Fall/Winter 2016 Adult Acute Care Bulletin

Fall/Winter 2016 Adult Acute Care Bulletin

Chair
Keith Lamb, RRT-ACCS
Adult Critical Care Supervisor
UnityPoint Health System
Des Moines, IA
keith.lamb@unitypoint.org
Editor
Joe Hylton, RRT-NPS, CPFT
Co-Editor
J. Brady Scott, MSc, RRT-ACCS, FAARC
Director of Clinical Education
Assistant Professor
Department of Cardiopulmonary Sciences
Division of Respiratory Care
Rush University
Chicago, IL 60612
Jonathan_B_Scott@rush.edu

In this issue:


ARDS & APRV: A Closer Look

Edwin Coombs, MA, RRT-NPS, ACCS, FAARC
Director of Marketing, Draeger, Inc.

Acute respiratory distress syndrome (ARDS) is reported to have a mortality rate of approximately 40%.1 The definition of ARDS has undergone several revisions based on research and a better understanding of the pathophysiology of the syndrome. In 1994, the American-European Consensus Conference (AECC) defined ARDS by establishing four key parameters: 1) acute onset, 2) P/F ratio of < 300, 3) no demonstrable left heart failure, and 4) presence of bilateral infiltrates.2 Then again in 2012, the Berlin definition included sub-stratifications to define the severity of ARDS; those being mild, moderate, and severe.3

Current practice

It is now known that improper mechanical ventilation can exacerbate ARDS-induced lung injury, leading to a secondary ventilator induced lung injury (VILI), which can significantly increase mortality. In 2000 the standard of care changed dramatically when the ARMA trial demonstrated that when clinicians limited tidal volumes to 6ml/Kg-IBW, as compared to previous tidal volume standards, there was a marked improvement of 9% in survival rates.4

However, recent analysis suggests that the absolute size of the tidal volume is not the mechanism driving VILI. Rather it has been shown that minimizing the driving pressure is the key to reducing ARDS mortality.5 Also we remain without a consensus regarding the methodology of defining the optimal level of PEEP necessary to maintain lung volume during expiration and prevent alveolar collapse and reopening with each breath.

The current understanding of an optimal lung protective strategy to minimize VILI is to open the lung and keep it open. A collaboration between Villar and Slutsky concluded that “ARDS is no longer a syndrome that must be treated, but is a syndrome that should be prevented.”6

Airway pressure release ventilation

Airway pressure release ventilation (APRV) was first described in 1987 and defined as continuous positive airway pressure (CPAP) with a brief release period while allowing the patient to breathe spontaneously throughout the respiratory cycle. APRV may be an ideal mode for the “open lung” strategy; the extended time at inspiration (i.e. CPAP) would continually recruit the lung, while minimal release time would prevent lung collapse during expiration.

Unfortunately, the settings that constitute an APRV breath have been inconsistently defined and significant variations in both clinical practice and laboratory experiments render any conclusions of APRV efficacy difficult. Variations in APRV strategies revolve around modifying the CPAP and release time durations; however, the most significant evolution of APRV has been the development of the ability to personalize the expiratory duration to precisely meet the needs of the patient’s changing lung physiology.7 This personalization is accomplished by analyzing the expiratory flow curve with each breath and adjusting expiratory duration accordingly.7

Since the initial concepts of APRV were formulated in 1987, there has been a major paradigm shift in the way in which APRV is set. Initially, settings that determined inspiratory and expiratory termination were fixed and not adjusted to an individual patient’s lung compliance. In 2005, Habashi published a novel method of setting expiratory duration based on expiratory mechanics of the slope of the expiratory flow curve.8

In humans, Putensen et al. showed that APRV with spontaneous breathing increased oxygenation, cardiac index, and pulmonary compliance with reduced sedation requirements as compared with conventional positive pressure ventilation.9 Our understanding of VILI is an evolution from a normal, homogenously ventilated lung to that of a heterogeneously ventilated lung that is characterized by collapse and edema-filled alveoli. This heterogeneity results in stress concentrators and recurrent alveolar collapse. Thus a ventilation strategy that restores or maintains homogeneity would minimize VILI and obstruct the progression of acute lung injury.10,11,12

Personalized APRV: alveolar stress and strain

As mentioned earlier, the most significant evolution of APRV has been an understanding of the need to personalize the mechanical breath that recruits alveoli, resulting in homogenous inflation of the lung, coupled with a brief release phase based on lung mechanics (expiratory curve of the flow-time waveform). The prevention of alveolar collapse and cyclical opening and closing of the alveoli prevents dynamic tissue strain.13,14 Kollish-Singule et al. conducted three micro-anatomic studies that demonstrated reduced alveolar and conducting airway micro-strain as well as increased alveolar homogeneity using a personalized APRV approach where the Tlow was set to maintain an end-expiratory flow/peak expiratory flow (EEF/PEF) ratio of 75%. Extending the EEF/PEF ratio to 10% resulted in alveolar collapse and instability.15

Clinical implications of APRV and current state

In a meta-analysis, Andrews et al. demonstrated a tenfold decrease in the incidence of ARDS as well as a threefold decrease in mortality when compared to trauma patients with similar injuries who were treated with standard of care ventilation in 15 trauma units.16

It is clear from the initial days of Stock and Downs and current reviews that the application and principle behind APRV have evolved over nearly 30 years. Although the acronym remains as “APRV” the mechanical properties of the breath are vastly different. The “personalized APRV breath approach” appears to be an exciting and novel approach to reduce the incidence of ARDS, as well as the morbidity and mortality of established ARDS.

Controversy remains

Despite recent animal laboratory studies and retrospective analysis of trauma sites, there is a lack of human trials that utilize a personalized APRV approach. This appropriately leads to questions that must be answered before a widespread change in clinical practice can be considered.

A pro-con discussion on the role of APRV has been conducted at a Respiratory Care Journal Conference. The authors and panel participants did not reference many of the contemporary research works that are enumerated in this paper.16 The published pro-con discussion focused on the technical characteristics of “fixed-APRV,” which as discussed can render a mechanical breath either protective or harmful based on current understandings of “personalizing” the mechanical breath.

APRV cannot simply be considered inverse ratio ventilation; the brief release phase (Tlow) must be set appropriately to prevent alveolar collapse. The pro/con discussion added that different manufacturers’ devices operate differently; to this there is no disagreement and clearly understanding these differences when using APRV clinically is of paramount importance. A White Paper from the AARC and UHC Respiratory Care Network provides guidance on best practices to define competency, training, and an interdisciplinary approach necessary for patient safety and improving outcomes.17

Lessons learned

The published pro/con debate also pointed out that for APRV to perform as intended and obtain the desired therapeutic goals, clinicians must set the device appropriately. However, optimal settings are critical for APRV to be lung protective, and the ability to set these optimal settings varies amongst different manufacturers’ devices.17 This is very true. Initiating and maintaining both invasive and noninvasive mechanical ventilation is a complex process. The licensed clinician must differentiate among various manufacturers, ventilator models, available modes, and breath types to determine which is appropriate for each individual patient.18 The suggestion of an evidence-based protocol or management strategy is valid, as is potentially the need to have an established nomenclature.

More study and education efforts required

Generally speaking, the ventilator management of ARDS should take into consideration the patient’s specific physiologic parameters with the objective of providing the greatest benefit with the least risk of complications. Although low tidal volume and high PEEPs have led to improved outcomes in ARDS, mortality remains high. To date, APRV remains a “tool in the toolbox” for clinicians. Further clinical trials will be required before it will be considered a mainstream treatment. Promising animal studies and retrospective reviews will continue to advance our understanding of the mechanical breath profile. Additionally, clinicians must be educated in the personalized breath approach to APRV to ensure effectiveness when the clinical decision is made to utilize this mode.

References

 

  1. Villar J. Sulemanji D. Kacmarek RM. The acute respiratory distress syndrome: incidence and mortality, has it changed? Curr Opin Crit Care 2014;20(1)3-9.
  2. Ranieri VM. Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin definition. JAMA 2012;307(23):2526-2533.
  3. Ferguson ND, Fan E, Camporata L, et al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med 2012;38910):1573-1582.
  4. Laffey JG, Kavanaugh, BP. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury. New Eng J Med 2000;343(11):812.
  5. Amato M, Meade M, et al. Driving pressure and survival in acute respiratory distress syndrome. New Eng J Med 372:747-755.
  6. Villar J, Slutsky A. Is acute respiratory distress syndrome an iatrogenic disease? Crit Care Med 2010;14(1):120.
  7. Jain S, Kollish-Singule M. et al. The 30 year evolution of airway pressure release ventilation. Intensive Care Med Exp 2016;4:11, 2.
  8. Habashi NM. Other approaches to open-lung ventilation: airway pressure release ventilation. Crit Care Med 2005;33:S228-S240.
  9. Putensen C, Zech S, et al. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Crit Care Med 2001;164;43-49.
  10. Protti A, Andreis DT, et al. Lung stress and strain during mechanical ventilation: any difference between statics & dynamics? Crit Care Med 2013;41:1046-1055.
  11. Retamal J, Bergamini BC, et al. Non-lobular atelectasis generates inflammation and structural alveolar injury in the surrounding healthy tissue during mechanical ventilation. Crit Care 2014;18:505.
  12. Caironi P, Cressoni M, et al. Lung opening and closing during ventilation of acute respiratory distress syndrome. Am J Crit Care Med 2010;181:578-586.
  13. Kollish-Singule M, Emr B., et al. Mechanical breath profile of airway pressure release ventilation: the effect on alveolar recruitment and microstrain in acute lung lnjury. JAMA Surg 2014;149:1138-1145.
  14. Kollish-Singule M, Jain S, et al. Effect of airway pressure release ventilation on dynamic alveolar heterogeneity. JAMA Surg 2016;151(1):64-72.
  15. Kollish-Singule M, Emr B, et al. APRV reduces conducing airway micro-strain in lung injury. J Am Coll Surg 2014;219:9.
  16. Andrews PL, Shiber JR, et al. Early application of APRV may reduce mortality in high-risk trauma patients: a systemic review of observational trauma ARDS literature. J Trauma Acute Care Surg 2013;75:635-641.
  17. Mirales-Cabodeveila E, Kacmarek RM. Should APRV be a primary mode in ARDS? Respir Care 2016;61:6, 761-773.
  18. Branson R, Godwin T, Hargett J, Papadakos P, Rodriguez D, Stampor L, Strickland S, AARC whitepaper “safe initiation & management of mechanical ventilation” 2016. staging.nifty-cows.flywheelsites.com.

High Flow Nasal Cannula: Simple and Effective

Meagan N. Dubosky, MS, RRT-ACCS, RRT-NPS, AE-C
Manager, Respiratory Care & Pulmonary Rehab Services, Rush Oak Park Hospital;
Assistant Professor, Rush University, Chicago, IL

The use of heated and humidified high-flow nasal cannula (HFNC) to manage patients with hypoxemia is growing in popularity. Capable of delivering up to 60 L/min, HFNC therapy can potentially exceed the patient’s inspiratory flow demands, resulting in a fixed delivery of fraction of inspired oxygen (FiO2) ranging from 0.21 to 1.0.1-3 Reports of improved patient comfort warrant clinicians to understand how to apply and manage this device.4,5 This article will explain the HFNC’s evolution, potential mechanisms of action, and use in various patient conditions. A recommended application will be suggested as well.

The history of HFNC

The use of oxygen therapy to treat hypoxemia has evolved in the past two decades.5 Low flow systems, 1-15 L/min, include the nasal cannula, simple mask, and partial/nonrebreathing mask. These devices deliver a variable FiO2 as oxygen mixes with room air being inspired by the patient. Large variance in FiO2 may occur breath to breath when the patient’s breathing pattern and peak inspiratory flow rates exceed the flow delivered by the device.1,5-7

High flow systems, such as entrainment masks, provide a more precise FiO2 than low flow systems but are less well tolerated due to mask discomfort and inadequate heat and humidification.5,8,9 A fixed FiO2 is associated with lower FiO2 settings when entraining. A targeted FiO2 of 0.40 or higher is associated with an air entrainment ratio that may not meet inspiratory flow demands.

A HFNC system combines an air/oxygen blender with an active humidity system, allowing for independent control of temperature and FiO2, and gas flow rates ranging from 2-8 L/min in infants to 16-60 L/min in adults.1,5,10 When a device delivers 60 L/min or higher, the device is considered to deliver a fixed FiO2. Typically this flow exceeds most inspiratory flow demands.10

First used in neonatal and pediatric respiratory care, HFNC is a first-line therapy for the management of respiratory distress syndrome, apnea of prematurity, hypoxic respiratory failure, and hypoxemia post extubation.5,11 HFNC is now being used for the management of patients who previously required CPAP, since low levels of positive expiratory pressure are generated. With nasal prongs now tailored to fit all adult sizes, the advantages for all patients with dyspnea and hypoxemia have increased.5,11,12

Mechanisms of action

Dead space washout: The washout of expired CO2 from anatomical dead space is reported as one of the primary mechanisms adding to the success of HFNC therapy.5,11,13 Reducing the fraction of inspired CO2 allows more FiO2 to participate in gas exchange and lower minute ventilation needs. This may result in a decreased respiratory rate and/or tidal volume, and thus, less work of breathing. Multiple animal studies and clinical trials have reported a reduction in PaCO2, tidal volume, minute ventilation, and dead space with use of HFNC.11,12

Metabolic expenditures: Decreasing the energy used by the respiratory muscles to breathe and the upper airway to condition gases may benefit those who are ill. Resistance is higher during the inspiratory phase of a breath than the expiratory phase and patients with an increased respiratory rate spend more time working to overcome this inspiratory resistance. Traditionally, CPAP splinted these airways open and normalized functional residual capacity (FRC), thus reducing the work load. It is likely that HFNC meets the flow demands and creates a positive expiratory pressure in the hypopharynx, decreasing energy used in resistive work of breathing.14,15 The nasal passage heats and humidifies well under normal conditions, but is stressed when cold, dry medical gas is administered. This issue too is resolved with the use of heated and humidified HFNC. Therefore, energy is conserved.5,11

Comfort and gas conditioning: Improved secretion clearance and patient comfort are yet another benefit of the HFNC. Unconditioned medical gas administration moves the isothermic saturation boundary further down the respiratory tract. This shift damages ciliary function and dehydrates mucosal tissue, creating retention of secretions. A study evaluating gas humidification and human airway epithelial cells found an increase in inflammatory markers following eight hours of low humidity.16 Numerous studies have also offered subjective data stating that patients better tolerated HFNC when compared to other devices, including noninvasive ventilation (NIV).1,5,11,12,17,18 Comfort often leads to compliance, and in patients refusing to wear oxygen or NIV masks, the HFNC has been shown to be more comfortable. It is less intrusive and does not inhibit the patient’s ability to eat, drink, and speak freely.19

Distending pressure: Providing distending pressure to the lungs can improve gas exchange and lung mechanics in patients with acute respiratory distress. Traditionally accomplished with CPAP, it is now being achieved with HFNC when flow rate and nasal prong sizes are appropriate.11,20 As flow increases there is a significant pressure increase, and this is exponentially enhanced with closed-mouth breathing.5,21 Parke et al. found that flows of 35 L/min created a mean nasopharyngeal airway pressure of 1.2 cm H2O (open mouth) and 2.7 cm H2O (closed mouth) in postoperative cardiac surgery adults.22 This benefit is thought to help potentially lower work and maintain airway patency.

Clinical applications: The primary indication for HFNC is to support spontaneously breathing patients with high oxygen and/or flow requirements and moderate to severe hypoxemia and increased work of breathing. Potential benefits include improved oxygenation, work of breathing, secretion clearance, and tolerance, along with avoidance of intubation. Contraindications include nasal passage abnormalities or recent nasal surgery, apnea, respiratory arrest, and hypercapnic respiratory failure requiring mechanical ventilation.9,11,12,23,24

Acute hypoxemic respiratory failure (AHRF): Hypoxemic respiratory failure (Type I) is a failure to oxygenate, while ventilatory failure (Type II) presents with the inability to clear carbon dioxide1,25 NIV is a treatment for Type II respiratory failure but data are lacking regarding NIV use in Type I or AHRF. Frat et al. recently published back to back studies exploring HFNC in this population. The first study compared HFNC, standard oxygen, and NIV in 310 patients with AHRF without hypercapnia. They found no significant difference in the primary outcome of 28 day intubation rates amongst the three devices, although the rate was higher in the NIV and standard oxygen groups. A difference was found favoring the HFNC in 90-day mortality. They also reported a benefit in intubation rates in patients with a P/F ratio of less than 200. The study team speculated that the lower mortality rate may have resulted from the overall effects of less intubation. Subjective measures of discomfort and dyspnea were highly improved in the HFNC arm.

Frat et al. also explored HFNC use alternating with NIV in AHRF, defined as a P/F ≤ 300 mm Hg with standard oxygen mask with an increased respiratory rate (> 30 breaths/min) or respiratory distress. Twenty-eight subjects were included and clinical efficacy was evaluated. The conclusion was that HFNC was better tolerated and resulted in improved oxygenation and tachypnea (mean PaO2 from 83 to 108 mm Hg). Although oxygenation with NIV (mean PaO2 from 83 to 125 mm Hg) did improve more dramatically, the improved tolerance with HFNC might serve as an alternative.23,25

Intubation: Intubation involves timeframes where the airway is occluded and oxygen delivery is interrupted. Tracheal intubation is common in the ICU and is often association with hypoxemic complications. Pre-oxygenation is routine practice but often neglected when airway protection is at risk. In a study involving 101 patients, Romain et al. compared pre-oxygenation with a nonrebreather (NRB) to HFNC during direct larygoscopy in the ICU. The use of HFNC when pre-oxygenating significantly decreased severe hypoxemia when compared with NRB during intubation. The ability to leave the device in place throughout the entire procedure potentially increased the oxygen delivery, delaying desaturation.26

Do-not-intubate: The use of NIV is common in patients at the end of life with a do-not-intubate (DNI) directive. The respiratory insufficiencies may be met with a face mask and NIV; however, there is often difficulty with mask fit and tolerance. The Mayo Clinic assessed the effectiveness of HFNC in 50 hypoxemic DNI patients with mild hypercapnia (PaCO2 < 65). Nine (18%) of the 50 subjects escalated to NIV, and the other 82% were maintained on HFNC for a median duration of 30 hours. HFNC was found to provide acceptable oxygenation and be considered as an alternative to NIV in DNI patients.18

Heart failure: Heart failure (HF) is a common cause of AHRF and is associated with poor outcomes. Patients with HF often have issues oxygenating, leading to the use of NIV and potential intubation. These therapies improve oxygenation, increase intrathoracic pressure, reduce the work of breathing, decrease preload, and are highly beneficial in HF.27

COPD: Many of the mechanisms of action for HFNC benefit COPD patients. The cornerstone treatment in this disorder is NIV, but treatment intolerance and mask discomfort are well documented. Potential benefits of HFNC include an increase in pressure and decrease in respiratory rate with high flow rates, which help to support inspiratory efforts. Positive expiratory pressures may splint open the airways, allowing a lower FRC similar to the effect associated with pursed lipped breathing. This support could lower the work of breathing while the higher flow rates flush carbon dioxide from dead space.28 The fact that FiO2 can be manipulated with HFNC therapy makes the device an option to deliver low FiO2 and high flows to COPD patients.

Delivery techniques: Physiologic response to flow and FiO2 are well studied and these are the two adjusted parameters. Flow rates in published studies have started at 30 L/min and gone up to 50 L/min.5,12,23,29 Our institution starts at a flow rate of 30 L/min and titrates in response to respiratory rate and work of breathing. This initial flow rate is increased to 60 L/min until observed respiratory distress lessens. Unless the patient is diagnosed with COPD, the FiO2 is started at 1.0 and adjusted to maintain a target saturation of 92-98%. Patients with COPD start at FiO2 of 0.50 or less and then titrate to a target saturation of 90-92%. This method has not been fully validated and further study is needed.

Nasal prong sizing is an important aspect and manufacturer guidelines and sizing tools should be followed. Typically, the nasal cannula prong diameter should be approximately half the size of the patient’s nostril for adequate delivery and potential benefit of distending pressure.

Patients receiving HFNC should be assessed often for comfort and physiologic response in the form of heart rate, respiratory rate, breath sounds, and SpO2. Flow and FiO2 should be monitored on the device along with patency of the circuit and cannula, with both being changed when visibly soiled.

Welcome addition

Use of HFNC in the adult patient population continues to evolve and is a welcome addition to the arsenal of noninvasive strategies. Patient tolerance is pivotal in the surge of usage and is likely due to the interface comfort and the heated and humidified gas. Clinicians also find the device easy to maneuver during procedures, providing a continual source of oxygen and dead space washout. Strategies for use will need to be further developed as the data from clinical trials increase.

References

  1. Schwabbauer N, Berg B, Blumenstock G, Haap M, Hetzel J, Riessen R. Nasal high-flow oxygen therapy in patients with hypoxic respiratory failure: effect on functional and subjective respiratory parameters compared to conventional oxygen therapy and non-invasive ventilation (NIV). BMC Anesthesiol 2014;14:66-2253-14-66. eCollection 2014.
  2. Ricard JD. High flow nasal oxygen in acute respiratory failure. Minerva Anestesiol 2012;78(7):836-841.
  3. Lenglet H, Sztrymf B, Leroy C, Brun P, Dreyfuss D, Ricard JD. Humidified high flow nasal oxygen during respiratory failure in the emergency department: feasibility and efficacy. Respir Care 2012;57(11):1873-1878.
  4. Rello J, Perez M, Roca O, Poulakou G, Souto J, Laborda C, et al. High-flow nasal therapy in adults with severe acute respiratory infection: a cohort study in patients with 2009 influenza A/H1N1v. J Crit Care 2012;27(5):434-439.
  5. Spoletini G, Alotaibi M, Blasi F, Hill NS. Heated humidified high-flow nasal oxygen in adults: mechanisms of action and clinical implications. Chest 2015;148(1):253-261.
  6. Wagstaff TA, Soni N. Performance of six types of oxygen delivery devices at varying respiratory rates. Anaesthesia 2007;62(5):492-503.
  7. El-Khatib MF. High-flow nasal cannula oxygen therapy during hypoxemic respiratory failure. Respir Care 2012;57(10):1696-1698.
  8. Chanques G, Constantin JM, Sauter M, Jung B, Sebbane M, Verzilli D, et al. Discomfort associated with underhumidified high-flow oxygen therapy in critically ill patients. Intensive Care Med 2009;35(6):996-1003.
  9. Kallstrom TJ, American Association for Respiratory Care (AARC). AARC Clinical Practice Guideline: oxygen therapy for adults in the acute care facility—2002 revision & update. Respir Care 2002;47(6):717-720.
  10. Sim MA, Dean P, Kinsella J, Black R, Carter R, Hughes M. Performance of oxygen delivery devices when the breathing pattern of respiratory failure is simulated. Anaesthesia 2008;63(9):938-940.
  11. Dysart K, Miller TL, Wolfson MR, Shaffer TH. Research in high flow therapy: mechanisms of action. Respir Med 2009;103(10):1400-1405.
  12. Frat JP, Brugiere B, Ragot S, Chatellier D, Veinstein A, Goudet V, et al. Sequential application of oxygen therapy via high-flow nasal cannula and noninvasive ventilation in acute respiratory failure: an observational pilot study. Respir Care 2015;60(2):170-178.
  13. Danan C, Dassieu G, Janaud JC, Brochard L. Efficacy of dead-space washout in mechanically ventilated premature newborns. Am J Respir Crit Care Med 1996;153(5):1571-1576.
  14. Miller MJ, DiFiore JM, Strohl KP, Martin RJ. Effects of nasal CPAP on supraglottic and total pulmonary resistance in preterm infants. J Appl Physiol (1985) 1990;68(1):141-146.
  15. Shepard JW, Jr, Burger CD. Nasal and oral flow-volume loops in normal subjects and patients with obstructive sleep apnea. Am Rev Respir Dis 1990;142(6 Pt 1):1288-1293.
  16. Chidekel A, Zhu Y, Wang J, Mosko JJ, Rodriguez E, Shaffer TH. The effects of gas humidification with high-flow nasal cannula on cultured human airway epithelial cells. Pulm Med 2012;2012:380686.
  17. Cuquemelle E, Pham T, Papon JF, Louis B, Danin PE, Brochard L. Heated and humidified high-flow oxygen therapy reduces discomfort during hypoxemic respiratory failure. Respir Care 2012;57(10):1571-1577.
  18. Peters SG, Holets SR, Gay PC. High-flow nasal cannula therapy in do-not-intubate patients with hypoxemic respiratory distress. Respir Care 2013;58(4):597-600.
  19. Del Sorbo L, Ferguson ND. High-flow nasal cannulae or noninvasive ventilation for management of postoperative respiratory failure. JAMA 2015;313(23):2325-2326.
  20. Riera J, Perez P, Cortes J, Roca O, Masclans JR, Rello J. Effect of high-flow nasal cannula and body position on end-expiratory lung volume: a cohort study using electrical impedance tomography. Respir Care 2013;58(4):589-596.
  21. Groves N, Tobin A. High flow nasal oxygen generates positive airway pressure in adult volunteers. Aust Crit Care 2007;20(4):126-131.
  22. Parke R, McGuinness S, Eccleston M. Nasal high-flow therapy delivers low level positive airway pressure. Br J Anaesth 2009;103(6):886-890.
  23. Frat JP, Thille AW, Mercat A, Girault C, Ragot S, Perbet S, et al. High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N Engl J Med 2015;372(23):2185-2196.
  24. Nishimura M. High-flow nasal cannula oxygen therapy in adults. J Intensive Care 2015;3(1):15-015-0084-5. eCollection 2015.
  25. Casserly B, Rounds S. Essentials in Critical Care Medicine. In: Andreoli TE, Benjamin IJ, Griggs RC, Wing EJ. Cecil Essentials of Medicine, 8th edition. Philadelphia, PA: Saunders Elsevier; 2010:259.
  26. Miguel-Montanes R, Hajage D, Messika J, Bertrand F, Gaudry S, Rafat C, et al. Use of high-flow nasal cannula oxygen therapy to prevent desaturation during tracheal intubation of intensive care patients with mild-to-moderate hypoxemia. Crit Care Med 2015;43(3):574-583.
  27. Roca O, Perez-Teran P, Masclans JR, Perez L, Galve E, Evangelista A, et al. Patients with New York Heart Association class III heart failure may benefit with high flow nasal cannula supportive therapy: high flow nasal cannula in heart failure. J Crit Care 2013;28(5):741-746.
  28. Braunlich J, Beyer D, Mai D, Hammerschmidt S, Seyfarth HJ, Wirtz H. Effects of nasal high flow on ventilation in volunteers, COPD and idiopathic pulmonary fibrosis patients. Respiration 2013;85(4):319-325.
  29. Stephan F, Barrucand B, Petit P, Rezaiguia-Delclaux S, Medard A, Delannoy B, et al. High-flow nasal oxygen vs noninvasive positive airway pressure in hypoxemic patients after cardiothoracic surgery: a randomized clinical trial. JAMA 2015;313(23):2331-2339.

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Next Bulletin Deadline: Spring Issue: February 1, 2017.