Winter 2015 Diagnostics Section Bulletin

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Notes from the Editor

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

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Highlights from AARC Congress 2014 in Las Vegas, NV

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:

• Arterial Blood Gas Quality Assurance — “Doing the Right Thing Right,” presented by the queen of quality herself, Susan Blonshine, RRT, RPFT, AE-C, FAARC
• Spirometry and Diffusion Capacity Is All You Really Need – Pro/Con, presented by Matt and Bulletin editor, Jeff Haynes, RRT, RPFT
• New ATS/ERS Recommendations for Methacholine Challenge & Mannitol Testing, presented by Jack Wanger, MS, RRT, RPFT, FAARC
• New ATS/ERS Recommendations for Field Testing, (e.g., 6-Minute Walk and Other Field Tests), presented by Carl Mottram, RRT, RPFT, FAARC
• Pulmonary Function Testing in the Elderly, presented by Jeff Haynes (who colorfully demonstrated nuances to consider when testing elderly patients!)
• Vaping: What is It and is It Safe?, presented by Ralph Stumbo, Jr., RRT, CPFT
• Are Your Patients Getting High? The Effects of Altitude on Our Patients and the Precautions They Need to Take, presented by Ralph Stumbo
• Developing a Bronchial Thermoplasy Program, presented by Tamela Carroll, RRT, RPFT

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.

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Meet Our Specialty Practitioner of the Year

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.

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Creating Levey-Jennings Charts in Excel

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.

1. Beginning with a blank Excel worksheet, the first step is to calculate the MEAN and SD (standard deviation) values.
2. To calculate the MEAN:
   • Click cell N1; in cells N1-N10 enter the ten FVC values from the biological control testing.
   • Click on cell N11 and enter the formula: =AVERAGE(N1:N10).
   • Click cell O11 and type MEAN.
3. To calculate the SD (standard deviation):
   • Click cell N12 and enter the formula: =STDEV.S(N1:N10).
   • Click cell O12 and type SD.

These equations can also be performed using the functions AVERAGE and STDEV.S.

4. In each cell listed below enter the corresponding heading:
   • Cell A1: Week
   • Cell B1: Date
   • Cell C1: FVC
   • Cell E1: MEAN
   • Cell F1: UCL (this will be the upper control limit on the chart)
   • Cell G1: LCL (this will be the lower control limit on the chart)
   • Cell H1: SD+1
   • Cell I1: SD+2
   • Cell J1: SD-1
   • Cell K1: SD-2

When finished the spreadsheet should look like the example above.

5. This step uses a function called AUTOFILL; the AUTOFILL function automatically generates a series of numbers, or copies a number into selected cells.
   • Click cell A2
   • Enter the first three numbers into the cells as directed below:
     Cell A2: 1
     Cell A3: 2
     Cell A4: 3
   • Left click cell A2, hold down the mouse and drag down to select cells A2, A3, and A4.
   • To AUTOFILL 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 column to row 53 and release the mouse.

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.).

6. In column B enter the date the biological control test was performed and enter the FVC value in column C. Leave all future entries blank.

7. The following steps will fill in our remaining columns. Click each cell listed below and enter the corresponding equation exactly:
   • Cell E2 enter the formula: =N$11
   • Cell F2 enter the formula: =N$11+(N$12*3)
   • Cell G2 enter the formula: =N$11-(N$12*3)
   • Cell H2 enter the formula: =N$11+(N$12*1)
   • Cell I2 enter the formula: =N$11+(N$12*2)
   • Cell J2 enter the formula: =N$11-(N$12*1)
   • Cell K2 enter the formula: =N$11-(N$12*2)

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.

8. To generate the chart click the Insert tab in the tool bar:
   • Click on the Line, then Graph, icons as shown below. (A blank/white rectangle will open on your screen):
        
   • Click the Select Data icon in the tool bar.
   • When the Select Data Source window opens move your cursor to cell C1.
   • Click and hold, selecting cells C1-C53.
   • Now press and hold the Ctrl key on the keyboard.
   • Move the cursor to cell E1 and click and hold, selecting cells E1 to K1 and down to row 53.
   • You should see a dotted line around the columns C, E, F, G, H, I, J, and K.
   • Click ok and the chart will appear.

9. To move the chart into its own sheet:
   • Click once on the chart, then click the Move Chart icon, located in the upper right hand corner.
   • Choose Sheet 2 in the drop down menu and click enter.

The following steps customize the chart. If you are satisfied with the chart as you see it, you may skip to step 15.

10. To remove the thin black line graph lines:
    • Click directly on one of the thin black lines. Small dots will appear on the ends of the lines.
    • Right click and click Delete.
11. To adjust the numbers on the left hand side of the chart:
    • Left click one of the numbers (a thin black rectangle with dots on the corners should surround the numbers).
    • Right click.
    • Click Format Axis.
    • In the Axis Options screen that opens, click the dot next to Fixed and enter a number slightly smaller than your LCL (Lower Control Limit)/bottom chart line.
      
    • Click Close.

If more changes are needed, repeat the steps and adjust the numbers again.

12. To customize line color:
    • Click on the line to be changed (little dots will appear on the line once selected).
    • Click the Format tab.
    • At the top of the screen click Shape Outline and select the desired color.
      
    • I prefer to change my lines as listed below. This helps to give me a visual reminder of whether or not my data are in control:
      UCL & LCL — Red
      SD+1 & SD-1 — Green
      SD+2 & SD-2 — Yellow
13. To add plot points to the data line:
    • Click the data line (this is the jagged line on the chart).
    • Right click and select Format Series Data.
    • Click Marker options.
    • Click Automatic (or if you wish to choose the marker shape, click Built In and select the shape you wish to use from the drop down).
      
    • Click Close.
    • Under the Format tab at the top of the screen click Shape Fill and select the desired color for the marker.
      
14. To add a title to the chart:
    • Click anywhere on the chart.
    • Click the Layout tab at the top of the screen.
    • Click the Chart Title icon and click Above Chart (a box containing Chart Title will appear on the chart).
      
    • Highlight “Chart Title” and type in the name of the chart.
15. To add Westgard Rules text:
    • Click the Insert tab at the top of the screen.
    • Click the Text Box icon.
      
    • Move the cursor to the right of the chart where you would like the rules to appear.
    • Click and hold the cursor and drag it over the screen. There should now be an empty white box. This is the text box.
    • Click inside the text box and type the following information:

Westgard Rules

• 1 observation exceeds the mean +/- 2 SD = Warning
• 1 observation exceeds the mean +/- 3 SD = Out of control
• 2 observations exceed the mean +/- 2 SD = Out of control
• 4 consecutive observations exceed the mean +/- 1 SD in the same direction = Out of control
• 10 consecutive observations fall on the same side of the mean = out of control

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Factors Influencing Nasal Nitric Oxide (NO) Values

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

Nasal NO in disease states

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

 

References

1. ATS/ERS Recommendations for Standardized Procedures for the Online and Offline Measurement of Exhaled Lower Respiratory Nitric Oxide and Nasal Nitric Oxide. 2005.
2. Palm JP, Graf P, Lundberg JO, Alving K. Characterization of exhaled nitric oxide: introducing a new reproducible method for nasal nitric oxide measurements. Eur Respir J 2000;16:236-241.
3. Chatkin JM, Djupesland PG, Qian W, McClean P, Furlott H, Gutierrez C, Zamel N, Haight JS. Nasal nitric oxide is independent of nasal cavity volume. Am J Rhinol 1999;13:179-184.
4. Kase Y, Hilberg O, Pedersen OF. Posture and nasal patency: evaluation by acoustic rhinometry. Acta Otolaryngol 1994;114:70-74.
5. Bartley J, Fergusson W, Moody A, Wells AU, Kolbe J. Normal adult values, diurnal variation, and repeatability of nasal nitric oxide measurement. Am J Rhinol 1999;13:401-405.
6. Rinder J, Lundberg JON, Anggaard A, Alving K, Lundberg JM. Effects of topical nasal decongestants, l-arginine and nitric oxide synthase inhibition on nasal cavity nitric oxide levels and nasal cavity volume in man. Am J Rhinol 1996;10:399-408.
7. Djupesland PG, Chatkin JM, Qian W, Cole P, Zamel N, McClean P,Furlott H, Haight JS. Aerodynamic influences on nasal nitric oxide output measurements. Acta Otolaryngol 1999;119:479-485.
8. Qian W, Sabo R, Ohm M, Haight J, Fenton R. Nasal nitric oxide and nasal cycle. Laryngoscope 2001;111:1603-1607.
9. Cobos Barroso N, Reverte Bover C, Gartner S, Linan Cortes S, Quinto Domech L. Exhaled and nasal nitric oxide in normal and asthmatic children [in Spanish]. An Esp Pediatr 1998;49:241-247.
10. Dotsch J, Demirakca S, Terbrack HG, Huls G, Rascher W, Kuhl PG. Airway nitric oxide in asthmatic children and patients with cystic fibrosis. Eur Respir J 1996;9:2537-2540.
11. Artlich A, Bush T, Lewandowsky K. Exhaled nitric oxide in preterm infants. Respir Physiol 1998;114:195-200.
12. Kharitonov SA, Robbins RA, Yates D, Keatings V, Barnes PJ. Acute and chronic effects of cigarette smoking on exhaled nitric oxide. Am J Respir Crit Care Med 1995;152:609-612.
13. Phillips CR, Giraud GD, Holden WE: Exhaled nitric oxide during exercise: Site of release and modulation by ventilation and blood flow. J Appl Physiol 1996;80:1865-1871.
14. Lundberg JON, Rinder J, Weitzberg E, Alving K: Heavy physical exercise decreases nitric oxide levels in the nasal airways in humans. Acta Physiol Scand 1997;159:51-57.
15. Olin AC, Hellgren J, Karlsson G, Ljungkvist G, Nolkrantz K, Toren K: Nasal nitric oxide and its relationship to nasal symptoms, smoking and nasal nitrate. Rhinology 1998;36:117-121.
16. Giraud GD, Nejadnik B, Kimberly B, Holden WE. Physical characteristics and gas composition of nasal air affect nasal nitric oxide release. Respir Physiol 1998;114:285-296.
17. Ferguson EA, Eccles R. Changes in nasal nitric oxide concentration associated with symptoms of common cold and treatment with a topical nasal decongestant. Acta Otolaryngol 1997;117:614-617.
18. Westerveld GJ, Voss HP, van der Hee RM, de Haan-Koelewijn GJ, den Hartog GJ, Scheeren RA, Bast A. Inhibition of nitric oxide synthase by nasal decongestants. Eur Respir J 2000;16:437-444.
19. Lundberg JON, Weitzberg E, Lundberg JM, Alving K: Nitric oxide in exhaled air. Eur Respir J 1996;9:2671-2680.

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Quarterly Case Report: Bronchoconstriction During Spirometry Testing

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, LV_pleth) 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.

Proposed mechanisms of deep inhalation induced bronchoconstriction

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

Teaching Points

• Declining spirometry values during testing may be physiologic. The technologist should be vigilant not to confuse deep inhalation-induced bronchoconstriction with poor effort since excessive repetition of spirometry efforts has the potential to worsen airflow obstruction.
• When bronchoconstriction is observed during spirometry testing, reporting the best values may be misleading, especially when these values are linked to tests that are performed after the bronchoconstriction has occurred. The best approach is to show all of the data to the interpreting physician.
• Pulmonary function data are better classified and interpreted in the context of CI ranges and z-scores than by relying solely on % predicted. Consideration of the pre-test probability of asthma should be included when assigning a post-test probability of asthma.

References

1. Burns GP, Gibson GJ. A novel hypothesis to explain the bronchoconstrictor effect of deep inspiration in asthma. Thorax 2002;57:116.
2. Lim et al. The effects of deep inhalation on maximal expiratory flow during intensive treatment of spontaneous asthmatic episodes. Am Rev Respir Dis 1989;140:340.
3. Krishnan et al. Airway smooth muscle and bronchospasm: fluctuating, fluidizing, freezing. Respir Physiol Neurobiol 2008;163:17.

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Section Connection

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.

Section discussion list: Go to the section website and click on “Discussion List” to start networking with your peers via the AARC’s social networking site, AARConnect.

Bulletin deadlines: Winter Issue: December 1; Spring Issue: March 1; Summer Issue: June 1; Fall Issue: September 1.