American Association for Respiratory Care's

Summer 2004

Chair & Editor
Timothy R. Myers, BS, RRT–NPS
Clinical Studies Coordinator, Dept. of Pediatrics
Rainbow Babies & Children's Hospital
Case Western Reserve University
11100 Euclid Avenue Suite 3001
Cleveland, OH 44106
(216) 844–7429
Fax (216) 844–5246
timothy.myers@uhhs.com

Co–Editors
Melissa K. Brown RCP, RRT–NPS
Instructor
Respiratory Therapy Program
Health Sciences Department
Grossmont Community College
8800 Grossmont College Dr.
El Cajon, CA 92020
619–743–4032
mkbrown@ucsd.edu

Kathleen Deakins, RRT–NPS
Rainbow Babies and Children's Hospital
11100 Euclid Ave
Cleveland OH 44110
(216) 844–1954
Fax: 216–844–5246
kathleen.deakins@uhhs.com

 

In This Issue...

Notes from the Chair Timothy R. Myers, BS, RRT–NPS
Nasal Ventilation and the Classics Douglas Petsinger, BS, RRT, RCP III
Room Air vs. Oxygen in the Delivery Room Wade Rich, RRT–NPS
Section Connection  
   
   
   
   
   
   
   
 
   
   
 
 
 
 

AARC Education Section Bulletin
AARC Education Section Bulletin

Notes from the Chair

Timothy R. Myers, BS, RRT–NPS

By the time this edition of the Bulletin comes to many of you, we will be well into the summer months and the accompanying increase in motor vehicle accidents, near–drownings, and surgical activity typical in many children’s hospitals at this time of the year. Despite this busy season, however, let me remind you of a very important task that we will need to address prior to the next edition of Bulletin: the selection of a new Specialty Practitioner of the Year (SPOY).

Every year, each of the AARC Specialty Sections sponsors a SPOY award, which is presented to the recipient at the Awards Ceremony during the AARC International Respiratory Congress (this year, in New Orleans, LA, in December). As the nomination August 31deadline for the Neonatal–Pediatric SPOY approaches, I encourage all members to brainstorm names of worthy candidates and prepare nominations for submission. Nominations may be made electronically by filling out the form on the section web site. A committee of volunteers will be assembled to assist with the selection of our SPOY. If you are interested in participating on the SPOY Committee, please send me an e–mail. SPOY Committee members will be named in an upcoming edition of the Bulletin.

The New Orleans Congress will also mark a change in leadership within the section. My term is ending, and our new chair, Michael Tracy, BS, RRT–NPS, will assume the chair for a three–year term (2005–07). Since our section had more than 1,000 members on December 31, 2003, Michael will also serve on the AARC’s Board of Directors.

As always, I want to encourage any section member who would like to contribute to the Bulletin to contact one of our co–editors, Melissa Brown or Kathy Deakins. They have worked very hard over the last several years to bring you Bulletins with exciting and clinically relevant articles.

I would also like to encourage everyone who hasn’t already joined us on the section e–mail list to do so soon. This is an excellent tool for exchanging thoughts, ideas and information with your colleagues across the country.

Now, without further ado, let’s get on with the exciting articles in this edition of the Neonatal–Pediatric Section Bulletin.

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AARC Education Section Bulletin
AARC Education Section Bulletin

Nasal Ventilation and the Classics

by Douglas Petsinger, BS, RRT, RCP III,
Sibley Heart Center, CICU, Children's Healthcare of Atlanta

A 50 kg, 19–year–old female with a surgical history of Truncus Type I defect repaired at two months of age, along with an RV–PA Conduit and Aortic Homograph requiring multiple interventions and a Pectus Excavatum repair at a later date, presented with Conduit Stenosis and underwent a replacement and Tricuspid Valve Annuloplasty with a minor complication of post–operative bleeding.  

Her initial ventilator support was minimal, although her PaO2 was 125 mm Hg on 40% and +6 cm H2O of PEEP. Once bleeding was under control on post–op day one, she was extubated to a 2 L/min nasal cannula with a PaO2 of 63 mm Hg. The morning chest film revealed LLL atelectesis, and the patient exhibited moderate hypoxemia on a 50% VM with a PaO2 of 52 mm HG on post–op day two.  

On post–op day three, her oxygen requirement worsened to a 100% requirement, with a PaO2 of 60 mm Hg and an increasing respiratory rate. Her chest film revealed left lung whiteout along with corresponding diminished–to–absent breath sounds over the left chest. She was then placed on nasal ventilation on a Drager XL ventilator (Drager Medical, Telford, PA, USA) at +8 cm H2O CPAP, + 15 cm H2O PS, and 100%. Over the next several hours the CPAP was optimized to +14 cm H2O and the PS was decreased to +3 cm H2O for triggering and comfort purposes. She tolerated a Petite nasal mask (Respironics, Inc, Murrysville, PA, USA) without evidence of breakdown. After six hours on CPAP, she was able to sit in a chair, as well as nap, without the previous symptoms of respiratory distress. The CPAP was slowly weaned over the next 24–hour period to a 5 L/min nasal cannula without compromising her oxygenation. On post–op day five she was ambulating without difficulty on a 2 L/min nasal cannula and discharged to the step–down unit.  

They say that hindsight is always 20/20. This was a classic case of refractory hypoxemia. In the second edition of Kacmarek’s “The Essentials of Respiratory Therapy,” hypoxemia is defined as inadequate quantities of oxygen in the blood. The causes range from an R–L intracardiac shunt to V/Q abnormalities to a decreased PvO2. Kacmarek then defines refractory hypoxemia as an unresponsive change in PaO2 to oxygen. Most likely, the patient had a mild reperfusion injury due to a long–term “low flow” state in the pulmonary vasculature bed that was reperfused at higher flow after the RV–PA Conduit replacement. The vascular bed needed time and an increase in intrathoracic pressure to reestablish the hydrostatic pressure gradient of the alveolar–pulmonary vascular bed. This physiology has been observed in long–term “low flow” states (conduit stenosis) and in the early post–operative lung transplantation period.  

The other question that arises from this experience is: Should endotracheal mechanical ventilation be prolonged for greater than 12 hours post–operatively for high–risk patients? The risk–benefit analysis leans towards a shorter duration of endotracheal ventilation in a post–operative cardiac patient. The argument can also be made that this physiologic phenomenon does not always occur with every patient who has a “low flow” state or a reperfusion potential.  

If refractory hypoxemia presents clinically, then a trial of nasal ventilation should be considered or attempted prior to reinstituting endotracheal mechanical ventilation. This then opens the discussion of the effectiveness of nasal ventilation compared to endotracheal mechanical ventilation. There are obviously pro and con arguments for both nasal and endotracheal ventilation. Ideally, an accurate delivery and measurement of mean airway pressure (Paw) is achievable with endotracheal ventilation. The risks for nosocomial infection are higher with endotracheal ventilation. However, the longer the patient wears a nasal mask, the greater the possibility for skin breakdown and orbital trauma. The long–term use of a nasopharyngeal airway (NPA) to deliver CPAP/PSV will also increase the risk for nares trauma and sinus infections. In both cases a sedative/analgesia must be used to decrease mental angst and trauma.  

Which modality is best? Is there a distinction between nasal and endotracheal ventilation for a positive outcome in developmental care for the neonate and younger child? The ultimate questions we should ask are, am I being proactive in my clinical choice and will this truly benefit this patient?  

A brief overview of the nasal ventilation experience  

The advent of “cradle to the grave” ventilators has enhanced the clinician’s ability to perform supportive mechanical ventilation without endotracheal intubation in some cases. These “noninvasive” capabilities may have decreased our frequency of reintubations, especially for our long–term mechanical ventilation patients. The clinician now has the ability to utilize the same modalities with either endotracheal or nasal ventilation. The indications for nasal ventilation in our specific cardiac population can be viewed as either a “bridge” from endotracheal ventilation to unassisted ventilation or a proactive attempt to avoid intubation and the possible sequella of endotracheal mechanical ventilation.  

The patient population we deal with in the CICU at the Sibley Heart Center ranges from neonates to adults, and the incidence of parenchymal lung disease is not the causative agent in the majority of patients with a cardio–respiratory failure clinical picture. The cardio–respiratory failure we deal with is more a hemodynamic–driven respiratory failure that then leads to a worsening carbon dioxide (CO2) clearance and increasing oxygen consumption (VO2). This being said, we still have a specific patient population that requires long–term endotracheal mechanical ventilation of greater than 20 days, and they then have parenchymal lung disease as well as hemodynamic issues. Specifically, our Norwood RV–PA conduit and the S/P obstructed TAPVR populations.  

Patients who fall into the category of extubation failure in the CICU can be classified as either mechanical failure or hemodynamic failure. Our observation is that if a proactive approach towards “treating” either type of extubation failure is either ignored or unrecognized then profound acidosis (metabolic and respiratory) will lead to hemodynamic collapse. The effect of acidosis on cardiac output is profound. We view mechanical failure as poor CO2 clearance due to airway edema and/or obstruction and alveolar abnormalities enhanced by peri–bronchial cuffing.  

Extubation hemodynamic failure is characterized as a rapid increase in metabolic acidosis (< –2 mEq/L), along with a profound decrease in urine output and falling transcutanous peripheral digit temperature (toe temperature). These are clinical physiologic responses to a falling cardiac output (C.O.), which is most likely related to the cardiopulmonary system’s reaction to the cessation of the after–load reducing effect of mechanical ventilation. Post extubation hemodynamic failure will also enhance the characteristics of mechanical failure as evidenced by both upper airway edema and poor CO2 clearance. Clinicians at the bedside must become observant historians of which physiological response manifested first, etc.  

The patient’s weight plays a significant role in determining which nasal ventilator we choose for “non–invasive” ventilation. For patients who weigh less than 3.5 kg, the Arabella CPAP generator (Hamilton Medical, Reno, NV, USA) is our preferred choice. We have found that the Infant NCPAP Mask (VIASYS Healthcare–Critical Care Division, Palm Springs, CA, USA) seems to perform the best, with minimal skin breakdown. The larger baby is somewhat challenging when it comes to the infant flow generator due to a need to meet an increase in flow requirements. We are pleased with the ability of the Drager Evita IV and XL (Drager Medical, Telford, PA, USA) to deliver nasal ventilation with relative ease. The nasal ventilation strategy has evolved into an optimized CPAP with a minimal amount of Pressure Support Ventilation (PSV) for triggering and patient comfort. The nasal ventilation is accomplished with a naso–pharyngeal airway (NPA) for the smaller patient (≈ 4.5 kg) or a nasal mask (Respironics, Murrysville, PA, USA).  

Our philosophy for an optimal CPAP and minimal PSV is that if you can meet the patient’s flow demands with optimal recruitment, he will tolerate nasal ventilation without a need for excessive sedation. The initial settings are CPAP +10–15 cm H2O pressure and PSV set at 3–5 cm H2O pressure. The sensitivity is set at a level for easy patient triggering without autocycling. The Drager has the ability to recognize noninvasive ventilation (NIV) as a type of patient airway. This enables the clinician to avoid “nuisance” alarms and to minimize some of the over–stimulation that the patient experiences –– and that the clinical team feels and hears. The end result is a high flow CPAP system that meets the patient’s flow requirements and increases CO2 clearance, improves oxygenation, and aids in stabilizing patient hemodynamics. This nasal ventilation strategy applies to avoiding intubation, as well as to bridging off endotracheal ventilation.  

Nasal ventilation is not a benign modality. Known complications may include skin integrity, nasal and orbital trauma, and tissue damage associated with high gas flow. Secretion clearance may be compromised. High gas flow amended with aggressive diuretic management may cause life–threatening acidosis requiring emergent airway management.  

The baby does not necessarily have to be convinced to tolerate nasal ventilation. The older child and the adult can be coerced and convinced to tolerate nasal ventilation. Parents, on the other hand, are sometimes skeptical. Questions like, “How does it feel?” or “What’s it like?” are addressed with the same analogy. It’s like sticking your head out of a car window traveling down the road at 50 or 60 MPH. Sometimes it will not bother you and other times you will just plain hate it. “Is it better than putting the breathing tube back in?” Honestly, there are advantages and disadvantages either way. Finally, there is the belief that once the endotracheal tube is out, it’s a successful extubation. The only thing we have done for the patient is removed the endotracheal tube; mechanical ventilation is still in place. Theoretically, ventilator days are still occurring and the CICU bed is still occupied by the same patient.  

Many nasal ventilation studies involving adults have been reported, with promising results. Unfortunately, the same does not hold truefor the neonatal–pediatric population. There are good data on CPAP generators used with extremely low birth weight (ELBW) infants, showing decreased length of stay and O2 requirements. The evidence for successful utilization of nasal ventilation for rescue or post–extubation management in a neonatal–pediatric CICU setting has not been available except in anecdotal form. The PICU groups are more likely to randomize therapies than the neonatal–pediatric cardiac world. We extrapolate neonatal through adult data as well. However, we find that if a therapy works, then we will use it. Why randomize? Many years ago, Barbara Wilson told me that I should randomize Nasal Assist Control Ventilation in the CICU. I’m a cardiac creature of comfort, so of course I said, “Why should I? It works!”  

Many questions come to mind regarding the utilization of nasal ventilation. Are we truly helping the patient from a physiological, infectious disease and psychological standpoint? What are the long–term effects of nasal ventilation in our younger and smaller patient populations? Is nasal ventilation more cost effective than appropriately timed intubation or extubation? Are we prolonging ICU stays? Will this work, and if not, why are we doing it? Hopefully, the establishment of data collection systems leading to an evidence–based practice model in the CICU will answer these questions.

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AARC Education Section Bulletin
AARC Education Section Bulletin

Room Air vs. Oxygen in the Delivery Room

by Wade Rich, RRT–NPS, Clinical Research Administrator, Division of Neonatology,
UCSD Medical Center, San Diego, CA

Almost all delivery room resuscitation for extremely low birth weight (ELBW) infants is performed using 100% oxygen. There have been a number of recent studies and commentaries regarding the ideal inspired oxygen (FiO2) level, and all have concluded that we are in need of further prospective studies on the use of lesser oxygen requirements for resuscitation of such infants.(1,2,3,4,5,6,7)

Vento, et al. performed a room air (RA) versus O2 resuscitation study in 106 term infants (37–40 weeks) with evidence of asphyxia, obtaining blood gases during the resuscitation. They reported that the RA infants required less ventilation to their first cry and had lower levels of superoxide dismutase at 15 minutes. They also found a significant association between the initial PaO2 obtained during resuscitation (72.2 torr vs. 126.3 torr for RA vs. O2 groups) and the enzyme activity of glutathione peroxidase, glutathione reductase, glutathione–S–transferase, and levels of oxidized glutathione.(8)  

The most recent comparison was performed by Ramji, et al who reported that the median time to first cry (2.0 versus 3.0 minutes) and median duration of resuscitation (2.0 versus 3.0 minutes) were significantly shorter in the RA group. There was no statistically significant difference in the overall or asphyxia–related mortality in the two treatment groups (12.4% and 10.0% in RA vs. 18.1% and 13.6% in O2 group).(9)  

Saugstad, et al. have recently provided a meta–analysis of the studies available comparing RA versus O2 for neonatal resuscitation. They report that the use of RA is associated with a significant decrease in mortality from 11% to 6% (p = 0.0021), with an odds ratio of .57 (95% CI .40, .81). No difference was observed for infants with a 1 minute of Apgar <4.(10) Saugstad, et al. recently reported the 18–24 month follow–up of the infants in the Resair 2 resuscitation trial. Of the original 591 enrolled infants, basic follow–up information was available for 213 of 323 surviving eligible infants from seven of the original ten centers. The authors report that there were no significant differences in neurologic handicap, somatic growth, or developmental milestones between infants who received 100% oxygen versus RA for initial resuscitation.(11)  

All these studies excluded the very premature infant. In the only randomized prospective trial to evaluate room air compared with oxygen in preterm infants, Lundstrom, et al resuscitated 66 infants of less than 33 weeks gestation who were randomized to receive either 80% O2 (36) or RA (34). They noted that two hours following delivery, the RA infants had a higher cerebral blood flow compared with O2 resuscitated infants.(12) Nine of the 34 infants (26.5%) in the RA group required O2 for resuscitation during the first ten minutes of life, none requiring more than 50% oxygen. They did not find any significant differences in short– or long–term outcomes.  

Despite mounting evidence suggesting that decreased oxygen exposure is beneficial for infants, including recent data reported from a single center that maintaining lower SpO2s from birth was associated with decreased retinopathy of prematurity,(13), no prospective study to date has looked at the option of blending oxygen during neonatal resuscitation. The use of inspired gas blenders has been standard practice in the NICU for many years, yet this option is seldom available on resuscitation beds, even when they are in an environment where both compressed air and oxygen are available.  

Pulse oximeters  

While pulse oximetry has been shown to provide useful information during the infant’s transition from fetal life (14,15,16,17,18), it is not common practice to use pulse oximeters during neonatal resuscitation. It is somewhat surprising to realize that the AARC’s 1993 Clinical Practice Guideline on Resuscitation in Acute Care Hospitals indicated that pulse oximetry should be utilized during neonatal resuscitation.(19) There is no mention of the use of pulse oximeters in the current textbook of the Neonatal Resuscitation Program, and to our knowledge pulse oximetry has not become an accepted standard of care during neonatal resuscitation.

At UCSD, we instituted the use of pulse oximeters during resuscitation over two years ago as a tool to provide continuous heart rate and a quantitative determination of oxygenation. Which are two of our previously established requirements for a well–controlled resuscitation. In reviewing resuscitations, we found that the current recommendation of intermittent heart rate checks using a stethoscope or cord palpation is inadequate for infants receiving advanced resuscitation, and that a having a team member assigned to visually indicate continuous heart rate is more helpful in assessing the benefit of any intervention. Oximeters can fulfill this function, although even with the most current generations of pulse oximeters, we have found that a useful signal is rarely available within one minute of birth in depressed infants, even when applied by a committed resuscitation team member.

The delayed time–to–function of the oximeter results from a combination of factors, including the site of application, poor perfusion, averaging algorithms, sensitivity settings, movement artifact, and sensor design and function. Our preferred site is the right hand in order to obtain a pre–ductal SpO2 value. Our current observations appear consistent with those of the previously cited work by Lundstrom, who placed a pulse oximeter on the right hand of 12 infants in each group of premature infants he studied, noting that useful information was obtained at approximately three minutes of age. He noted that SpO2 was lower in the RA infants, with values at five and seven minutes of 75% and 80%, compared with 92% and 94% in the 80% oxygen group (p < 0.001).

The use of shorter averaging intervals, maximal sensitivity, and pulse oximeters with excellent motion artifact rejection should decrease the interval between application and function of the pulse oximeter in the delivery room, while development of neonatal reflectance sensors may further improve their utility during resuscitation. Continuous palpation/auscultation of heart rate during resuscitation is vital to gauge the effects of resuscitation interventions and should continue until the pulse oximeter is operational.  

References

  1. Lefkowitz, W. Oxygen and resuscitation: Beyond the myth. Pediatrics. 2002; 109(3):517–519.
  2. McIntosh, N. High or low oxygen saturation for the preterm baby. Archives of Disease in Childhood. 2001; 84(3):F149.
  3. Friel, JK; Widness, JA; Jiang, TN; Belkhode, SL; Rebouche, CJ; Ziegler, EE. Antioxidant status and oxidant stress may be associated with vitamin E intakes in very low birth weight infants during the first month of life. Nutrition Research. 2002; 22(1–2):55–64.
  4. Saugstad, Ola and others. Oxygen toxicity in the neonatal period. Acta Pediatr Scand 1990;79: 881–92.
  5. Ramji, S; Ahuja, S; Thirupuram, S; Rootwelt, T; Rooth, G; Saugstad, OD. Resuscitation of Asphyxic Newborn Infants with Room Air or 100% Oxygen. Pediatric Research. 1993 Dec; 34(6):809–812.
  6. Vento, M; Asensi, M; Sastre, J; GarciaSala, F; Pallardo, FV; Vina, J. Resuscitation with room air instead of 100% oxygen prevents oxidative stress in moderately asphyxiated term neonates. Pediatrics. 2001; 107(4):642–647.
  7. Saugstad, OD; Rootwelt, T; Aalen, O. Resuscitation of asphyxiated newborn infants with room air or oxygen: An international controlled trial: The Resair 2 study. Pediatrics. 1998; 102(1):E11–E17.
  8. Vento, M; Asensi, M; Sastre, J; Lloret, A; Garcia–Sala, F; Vina, J. Oxidative stress in asphyxiated term infants resuscitated with 100% oxygen. J Pediatr. 2003 Mar; 142(3):240–6. (Author’s Note: This study comparing room air and oxygen for resuscitation demonstrates a relationship between the arterial oxygen levels and the measures of oxidative stress.)
  9. Ramji S; Rasaily R; Mishra PK; Narang A; Jayam S; Kapoor AN; Kambo I, Mathur A, Saxena BN. Resuscitation of asphyxiated newborns with room air or 100% oxygen at birth: a multicentric clinical trial. Indian Pediatr. 2003 Jun;40(6):510–7. (Author’s Note: The most recent trial comparing room air with oxygen for resuscitation.)
  10. Saugstad, OD; Ramji, S; Vento, M. Neonatal mortality is less in depressed infants if resuscitation is performed with ambient air instead of pure oxygen. A meta–analysis. Pediatr Res 2003;53:345A.
  11. Saugstad OD; Ramji S; Irani SF; et al. Resuscitation of Newborn Infants With 21% or 100% Oxygen: Follow–Up at 18 to 24 Months. Pediatrics 2003; 112:296–300. (Author’s Note: This is the first publication of the follow–up of infants randomized to resuscitation with either room air or oxygen and demonstrates that the outcome was similar for both groups.)
  12. Lundstrom, KE; Pryds, O; Greisen, G. Oxygen at birth and prolonged cerebral vasoconstriction in preterm infants. Archives of Disease in Childhood. 1995 Sep; 73(2 Sp. Iss.):F81–F86.
  13. Chow, LC; Wright, KW; Sola, A. Can changes in clinical practice decrease the incidence of severe retinopathy of prematurity in very low birth weight infants? Pediatrics. 2003; 111(2):339–345.
  14. Sendak, M J; Harris, A P; Donham, RT. Use of pulse oximetry to assess arterial oxygen saturation during newborn resuscitation. Crit Care Med. 1986 Aug; 14(8):739–40.
  15. Maxwell, LG; Harris, AP; Sendak, MJ; Donham, RT. Monitoring the resuscitation of preterm infants in the delivery room using pulse oximetry. Clin Pediatr 1987 Jan; 26(1):18–20.
  16. Reddy, VK; Holzman, IR; Wedgwood, JS. Pulse Oximetry Saturations in the First 6 Hours of Life in Normal Term Infants. Clinical Pediatrics. 1999 Feb; 38(2):87–92.
  17. Meier–Stauss, P; Bucher, HU; Hurlimann, R; Konig, V; Huch, R. Pulse oximetry used for documenting oxygen saturation and right–to–left shunting immediately after birth. Eur J Pediatr. 1990; 149:35.
  18. Harris, AP; Sendak, MJ; Donham, RT. Changes in arterial oxygen saturation immediately after birth in the human neonate. J Pediatr. 1986 Jul; 109(1):117–9.
  19. The American Association for Respiratory Care. Clinical practice guidelines for resuscitation in acute care hospitals. Respir Care. 1993; 38:1179–1188.

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AARC Education Section Bulletin
AARC Education Section Bulletin

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 E–mail list: Start networking with your colleagues via the section e–mail list.

Specialty Practitioner of the Year: Submit your 2004 nominations now.

Bulletin Deadlines: Winter Issue: December 10; Spring Issue: March 10; Summer Issue: June 10; Fall Issue: September 10.

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