Katrina Hynes, BAS, RRT, CPFT
Special Pulmonary Evaluation Laboratory
Rochester, MN 55905
Matthew J O’Brien, RRT, RPFT
Pulmonary Diagnostic Lab
University of Wisconsin Hospital and Clinics
600 Highland Ave Room E5/520
Madison, WI 53792-5772
Fax: (608) 263-7002
Jeffrey M. Haynes, RRT, RPFT
I would like to thank Katrina Hynes and Matt O’Brien for the opportunity to serve as your Bulletin editor this past year. I’m also very appreciative of the invaluable assistance and support I’ve received from Debbie Bunch. It’s been a pleasure to work with new friends from all over the country, and I look forward to working with more of you in 2015. The Diagnostics Section membership really came through with great submissions on a wide array of topics. I’d like to give a big thanks to the following authors:
Danielle Bonagura, RRT
Katrina Hynes, BAS, RRT, RPFT
Brad Knudson, RRT
Elizabeth Koch, BHS, RRT, RPFT
Matt O’Brien, MS, RRT, RPFT
Balamurugan Panneerselvam, BS, CPFT, RPSGT
Gregg Ruppel, MS, RRT, RPFT
Jennifer Weltz Horpedahl, RRT-NPS, RPFT, AE-C
Holly Wilson, RPFT
Matthew O’Brien, MS, RRT, RPFT, and Katrina Hynes, BAS, RRT
Respiratory therapists from around the globe attended AARC Congress 2014 in “the city that never sleeps” last December. Our section was privileged to have an array of talents presenting, from the profession’s giants (Jack Wanger, Susan Blonshine, and Carl Mottram, to name a few) to first-time presenters.
Our featured presentations included:
The diagnostics, sleep, and pulmonary rehabilitation Open Forum presenters did a fantastic job sharing a variety of interesting research topics as well, and as always, the vendor exhibits were a great draw, showcasing new and upcoming products.
We held our annual business meeting during the Congress too, and congratulations were issued to Ann Wilson, BS, RRT, RPFT, AE-C, on receiving the our section’s Specialty Practitioner of the Year award. (See Matt’s article in this issue for more on Ann.)
Katrina was officially introduced as the incoming chair as well. She currently serves as assistant supervisor of the pulmonary function laboratory at the Mayo Clinic in Rochester, MN, and is also an adjunct faculty member for the University of Minnesota/Mayo School of Health Sciences Respiratory Care Program and a faculty member for the NIOSH Spirometry course. She recently co-authored Chapter 5, Pulmonary Function Testing and Bedside Pulmonary Mechanics, in a text by Brian Walsh and is currently enrolled in the Executive Masters of Healthcare Administration program at the University of Minnesota.
The Diagnostic Section continues to seek out new authors for the Bulletin. This is a great venue to share your knowledge with colleagues in the field, as well as get your name out into the public. If you have a topic you feel would be of interest to fellow respiratory therapists and/or you’d enjoy the opportunity/challenge to author a Bulletin article, please contact Jeff Haynes and/or Katrina via AARConnect or the contact info listed in the masthead. We would love to mentor you through the process and help you shine!
As we enter 2015, we encourage everyone to begin planning their attendance at AARC Congress 2015 in Tampa, FL. If you plan to submit an abstract to the 2015 Open Forum, the deadline is May 1.
Matthew J. O’Brien, MS, RRT, RPFT
Congratulations to Ann Wilson, BS, RRT, RPFT, AE-C! Ann received our 2014 Specialty Practitioner of the Year award at AARC Congress 2014 in Las Vegas.
Ann is the practice manager at Wellspan Medical Group, Valley Green Family Medicine, in Felton, PA. She has a long track record of involvement in respiratory care and diagnostics. Since the start of her membership in the AARC in 1986 she has worked for York Hospital and its affiliates in respiratory and pulmonary rehabilitation, and as an advanced practitioner respiratory therapist in the pulmonary physiology lab. She is also the director of Camp Green Zone, an asthma camp for kids. In addition to her growth within her organization Ann has been an active participant in the Pennsylvania Society for Respiratory Care, where she has served as district director, secretary, president, and delegate.
As part of a Lean Project, Ann has recently improved the efficiency of the BioQC and Preventative Maintenance Program at the Wellspan York Pulmonary Physiology Lab. Among her many other accomplishments are implementing an alpha 1 antitrypsin screening program and recruiting speakers for the York Hospital Excellence in Respiratory Care Conference.
Ann is currently enrolled in the MBA program at Eastern University for Health Administration as well.
Thanks to Karen Engle, RRT, CPFT, for nominating our 2014 Diagnostics Specialty Practitioner of the Year.
Jennifer Weltz Horpedahl, RRT-NPS, RPFT, AE-C, Kadlec Regional Medical Center, Richland, WA
This tutorial is designed for use with Microsoft Excel Professional 2010. It may be used with other versions of Excel as well, although some functions may appear differently.
The chart is designed for input of one biological control value each week of the year. The spreadsheet will update the chart automatically as data are entered. Ten biological control tests are needed to start; these will be used to calculate the mean and standard deviation values. FVC headings and values are used in the tutorial, however this can be customized (FEV1, FRC, DLCO, etc.) by replacing the headings and biological control test values.
These equations can also be performed using the functions AVERAGE and STDEV.S.
When finished the spreadsheet should look like the example above.
In step 6 the weekly biological control test data will be entered. As mentioned in the instructions, the tutorial and examples refer to FVC data, but this can be customized to the value you are monitoring (FEV1, DLCO, etc.).
Left click on cell E2, hold, and drag to cell K2. To AUTOFILL the remaining cells move the cursor over the small black square in the bottom right corner. When it changes to a black + sign LEFT click the mouse, hold, and drag it down the columns to row 53 and release the mouse.
The following steps customize the chart. If you are satisfied with the chart as you see it, you may skip to step 15.
If more changes are needed, repeat the steps and adjust the numbers again.
Balamurugan Panneerselvam, BS, CPFT, RPSGT, Hamad Medical Corporation, Doha YT, Qatar
Nitric oxide (NO) produced in the upper airways can regulate several lung functions and keep the lungs free of infection. Several local and systemic factors can modify nasal NO levels, the most important being obstruction of the osteomeatal complex. Conditions that may affect exhaled and nasal NO release should be avoided, or recorded and considered during the interpretation of the data.
Ambient air: Methods that use ambient air as the gas source for the transnasal flow may introduce considerable NO concentrations (up to several hundred parts per billion) into the nasal cavity. It is conceivable that this exogenous NO may influence nasal physiology, but more importantly, reduce the gradient for NO diffusion from nasal epithelium to lumen. In any case, ambient NO should always be recorded at the time of each test and must be taken into account when assessing results.1
Circadian change: A circadian effect on nasal NO was suggest by one study,2 so it is reasonable to record the time of testing and to attempt to measure nasal NO at the same time each day when performing serial measurements.
Posture: It would seem advisable to study patients in the seated position, which is the most convenient. In one study, nasal NO was unchanged when assuming the supine posture,3 although this position increases nasal volume.4 However, NO levels are independent of nasal cavity volume.
Nasal volume: Nasal cavity volume in healthy people can vary with changes in nasal blood volume, but nasal NO levels are independent of nasal cavity volume.3,5 In another study nasal NO has been reported to be volume-dependent at low transnasal flows6 and may be affected by changes in nasal aerodynamics.7
Nasal aerodynamics: The physics of airflow through the nasal cavity could alter the sampling of nasal NO. However, at low flow rates, laminar flow patterns may predominate and certain areas of the cavity may contribute less NO to the sample.1
Physiological nasal cycle: One study indicates that an increase in nasal NO may be related to the increase in resistance that occurs during the nasal cycle.8
Age: Nasal NO concentrations in adults are not affected by aging.5,9 In children, nasal NO does not appear to be age-dependent after the age of 11 years, but for those children younger than 11 years, age may affect NO output.10
Sex: There is no effect of sex on nasal NO.5 The effects of menstrual cycle or pregnancy on nasal NO outputs are unknown, so these characteristics should be noted in the record.
Body size/surface area: When related to body weight, NO output in preterm infants was shown to be similar to adults.11 But NO output, corrected for body surface area, is higher in children younger than 11 years.12 In any case, height and weight should always be reported to allow calculations of NO output/body surface area (V̇ no/m2).
Physical exercise: Nasal NO concentrations decrease by about 50% during physical exercise and reach normal baseline concentrations in about 15-20 minutes.13,14 It is therefore prudent to refrain from exercise for one hour prior to the measurements.
Smoking: The effect of prenatal or postnatal tobacco smoke exposure on nasal NO concentration has not been investigated in children. Nasal NO concentrations are slightly lower in smokers.15,16
Drugs: Data on the effect of pharmacological substances on nasal NO output are limited. Nasal decongestants, such as oxymetazoline and xylometazoline, decrease nasal NO concentrations by about 15% and have a dose-dependent inhibitory effect on total iNOS activity in vitro.17,18 Histamine, topical and systemic steroids, and antibiotics have no effect on nasal NO concentrations in healthy persons.19
There is a profound decrease in nasal NO in the primary ciliary dyskinesia syndromes, and nasal NO may become a useful screening test for this disorder as stated previously.1 The findings in allergic rhinitis, however, have been inconsistent, and it is uncertain what role nasal NO will play in the management of this condition.1 However, several studies have indicated that nasal NO levels are increased in patients with allergic rhinitis. For example, Kharitonov and co-workers reported nasal NO levels to be 1527 ± 87 ppb in untreated patients with allergic rhinitis, whereas levels of 996 ± 39 ppb were found in healthy controls. Nasal NO has been reported to be low in nasal polyposis HIV infection, panbronchiolitis, and cystic fibrosis.1
Table: Factors Influencing Nasal NO Values
Jeffrey M. Haynes, RRT, RPFT
A 49-year-old male arrived at the PFT laboratory for a complete PFT and methacholine challenge test. The patient was a former smoker who quit in 2013. The patient reported allergies to cats, dogs, horses, pollen, grass, and trees. The patient also had a history of childhood asthma, which had been quiescent during adult life; however, recently he has experienced wheezing and chest tightness, especially with exercise and cold air exposure. The local temperature was 12° F on the day of testing. The patient was being treated with albuterol as needed, which he found to be effective in ameliorating symptoms.
Serial pre-bronchodilator spirometry values are listed below:
As shown above, FVC and FEV1 decline with repeated measurements. Flow-volume loops from effort #1 and #6 are superimposed below:
The concave nature of the smaller flow-volume loop supports the suspicion of bronchoconstriction due to deep inhalation rather than poor effort (i.e. submaximal inhalation).
Typically, the decision of which values to report is straightforward: the best FVC and FEV1. However, in this situation I chose to report the best values from the last four efforts because the yet-to-be-performed tests (sGaw, LVpleth) should be linked to the current state of ventilation, which is reflected by an FEV1 of 2.74 L. The best FEV1 of 3.28 L is reflective of a state of ventilation which no longer exists due to deep inhalation induced bronchoconstriction. Because of baseline obstruction, methacholine challenge testing wasn’t appropriate so the patient was administered bronchodilator. Pre and post bronchodilator PFT data and flow-volume loops are shown below:
My Interpretation (yes, RPFTs are capable of interpreting PFT data!):
Spirometry shows an obstructive process with FEV1 and FEV1/FVC below the lower confidence interval (CI) and z-scores less than -1.64. In addition, serial baseline spirometry data suggest deep inhalation induced bronchoconstriction. There is a significant response to bronchodilator, normalizing nearly all indices except FEV1/FVC, which remains abnormal with a z-score of slightly more negative than -1.64.
Lung Volumes show significant air trapping with the RV and RV/TLC greater than the upper CI. The air trapping is completely reversed after bronchodilator.
Specific Conductance is markedly reduced and below the lower CI. Bronchodilator increased sGaw 200%, producing a value within the normal CI range.
My Impression: The pre-test probability of asthma is greater than 50% based on a childhood asthma history, atopy, suggestive symptoms, and a favorable response to albuterol. Given the above-mentioned PFT results, the post-test probability of asthma is very high. Any suspicions of COPD or restrictive lung disease can be ruled out.
The physiology of deep inhalation is very complicated and often counterintuitive. Imaging studies have indicated that bronchoconstriction in asthma is not the diffuse, homogenous process suggested by the stethoscope. In fact, airflow obstruction in asthma is very heterogeneous and patchy. These patchy areas are referred to as ventilation defects (VDefs). The airways neighboring the VDefs actually dilate through radial traction and receive a higher proportion of ventilation. When the neighboring parenchyma is hyper-expanded by deep inhalation the unstable edges of the VDefs succumb to the pressure, extending the size of the VDef.
Other proposed mechanisms of deep inhalation bronchoconstriction include airway edema due to trans luminal negative pressure,1 relative airway-parenchymal hysteresis (reduced deflation elastic recoil),2 and amplified actin-myosin latching in airway smooth muscle due to airway remodeling.3
Recruit a new member: Know an AARC member who could benefit from section membership? Direct them to section sign-up. It’s the easiest way to add section membership to their overall membership package.
Bulletin deadlines: Winter Issue: December 1; Spring Issue: March 1; Summer Issue: June 1; Fall Issue: September 1.