the DLCO test and consider the patient’s spirometry and lung volume results and perhaps something of the patient’s medical history as well

References:

Brusasco V, Crapo R, Viegl G.  Standardisation of the single-breath determination of carbon monoxide uptake in the lung.  Eur Respir J 2005; 26: 720-735.

Hughes JMB.  The single breath transfer factor (TL,CO) and the transfer coefficient (KCO)L a window onto the pulmonary microcirculation.  Clin Physiol & Func Im 2003; 23:63-71.

Hughes JMB, Prie ND.  In defense of the carbon monoxide transfer coefficient KCO (TL/VA)  Eur Respir J. 2001; 17: 168-174

Hughes MB, Pride NB.  Examination of the carbon monoxide diffusing capacity (DLCO) in relation to its KCO and VA compenents.  Am J Respir Crit Care Med 2012; 186: 132-139.

Lipscomb DJ, Patel K, Hughes JMB.  Interpretation of increases in the transfer coefficient for carbon monoxide (TLCO/VC or KCO).  Thorax 1978; 33: 728-733.

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

I’ve mentioned previously that the PFT Lab I am associated with recently went through a major hardware and software update. As part of this update we decided to change spirometry predicted equations to NHANESIII. The lab has used the Morris equations for at least the last 25 years and this has caused us to revisit a number of issues associated with interpretation of results, one of which is age.

The software update included the NHANESIII equation set but when we selected it we found that the software would not calculate predicted values for patients over the age of 80. The manufacturer said that this was because that was as far as the age range went in the original NHANESIII study and for this reason they could not extend it. Furthermore, their recommendation was to use the Crapo or Knudsen equations for ages above 80 because they were “more linear”.Our PFT Lab has a substantial population of patients who are older than 80 and I suspect that this is true for many other PFT Labs as well. Our decision was to use the NHANESIII equations for all ages because the study they came from has the largest number of well characterized subjects and that the results were extensively analyzed. We also felt that using a different equation set above 80 would lead to discontinuities in the predicted values.

I was able to modify the age limits imposed by the manufacturer on the NHANESIII equations but also decided to investigate the issue of age and prediction equations further.

The ATS/ERS indicates that it is the responsibility of each PFT Lab to choose for itself which equation set matches its local population but I’ve always wondered how it is possible to do this. Even if you are capable of performing an adequate statistical analysis (something I am not sure I could do), most patients seen in a pulmonary function lab are there because they are having respiratory problems and if you try to select only “normal” patients for analysis how are you determining they are “normal”? This is even more difficult when considering patients above the age of 80 because being survivors they already are, by definition, outliers.

I was able to find three studies with a subject population between the ages of 65 and 85 and entered their equations into a spreadsheet. To be able to compare them to more conventional studies I also entered the equations for NHANESIII, Knudsen and Morris and then graphed the results.

What was first evident is that patient height makes a big difference in the distribution of the predicted values. Depending on what height you are looking at, the question as to which equations produce the highest values and which produce the lowest values changes. No single equation set was always highest or always lowest. In order to look at just the effect of age I chose to look at the values from the average height for men (178 cm) and women (164 cm).

Using age 75 as a point of comparison since that is an age within all predicted sets, for males there was one equation set that was an excessively low for both FVC and FEV1 when compared to the other studies. If those results are ignored, the male FVC values clustered within 0.24 L and FEV1 clustered within 0.36 L. For females at age 75 there was both an excessively low (same set as males) and an excessively high set of equations. If those results are ignored the FVC values clustered within 0.16 L and the FEV1 clustered within 0.12 L. This at least gives an indication that these studies may not be all that different from each other. Interestingly all of the outlying male and female values were from the elder population studies.

However, although the actual FVC and FEV1 values are of course important, when judging obstruction the FEV1/FVC ratio is critical. Looking at this it is evident that the underlying equations and data sets from several studies appear to have problems. We could argue about the actual slope that the FEV1/FVC ratio takes with advancing age but a ratio that rises or remains essentially unchanged should be viewed with suspicion. As importantly, when these are taken out of the mix and the remaining ratios are considered there is actually quite a broad range of predicted ratios. The highest value for males was about 79% and the lowest was about 66%. For females the highest predicted ratio was 81% and the lowest about 68%. I find this excessively broad range of predicted FEV1/FVC ratio to be concerning, particularly for the implications it has about including or excluding a diagnosis of airway obstruction.

Is a linear equation more accurate for the elderly than one that uses exponentials and shows an increasing rate of decrease with age? Up to age 80 the NHANESIII data set shows an accelerating rate of decrease and notably Knudsen as well has a different equation for females above the age of 70 than it has below that age, and the rate of decrease is higher for the over 70 equations. All of the equations from the elder studies of spirometry are linear but that may be an aspect of the limited age range and number of subjects in each study rather than a true indication.

I am not sure that looking at the equations from the elder spirometry studies was at all helpful. These studies were limited and the results from their equation sets tended to be the outliers, both high and low. Having said that, even if the results from those equation sets are ignored there are still substantial differences in the FEV1/FVC ratio amongst the remaining equation sets. For that reason I think that anybody evaluating new equation sets should pay close attention to the predicted FEV1/FVC ratios because they showed far greater differences there than did the predicted FVC and FEV1. That doesn’t mean that a more realistic predicted FEV1/FVC ratio means that the predicted FVC and FEV1 are also realistic but I think it is a good first step.

I would also suggest avoiding the thought that any equation set that is closest to the average of other equation sets is more likely to be the “best” equation set. Given the differences in populations and the number of subjects between studies this is more like comparing apples to oranges than not.

There are professionals in our field who have spent their entire career exploring the issue of predicted values. Selection of a proper equation set is a long-standing conundrum and as it’s been said, you can’t solve a conundrum, you can only survive it. Any equation set is a line drawn in the sand and I hope that any staff involved in the review and interpretation of results realizes this. Our choice was to use the NHANESIII equation set because it is the largest and best characterized study of its kind. The PFT Lab I am associated with sees a very cosmopolitan population, with broad range of races and ethnicities and I think this was the best choice we could make. PFT Labs that see a more homogeneous population may well find a different equation set to be more appropriate.

References:

Enright P, Kronmal RA, Higgins M, Schenker M, Haponik EF. Spirometry reference values for women and men 65 to 85 years of age. Am Rev Respir Dis 1993; 147: 125-133.

Garcia-Rio F, Pino JM, Dorgham A, Villamor AJ. Spirometric reference equations for European females and males aged 65-85 years. Eur Respir J 2004; 24: 397-405.

Hankinson JL, Odencrantz JR, Fedan KB. Spirometric Reference Values from a sample of the general U.S. Population. Am J Respir Crit Care Med 1999; 159: 179-187.

Knudsen RJ, Lebowitz MD, Holberd CJ, Burrows B. Changes in the normal maximal expiratory flow-volume curve with growth and aging. Am Rev Respir Dis 1983; 127: 725-734

Morris JF, Koski A, Temple WP, Claremont A, Thomas DR. Fifteen year interval spirometric evaluation of the Oregon predictive equations. Chest 1988; 92: 123-127

Narancic NS, Pavlovic M, Zuskin E, Milicic J, Skaric-Juric T, Barbalic M, Rudan P. New reference equations for forced spirometry in elderly persons. Respir Med 2009; 103: 621-628.

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

The respiratory system is in part a mechanical pump or bellows. The Maximum Voluntary Ventilation test (MVV, aka Maximum Breathing Capacity, MBC) is intended to measure the maximum ventilation a patient is capable of. As such the results are dependent on a patient’s lung volume, respiratory muscle strength and endurance, airway resistance and overall inertia of the thoracic cage.

When I started doing PFT’s in the early 1970’s the MVV was a standard part of a complete workup. This has long since changed and I have not performed the MVV test routinely in over 25 years but I’ve always wondered what the MVV test is actually supposed be measuring in a clinical sense.

The ATS/ERS statement on spirometry recommends that the MVV test be 12 seconds long and that for optimum results the patient’s tidal volume should be approximately 50% of their VC at a respiratory rate of 90 breaths per minute. Tidal volume is accumulated during exhalation and at the end of the test the accumulated volume is then multiplied by 5. The ATS/ERS statement also suggests that MVV values that are less than FEV1 (L) x 40 indicate suboptimal patient effort.

The Maximum Voluntary Ventilation has been studied in a variety of disease states and has been shown to be reduced in upper airway obstruction, COPD, obesity, restraint position, dystonia, multiple sclerosis, diabetes, malnourishment, ALS, scoliosis, fatigue, Lupus, cervical spondylotic myelopathy, toxic chemical exposure, atrial fibrillation, polymyositis and chronic kidney failure. That MVV is reduced in these cases should not be a surprise as any reduction in lung volume, muscle strength or endurance, or any increase in airway resistance or inertia will act to limit MVV. A reduction in MVV is not specific however, and the fact that MVV is reduced does not by itself give any indication as to why it is reduced. This means that although the results may give a sense of a patient’s ventilatory status (i.e. good, fair, poor) they are not particularly diagnostic.

MVV has been most often used to evaluate maximum ventilation during cardiopulmonary exercise testing. Although it would seem that there should be a good correlation between maximum exercise ventilation and MVV this tends not to be the case. In particular MVV has been shown to be able to both under- and over-estimate Ve max in patients with airway obstruction. I think a legitimate criticism of comparing MVV and Max Ve results is that the MVV test requires the patient to adopt an artificial breathing pattern that has little relevance to actual exercise breathing patterns. At least one study has shown a higher MVV in what was termed the running position (standing, upper body angled forward 11 degrees, neck extended) when compared to the MVV performed while sitting upright. My personal experience, based on several years of performing both spirometry and MVV tests prior to CPET testing is that FEV1 x 40 is a far better predictor of Ve max than MVV.

One of my biggest concerns about the clinical use of MVV test results to monitor patient status is that patients often perform it poorly. As a technician, during the test you can try get the patient to breathe at the correct respiratory rate and tidal volume but too often I’ve seen patients either pant at very high respiratory rates and low tidal volumes or breathe slowly with very large tidal volumes. Repeated instructions and demonstrations on how to perform the test often make no difference in how well the patient is able to perform the test. In addition patients often refuse to repeat the test because of dizziness.

Although poor performance often leads to reduced MVV values I’ve also seen a number of patients with COPD get into what could best be described as a “resonance” with the testing system and produce MVV results that are well above what they should be capable of.

MVV can be be used as part of an overall assessment and has been used to evaluate patients pre- and post-operatively and pre- and post-exercise training. Because it is non-specific it cannot be a diagnostic test and because of patient performance issues it may be of limited value in monitoring patient outcomes. I strongly suspect that other non-specific multi-system tests like the 6-minute walk may be more clinically relevant than the MVV test and for these reasons I think any clinical usefulness of the MVV is quite limited.

Update:  The normal values for the MVV and the problems involved in assessing MVV test quality was discussed in Assessing MVV Quality.

References:

Bartlett RG, Phillips NE, Wolski G. Maximum voluntary ventilation prediction for the velocity-volume loop. Chest 1963; 43: 382-392

Carter R, Peavlre M, Zinkgraf S, Williams J, Fields S. Predicting maximal exercise ventilation in patients with chronic obstructive pulmonary disease. Chest 1987; 92: 253-259

Dillard TA, Hnatiuk OW, McCumber TR. Maximum Voluntary Ventilation. Spirometric determinants in chronic obstructive pulmonary disease and normal subjects. Amer Rev Resp Dis 1993; 147: 870-875

Haas F, Simnowitz M, Axen K, Gaudino D. Haas A. Effect of upper body posture on forced inspiration and expiration. J Appl Physiol 1982; 52: 879-886.

Matheson HW, Spies SN, Gray JS, arnum DR. Ventilatory Function Tests: II. Factors affecting the voluntary ventilation capacity. J Clin Invest 1950; 29: 682-687.

Miller MR, et al. ATS/ERS Task Force: Standardization of Spirometry. Eur Respir J 2005; 26: 319-338.

Pineda H, Haas F, Axen K, Haas A. Accuracy of pulmonary function tests in predicting exercise tolerance in chronic obstructive pulmonary disease. Chest 1984; 86: 564-567

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

This spirometry report came across my desk today.

                   Obs:    %Pred:    Pred:

FVC (L):         5.14     101%     5.10

FEV1(L):        4.07     105%    4.07

FEV1/FVC:     79       104%     76

On the face of it, this looks like an eminently normal spirometry test. If you look carefully at the flow-volume loop however, you will see that the inhaled volume is greater than the exhaled volume. The test system did not report the inspiratory vital capacity (FIVC) but by eyeball I would estimate the difference to be about 0.60 liters. The ATS recommends that the largest vital capacity, regardless of where it comes from should be used to calculate the FEV1/VC ratio. This means that the FEV1/FIVC ratio is actually about 70.9 not 79.2 which is 93% of predicted, not 104% and that this is probably mild airway obstruction.

This spirometry effort met all ATS/ERS criteria. It was longer than 6 seconds and met end-of-exhalation flow rate criteria. Is this gas trapping? Given the FEV1, probably not in the same way that somebody with COPD might have gas trapping, but maybe yes. The patient was 68 years old and since closing volume rises with age a certain amount of gas trapping is a normal consequence of aging and I think this may be what this spirometry effort is showing. Or, despite meeting end-of-exhalation criteria maybe the patient should have exhaled longer.

This spirometry effort also got me curious about why the test system did not report the FIVC. The PFT Lab I am associated with does not normally report FIVC. For those patients whose inspiratory flows are important we tend to look solely at the contour of the flow-volume loop and not at any specific inspiratory flow rate numbers or ratios. There were no settings in the software for FIVC and the test system’s manual did not address this issue at all so with some simple experimentation I found that it would report an FIVC only if the inspiratory effort was performed immediately following the FVC effort.

This is a point of some concern because the ATS/ERS statement on spirometry says you can perform an FIVC maneuver either before or after a forced expiratory effort and that as already mentioned the largest VC should be used for the FEV1/VC ratio. Because the software for our testing system (and I suspect many other test systems) only allows the FIVC to be measured after the FVC it is missing, at least in those cases like this one, an accurate assessment of the patient’s largest VC.

In addition, from a procedural point of view I suspect that some patients may be able to exhale further towards RV and therefore produce a larger inspiratory vital capacity when the exhalation starts with a steady exhalation from FRC than immediately after a prolonged forced expiratory effort and our test system will not allow FIVC to be measured this way.

Strictly speaking, forced inspiratory flow rates and vital capacity are not values that normally need to be measured. Inspiratory airway obstruction is much less common than expiratory airway obstruction and in addition my experience has been that patient inspiratory efforts tend to be far more variable and irreproducible than expiratory efforts. This particular spirometry effort was unusual in that the reported values were essentially normal and this kind of discrepancy between inspiratory and expiratory vital capacity is something that is more commonly seen with moderate to severe COPD.

References:

Miller MR, et al. ATS/ERS Task Force: Standardization of Spirometry. Eur Respir J 2005; 26: 319-338.

Pellegrino R, et al. ATS/ERS Task Force: Interpretive strategies for lung function tests. Eur Respir J 2005; 26: 948-968.

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