2008 NCSRC Newsletter, Issue 1

HRMC Respiratory Therapy Department receives Practitioner of the Year award

The respiratory therapy staff at Haywood Regional Medical Center include, from left in front, Anne Frady, Sherry Crawford, Brooke Hill, Tracy Baker, Michelle Caldwell, Kathy Edwards, Angie Carver, Janice Boone, Patty Teague, Anita Cope, Bill Rodgers; not pictured, Shane Sutton, Tracy Mehaffey and Angie Medford.

The staff of Haywood Regional Medical Center's Respiratory Therapy Department has overcome adversity and for their extraordinary efforts has been recognized by the N.C. Society for Respiratory Care with the Practitioner of the Year award.

"This award has never been given to a department before," said Susan Collins, spokeswoman for the N.C. Society for Respiratory Care.

Being the first respiratory therapy department in the state to be named Practitioner of the Year was a fitting reward for a challenge that began in January with the resignation of the department's director and then continued a month later with the hospital's loss of its Medicare and Medicaid contract.

"When our hospital was in a state of uncertainty, we pulled together as a department, corrected the problems and at the same time was able to get our arterial blood gas lab recertified," said Tracy Baker, a registered respiratory therapist at HRMC.

To add to those problems, the respiratory therapy department's director had resigned in January, leaving employees to manage without a director.

Angie Carver, lead respiratory therapist for HRMC, said the award exemplifies the dedication and perseverance of each of the department's 17 employees.

"We basically had no leadership. We all had to step up and work hard," Carver said. "I think it's a great honor to be chosen for this for the entire state. It proves we have a great department," she said.

"We worked diligently to get our hospital back up and running so the community would have a hospital and would not have to travel 30 minutes or more to receive healthcare," Baker said.

Respiratory therapist Anne Frady said she is proud of the department for winning the award.

"This is what team work is all about. Tracy and Mike Puttkammer led us through a time when we would have buckled. Other respiratory departments across the state and nation were aware of the CMS situation and lent their support any way they could to help get our hospital accreditation back. Finding other jobs would have been the easiest option, but we came together and kept the hospital running for our families, our hospital family and Haywood County," Frady said.

The department had 11 employees covering two shifts during the Medicare crisis. Since then, six new employees have been added and the department has a new director - David Capraun.

"I would like to welcome our new therapists to the family," Frady said. "They chose to come and work with us and we appreciate them coming to our respiratory family."

Therapist Janice Boone said the significance of the award is it proves that Haywood County residents can receive the best care possible within their own county.

"This proves to the community that even though we are a small hospital, we are among the best respiratory therapy departments in the state," Boone said.

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Information on the Forrest M Bird Endowment

July 31, 2008

Dear Colleague,

We are contacting you about a special person being recognized for his outstanding contributions to respiratory medicine, Forrest M Bird, MD, PhD, ScD. Many of you are familiar with Dr. Bird because his inventions help you save the lives of patients daily.

The American College of Chest Physicians and The CHEST Foundation are recognizing Dr. Bird for his development of the first mass-produced mechanical ventilators for acute and chronic cardiopulmonary care. Dr. Bird invented one of the first respirators in the 1950s and has been working on ways to improve mechanical ventilation since. His TBird Ventilator Series was the world's first ventilator that moved with the patient from one clinical setting to the next without interruption. In 1970, he introduced the BABYbird respirator, which may have reduced infant mortality due to respirator problems from 70% to less than 10%. The Bird oxygen blender, developed for use with the BABYbird, is still used today to titrate the gas source for ventilators.

The CHEST Foundation has established the Forrest M. Bird, MD, PhD, ScD Endowment to honor his achievements and to support educational opportunities in mechanical ventilation for respiratory therapists and health professionals working in the area of pulmonary medicine. An endowment brochure with more details is available online.

Please consider making a donation of $25 or more to pay tribute to Dr. Bird's lifelong achievements and to benefit our patients for generations to come. You can make a tax-deductible gift online today. Or, mail your gift using the response form from the brochure.

If you have questions about the endowment, please contact Marilyn Lederer, Executive Director of The CHEST Foundation, at (847) 498-8370 or mlederer@chestnet.org. Thank you in advance for considering a donation. Together, all of us can help to build this endowment to the level it deserves.

Sincerely,

Robert C. Miglino, RRT, BSRT, MPS
President
Focus Publications, Inc.

Robert G. Johnson, MD, FCCP
President, The CHEST Foundation

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The Role Inhaled Nitric Oxide in the Management of Acute Respiratory Failure

Michael A. Gentile RRT FAARC FCCM
Associate in Research
Divisions of Pulmonary and Critical Care Medicine
Duke University Medical Center
Durham, NC USA 27710
Email: michael.gentile@duke.edu

History and Physiology

Nitric oxide is a naturally occurring substance found in the human body that acts as a neurochemical transmitter. It is also in human airways at concentrations of 10 to 100 parts per billion (ppb), in smog at10 to 1000 ppb, and 400 to 1000 parts per million (ppm) in cigarette smoke [1]. Medical dosing of inhaled nitric oxide (iNO) gas is generally 1 to 40 ppm. [2]

The role of iNO for clinical use has increased remarkably over the last decade. It was first described in 1987 as “endothelial-derived growth factor. ”[3] Since that time, iNO has been the subject of incredible study for the physiologic response in patients with impaired hemodynamics and/or gas exchange. The discovery of iNO’s role in pulmonary vascular tone led to a flood of research from basic science to large randomized clinical trials in patients of all ages, resulting in thousands of publications. In 1992, the journal Science named nitric oxide the “Molecule of the Year. ”[4] Several researchers received a Nobel Prize in Medicine and Physiology for their work with nitric oxide in 1998. [5]

So how does it work? The medical significance of iNO as a selective pulmonary vasodilator rests on its characteristic of being delivered as a gas directly to the pulmonary circulation without systemic side effects. Nitric oxide activates guanylate cyclase and converts it into cyclic guanine monophosphate (cGMP). The presence of cGMP at the smooth muscle causes relaxation. When this occurs in the pulmonary vasculature, the result is reduced pulmonary vascular resistance, redistribution of pulmonary blood flow, and a reduction in right heart work. iNO is instantly inactivated by hemoglobin, which leads to rapid results after inhalation of gas begins. As soon as nitric oxide is inhaled, pulmonary blood is redistributed to areas of the lung where ventilation is more efficient, thus improving ventilation–perfusion matching and oxygenation. [6] When iNO is delivered to better ventilated regions of the lung, blood flow is redistributed to maximize gas exchange. Once nitric oxide enters the circulation, it quickly combines with hemoglobin and forms methemoglobin preventing systemic effects and, thus, making it a selective pulmonary vasodilator. This property alone makes iNO a very appealing research topic for many pulmonary disorders.

Indications

The only FDA-approved indication for iNO is for the treatment of term neonates with hypoxic respiratory failure associated with pulmonary hypertension as a means to improve oxygenation and, therefore, avoiding Extracorporeal Membrane Oxygenation (ECMO) while improving mortality. All other uses are considered “off label.” However, many medications are used outside of their approved indication as science discovers new applications and indications for most drugs.

Important components of acute respiratory distress syndrome (ARDS) are ventilation-perfusion mismatch, intrapulmonary right-to-left-shunt, pulmonary hypertension and accompanying hypoxemia. [7, 8, 9] The rationale for delivery of iNO in ARDS patients is to reduce pulmonary hypertension and direct blood flow toward ventilated alveoli. In 1993, Rossaint et al first described improved oxygenation and reduced pulmonary artery hypertension in patients with ARDS.[10] iNO produces vasodilatation in ventilated lung units and decreases pulmonary hypertension, thereby reducing V/Q mismatch by redistributing pulmonary perfusion toward ventilated regions and enhancing oxygenation. The importance of delivering iNO to well ventilated alveoli cannot be stressed enough. Several reports show a synergistic effect of iNO and high frequency oscillatory ventilation (HFOV). [29, 30, 32] Simply stated, if the lung is not “open”, iNO is unable to enter the blood stream and vasodilatation cannot occur. HFOV utilized elevated mean airway pressures to recruit the lung and provide increased surface area for gas exchange.

Hundreds of reports have been published regarding the use of iNO in humans. These reports can be divided into many areas of interest and patient population. More than 20 clinical trials of pediatric and adult patients with ARDS treated with iNO have been published. [11-31] Generally, 60% to 80% of ARDS patients respond to iNO with a 20% improvement in oxygenation and a 10% reduction in pulmonary artery pressure. Despite these improvements in oxygenation, in randomized, controlled trials in both adult and pediatric patients with ARDS, iNO was found to have no effect on mortality or the duration of mechanical ventilation. However, the improvement in oxygenation allows for the reduction in possibly harmful ventilator settings such as high concentrations of FiO2 and elevated peak inspiratory and plateau pressures. In addition to the positive effect of iNO on pulmonary blood flow and gas exchange, iNO plays a role in other processes during ARDS, inhibiting platelet aggregation and inflammatory mediator release.

Conversely, in newborns with hypoxic respiratory failure who are ECMO candidates, multiple trials have shown positive outcomes with the use iNO. [32-35] This is an important finding due to the invasive nature and resources needed for ECMO versus iNO.

Adverse Effects.

Abrupt discontinuation of iNO can precipitate a rapid increase in intrapulmonary right to left shunting, a decrease in PaO2, and severe rebound pulmonary hypertension. The reasons for this rebound phenomenon are not entirely known, but it may relate to feedback inhibition of nitric oxide synthase activity and/or elevated endothelin-1 (ET-1) levels. With some patients, the hypoxemia and pulmonary hypertension can be worse after discontinuation of iNO then prior to instituting treatment.

Several strategies may help avoid the deleterious effects of rebound during withdrawal of iNO. First, use the lowest effective iNO dose (generally 5 ppm or less). Second, do not withdraw iNO until the patient’s clinical status improves sufficiently (FiO2 = 0.40, PEEP = 5 cm H2O, and hemodynamics optimized). Third, set the iNO dose at 1 ppm (or less) for 30 minutes to 1 hour before discontinuing. Fourth, increase the FiO2 by 0.10 when discontinuing iNO. While these are general guidelines, every patient’s iNO plan must be handled individually.

Administration of the nucleotide phosphodiesterase (PDE) inhibitor dipyridamole has been reported to prevent rebound pulmonary hypertension. It has also been suggested that the use of sildenafil, a selective inhibitor of a cGMP-specific phosphodiesterase, can improve the harmful effects related to the discontinuation of iNO. Sildenafil is reported to possibly potentiate and/or prolong the pulmonary vasodilating effects of iNO. Further studies on dipyridamole and sildenafil are warranted to evaluate their effectiveness in this clinical setting.

In the presence of oxygen, iNO is rapidly oxidized to nitrogen dioxide. To minimize production of nitrogen dioxide, both the concentration of oxygen and nitric oxide and the contact between them should be kept to the minimal amount. The Occupational Safety and Health Administration (OSHA) in 1988 set safety limits for nitrogen dioxide at 5 ppm for 8 hours. Although increased airway reactivity and parenchymal lung injury have been reported in humans with inhalation of 2 ppm or less, toxicity is unlikely with inhaled nitric oxide at less than 40 ppm. [33]

Increasing doses of iNO may lead to methemoglobinemia. [33, 36] Methemoglobinemia toxicity occurs when inhaled nitric oxide at higher doses binds with hemoglobin in red blood cells. This results in the reduction of the oxygen-carrying capacity of the blood, which in turn, decreases oxygen delivery and creates a functional anemia. The oxyhemoglobin dissociation curve is also affected and leads to a shift to the left, diminishing the release of oxygen from red blood cells to the tissues.

Methemoglobin reductase within erythrocytes converts methemoglobin to hemoglobin. The incidence of methemoglobin (metHb) is low when iNO is administered within the accepted dose range of less than 40 ppm (and usually much less than 40 ppm). It should be noted that methemoglobinemia can also be caused by other substances, including nitrates, prilocaine, benzocaine, dapsone, and metoclopramide. MetHb is reported with blood gas co-oximetry and should be monitored during iNO therapy. Normal metHb is less than 2%, and levels below 5% do not require treatment. If metHb levels are gradually increasing, a lower but still effective iNO dose may be used. If metHb levels are significant, then iNO should be discontinued, and methylene blue, which increases reduced nicotinamide adenine dinucleotide-methemoglobin reductase, should be infused. Ascorbic acid can also be used to treat methemoglobinemia.

Inhaled nitric oxide may have adverse hemodynamic effects in patients with preexisting severe left ventricular dysfunction. The acute reduction in right ventricular afterload may lead to an increase in pulmonary venous return to the left heart, thereby increasing left ventricular filling pressures and worsening pulmonary edema.

Summary and Future Direction

The role of iNO as an adjunct to mechanical ventilation in pediatric patients with ARDS remains unclear. The question remains whether to use iNO beyond its approved indication. Although iNO has scientific and physiologic merits by increasing PaO2 and reducing pulmonary artery hypertension, no study has ever demonstrated its role for improving outcomes in patients with ARDS. In selected patients, iNO may be used to minimize FiO2 and reduce lung distention pressures. The increase in PaO2 may allow for patients to overcome a critical phase of ARDS. However, the lack of evidence that iNO administration affects survival or outcome is generally not sufficient to justify use of this adjunctive therapy for most ARDS patients.

Future iNO research will further evaluate the role of iNO in lung injury and inflammation as well as other disease states. As more knowledge is gained about the interaction of iNO and the human body, new and promising therapies may emerge to treat cardiopulmonary diseases.

References

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2. Brett SJ, Hansell DM, Evans TW. Clinical correlates in acute lung injury: response to inhaled nitric oxide. Chest 1998;114:1397-1404.
3. Palmer RM, Ferrige AG, Moncada S. Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor. Nature 1987;327:524-526.
4. Koshland DE. The molecule of the year. Science 1992;258:1861.
5. Bian K, Murad F. Nitric oxide biogeneration, regulation, and relevance to human diseases. Frontiers in Bioscience 2003;8:264-278.
6. Miller CC, Miller JW. Pulmonary Vascular smooth muscle regulation: the role of inhaled nitric oxide gas. Respiratory Care 1992;37:1175-1185.
7. Kaisers U, Busch T, Deja M, Donaubauer B, Falke KJ. Selective pulmonary vasodilation in acute respiratory distress syndrome. Critical Care Medicine.2003;31:S337-342.
8. Villar J, Blazquez MA, Lubillo S, Quintana J, Manzano JL. Pulmonary hypertension in acute respiratory failure. Critical Care Medicine 1989; 17:523-526.
9. Zapol WM, Snider MT. Pulmonary hypertension in severe acute respiratory failure. New England Journal of Medicine 1977; 296:476-480.
10. Rossaint R, Falke KJ, Lopez F, Slama K, Pison U, Zapol WM. Inhaled nitric oxide for the adult respiratory distress syndrome. New England Journal of Medicine 1993;328:399-405.
11. Bigatello LM, Hurford WE, Kacmarek RM, Roberts JD Jr, Zapol WM (1994) Prolonged inhalation of low concentrations of nitric oxide in patients with severe adult respiratory distress syndrome. Effects on pulmonary hemodynamics and oxygenation. Anesthesiology 80:761–770.
12. Dellinger RP, Zimmerman JL, Taylor RW. Effects of inhaled nitric oxide in patients with acute respiratory distress syndrome: Results of a randomized, phase II trial. Critical Care Medicine 1998;26:15–23.
13. Taylor RW, Zimmerman JL, Dellinger RP. Low-dose inhaled nitric oxide in patients with acute lung injury: A randomized controlled trial. JAMA 2004;291:1603–1609.
14. Bigatello LM, Hurford WE, Kacmarek RM, Roberts JD Jr, Zapol WM. Prolonged inhalation of low concentrations of nitric oxide in patients with severe adult respiratory distress syndrome. Effects on pulmonary hemodynamics and oxygenation. Anesthesiology 1994;80:761–770.
15. Gerlach H, Pappert D, Lewandowski K, Rossaint R, Falke KJ. Long-term inhalation with evaluated low doses of nitric oxide for selective improvement of oxygenation in patients with adult respiratory distress syndrome. Intensive Care Med 1993;19:443–449.
16. Michael JR, Barton RG, Saffle JR, Mone M, Markewitz BA, Hillier K, Elstad MR, Campbell EJ, Troyer BE, Whatley RE, Liou TG, Samuelson WM, Carveth HJ, Hinson DM, Morris SE, Davis BL, Day RW. Inhaled nitric oxide versus conventional therapy: effect on oxygenation in ARDS. Am J Respir Crit Care Med 1998;157:1372–1380.
17. Gerlach H, Keh D, Semmerow A, Busch T, Lewandowski K, Pappert DM, Rossaint R, Falke KJ. Dose-response characteristics during long-term inhalation of nitric oxide in patients with severe acute respiratory distress syndrome: a prospective, randomized, controlled study. Am J Respir Crit Care Med 2003;167:1008–1015.
18. McIntyre RC, Moore FA, Moore EE, Piedalue F, Haenel JS, Fullerton DA. Inhaled nitric oxide variably improves oxygenation and pulmonary hypertension in patients with acute respiratory distress syndrome. J Trauma 1995;39:418–425.
19. Papazian L, Bregeon F, Gaillat F, Thirion X, Gainnier M, Gregoire R, Saux P, Gouin F, Jammes Y, Auffray JP. Respective and combined effects of prone position and inhaled nitric oxide in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 1998;157:580–585.
20. Krafft PP, Fridich RD, Fitzgerald D. Effectiveness of nitric oxide inhalation in septic ARDS. Chest 1996;109:486-493.
21. Mehta S, MacDonald R, Hallett DC, Lapinsky SE, Aubin M, Stewart TE. Acute oxygenation response to inhaled nitric oxide when combined with high-frequency oscillatory ventilation in adults with acute respiratory distress syndrome. Critical Care Medicine 2003;31:383-389.
22. Brett SJ, Hansell DM, Evans TW. Clinical correlates in acute lung injury: response to inhaled nitric oxide. Chest 1998;114:1397-1404.
23. Abman SH, Griebel JL, Parker DK, Schmidt JM, Swanton D, Kinsella JP. Acute effects of inhaled nitric oxide in children with severe hypoxemic respiratory failure. J Pediatr 1994;124:881–888.
24. Okamoto K, Hamaguchi M, Kukita I, Kikuta K, Sato T. Efficacy of inhaled nitric oxide in children with ARDS. Chest 1998;114:827-833.
25. Day RW, Allen EM, Witte MK. A randomized, controlled study of the 1-hour and 24-hour effects of inhaled nitric oxide therapy in children with acute hypoxemic respiratory failure. Chest 1997;112:1324-1331.
26. Goldman AP, Tasker RC, Hosiasson S, Henrichsen T, Macrae DJ. Early response to inhaled nitric oxide and its relationship to outcome in children with severe hypoxemic respiratory failure. Chest 1997;112:752-758.
27. Fioretto JR, de Moraes MA, Bonatto RC, Ricchetti SM, Carpi MF. Acute and sustained effects of early administration of inhaled nitric oxide to children with acute respiratory distress syndrome. Pediatric Critical Care Medicine 2004;5:469-474.
28. Dobyns EL. Anas NG. Fortenberry JD. Deshpande J. Cornfield DN. Tasker RC. Liu P. Eells PL. Griebel J. Kinsella JP. Abman SH. Interactive effects of high-frequency oscillatory ventilation and inhaled nitric oxide in acute hypoxemic respiratory failure in pediatrics. Critical Care Medicine. 30(11):2425-9, 2002 Nov.
29. Kinsella JP. Abman SH. High-frequency oscillatory ventilation augments the response to inhaled nitric oxide in persistent pulmonary hypertension of the newborn: Nitric Oxide Study Group. Chest. 114(1 Suppl):100S, 1998 Jul.
30. Mehta S, MacDonald R, Hullett DC, et al. Acute oxygenation response to inhaled nitric oxide when combined with high-frequency oscillatory ventilation in adults with acute respiratory distress syndrome. Crit Care Med 2003;31(2):383–389.
31. Baldauf M, Silver P, Sagy M. Evaluating the validity of responsiveness to inhaled nitric oxide in pediatric patients with ARDS: an analytic tool. Chest 2001;119:1166-1172.
32. Clark RH, Kueser TJ, Walker MW, Southgate WM, Huckaby JL, Perez JA, Roy BJ, Keszler M, Kinsella JP. Low-dose nitric oxide therapy for persistent pulmonary hypertension of the newborn. Clinical Inhaled Nitric Oxide Research Group. New England Journal of Medicine. 2000;342:469-474.
33. Davidson D, Barefield ES, Kattwinkel J, Dudell G, Damask M, Straube R, Rhines J, Chang CT. Inhaled nitric oxide for the early treatment of persistent pulmonary hypertension of the term newborn: a randomized, double-masked, placebo-controlled, dose-response, multicenter study. The I-NO/PPHN Study Group. Pediatrics 1998; 101:325-34.
34. Roberts JD Jr, Fineman JR, Morin FC 3rd, Shaul PW, Rimar S, Schreiber MD, Polin RA, Zwass MS, Zayek MM, Gross I, Heymann MA, Zapol WM. Inhaled nitric oxide and persistent pulmonary hypertension of the newborn. The Inhaled Nitric Oxide Study Group. New England Journal of Medicine 1997; 336:605-610.
35. The Neonatal Inhaled Nitric Oxide Study. Inhaled nitric oxide in full-term and nearly full-term infants with hypoxic respiratory failure. New England Journal of Medicine 1997;336:597-604.
36. Weinberger B, Laskin DL, Heck DE Laskin JD. The toxicology of inhaled nitric oxide. Toxicol Sci 2001;59:5–16.

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A Word From the President:

Congratulations on being an integral part of the greatest patient and professional advocacy group in the US for patients and their families who suffer from pulmonary and cardiac disease and those of us who treat and educate them, the American Association for Respiratory Care and its North Carolina affiliate, the North Carolina Society for Respiratory Care! I am proud to be a respiratory therapist with the opportunity to serve as the President of such an outstanding organization.

Our profession is ever-changing and continuously adaptable to every healthcare situation. It is exactly that quality which has contributed to our current position in the marketplace and which will lead us into our future. We are a group of highly skilled, well educated, credentialed, licensed healthcare providers who have dedicated our lives to helping our fellow humans breathe well. It sounds simple, doesn’t it? Air goes in, gas is exchanged and air goes out! But this terrifically complicated physiologic activity is the source of life, because in the end, we will all die from hypoxia! I thank each of you for your individual contributions to our profession and the care of those entrusted to our care!

We’ve done really well to be such a young profession. We’ve come a long way in a short time to carve ourselves out a place at the healthcare table and our future is assured, as long as we maintain our primary focus, excellence in patient care and advocacy for them and ourselves! We’ve grown from oxygen orderlies to pulmonary and cardiac professionals in only 2 generations. It hasn’t been an easy process for us and at times it has been a real fight! It still is a fight at times today, and I encourage you to work for yourselves, your profession and our patients through your professional organization, because there is power in numbers and focused effort!

This has been a busy year for our profession and this organization. We have faced challenges in homecare reimbursement with yet another round of cuts by CMS and competitive bidding which has finally hit North Carolina, challenges to our licensure from the American Academy of Sleep Medicine who has backed the introduction of bills which would virtually exclude RCPs from attaining the RPSGT credential or working in sleep centers, and challenges in acute care hospitals statewide on timely delivery of medications through inspectors from the Division of Facility Services of the North Carolina Department of Health and Human Services. As insurers and governmental agencies seek to reduce healthcare spending and reimbursement while simultaneously dumping the cost of healthcare on us, the consumers, we will continue to face these and many other challenges. To help face these challenges, the NCSRC sponsored a contingency of therapists, students and educators in the annual AARC Capitol Day where we descend on Washington to plead our case to our Representatives and Senators in a direct manner. Funds for part of this trip came from the NCSRC through your membership fees. I would urge you to get politically active and become a part of our PACT Committee. You may also get active by writing, calling or emailing your Representative or Senator at the state or national level by using the AARC’s Capitol Connection on the AARC website: www.aarc.org or via the NCSRC website: www.ncsrc.org . As far as I’m concerned, there is no excuse for not utilizing these websites to advocate for your patients and your profession! If you have used this method of communicating with our government, my sincere thanks! If you have not, I urge you to do so now!

Currently, the NCSRC represents about 35% on the respiratory therapists practicing in North Carolina. To me, this is an unacceptably low number, and this is in spite of a concerted effort over the last 2 years by our Membership Committee. If you’re reading this, you need to work to increase our membership numbers. More members equals more voices for our profession, and we can use all the voices we can muster since we are a minority in the allied healthcare field. More members also equals more funds to purchase the services of a professional lobbyist to represent our interests here in North Carolina, and we could desperately use a lobbyist! My challenge to each of you is to stop thinking membership is somebody else’s job, or the Membership Committee’s job, or the NCSRC’s job and realize it’s really YOUR job! So, let’s do this together, and do it NOW!

Our annual Symposium is coming in September and it will be another great meeting! This year and again in 2009, the Symposium will be held in Winston-Salem at the Benton Convention Center downtown. For 2010 and 2011 we will be in Wilmington at the Riverside Hilton Inn in downtown Wilmington. I look forward to seeing all of you there!

Each year it seems we lose friends, colleagues and heroes. This year has been no exception. Please take the time to honor those who have died. Honor them in a manner befitting the service they gave to us, our patients and our profession. Remember their families, their co-workers and colleagues and friends and support them as you see fit. We all leave a legacy of caring behind when we go, and it’s only right that those who survive us honor our legacy. We all are standing on the shoulders of giants in our profession, and may we never take that for granted.

It has been an honor to serve as your President this year. As Terry Smith takes over this September, give Terry all the support you can. Support the NCSRC and take an active role in whatever area you choose to participate in. Nominate someone for an office, offer to serve on a Committee, vote when the ballots come out, work to increase membership, and always have a servant attitude!

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Airway Management in the Obstetric Patient

By Scott Prater, RRT, NREMT-P
Flight Respiratory Therapist, MedCenter Air
Carolinas Medical Center
Charlotte, NC

Has anyone participated in rapid sequence intubation (RSI) of an obstetric patient, only to have them become hypoxic, have an episode of bradycardia, and the fetus have heart rate decelerations? An obstetric patient requiring advanced airway management techniques presents some very difficult issues with RSI. The leading cause of morbidity and mortality in this patient population are airway management issues relating to the inability to intubate, aspiration, unrecognized esophageal intubation, and inadequate ventilation and/or oxygenation. Failed intubations in the obstetric population are eight times greater than the normal patient population. Morbidity in this patient population is 13 times greater than the general population. Maternal disorders, including pregnancy induced hypertension (PIH) and pre-eclampsia have been proven to increase the chance that laryngeal edema might go unrecognized.

Anatomical differences in the obstetric patient can present difficulties in this patient population. Anatomical differences include weight gain, breast enlargement, engorged mucous membranes, and cephalad displacement of the stomach by the uterus. Physiological changes also present cause for concern. Obstetric patients have increased oxygen consumption (by as much as 20%), decreased functional residual capacity (FRC) and a decrease in minute ventilation (VE). Due to the decrease in FRC, these patients will present a greater risk for hypoxia and hypercarbia. The administration of narcotics may accelerate and worsen oxygen desaturation during intubation attempts. Other changes may include delayed gastric emptying, reduced esophageal sphincter tone and an increase in gastric acid production, which can increase the risk of aspiration. Aspiration pneumonia is seven times greater in these patients, resulting from increased capillary permeability, increased interstitial lung water and decreased colloid osmotic pressure. Notable changes in the cardiovascular system include an increase in cardiac output, largely due to an increase in stroke volume. There is an increase in circulating blood volume, caused by as much as a 40% increase in plasma, with a dilutional anemia present and aortocaval compression due to the gravid uterus.

Prior to intubation, application of high- flow O2 is of vital importance to assist in minimization of desaturation. To help minimize the risk for aspiration, you should also utilize the sellicks maneuver (cricoid pressure). Oral intubation is always preferred over nasal due to mucosal engorgement. If after one unsuccessful attempt, further attempts should be done with continual cricoid pressure and utilization of a different laryngoscope blade, a change in head position if able, or direct laryngoscopy by another practitioner. If unsuccessful, you should immediately move to your rescue airway; intubation should be done with the fast-track LMA. For this reason, all providers should be well trained on the use of their back-up devices. If still unable to secure airway and you are unable to BVM patient, this becomes a “can not ventilate, can not intubate patient.” At this time you should move to securing a surgical airway.

Airway management of the obstetric patient presents several important considerations. It must be strongly emphasized that the obstetric patient requiring advanced airway management techniques and RSI has a very low threshold for oxygenation and/or ventilation compromise and cardiovascular decompensation. Knowledge of the physiologic and anatomic changes present in this population, strong airway management skills and proper planning is of utmost importance in successfully managing the airway of an OB patient.

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Congenital Heart Defects

According to the National Heart Lung and Blood Institute, congenital heart defects (CHD) are the most common birth defects. CHD affects 8 of every 1000 newborns each year. These defects range from simple, that show no signs or symptoms, to complex, which can be life threatening and require urgent medical / surgical treatment. In most cases, it is unclear what causes these problems, however viral infections and ceratin drugs, both illegal and over the counter, may increase the risk.

Congenital Heart Diseases are divided into two categories, cyanotic and acyanotic. The most common cyanotic defects are Tetralogy of Fallot, Transportation of the Great Vessels, and Total Anomalous Pulmonary Venous Return (TAPVR). The biggest concern with cyanotic defects is hypoxia due to oxygenated blood shunting back to the venous system. Surgical repair is the most common treatment. Acyanotic defects include Patent Ductus Arteriosus (PDA), Atrial Septal Defect (ASD), Ventricular Septal Defect (VSD), Aortic Stenosis (AS), Pulmonary Stenosis (PS), Atrioventricular Canal Defect (A-V Canal), and Coarctation of the Aorta (Coarct). The biggest concerns with acyanotic defects are developing congestive heart failure and pulmonary hypertension due to heart pumping harder to bypass obstructions and shunts.

Early diagnosis is the key in the treatment if CHD. According to the American Family Physician magazine, one third of infants born with CHD will develop life threatening symptoms within the first few days of life and the infant mortality rate in these cases are as high as 90%. Common signs and symptoms include: cyanosis, retractions, tachypnea, rales, and difficulty feeding. A murmur may be heard, however, this is not always the case because some severe forms of CHD will not have a murmur. Once CHD is suspected, an echocardiogram should be done to confirm or rule out CHD.

Chris Pilkenton, RRT-NPS, RCP

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