Numero 0 Anno 8 3 Selezione ARIR - arirassociazione.org · American Association for Respiratory Care Continuing Medical Education from International Experts AARC Educational Programs

INTERNATIONALAFFILIATE

• Numero 01

• Anno 8

• 2013

High-Flow Nasal Cannula Oxygen in Critically Ill Adults:

Bryan A Wattier RRT

Short-Term Effects of Humidification Devices onRespiratory Pattern and Arterial Blood Gases

Francois Lellouche MD PhD et al.

Selezione ARIRda e AARC Times

EDIZIONI

Copertina:Copertina_01-02 28-12-2009 15:13 Pagina 2

Jeffrey J Ward MEd RRT FAARC

During Noninvasive Ventilation

Humidified High Flow Nasal Oxygen DuringRespiratory Failure in the Emergency Department:

Hugo Lenglet MD et al.Feasibility and Efficacy

A Preliminary Randomized Controlled Trial to AssessEffectiveness of Nasal High-Flow Oxygen

Rachael L Parke MHSc et al.in Intensive Care Patients

Is Humidification Always Necessary During

Do the Nose or Lungs Know There’s a Difference?

Noninvasive Ventilation in the Hospital?Richard D Branson MSc RRT FAARC

Michael A Gentile RRT FAARC

Giancarlo

Typewritten Text

PRESIDENTE PRESIDENT AND FOUNDING MEMBER

MARTA LAZZERI

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VICE PRESIDENTE VICE PRESIDENT

ANDREA LANZA

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SEGRETERIASECRETARY

ANNA BRIVIO

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TESORIERETREASORER

ALESSIA COLOMBO

CONSIGLIERIBOARD

EMILIA PRIVITERA

GIANCARLO PIAGGI

ELISA DE MATTIA

SIMONE GAMBAZZA

FRANCESCO D'ABROSCA

SERGIO ZUFFO

CONSIGLIERI ONORARIHONORARY BOARD

ROBERTO ADONE

MONICA BASSI

ANDREA BELLONE

ITALO BRAMBILLA

DALLO STATUTO DELLA ASSOCIAZIONE

Art. 1: è costituita l’Associazione Riabilitatori dell’Insufficienza Respiratoria (A.R.I.R.).

Art. 3: l’Associazione non ha finalità di lucroe intende promuovere la prevenzione e lariabilitazione delle patologie respiratorie. Per il conseguimento dei suoi scopil’Associazione concorre a:• Diffondere in campo clinico terapeuticoe home care, la pratica della fisioterapiae riabilitazione respiratoria.• Organizzare la formazione, l’aggiornamento,il coordinamento, la promozione dello sviluppoprofessionale dei fisioterapisti con specifichecompetenze in ambito respiratorio.• Sostenere in campo scientifico e socialel’educazione e l’igiene respiratoria.• Promuovere la ricerca scientifica nel campodella fisioterapia e della riabilitazionerespiratoria.

Art. 4: sono soci le persone e gli enti cheverranno ammessi dal Consiglio e cheverseranno la quota di Associazione.

Art. 5: i soci si dividono in quattro categorie:1. soci fondatori2. soci ordinari3. soci sostenitori4. soci onorariSono soci fondatori coloro che hanno sottoscrittol’atto Costitutivo dell’Associazione e coloro i qualipur non avendo sottoscritto l’atto costitutivo siaattribuita dal Consiglio tale qualifica.Sono soci ordinari i fisioterapisti accettati dalConsiglio direttivo e che versano annualmentela quota associativa stabilita Sono soci sostenitori persone fisiche egiuridiche che intendono sostenere gli scopiche l’Associazione si prefigge. Sono soci onorari le persone e gli enti ai quali il Direttivo attribuisce tale qualifica, ritenendolein grado, per qualità, titoli o attività, di dareall’Associazione un contributo d’opera o di prestigio.

Art. 6: l’Associazione trae mezzi perconseguire i propri scopi dai contributi dei socie da ogni altro provento che le confluisca.

Art. 9: i soci hanno diritto: di partecipare alle assemblee e di usufruiredel materiale tecnico e didatticodell’Associazione, così come, in viaprioritaria, di beneficiare delle iniziativepromosse dall’Associazione,

FROM THE STATUTE OF THE ASSOCIATION:

Art.1: The Associazione Riabilitatoridell’Insufficienza Respiratoria (A.R.I.R.) wasestablished in Milan on October 25, 1989.

Art.3: PURPOSE OF THE ASSOCIATIONARIR is a no profit entity, promoting theprevention and rehabilitation of respiratorydisease. In order to do this ARIR strives to:• Promote the practice of respiratory therapyand pulmonary rehabilitation within theclinical and therapeutic fields;• Organize the training, continuing education,coordination, and the promotion and theprofessional development of physiotherapisthaving specific competencies in therespiratory fields;• Support respiratory care understanding thehygiene within the scientific and social realms;• Promote scientific research in the field ofphysiotherapy and respiratory rehabilitation.

Art. 4: All persons and entities that areaccepted by the Board of Directors and whopay the associational fee are consideredmembers.

Art. 5: There are four categoriesof membership:1. Founding members2. Regular members3. Sustaining members4. Honorary members.Those who have taken part in the signing of the associational statute and those whom,thought not having signed the statute, aredeemed valid candidates by the Board ofDirectors are founding members.Physiotherapists accepted by the Board of Directors and who pay the establishedyearly associational fee are consideredregular members.Natural and juridical persons who wish tosupport the pre-established purpose of theassociation are considered sustainingmembers.Persons and entities to which the Board of Directors deems such status appropriate,for reasons of capabilities, qualities, titles or activities able to give the Association a contribution of work or prestige, areconsidered honorary members.

Art. 6: The Association obtains the means ofcarrying out its purpose from the contributionsof its members and from any other proceedsgoing towards it.

Art. 9: MEMBER RIGHTS The members have the right to: participate at he assemblies, utilize the technical andteaching materials of the Association, as wellas enjoy, as privileged members, the benefitsof the activities promoted by the Association.

DIRETTORE RESPONSABILEEDITOR IN CHIEF

GIOVANNI OLIVA

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REDAZIONEEDITORIAL STAFF

ANTONELLA SANNITI,

RESPONSABILI SCIENTIFICISCIENTIFIC ACCOUNTEES

ENRICO CLINI,ELENA REPOSSINI

BOARD EDITORIALEEDITORIAL BOARD

ANNA BRIVIO, PAOLA CAPONE,MARTA CORNACCHIA,EMILIA PRIVITERA,MARTA LAZZERI,GIANCARLO PIAGGI,MAURIZIO SOMMARIVA,SERGIO ZUFFO

ARIR:www.arirassociazione.org

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EDITOREEDITOR

ARIR EDIZIONI

ASSOCIAZIONE RIABILITATORI

DELL’INSUFFICIENZA RESPIRATORIA

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REG. TRIBUNALE DI MILANO N.967DEL 06-07-06

Il periodico “Selezione ARIR da Respiratory

Il periodico “Selezione ARIR da RespiratoryCare e AARC Times” costituisce il secondoimpegno editoriale dell’AssociazioneRiabilitatori dell’Insufficienza Respiratoria(ARIR).Le motivazioni di questa realizzazione si delineano nell’ambito dell’attività di didattica e aggiornamento chel’associazione svolge ormai da 20 anni. È proprio realizzando corsi per Fisioterapistiin molti ospedali italiani che l’Associazioneha conosciuto direttamente quali sono i principali problemi ed ostacoli che il Fisioterapista incontra nel processocontinuo di aggiornamento in materia di Fisioterapia e Riabilitazione Respiratoria.Uno degli aspetti cruciali per mantenersi “al passo con i tempi” ,oltre a partecipare a corsi specifici, è rappresentato dallapossibilità di entrare in contatto conesperienze e realtà più evolute ma al tempo stesso applicabili alla realtàitaliana.I criteri di valutazione e monitoraggio, le tecniche operative, gli approcci e le metodiche sono ciò che il Fisioterapistadeve acquisire per incrementare l’efficaciadel suo intervento.La realtà della Fisioterapia e RiabilitazioneRespiratoria è molto diversa da paese a paese ed in particolare rispetto alla realtàamericana e questo rende l’aggiornamentoun’operazione complessa e difficoltosaoltre che onerosa.L’ARIR dagli inizi della sua costituzione si è posta tra i vari obiettivi anche quello di ridurre le difficoltà e facilitarel’aggiornamento dei Fisioterapisti Italianiorganizzando corsi e convegni a cui hainvitato e invita numerosi colleghi stranieri,esperti nei diversi ambiti della Fisioterapia e Riabilitazione Respiratoria, promuovendocosì lo scambio culturale e professionale tra le diverse realtà europee e ancheextra-europee.Con la realizzazione di “Selezione ARIR da Respiratory Care e AARC Times” l’ARIR intende rispondere ulteriormente e in modo concreto ad una esigenzacentrale della formazione: l’accesso alle pubblicazioni scientifiche. Questo periodico offre a chi si occupa di Fisioterapia e Riabilitazione Respiratoria la possibilità di accedere ad alcune dellepubblicazioni scientifiche della AmericanAssociation for Respiratory Care (AARC),selezionando quelle più vicine alla realtàitaliana. “Selezione ARIR da Respiratory Care e AARC Times” è un periodico semestraleche nasce dalla volontà congiunta di ARIR e AARC frutto dell’affiliazione delle dueAssociazioni e sarà distribuito gratuitamenteai soci ARIR e verrà pubblicato nel websitedell’Associazione www.arirassociazione.orgnello spazio riservato ai soci.

A nome del Direttivo ARIRIl Presidente ARIR

Ft Marta Lazzeri

The review “ARIR selection from Respiratory

The review "ARIR selection from RespiratoryCare and AARC Time" is the second editorialengagement of the Italian AssociazioneRiabilitatori della Insufficienza Respiratoria(ARIR)The reasons of this workmust be found in the educational and updating activity that the association has been developingfrom more than 20 years.The association has directly known, during its courses which are the principalproblems and obstacles in many italianhospitals. Above all, the necessity of acontinuous updating in physiotherapy and respiratory care.In addition to attend specific courses, one of the meaning aspect to bring up to date, is to meet more developedexperiences and reality suitable to the italian ones.The evaluation criteria and the operativetechniques are the elements that any physiotherapist must study toameliorate the efficacy of his/her job.The reality of physiotherapy andrespiratory care is very different fromcountry to country, particularly from the US one, thus making the updating a very difficult and expensive operation.From the beginning, one of ARIR objectivehas been that of making easy the updatingof the italian physiotherapists, thusorganizing events on specific topics(courses and congress). So far, manyforeign people, experts in physiotherapyand respiratory care, has been invited from ARIR with the goal of promoting the cultural and professional exchange from european and extra Europeanexperiences.With the realization of "ARIR selection from Respiratory Care and AARC Time",ARIR wants to answer in a concrete way to a principal exigence of the professionaleducation: the access to the scientificarticles.This review offers to people who areencharged in physiotherapy and respiratorycare the access to scientific articles of theAmerican Association for Respiratory Care(AARC), selecting the ones closer to theitalian reality."ARIR selection from Respiratory Care and AARC Time" is a six month review born from the ARIR and AARC agreement,and it will be distributed for free to the ARIR members and published in the ARIR website (www.ariassociazione.org) in the page reserved to its members.

From the Board of DirectorsThe President of Arir

Marta Lazzeri


Selezione ARIR da Respiratory Care e AARC Times 1

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Editorials

High-Flow Nasal Cannula Oxygen in Critically Ill Adults:Do the Nose or Lungs Know There’s a Difference?

Intra-nasal oxygen was introduced by Arbuthnot Lanein 1907, using rubber nasal catheters. This approach wasadvocated by Adrian Stokes for use in critically ill victimsof phosgene gas warfare during World War I.1 However,placement of rubber catheters into the nasal cavity (andoften removal) was quite uncomfortable and required someskill (it makes our eyes water just thinking about the pro-cedure). Nasal catheter use was gradually abandoned andreplaced by the minimally invasive nasal cannula, as it wassimple to apply and better tolerated. By 1929, Dr AlvanBarach had developed a bifurcated malleable-metal can-nula that was held in position by a cloth headband.2 To-day’s nasal cannula has evolved to be the most commonappliance for oxygen therapy; modern plastics now pro-vide soft intra-nasal prongs. Its low cost and simple tech-nology support administration with minimal training byhealthcare providers and patients and their family mem-bers. The basic cannula system includes an oxygen flowmeter, small-bore connecting tubing attached to either ablind-ended tube with elastic headband or an over-the-earlariat with under-the-chin adjustment. Permutations of thestandard device include:

• Models sized for perinatal and pediatric patients3

• Incorporation with eye glasses

• A single prong for sidestream sensing of exhaled carbondioxide4

• Reservoir systems (moustache and pendant) (used pri-marily in long-term ambulatory care)5,6

• A sensor to allow flow only on inspiratory demand (alsoused primarily in long-term ambulatory care)7

• High-flow designs for adult and perinatal/pediatric pa-tients8-10

Nasal masks have also been applied to the nose specif-ically for oxygen delivery.11 Humidification of oxygen tocannulas, for non-ambulatory low-flow applications, hastraditionally been accomplished using unheated low-flow(� 6 L/min) diffuser humidifiers (“bubblers”) despite lackof efficiency and evidence of benefit.12 There are someunheated humidifiers available with adequate humiditycharacteristics for use with a larger-bore cannula for flowsin the 6–15 L/min range (Salter Labs, Arvin, California).

Heated water systems capable of providing 100% bodyhumidity have recently been incorporated into high-flownasal cannulas (HFNCs) to preserve nasal mucosa andimprove comfort. The Vapotherm 2000i (Vapotherm,Stevensville, Maryland) uses a heater and single-use car-tridge in line with an air-oxygen blender. The mixed gasflow is independently controlled (range 1–40 L/min). Thedown side of such systems is that they add substantial costand technology to the basic cannula system.

SEE THE ORIGINAL STUDY ON PAGE 265

In this issue of RESPIRATORY CARE, Parke and colleaguespresent original research on an HFNC in an intensive careunit setting to provide supplemental oxygen to patientswith mild to moderate hypoxemic respiratory failure.13

Sixty patients were enrolled, and data were analyzed from56 patients. The patients were randomized to either HFNCor high-flow oxygen via aerosol-type face mask (HFFM),which had been their institution’s standard therapy. TheHFNC group used an Optiflow cannula with humidifica-tion by an MR880 heated humidifier (both from Fisher &Paykel Healthcare, Auckland, New Zealand). Although itwas not explicitly described, we presume that an oxygen-air blender delivered the blended source gases to the can-nula. They used a face mask designed for high-flow aero-sol applications (Hudson RCI, Research Triangle Park,North Carolina). Oxygen from a flow meter was mixedusing a “venturi” air entrainer and they used a humidifiersystem similar to that used with the HFNC (MR850, Fisher& Paykel Healthcare, Auckland, New Zealand). Both hu-midifiers were equipped with similar heated-wire corru-gated tubing devices.

The study objective was to determine if HFNC wouldbe better tolerated and/or result in fewer treatment failuresthan HFFM. Treatment failure was defined as worseningrespiratory failure that required a change in the deviceproviding respiratory support within 24 hours of studyenrollment.13

Respiratory therapists and physicians have benefited froma growing collection of medical literature supporting evi-dence-based guidelines and decision-making pathways formedical gas therapy. Guidelines are currently available forpatients in general wards, emergency departments, and inten-


sive care units.14,15 Parke and colleagues are to be congratu-lated for a lucid evaluation of an alternative oxygen-deliverydevice compared to previous standard therapy for patientswith mild to moderate hypoxemia. All too frequently, appli-cation of new therapy is based on administrative decisions,without using research to guide clinical practice.

An evidence-based and comprehensive approach for rec-ommending supplemental oxygen and then (if needed) toinitially select a specific oxygen-delivery appliance can becomplex. The determination requires evaluation of the pa-tient scenario, age, preexisting medical conditions, treat-ment setting, technical limitations, cost constraints, andissues related to convenience. Often, institutional traditionor protocols are imposed. Assessment of hypoxemic re-spiratory failure is often complicated by cardiovasculardisease or neuromuscular disorders, either or both of whichmay cause hypercapnic failure that requires mechanicalventilatory support. In addition, treatment also necessitateselucidating the pathophysiologic cause of the hypoxemia,which is often only determined by response to initial ther-apy. Hypoxemia from pulmonary pathology with predom-inant right-to-left pulmonary shunting tends to respondpoorly to only increasing the FIO2

. Noninvasive continuouspositive airway pressure (CPAP) (during spontaneousbreathing) or applied PEEP (during mechanical ventila-tion) may be needed to elevate PaO2

and saturation. As theParke study notes in the discussion section, changing theoxygen-therapy device from a protocol or escalating ther-apy is tempered by both clinical judgment of objectivepatient data and subjective decision making.

After reading the Parke paper, the following questionshould be reviewed as clinicians put the study into per-spective and for further consideration when incorporatingHFNC into their armamentarium of oxygen-delivery ap-pliances: did the study attend to the hypotheses that HFNCwould be better tolerated and result in fewer treatmentfailures than HFFM?

Treatment failure was defined as worsening respiratoryfailure necessitating changing either device within 24 hoursof initiating oxygen therapy. Parke et al acknowledge thatthe clinicians were not held to strict criteria for identifyingworsening respiratory failure. A combination of clinicalfindings, in no particular order, made up the clinicians’decision tree: dyspnea; fatigue; worsening gas exchange;and intolerance of the oxygen-delivery appliance.

An independent analysis of patient tolerance is a diffi-cult task. It is dependent on a patient’s perception of com-fort in wearing a medical device. There may be individualbias in wearing a nasal versus facial appliance that mayhave nothing to do with their sensation of dyspnea butrelate to problems in claustrophobia, communication, ororal access. A study by Roca and colleagues analyzedtolerability based on patient perceptions of comfort, mu-cosal drying (“dry mouth”), and dyspnea during a com-

parison of HFNC versus oxygen mask.16 No numericalcomfort scale survey was performed as part of the Parkeet al study, similar to patients’ subjective perception ofpain on a visual analog 0–10 scale.

It would appear that the 60 subjects in the study byParke et al13 were selected randomly from a cardiothoracicand vascular intensive care unit. Their Table 1 suggeststhat the patients were tachypneic and required more than4 L/min via cannula or 6 L/min via oxygen mask. For thepurposes of the study design, the randomization was toeither HFNC or HFFM, although neither of the devicesmay have been able to meet the FIO2

and/or inspiratoryflow requirements.

The ranges of hypoxemia and respiratory breathing fre-quency were substantial. Based on one standard deviation,the room air PaO2

range was 56–88 mm Hg in the HFNCgroup and 62–92 mm Hg in the HFFM group. Of interestis the lack of significant difference between the 2 groupsin their PaO2

/FIO2ratios during the first 4 hours of oxygen

administration. Although the mean respiratory rates weresimilar, the upper level of one standard deviation for bothgroups exceeded 25 breaths/min.

One of the most interesting findings in the Parke et alstudy was the frequency of desaturation events amongpatients in the 2 treatment groups. Although not specifi-cally defined, they were far more common in the HFFMgroup: a mean of 1.86 desaturations/patient, compared to0.79 desaturations/patient in the HFNC group. The firstconsideration would be to determine if these events wererelated to technical differences in the systems’ ability todeliver the expected FIO2

at flows adequate for the pa-tients’ often increasing flow demand. The Methods sectionand Figures 1 and 2 shed some light on this issue. TheHFNC had an initial flow of 35 L/min and FIO2

titrated asnecessary to attain SpO2

� 95%. Unfortunately, Figure 1does not identify the means by which the air/O2 mixtureswere provided and independently adjusted. We must pre-sume that an air/O2 blender with independent flow controlwas used. (To allow other clinicians to reproduce the re-search, more detailed equipment specifications are recom-mended.) Gas flow to the HFFM was generated from aflow meter; a diluter device provided the means to adjustFIO2

. However, with a diluter there is potential for the totalflow of mixed gas to decrease as FIO2

is increased. This isespecially critical with a face mask with an open design,no gas reservoir, and outlet holes, through which room aircan easily be secondarily entrained.17-19 We have observedthis problem in recently extubated patients who were placedon similar masks with standard large-volume aerosol nebu-lizers. Failure of the system to meet patient inspiratoryflow demand and allow secondary room air entrainment atthe mask has been interpreted as patient deterioration. Of-ten this occurs as the respiratory rate exceeds approxi-mately 25 breaths/min. The spiral of worsening hypox-

HIGH-FLOW NASAL CANNULA OXYGEN IN CRITICALLY ILL A


emia is accelerated if the FIO2of the nebulizer is mistakenly

increased, further decreasing total flow. We have beenable to simulate this phenomenon in the lab, using anintubation manikin attached to a mechanical double-lunganalog with one side being driven by a mechanical venti-lator, causing the adjacent lung to ventilate the manikin.An oxygen analyzer placed in the trachea documenteddeclining FIO2

with tachypnea and/or increasing the FIO2

from the nebulizer. An air/O2 blender or high-flow large-volume nebulizer may remedy the clinical problem.20,21

The HFNC design has the potential to allow inboard leaksthrough the mouth, but at the same time may set up the nasalcavity and pharynx as an oxygen reservoir. There are no datato help determine if the increased number of desaturationevents in the HFFM group could be directly correlated withthe patient’s tachypnea. If that were the case, failure of thesystem’s inherent design (mask dilution and/or flow limita-tion) could be implicated as the cause of desaturation eventsand identify the advantage of the blender-driven HFNC.

A potential major feature that may also identify thetechnical advantage of the HFNC is its ability to generateCPAP. Parke and colleagues demonstrated this effect withtheir HFNC system in a previous publication.22 The HFNCused in this study is an example of using an adjustableflow of humidified gas to create CPAP as it meets resis-tance in the anatomical upper airways. This approach hasbeen documented for use in both perinatal/pediatric andadult patients.23-26 The attributed mechanism of the actionof positive pressure is multifaceted: improved work ofbreathing by the mechanical effect on respiratory muscu-lature; improved gas exchange by decreasing low ventila-tion-perfusion in the lung; and purging the anatomical air-ways of carbon dioxide while using them as an oxygenreservoir.27 Unlike the tighter-sealing nasal CPAP masksor nasal pillows, the HFNC used in the Parke et al study isnot well suited for obstructive sleep apnea or noninvasiveventilation, and not requiring a tight seal may preventsome discomfort. However, both mask designs are depen-dent upon a level of seal by the oropharynx and mouth tomaintain CPAP in the major airways and lung.

The lessons provided by the Parke et al study13 may bemore valuable than its objective of demonstrating superi-ority of one oxygen-delivery device over another for pa-tients with moderate hypoxemia. The study illustrates thatthe challenges of clinical research when matching a deviceto a patient problem are based on “hard science,” criticalthinking, and the art of responding to often subtle clues.Parke et al note the study’s limitations and the difficulty ofperforming detailed, real-time analysis of factors thatprompted oxygen desaturation episodes and treatment fail-ure. A number of factors may have introduced bias into thefindings. Besides knowing the oxygen-delivery apparatusto elevate FIO2

and meet flow demand, a few other factors

may have included air dilution systems, mask design, andpotential deteriorating cardiopulmonary disease states.

This randomized controlled study by Parke and col-leagues has advanced the evidence for clinical use of thehigh-flow cannula beyond the bench or case series. It hasmodeled an approach for respiratory care clinicians tothoughtfully review new equipment as it is made availablefrom manufacturers. The study does appear to uncoverboth the benefits and limitations of HFNC. Although HFNCmay not be needed for many patients with mild hypoxemiaand moderate respiratory rate, it does appear to be ideal forsome patient problems. HFNC probably requires greatercaution when applied to patients with pathophysiologiesthat induce intrinsic PEEP, such as unstable COPD orasthma, as its role remains controversial. A low level ofextrinsic CPAP may not be effective in counteracting PEEPiand could lead to unintended increase in lung volume.28,29

These insights should allow further investigations to betterselect specific patient problems for which it is best suited,including patients with moderate hypoxemia who initiallydo not respond well to low-flow cannula, do not tolerateface mask, or have pathophysiology that would benefitfrom a low level of CPAP. In retrospect, it would appearthat the nasal catheter might have been well suited to treatWorld War I victims of gas exposure.30

Bryan A Wattier RRTJeffrey J Ward MEd RRT FAARC

Respiratory Care ProgramUniversity of Minnesota

Mayo ClinicRochester, Minnesota

REFERENCES

1. Leigh JM. The evolution of the oxygen therapy apparatus. Anaes-thesia 1974;29(4):462-485.

2. Barach AL. Principles and practices of inhalation therapy. Philadel-phia: JB Lippincott; 1944.

3. Vain NE, Prudent LM, Stevens DP, Weeter MM, Maisels MJ. Reg-ulation of oxygen concentration delivered to infants by nasal cannu-las. Am J Dis Child 1989;143(12):1458-1460.

4. Soto RG, Fu ES, Fila H, Miguel RV. Capnography accurately detectsapnea during monitored anesthesia care. Anesth Analg 2004;99(2):379-382.

5. Gould GA, Hayhurst MD, Scott W. Clinical assessment of oxygenconserving devices in chronic bronchitis and emphysema. Thorax1985;40(11):820-824.

6. Collard P, Wautelet F, Delwiche JP, Prignot J, Dubois P. Improve-ment of oxygen delivery in severe hypoxaemia by a reservoir can-nula. Eur Respir J 1989;2(8)778-781.

7. Bliss PL, McCoy RW, Adams AB. Characteristics of demand oxy-gen delivery systems: maximum output and setting recommenda-tions. Respir Care 2004;49(2):160-165.

8. Waugh JB, Granger WM. An evaluation of two new devices fornasal high-flow gas therapy. Respir Care 2004;49(8):902-906.

HIGH-FLOW NASAL CANNULA OXYGEN IN CRITICALLY ILL ADULTS


9. Wettstein RB, Shelledy DC, Peters JI. Delivered oxygen concentra-tions using low-flow and high-flow nasal cannulas. Respir Care 2005;50(5):604-609.

10. Spentzas T, Minarik M, Patters AB, Vinson B, Stidham G. Childrenwith respiratory distress treated with high-flow nasal cannula. J IntCare Med 2009;24(5):323-328.

11. Ward JJ, Gracey DR. Arterial oxygen values achieved by COPDpatients breathing oxygen alternatively via nasal mask and nasalcannula. Respir Care 1985;30(4):250-255.

12. Darin JD, Broadwell J, MacDollell R. An evaluation of water vaporoutput from four brands of unheated prefilled bubble humidifiers.Respir Care 1982;27(1):41-47.

13. Parke RL, McGuinness SP, Eccleston ML. A preliminary random-ized controlled trial to assess effectiveness of nasal high-flow oxy-gen in intensive care patients. Respir Care 2011;56(3):265-270.

14. American Association for Respiratory Care. Clinical practice guide-line: oxygen therapy for adults in the acute care facility: 2002 revi-sion and update. Respir Care 2002;47(6):717-720.

15. O’Driscoll BR, Howard LS, Davison AG; British Thoracic Society.BTS guideline for emergency oxygen use in adult patients. Thorax2008;63(Suppl 6):vi1-vi68. Erratum in: Thorax 2009;64(1):91.

16. Roca O, Riera J, Torres F, Masclans JR. High-flow oxygen therapyin acute respiratory failure. Respir Care 2010;55(4):408-413.

17. Monsat RL, Kaye W. Problems in delivering desired gas concentra-tions from jet nebulizers to patients via face tents. Respir Care 1984;29(10):994-1000.

18. Chechani V, Scott G, Burnham B, et al. Modification of an aerosolmask to provide high concentrations of oxygen in the inspired air.Chest 1991;100(6):1582-1585.

19. Foust GN, Potter WA, Wilons MD, Golden EB. Shortcomings ofusing two jet nebulizers in tandem with an aerosol face mask foroptimal oxygen therapy. Chest 1991;99(6):1346-1351.

20. Peters J, Shelledy DC, Higgins J, Hernandez J, Angel L. The effec-tiveness of a high flow oxygen nebulizer (Misty-Ox) versus not-rebreathing mask (NRB) in delivering high oxygen concentrations.Chest 1999;116(4):364S.

21. Ward JJ. Medical gas therapy. In: Burton GG, Hodgkin JE, Ward JJ,editors. Respiratory care: a guide to clinical practice. Philadelphia:JB Lippincott; 1997:335-404.

22. Parke R, McGinness, Eccleston M. Nasal high-flow therapy deliverslow level positive airway pressure. Br J Anaesth 2009;103(6):886-890.

23. de Klerk A. A humidified high-flow nasal cannula: is it the new andimproved CPAP? Adv Neonatal Care 2008;8(2):98-106.

24. Dani C, Pratesi S, Migliori C, Bertini G. High flow nasal cannulatherapy as respiratory support in the preterm infant. Ped Pulmonol-ogy 2009;44(7):629-634.

25. Finer NN, Mannino FL. High-flow nasal cannula: a kinder gentlerCPAP? (editorial) J Pediatr 2009;154(2):160-162.

26. Lampland AL, Plumm B, Meyers PA, Worwa CT, Mammel MC.Observational study of humidified high-flow nasal cannula com-pared with nasal continuous positive airway pressure. J Pediatr 2009;154(2):177-182.

27. Dysart K, Miller TL, Wolfson MR, Shaffer TH. Research in highflow therapy: mechanism of action. Respir Med 2009;103(10):1400-1405.

28. O’Donoghue FJ, Catcheside PG, Jordan AS, Bersten AD, McEvoyRD. Effect of CPAP on intrinsic PEEP, inspiratory effort, and lungvolume in severe stable COPD. Thorax 2002;57(6):533-539.

29. Medoff BD. Invasive and noninvasive ventilation in patients withasthma. Respir Care 2008;53(6):740-748.

30. Borak J, Diller WF. Phosgene exposure: mechanisms of injury andtreatment strategies. J Occup Environ Med 2001;43(2):110-119.

The authors have disclosed no conflicts of interest.

Correspondence: Bryan Wattier RRT, Respiratory Care Program, Uni-versity of Minnesota, Mayo Clinic, 200 First Street SW, Siebens 10-12C,Rochester MN 55905.

DOI: 10.4187/respcare.01250

HIGH-FLOW NASAL CANNULA OXYGEN IN CRITICALLY ILL ADULTS


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Short-Term Effects of Humidification Devices on Respiratory Patternand Arterial Blood Gases During Noninvasive Ventilation

Francois Lellouche MD PhD, Claudia Pignataro MD,Salvatore Maurizio Maggiore MD PhD, Emmanuelle Girou PharmD PhD,

Nicolas Deye MD MSc, Solenne Taille Eng,Marc Fischler MD, and Laurent Brochard MD

BACKGROUND: The impact of humidification devices on ventilatory and arterial blood gasesparameters during noninvasive ventilation (NIV) remains controversial. The aim of the study wasto compare the short-term impact of heat and moisture exchangers (HMEs) and heated humidifiers(HHs) during NIV for either hypercapnic or hypoxemic acute respiratory failure. METHODS:Consecutive subjects receiving NIV were successively treated with HME and HH in randomizedorder for 30 min each. At the end of each period, arterial blood gases were measured and venti-latory parameters were recorded. RESULTS: Eighty-one subjects were enrolled, of whom 52 werehypercapnic (with or without acidosis) and 29 hypoxemic. Minute ventilation was greater with theHME, in comparison with the HH (15 [12–18] vs 12 [10–16] median [interquartile range], P < .001),while PaCO2

was increased when using HME, indicating a dead space effect. This effect was observedin all subjects, but was more pronounced in hypercapnic subjects (PaCO2

62 � 17 mm Hg with HMEvs 57 � 14 with HH, P < .001). In a subgroup of 19 subjects with respiratory acidosis, alveolarhypoventilation improved only with the HH. The amplitude of the dead space impact was a functionof the degree of hypercapnia. CONCLUSIONS: Use of an HME decreased CO2 elimination duringNIV, despite increased minute ventilation, especially in hypercapnic subjects. Key words: noninva-sive ventilation; humidification; heated humidifiers; heat and moisture exchangers; dead space; alveolarhypoventilation; acute respiratory failure; COPD. [Respir Care 2012;57(11):1879–1886. © 2012 Daeda-lus Enterprises]

Drs Lellouche, Pignataro, Taille, Fischler, and Brochard are affiliatedwith the Service de Reanimation Medicale, Assistance Publique Hopi-taux de Paris, Centre Hospitalier Albert Chenevier-Henri Mondor, Cre-teil, France. Drs Lellouche, Maggiore, and Brochard are affiliated withthe Institut National de la Sante et de la Recherche Medicale Unit 955,Equipe 13, Creteil, France. Dr Girou is affiliated with the Unite deControle, Epidemiologie et Prevention de l’Infection, Assistance Pub-lique Hopitaux de Paris, Hopital Henri Mondor, Creteil, France. Dr Deyeis affiliated with the Service de Reanimation Medicale, Hopital Lari-boisiere, Paris, France. Dr Lellouche is also affiliated with Service deSoins Intensifs de Chirurgie Cardiaque, Centre de Recherche InstitutUniversitaire de Cardiologie et de Pneumologie de Quebec, UniversiteLaval, Quebec City, Quebec, Canada. Dr Pignataro is also affiliated withthe Departement d’Anesthesie et Reanimation, Hopital Lariboisiere, Paris,France. Dr Maggiore is also affiliated with the Istituto di Anestesiologiae Rianimazione, Universita Cattolica Policlinico A Gemelli. Rome, Italy.Dr Brochard is also affiliated with the Universite Paris 12, Creteil, France.

Dr Lellouche presented a version of this paper at the International Con-ference of the American Thoracic Society, held May 17–22, 2002, inAtlanta, Georgia.

The humidifiers for this study were supplied free of charge by Fisher &Paykel, which was not involved in the design or conduct of the study,collection, management, analysis, or interpretation of the data; or prep-aration, review, or approval of the manuscript.

Dr Brochard has disclosed relationships with Hudson and Fisher & Paykel.

Correspondence: Francois Lellouche MD PhD, Unite de Soins Intensifsde Chirurgie Cardiaque, Groupe de Recherche en Sante Respiratoire,Centre de Recherche de l’Institut Universitaire de Cardiologie et dePneumologie de Quebec, 2725 Chemin Sainte-Foy, Ville de Quebec,Quebec Canada G1V 4G5. E-mail: [email protected].



Introduction

Noninvasive ventilation (NIV) delivered via a face maskreduces the need for endotracheal intubation and the sub-sequent risk of morbidity and mortality.1-3 NIV is partic-ularly useful in patients with acute hypercapnic exacerba-tions of COPD.1,4,5 NIV failure, which has been reportedin 20–50% of patients,6,7 is ascribed to inadequate CO2

removal8-12 and poor tolerance of the technique.6,7

It is well established that gases delivered through anendotracheal tube must be humidified, because dry in-spired gases have deleterious effects.13,14 This statement isnot so clear during NIV.15 However, there are severalarguments favoring the use of humidification during NIV.First, the complications related to dry gases application arevery frequent during NIV16 and may reduce tolerance ofthis technique. When NIV is delivered using a standardintensive-care ventilator, the upper airways are not by-passed, but receive dry inspired gases.17 The upper air-ways may be unable to humidify these gases adequately,particularly in mouth-breather patients or when high in-spiratory flows are used. Another argument is the fre-quency of bronchial hyper-reactivity among patients re-quiring NIV,18,19 while dry gases are known to aggravatethis state20 and can be used to measure airway responsive-ness equally to methacholine and other cholinergic ana-logues or histamine.21 Two humidifying devices are com-monly used with intensive care ventilators: heatedhumidifier (HH) and heat-and-moisture exchanger (HME).Both devices can adequately humidify inspired gas, eventhough leaks reduce inspired humidity with HME.17 HMEdevices are frequently used because of their simplicityand lower cost.22 Since they are placed between theY-piece and the patient, they add substantial dead spaceto the circuit, leading to well known dead-space effectsduring assisted mechanical ventilation,23-25 and can alsomarginally increase the resistance to flow.26 The nega-tive impacts of HME dead space during NIV were notfound in a recently published study27 but have beenpreviously demonstrated in 2 previous physiologic stud-ies, including limited number of subjects.28,29 Jaber et alfound that HME was associated with significantly re-duced CO2 clearance, compared to HH, in spite of in-creased minute ventilation.28 We showed that the HMEdevice causes a large increase in work of breathing,compared to HH, as well as an increase in minute ven-tilation.29 The number of subjects was too small to dem-onstrate an impact on arterial blood gases in our previ-ous work. We thus addressed this question through asimple clinical study, with no assessment of subjecteffort, but including a large number of subjects with alldegrees of severity or type of respiratory failure.30

Methods

The study protocol was approved by an independentreview board (Comite d’Ethique de la Societe de Reani-mation de Langue Francaise). The subjects were givenwritten information on the protocol and signed a consentwaiver.

Subjects

Subjects were recruited in the medical ICU of HenriMondor hospital over a one-year period. Inclusion criteriawere recent dyspnea exacerbation and one of the follow-ing: respiratory rate � 25 breaths/min, PaO2

� 60 mm Hgwith room air, or arterial pH � 7.38. Exclusion criteriawere a need for immediate endotracheal intubation, severehypoxemia (FIO2

� 0.80 to obtain SaO2� 90%), respira-

tory rate � 12 breaths/min, pneumothorax, and hemody-namic instability.

Protocol

Consecutive subjects treated using NIV with pressuresupport were prospectively recruited. Ventilatory supportwas provided based on local recommendations.31 All sub-jects were ventilated with an ICU ventilator having in-spiratory and expiratory lines. The HH was placed in theinspiratory line, as recommended by the manufacturer, andthe HME was placed at the Y-piece. Each subject sat in achair or in bed at an angle exceeding 30°, and the size ofthe interface was selected to fit the subject. Standard oro-nasal masks with different shapes and sizes were used toensure a proper fit for each subject and to maximize com-fort. No flex-tube was placed between the Y-piece and themask. Hydrocolloid dressings were used to protect the

QUICK LOOK

Current knowledge

Humidification during noninvasive ventilation impactspatient comfort and tolerance, and physical character-istics of these devices can affect minute ventilation re-quirements.

What this paper contributes to our knowledge

The use of a heat and moisture exchanger during non-invasive ventilation is associated with reduced carbondioxide elimination, compared to heated humidifica-tion. The effect was more pronounced in patients withhypercapnic respiratory failure, high PaCO2

, low tidalvolume, and low PEEP.

SHORT-TERM EFFECTS OF HUMIDIFICATION DEVICES


skin. The subject placed the mask on his or her face beforethe procedure began, when possible. A head strap wasused to hold the mask in place. Strap tension was mini-mized. The first breaths were made with no expiratorypressure, and an inspiratory pressure not exceeding8 cm H2O. Inspiratory and expiratory pressures were in-creased in increments not exceeding 2 cm H2O. The ex-piratory pressure was gradually increased to 3 cm H2O inCOPD subjects, and to a maximum of 10 cm H2O inhypoxemic subjects. The inspiratory pressure was increasedto obtain an expired tidal volume between 7 and 9 mL/kg,or 6 and 8 mL/kg in COPD subjects. Low doses of seda-tive were given infrequently to agitated subjects. The phy-sician and nurses explained the different periods and set-ting modifications to reassure the subjects.

An HME (Hygrobac, DAR, Mirandola, Italy) and anHH (MR850, Fisher & Paykel Healthcare, Auckland, NewZealand) with heated circuits were compared with a cross-over design. HME dead space was 95 mL,32 while HMEresistance, measured in a previous paper, were equivalentto HH inspiratory circuit resistances.29

We a priori separated 3 groups of subjects:

• Subjects with hypercapnia and respiratory acidosis (usuallycorresponding to the initiation of NIV treatment)

• Subjects with hypercapnia and without respiratory aci-dosis (usually corresponding to the stabilization of NIVtreatment)

• Hypoxemic non-hypercapnic subjects

Hypercapnia was defined as a PaCO2exceeding

42 mm Hg. Acidosis was defined as a pH � 7.38. Hypox-emia was defined as a SpO2

� 90% when breathing roomair. Subjects were ventilated for 30 min with an HH deviceand for 30 min with an HME device. The sequence of thehumidification device was randomized. At the end of eachperiod (during the 5 last minutes), the ventilatory param-eters were recorded from the ventilator (respiratory rateand minute ventilation), and arterial blood gases were mea-sured. The ventilatory settings were selected by the attend-ing physician, and no changes occurred during the wholestudy time for these settings.

Arterial blood gas measurements were also available for19 subjects in the respiratory acidosis group at baseline,immediately before the initiation of NIV.

Statistical Analysis

The primary outcome was the impact of humidificationdevice on physiological parameters (arterial blood gasesand breathing pattern). Descriptive statistics, includingmeans, standard deviations, medians, and interquartileranges, were used to summarize the data. Categorical vari-ables were compared using the Mann-Whitney 2-sample

rank sum test. Continuous variables were compared usingthe Spearman rank correlation. Continuous variables werenot dichotomized, except PEEP level. We tested the carry-over effect to determine the impact of the sequence order(first NIV period with HH or with HME) and the impact ofthe period (first vs second NIV period). We analyzed theassociation between the �PaCO2

between the 2 humidifi-cation systems and PaCO2

under the HME with univariateanalysis. We then used multiple linear regression to iden-tify variables that made an important contribution to thevariability of �PaCO2

, to adjust for possible confoundingvariables. Despite being significant in the univariate anal-ysis, the type of respiratory failure was not entered in themultiple regression model, due to its close relationshipwith the variable PaCO2

under HME. The model was checkedfor normality, linearity, homoscedasticity, and multicol-linearity. Statistical analysis was performed using statisticssoftware (Stata 8.2, StataCorp, College Station, Texas). AP value � .05 was considered significant.

Results

Eighty-one subjects were included in our study. Theindications for NIV were acute hypoxemic respiratory dis-tress (from unilateral pneumonia or ARDS) in 26 subjects,exacerbation of COPD in 28, post-extubation respiratorydistress in 7, cardiopulmonary edema in 12, and otherindications in 8. The sex ratio (M/F) was 54/27, the meanage was 63 � 14 years, and the mean Simplified AcutePhysiology Score II score was 41 � 28. Ventilatory set-tings were as follows: the pressure support level was14 � 3 cm H2O, PEEP was set at 5 � 2 cm H2O, and FIO2

was 0.51 � 0.23.Table 1 and Figure 1 present the impact of the humid-

Table 1. Influence of the HME and HH Devices on Arterial BloodGases and Respiratory Parameters of All Patients

HME(n � 81)

HH(n � 81)

P*

pH 7.38 (7.32–7.43) 7.40 (7.35–7.45) � .001PaCO2

, mm Hg 47 (40–58) 46 (39–56) � .001PaO2

, mm Hg 86 (73–106) 84 (71–102) .45Respiratory rate,

cycles/min27 (23–33) 24 (20–30) � .001

Expired tidal volume,mL

535 (456–638) 545 (453–667) .89

Minute ventilation,L/min

15 (12–18) 12 (10–16) � .001

Results are expressed as median (interquartile range).* Statistical test used for comparison: Wilcoxon matched-pairs signed-rank test (nonparametrictest).HME � heat and moisture exchangerHH � heated humidifier



ification devices on arterial blood gases and respiratoryparameters for the whole population. The results for thedifferent populations (hypercapnia with or without acido-sis and hypoxemia) are presented in Table 2.

In all groups, the HME led to small but significantincrease in PaCO2

, despite significantly higher minute ven-tilation (see Table 2). These effects were more pronouncedin hypercapnic subjects (see Table 3 and Fig. 2). Baselinearterial blood gases prior to NIV were available for 19subjects with respiratory acidosis. CO2 removal improvedover baseline only with the HH device, and not with theHME. Figure 3 shows the evolution of PaCO2

according tothe device used in these subjects.

The evaluation of a carry-over effect demonstrated thatthere is a period effect (first vs second), as expected due tothe impact of NIV (P � .010), but no sequence effect(P � .70), indicating that beginning with HH or HME didnot have any effect on the results for PaCO2

variations.In univariate analysis, the most influential factors on the

difference in PaCO2between the 2 humidification systems

(PaCO2with HME – PaCO2

with HH) were the presence ofhypercapnic respiratory failure, the level of initial PaCO2

,and the expired tidal volume (see Table 3). Multiple re-gression analysis showed that PaCO2

level under HME wasthe best significant predictor of �PaCO2

after adjustmentfor PEEP level, expired tidal volume, and pH (Table 4).

Discussion

The present study assessed the effect of the main hu-midification devices on breathing pattern and arterial bloodgases in a large number of consecutive subjects with var-ious indications for NIV. The HME had a negative impacton CO2 elimination, compared to the HH (see Table 1).CO2 removal was reduced in all subject groups (see Ta-bles 2 and 3), despite increased minute ventilation trig-gered by the added dead space of the HME. The effectswere more pronounced in subjects with hypercapnic re-spiratory failure, high PaCO2

, low tidal volume, and lowPEEP (see Table 3).

Few data are available on humidification during NIV,and very few studies in the literature can be compared tothe present study. Our group previously conducted a phys-iologic study comparing HH and HME devices duringNIV in hypercapnic subjects.29 It showed that there is asignificant increase in work of breathing, combined withan increase in minute ventilation, with the HME. How-ever, a number of limitations due to experimental condi-tions made it impossible to evaluate the effect of the hu-midification devices on arterial blood gases in the previousstudy. First, the added dead space due to the pneumota-chograph (almost 30 mL) may have reduced the differencein the volume of dead space of the devices studied. Sec-ond, the transdiaphragmatic pressure measurements usinga double balloon eso-gastric catheter required patient co-operation. Because of this, patients with high PaCO2

andencephalopathy were excluded from the previous study.Patients were included after a mean ICU stay of 48 hours,and by then most of them had almost recovered fromacidosis.29

In the present study the experimental conditions weresimilar to real-life clinical conditions, with no interven-tions except for changing the humidification device after30 min. This large subject population made it possible todetect the deleterious effect of dead space on minute ven-tilation and breathing pattern in different categories ofsubjects (see Table 2).

Fig. 1. Comparison of the PaCO2at the end of each study period:

heat and moisture exchanger (HME) versus heated humidifier (HH)in the entire study population. PaCO2

was significantly higher withthe HME than with the HH (51 � 17 mm Hg vs 47 � 13 mm Hg,P � .001).



In the group of subjects on NIV for decompensation ofchronic respiratory failure (respiratory acidosis), there wasa marked difference in median minute ventilation betweenthe HH and HME devices (11.4 L/min vs 13.8 L/min,P � .001), respiratory rate, and PaCO2

. The deleteriouseffect of dead space in this category of subject was presentin the group of subjects with acidosis, corresponding to theinitiation of NIV, as well as in the group without acidosis,corresponding to the end of NIV. Jaber et al28 reportedthe same HME dead-space effect in less severe hyper-capnic patients. In their study, most of the patients hadno acidosis and hypercapnia was moderate (PaCO2

46.0 � 10.2 mm Hg at baseline).28

More striking was the finding that using the HME de-vice for 30 min with NIV impeded pH correction in thegroup of subjects with respiratory acidosis, compared tobaseline values (before NIV), while pH levels significantlyincreased with the HH device. Interestingly, many studieshave reported that a decrease in CO2 during NIV is astrong predictor of success.8-12 The effect of HME in sub-jects treated for hypoxemic respiratory failure was lesspronounced. These results are in agreement with those ofJaber et al.28

Table 2. Influence of Humidification Device on Arterial Blood Gases and Ventilator Parameters in Patients With Hypercapnia and Acidosis (EarlyNIV), Hypercapnia (End of NIV), and in Patients With Hypoxemia

Hypercapnia With Acidosis(n � 35)

Hypercapnia Without Acidosis(n � 17)

Hypoxemia(n � 29)

HME HH HME HH HME HH

pH 7.31 (7.28–7.34) 7.34 (7.30–7.36)* 7.41 (7.39–7.44) 7.42 (7.40–7.46)* 7.43 (7.38–7.45) 7.44 (7.41–7.47)*PaCO2

, mm Hg 60 (52–70) 56 (47–64)* 50 (47–55) 48 (45–53)* 36 (34–40) 35 (32–39)*PaO2

, mm Hg 85 (72–104) 79 (70–102) 80 (66–97) 75 (68–96) 92 (77–116) 92 (76–109)f, breaths/min 27 (22–33) 22 (18–28)* 23 (18–28) 20 (18–26)* 30 (26–34) 29 (24–32)†VT, mL 497 (437–584) 509 (438–585) 571 (517–696) 667 (500–737) 611 (484–692) 585 (454–668)VE, L/min 13.8 (11.1–15.1) 11.4 (9.4–12.1)* 15.1 (11.5–17.0) 12.2 (10.0–16.0)* 17.3 (14.5–23.0) 16.3 (11.7–19.8)*

Results are expressed as median (interquartile range).* P � .001 for heat and moisture exchanger (HME) vs heated humidifier (HH).† P � .01 for HME vs HH.f � respiratory frequencyVT � expiratory tidal volumeVE � minute ventilation

Table 3. Factors Influencing the �PaCO2*

�PaCO2P

Type of Respiratory FailureHypercapnic 3.4 (1.0 to 7.0) .005Hypoxemic 1.4 (0.4 to 2.5)

PaCO2, mm Hg† Rho � 0.53 � .001

pH† Rho � –0.41 .001Expired tidal volume, mL† Rho � –0.28 .01PEEP, cm H2O

0–5 2.8 (1.0 to 5.9) .026–10 0.8 (–1.1 to 3.5)

Minute ventilation, L/min† Rho � –0.16 .15Respiratory rate, cycles/min† Rho � 0.11 .36

Results are expressed as median (interquartile range). Statistical test used for comparison ofcontinuous variables: Spearman rank correlation. Statistical test used for comparison ofcategorical variables: Mann-Whitney 2-sample rank sum test.* �PaCO2 � PaCO2 with HME–PaCO2 with HH.† Level with HME.HME � heat and moisture exchangerHH � heated humidifier

Fig. 2. Comparison of the PaCO2at the end of each study period:

heat and moisture exchanger (HME) versus heated humidifier (HH)in hypercapnic subjects. PaCO2

was significantly higher with theHME than with the HH (62 � 17 mm Hg vs 57 � 14 mm Hg,P � .001).



Our results were also in agreement with studies on in-tubated patients.25,33-36 With intubated patients on assistedventilation, HMEs reduce CO2 elimination and increaseminute ventilation and work of breathing, compared toHHs. This requires an increase in pressure support from 5to 8 cm H2O, to compensate for the dead space of theHME.25,34,35 However, increasing pressure support duringNIV is not always feasible because it can increase leaksand patient/ventilator asynchrony.37 In the current studythe mean pressure support level was already 14 � 3 cm H2O.

In a recently published study, Boyer et al comparedHMEs with small dead space with HH during NIV and didnot find differences in CO2 elimination.27 The absence ofimpact of dead space in this study may be explained byseveral factors. First, the difference of dead space betweenHME and HH was small (90 mL vs 33 mL when flex-tubewas used and 38 mL vs 0 mL when no flex-tube was used).Also, the pressures used during NIV were very high (around20 cm H2O of total inspiratory pressure or higher in pa-tients with acute hypoxemic respiratory failure). Thesehigh pressures translated to high tidal volumes (around750 mL in patients with exacerbation of COPD), whichmay be difficult to obtain in the real-life setting. Even ifthere is incontrovertible evidence that dead space impact

exists during invasive and noninvasive mechanical venti-lation,23-25,29,33-36,38-42 it is important to keep in mind thatthis effect is usually related to the amount of additionaldead space.40 This impact may have little clinical impor-tance, however, in specific conditions when small deadspace HMEs are used.27

The effects observed in the present study were related tothe dead space and not to the resistance of the humidifi-cation devices. Indeed, the inspiratory and expiratory re-sistance of the HME and HH devices were similar (2.5 vs3 cm H2O/L/s), as previously reported.29 We used thesame devices without flex tubes, as in our previous study.29

The physiologic dead space is usually around 150 mL,43

while the interface dead space is approximately 70 mL.44

The instrumental dead space of the HME device used inthe present study was 95 mL. Instrumental dead spaceduring NIV should be reduced as much as possible, sincethe aim of NIV is to reduce the work of breathing and todecrease PaCO2

.45

In a previous study29 the HME device reduced the workof breathing but had no effect on minute ventilation whena PEEP of 5 cm H2O was applied. Interestingly, in thepresent study, mean PEEP was 5 � 2 cm H2O (settingswere performed by the attending physician). The negativeimpact of HME dead space on short-term physiologic pa-rameters such as minute ventilation and arterial blood gaseswas present within these real-life settings.

The main limitation of the present study was that noconclusions could be reached regarding the impact of theHH and HME devices on the outcome and efficacy ofNIV. However, in patients with marked hypercapnic en-cephalopathy and clinical signs of increased work of breath-ing, the dead space should be taken into account and thepresent results are relevant. An NIV session with a max-imal reduction of the dead space should be attempted be-fore proceeding to intubation, although this should notunduly prolong NIV and delay intubation if required. Theother limitation of the present study was the absence of aperiod with no humidification. While this is possible withdedicated NIV turbine-based ventilators, it is not accept-able when using ICU ventilators because of the risk ofincreased bronchial hyperreacticity with dry gases and dry-ness of secretions.18-20 Another limitation of this study isthe short time of the study periods (30 min each), whichmay have influenced the results.

Conclusions

In conclusion, the present study revealed that the deadspace of the HME device had a short-term negative impacton CO2 elimination and minute ventilation in subjectstreated with NIV delivered using an ICU ventilator. Thisimpact was more pronounced in the hypercapnic population.

Fig. 3. Influence of the heat and moisture exchanger (HME) andheated humidifier (HH) devices on the pH correction in hypercapnicsubjects with acidosis (n � 19); comparison with baseline valuesbefore NIV initiation.

Table 4. Multiple Linear Regression Model for �PaCO2

Independent Variable � (95% CI) P

PaCO2* 0.15 (0.07 to 0.24) .001

PEEP level –0.91 (–3.28 to 1.47) .45Expiratory tidal volume* –0.003 (–0.009 to 0.004) .40pH* –6.95 (–23.06 to 9.16) .39

* Level with heat and moisture exchanger.R2 for the model � 0.40.



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26. Ploysongsang Y, Branson R, Rashkin MC, Hurst JM. Pressure flowcharacteristics of commonly used heat-moisture exchangers. Am RevRespir Dis 1988;138(3):675-678.

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28. Jaber S, Chanques G, Matecki S, Ramonatxo M, Souche B, Perri-gault PF, et al. Comparison of the effects of heat and moistureexchangers and heated humidifiers on ventilation and gas exchangeduring non-invasive ventilation. Intensive Care Med 2002;28(11):1590-1594.

29. Lellouche F, Maggiore SM, Deye N, Taille S, Pigeot J, Harf A, et al.Effect of the humidification device on the work of breathing duringnoninvasive ventilation. Intensive Care Med 2002;28(11):1582-1589.

30. Lellouche F, Pignatarro C, Maggiore SM, Deye N, Fischler M, HarfA, et al. Influence of the humidification device during non-invasiveventilation (abstract). Am J Respir Crit Care Med 2002;165(Suppl):A384.

31. Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit CareMed 2001;163(2):540-577.

32. Lellouche F, Taille S, Lefrancois F, Deye N, Maggiore SM, JouvetP, et al. Humidification performance of 48 passive airway humidi-fiers: comparison with manufacturer data. Chest 2009;135(2):276-286.

33. Campbell RS, Davis K Jr, Johannigman JA, Branson RD. The effectsof passive humidifier dead space on respiratory variables in para-lyzed and spontaneously breathing patients. Respir Care 2000;45(3):306-312.

34. Girault C, Breton L, Richard JC, Tamion F, Vandelet P, Aboab J,et al. Mechanical effects of airway humidification devices in difficultto wean patients. Crit Care Med 2003;31(5):1306-1311.

35. Iotti GA, Olivei MC, Palo A, Galbusera C, Veronesi R, Comelli A,et al. Unfavorable mechanical effects of heat and moisture exchang-ers in ventilated patients. Intensive Care Med 1997;23(4):399-405.

36. Le Bourdelles G, Mier L, Fiquet B, Djedaini K, Saumon G, Coste F,et al. Comparison of the effects of heat and moisture exchangers andheated humidifiers on ventilation and gas exchange during weaningtrials from mechanical ventilation. Chest 1996;110(5):1294-1298.



37. Pertusini E, Lellouche F, Catani F, Heili S, Taille S, Rodriguez P,et al. Patient-ventilator asynchronies during NIV does level of pres-sure support matter ? Intensive Care Med 2004;30(Suppl):S65.

38. Hinkson CR, Benson MS, Stephens LM, Deem S. The effects ofapparatus dead space on PaCO2 in patients receiving lung-protectiveventilation. Respir Care 2006;51(10):1140-1144.

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41. Prin S, Chergui K, Augarde R, Page B, Jardin F, Veillard-Baron A.Ability and safety of a heated humidifier to control hypercapnic acidosisin severe ARDS. Intensive Care Med 2002;28(12):1756-1760.

42. Richecoeur J, Lu Q, Vieira SR, Puybasset L, Kalfon P, Coriat P,et al. Expiratory washout versus optimization of mechanical venti-lation during permissive hypercapnia in patients with severe acuterespiratory distress syndrome. Am J Respir Crit Care Med 1999;160(1):77-85.

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Humidified High Flow Nasal Oxygen During Respiratory Failurein the Emergency Department: Feasibility and Efficacy

Hugo Lenglet MD, Benjamin Sztrymf MD, Christophe Leroy MD, Patrick Brun MD,Didier Dreyfuss MD, and Jean-Damien Ricard MD PhD

OBJECTIVE: Heated and humidified high flow nasal cannula oxygen therapy (HFNC) representsa new alternative to conventional oxygen therapy that has not been evaluated in the emergencydepartment (ED). We aimed to study its feasibility and efficacy in patients exhibiting acute respi-ratory failure presenting to the ED. METHODS: Prospective, observational study in a universityhospital’s ED. Patients with acute respiratory failure requiring > 9 L/min oxygen or with ongoingclinical signs of respiratory distress despite oxygen therapy were included. The device of oxygenadministration was then switched from non-rebreathing mask to HFNC. Dyspnea, rated by theBorg scale and a visual analog scale, respiratory rate, and SpO2

were collected before and 15, 30, and60 min after beginning HFNC. Feasibility was assessed through caregivers’ acceptance of the devicein terms of practicality and perceived effect on the subjects, evaluated by questionnaire. RESULTS:Seventeen subjects, median age 64 y (46–84.7 y), were studied. Pneumonia was the most commonreason for oxygen therapy (n � 9). HFNC was associated with a significant decrease in bothdyspnea scores: Borg scale from 6 (5–7) to 3 (2–4) (P < .001), and visual analog scale from 7 (5–8)to 3 (1–5) (P < .01). Respiratory rate decreased from 28 breaths/min (25–32 breaths/min) to25 breaths/min (21–28 breaths/min) (P < .001), and SpO2

increased from 90% (88.5–94%) to 97%(92.5–100%) (P < .001). Fewer subjects exhibited clinical signs of respiratory distress (10/17 vs 3/17,P � .03). HFNC was well tolerated and no adverse event was noted. Altogether, 76% of healthcaregivers declared preferring HFNC, as compared to conventional oxygen therapy. CONCLUSIONS:HFNC is possible in the ED, and it alleviated dyspnea and improved respiratory parameters insubjects with acute hypoxemic respiratory failure. Key words: acute lung injury; acute respiratorydistress syndrome; dyspnea; oxygen inhalation therapy; mouth dryness; intensive care equipment andsupplies. [Respir Care 2012;57(11):1873–1878. © 2012 Daedalus Enterprises]

Introduction

Dyspnea is one of the most common complaints in pa-tients presenting to the emergency department (ED). Ox-ygen therapy is then one of the first treatments provided,according to current guideline.1,2 It can be delivered—

depending on the severity of the patient’s respiratory dis-tress—during either unassisted (via nasal cannulas or facemasks) or assisted breathing with noninvasive or invasivemechanical ventilation.3 In patients who do not requireimmediate mechanical ventilation, important drawbacksare associated with conventional oxygen therapy. Theseinclude the limited amount of oxygen supplied (15 L/minis usually the maximum flow delivered via a face mask),

Drs Lenglet, Sztrymf, Dreyfuss, and Ricard are affiliated with AssistancePublique-Hopitaux de Paris (APHP), Service de Reanimation Medicale;and Drs Lenglet, Leroy, and Brun are affiliated with Service d’Accueildes Urgences, Hopital Louis Mourier, F-92700, Colombes, France.Drs Dreyfuss and Ricard are also affiliated with the Universite ParisDiderot, Sorbonne Paris Cite, F-75018, Paris, France.

Dr Ricard presented a version of this paper at the International Confer-ence of the American Thoracic Society, held May 14–10, 2010, in NewOrleans, Louisiana.

The authors have disclosed no conflicts of interest.

Correspondence: Jean-Damien Ricard MD PhD, Service de ReanimationMedico-Chirurgicale, Hopital Louis Mourier, 178 Rue Des Renouillers,F-92700 Colombes, France. E-mail: [email protected].



the considerable imprecision regarding the exact deliveredFIO2

,4 and the poor tolerance of oxygen in some patientsbecause of insufficient heating and humidifying.5-7

Recently, an alternative to conventional oxygen therapyhas received growing attention: heated, humidified highflow nasal cannula oxygen (HFNC) is a technique that candeliver up to 100% heated and humidified oxygen at amaximum flow of 60 L/min of gas via nasal prongs orcannula under body temperature (37°C) and pressure withsaturated water conditions (100% of relative humidity)(Fig. 1). Most of the available data with this techniquehave been published in the neonatal field, where it is in-creasingly used.8 Several devices have been tested so far,9

but evaluation of HFNC in adults remains limited.7 Ben-eficial effects on respiratory parameters have been recentlyreported in ICU patients with acute respiratory failure10-14

and during heart failure.15 In addition, low levels of pos-itive pressure have been measured in patients recoveringfrom cardiac surgery with HFNC,16 as well as in healthyvolunteers.17 There are no data concerning the use of sucha device in the ED, despite dyspnea and respiratory failurebeing common features of patients and specificities in themanagement in response to the environment. Hence, theaim of this study was to determine the feasibility and theeffect of HFNC in patients with acute respiratory failurepresenting to the ED.

Methods

Study Design

A prospective, observational study was conducted in theED of a university hospital. The ethics committee of the

French Society of Intensive Care Medicine approved thestudy and waived informed consent, since the procedureswere all part of routine care. Subjects were informed of thestudy, its design and purpose, and all healthcare givers(nurses and physicians) were educated to this new systemwith theoretical information and demonstration providedby the manufacturer before the beginning of the study.

Population

Between January and April 2009, all consecutive adultpatients who presented in our ED and who received con-ventional oxygen therapy with a non-rebreathing high FIO2

face mask with reservoir (Hudson RCI, Teleflex Medical,High Wycombe, United Kingdom) were screened for eli-gibility. They were included if they remained dyspneicdespite aggressive conventional therapy (including a min-imum of 9 L/min oxygen via the face mask, and a maxi-mum of 15 L/min, although it is possible to deliver greatervalues, but without knowing precisely how much). Theywere excluded if they required immediate invasive or non-invasive mechanical ventilation or if they had hypercapnicrespiratory failure.

Sequence and Data Collection

General and demographic data were collected. WhileHFNC was prepared, all variables were measured underthe face mask. HFNC was delivered via a dedicated highflow delivery system (Optiflow, Fisher & Paykel, Auck-land, New Zealand). HFNC settings were left to the at-tending physician’s discretion, but internal discussion withthe medical team recommended for most cases an FIO2

� 60% with initial flow of 40 L/min. These settings couldobviously be adapted depending on the subject’s severity

QUICK LOOK

Current knowledge

High flow, heated, humidified oxygen delivered via anasal cannula has become a common therapy for treat-ing hypoxemia. This therapy has not been commonlyused in the emergency department.

What this paper contributes to our knowledge

The use of high flow, heated, and humidified oxygen bynasal cannula was associated with a lower respiratoryrate, higher oxygen saturation, and improved comfortscales, compared to conventional oxygen therapy in agroup of patients with hypoxemia in the emergencydepartment.

Fig. 1. Scheme of the high flow nasal cannula Optiflow device. Itconsists of an air-oxygen blender with adjustable FIO2

(0.21–1.0)that delivers a modifiable gas flow (up to 60 L/min) to a heatedchamber where the gas is heated and humidified. The gas mixtureis then routed through a high performance circuit to be deliveredat 37°C containing 44 mg H2O/L to the patient via short, wide borebinasal prongs. (Courtesy of Fisher & Paykel.)

HUMIDIFIED HIGH FLOW NASAL OXYGEN DURING RESPIRATORY FAILURE


and tolerance of HFNC. Its efficacy was assessed on itscapacity: to alleviate dyspnea, using the Borg scale18 anda visual analog scale (in those subjects whose neurologicalstatus allowed them to complete the evaluation); to de-crease respiratory rate); and to increase SpO2

. All thesevariables were collected before HFNC, while the subjectwas breathing through the high-FIO2

face mask, and 15, 30,and 60 min after using HFNC. To keep this study the leastinvasive, we decided not to systematically sample arterialblood for blood gas assessment. Arterial blood gases wereperformed at the attending physician’s discretion, whichexplains their being performed in only a subset of subjects,before and after HFNC therapy. At the end of the firsthour’s use of HFNC, subjects were asked to rate, by meansof a simple questionnaire, their appreciation of the devicein terms of overall comfort and noise, in comparison withthe face mask (more, less, or similar to conventional ox-ygen therapy). To ensure a more objective assessment,ambient noise, HFNC and conventional therapy generatednoise were measured with a sound level meter (SdB02,Calright Instruments, San Diego, California). Measure-ments were performed in the room, 1 m away from thedevice. Finally, healthcare givers were asked their opinionof HFNC preparation and setup and its efficacy, with thesame rating as subjects: more, less, or similar. The feasi-bility was determined according to these ratings.

Statistical Analysis

Statistical analysis was performed using statistics soft-ware (Prism 4, GraphPad Software, San Diego, Califor-nia). Results are expressed as median and interquartilerange (1QR). The Friedman test was used to comparepaired repeated measurements. The Wilcoxon test was usedto compare paired measurements. The chi-square test wasused for categorical variables. A P value � .05 was con-sidered significant.

Results

During the study period, 386 patients admitted to theED experienced dyspnea, among whom 17 met the afore-mentioned inclusion criteria for this study (see subjectflow chart, Fig. 2). The median age was 64 years (46–84.7 y), and the sex ratio was 9/8 (female/male). Themedian Simplified Acute Physiology Score II was 33 (18.5–39.5). The main causes of respiratory failure were pneu-monia, (n � 9), cardiogenic pulmonary edema (n � 4),pneumothorax (n � 1), acute asthma (n � 1), pleuraleffusion (n � 1), and septic shock (n � 1). Eight subjects’initial neurological status prevented them from fulfillingthe Borg and visual analog scale evaluation, which is avail-able for the 9 remaining subjects. The median oxygen flowthrough the face mask prior to HFNC was 15 L/min (10.5–

15 L/min). The median SpO2was 90% (88.5–94%), and the

median respiratory rate was 28 breaths/min (25–32 breaths/min). HFNC was instituted 94.5 min (53.5–139.5 min)after subjects crossed the emergency room door, with amedian flow of 40 L/min (30–40 L/min) and a medianFIO2

of 1.0 (0.70–0.10). Compared to the variables at hourzero, while receiving oxygen therapy through face mask,HFNC was associated with a significant decrease in dys-pnea intensity in both the Borg score and the visual analogscale as early as 15 min (Table). After 15 min, respiratoryrate decreased significantly (P � .05) and SpO2

increasedsignificantly (P � .01) (see Table). These beneficial ef-fects were maintained throughout the study period (seeTable). Fewer subjects exhibited clinical signs of respira-tory distress after one hour of HFNC (10/17 vs 3/17,P � .03).

Some subjects had arterial blood gases performed im-mediately upon arrival (before oxygen therapy was started),and the attending physician did not repeat them duringconventional oxygen therapy. Similarly, some subjects im-proved so dramatically under HFNC that the attendingphysician did not require additional arterial blood gases. Inthe remaining subjects (n � 6) in whom arterial bloodgases were performed before and during HFNC, PaO2

in-creased significantly, from 61 mm Hg (56–74 mm Hg) to129 mm Hg (96–194 mm Hg) (P � .04), with no signif-icant changes in pH (7.40 [7.35–7.44] vs 7.42 [7.35–7.44],P � .80) or PaCO2

(40 mm Hg [34.5–47 mm Hg] vs 40[35.5–46] mm Hg, P � .90).

Nine subjects were hospitalized in the ICU and 8 in theED’s short course hospitalization unit. HFNC was contin-

Fig. 2. Subject flow chart.



ued for all subjects admitted to the ICU. Seven were suc-cessfully weaned from HFNC after a median time of useof 13.5 h (4–34.5 h) and fully recovered. Two requiredinvasive mechanical ventilation, and one subject ultimatelydied. In the ED’s hospitalization unit, 5 subjects for whomdo-not-resuscitate orders had been given died; the remain-ing 4 subjects were ultimately discharged.

Nine subjects were able to give their opinion of thedevice. All but one stated greater comfort with HFNC thanwith the face mask. Two of them declared having beendisturbed by the noise. Objective sound level measurementindicated that HFNC generated 55 dB, oxygen via the facemask 50 dB, and ambient noise in the ED oscillated be-tween 60–70 dB.

All caregivers (n � 17) judged HFNC more efficientthan conventional oxygen therapy through the face mask.There were 82% who estimated that subjects were morecomfortable with this device. In terms of set-up and man-agement, 65% found no difference between HFNC andconventional oxygen therapy, while 24% found HFNCless difficult and 12% more difficult to set up and manage.Altogether, 76% of healthcare givers declared preferringHFNC, as compared to conventional oxygen therapy.

Discussion

Our study shows for the first time the beneficial effectsof HFNC to alleviate dyspnea and improve respiratorystatus of patients presenting to the ED with respiratoryfailure. These beneficial effects were seen in both objec-tive parameters (respiratory rate and SpO2

) and subjectiveones (Borg score and visual analog scale). Our resultshighlight the fact that this technique is feasible and effec-tive in the ED and that it could be used as the first linetherapy in the most severe patients. Whether or not thistechnique can reduce the number of patients requiring ICUadmission and mechanical ventilation remains to be fur-ther addressed.

Several factors can account for the beneficial effects ofHFNC observed in our study. High gas flow enhanceswashout of the nasopharyngeal dead space19 and improves

oxygenation through greater alveolar oxygen content.20 Inaddition, high oxygen flow reduces ambient air entrain-ment by providing a better matching between patient’sinspiratory demand and oxygen flow, thus considerablyreducing oxygen dilution. The increase in patient oxygen-ation may blunt the respiratory drive induced by hypox-emia and decrease the sensation of dyspnea. A decrease ininspiratory nasopharyngeal resistance may also result fromthe use of high oxygen flow, enabling a decrease in thework of breathing.20 The use of high flows also generate acertain level of positive pressure,16,17,21 contributing to thepulmonary distending pressure and recruitment. Finally,by providing heated and humidified oxygen, HFNC re-duces the metabolic cost of gas conditioning and improveslung and airway mechanics through adequate inspiratorygas flow rheology.

Of note, we were able to start HFNC very shortly afterthe patients’ admission to the ED. Whether a prompt al-leviation of respiratory distress and a faster correction ofhypoxemia can alter the course of these patients and leadto less ICU admission and potential intubation, in com-parison with conventional oxygen therapy, remains to beproven in a randomized controlled trial. Nonetheless, ourresults constitute a prerequisite for this trial to be con-ducted.

One noticeable aspect of HFNC is its good tolerance.Some patients in respiratory distress receiving high flowoxygen through face masks often tend to pull off their facemask after some time because of discomfort or claustro-phobia, and whenever they want to talk or drink. HFNCoffers the advantage of enabling oral intake, and patientsare able to speak. In addition, nasal cannulae are less oftendislodged at nighttime then face masks.22 Finally, accep-tance of the new device by the caregivers was good; it wasnot found more difficult to set up than ordinary oxygentherapy. Potential indications for HFNC encompass acutehypoxemic respiratory failure, whatever its origin, al-though, because of the limited PEEP effect with HFNC,patients with severe cardiogenic pulmonary edema shouldbe initially managed with CPAP.23,24

Table. Changes in Dyspnea and Respiratory Parameters Comparing Conventional Oxygen Therapy to High Flow Nasal Cannula

H0 H � 15 min H � 30 min H � 60 min

Borg scale (n � 9) 6 (5–7) 4 (3–4)* 4 (2–4)† 3 (2–4)†Visual analog scale (n � 9) 7 (5–8) 5 (2–6)* 4 (2–6)† 3 (1–5)‡Respiratory rate, breaths/min (n � 17) 28 (25–32) 25 (23–30)* 25 (21–30)‡ 25 (21–28)†SpO2

, % (n � 17) 90 (88.5–94) 96 (90–99)‡ 95 (90–100)† 97 (92.5–100)†

Values are median (1QR).* P � .05.† P � .001.‡ P � .01.H0 � time just before switching from conventional oxygen therapy to high flow nasal cannula;



Due to preliminary attributes and because we wanted tocapture the feasibility and the potential benefits of HFNCas close as possible to the “real life” of the ED setting, thisstudy had several limitations. First, this study is limited bythe fact that it was conducted on a small number of sub-jects with varied diseases and incomplete data. The prin-cipal reason for this small sample was the availability ofthe device because just one device was used. Second, dueto the observational nature of the study in an unfavorableenvironment for clinical research, blood gases were per-formed in a limited number of subjects. The noticeableincrease in SpO2

seen in all the subjects suggests an in-crease in PaO2

in those subjects in whom arterial bloodgases were not performed, even if the magnitude of thisincrease is unknown. Third, as in other studies on HFNC,we did not measure actual delivered FIO2

or the level ofPEEP. Part of the improvement in oxygenation observedwith HFNC might thus be related to the delivery of higherFIO2

, in comparison with the face mask. The true deliveredFIO2

with these masks is an ongoing quest, and variesconsiderably, depending on the design of the mask, theflow rate, and the subject’s minute ventilation. Given thecharacteristics of our face mask (non-rebreathing with areservoir) and the high oxygen flow rates used, we believethat most of our subjects, if not all, had similar FIO2

tothose during HFNC. Recently, Roca et al, using similaroxygen flows, made the same assumption.10 Moreover,this study was not designed to be a randomized or con-trolled trial, so the ability to compare the improvementbetween the 2 devices would be prudent. In addition, be-cause of the considerable difference in gas temperature,level of humidification, and interface between the 2 de-vices, this study could not be blinded.

We are also aware that treatments other than oxygensupply provided in the ED might have contributed to thesubjects’ improvement. Nevertheless, given the very rapidimprovement observed in our subjects, we believe thatthese other treatments, such as antibiotics in case of pneu-monia, would not have had sufficient time to contributesignificantly to the observed improvement. A larger scalestudy is warranted to analyze the effect of HFNC accord-ing to the etiology of respiratory distress and perform asensitivity analysis.

Finally, the clinical relevance of a 3-point decrease inrespiratory rate may be questioned. High respiratory ratehas been shown, however, as an important predictor ofcardiac arrest or critical illness in hospitalized patients.25,26

Even subtle changes in this often-neglected vital sign27

may have an important prognostic impact.

Conclusions

Taken together, our results show rapid and sustainedalleviation of dyspnea and improvement in oxygenation

with HFNC in subjects with respiratory distress presentingto the ED. HFNC was well tolerated, more comfortable,and not more difficult to use than conventional oxygentherapy via a face mask. Our results suggest that HFNCcould constitute a first line therapy for selected patientspresenting to the ED with acute respiratory failure andunderline the need for more data in that setting.

ACKNOWLEDGMENTS

The authors would like to thank the nurses and the medical staff of thehospital’s emergency department for their active collaboration in the study.

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18. Borg GA. Psychophysical bases of perceived exertion. Med Sci SportsExerc 1982;14(5):377-381.

19. Dewan NA, Bell CW. Effect of low flow and high flow oxygendelivery on exercise tolerance and sensation of dyspnea. A studycomparing the transtracheal catheter and nasal prongs. Chest 1994;105(4):1061-1065.

20. Dysart K, Miller TL, Wolfson MR, Shaffer TH. Research in high flowtherapy: mechanisms of action. Respir Med 2009;103(10):1400-1405.

21. Spence KL, Murphy D, Kilian C, McGonigle R, Kilani RA. High-flow nasal cannula as a device to provide continuous positive airwaypressure in infants. J Perinatol 2007;27(12):772-725.

22. Costello RW, Liston R, McNicholas WT. Compliance at night withlow flow oxygen therapy: a comparison of nasal cannulae and Ven-turi face masks. Thorax 1995;50(4):405-406.

23. Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD.Effect of non-invasive positive pressure ventilation (NIPPV) on mor-

tality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet 2006;367(9517):1155-1163.

24. Vital FM, Saconato H, Ladeira MT, Sen A, Hawkes CA, Soares B,Burns KE, Atallah AN. Non-invasive positive pressure ventilation(CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Co-chrane Database Syst Rev 2008;(3):CD005351.

25. Fieselmann JF, Hendryx MS, Helms CM, Wakefield DS. Respira-tory rate predicts cardiopulmonary arrest for internal medicine inpa-tients. J Gen Intern Med 1993;8(7):354-360.

26. Hodgetts TJ, Kenward G, Vlachonikolis IG, Payne S, Castle N. Theidentification of risk factors for cardiac arrest and formulation ofactivation criteria to alert a medical emergency team. Resuscitation2002;54(2):125-131.

27. Cretikos MA, Bellomo R, Hillman K, Chen J, Finfer S, Flabouris A.Respiratory rate: the neglected vital sign. Med J Aust2008;188(11):657-659.

This article is approved for Continuing Respiratory Care Educationcredit. For information and to obtain your CRCE

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Original Research

A Preliminary Randomized Controlled Trial to Assess Effectivenessof Nasal High-Flow Oxygen in Intensive Care Patients

Rachael L Parke MHSc, Shay P McGuinness, and Michelle L Eccleston RN

OBJECTIVE: In a cardiothoracic and vascular intensive care unit, to compare nasal high-flow(NHF) oxygen therapy and standard high-flow face mask (HFFM) oxygen therapy in patients withmild to moderate hypoxemic respiratory failure. METHODS: In a prospective randomized com-parative study, 60 patients with mild to moderate hypoxemic respiratory failure were randomizedto receive NHF or HFFM. We analyzed the success of allocated therapy, noninvasive ventilationrate, and oxygenation. RESULTS: Significantly more NHF patients succeeded with their allocatedtherapy (P � .006). The rate of noninvasive ventilation in the NHF group was 3/29 (10%), comparedwith 8/27 (30%) in the HFFM group (P � .10). The NHF patients also had significantly fewerdesaturations (P � .009). CONCLUSIONS: NHF oxygen therapy may be more effective thanHFFM in treating mild to moderate hypoxemic respiratory failure. Key words: ventilation; nonin-vasive; nasal high flow therapy; oxygen; humidification. (Australian Clinical Trials Registry, http://www.actr.org.au, ACTRN012606000139572) [Respir Care 2011;56(3):265–270. © 2011 Daedalus En-terprises]

Introduction

High-flow oxygen therapy is a routine treatment forhypoxemic respiratory failure in extubated, self-ventilat-ing patients in the intensive care unit (ICU). This therapyis traditionally delivered via a face mask rather than nasalcannula, because of the flow limits of traditional nasal

cannula (4–6 L/min)1,2 and the tendency for patients inrespiratory distress to breathe through their mouths. Opti-flow (Fisher & Paykel Healthcare, Auckland, New Zea-land) is a new nasal high-flow (NHF) oxygen system thatallows the delivery of up to 60 L/min of heated and hu-midified, blended air and oxygen via wide-bore nasal can-nula. The system conditions the inspired gas to 37°C and44 mg H2O/L, which is considered thermodynamicallyneutral to the airway,3 preserving the function of the cil-iated mucosa.4 Recent work described complications asso-ciated with unhumidified high-flow face mask (HFFM) ox-ygen therapy, which include discomfort and airway drying.5

SEE THE RELATED EDITORIAL ON PAGE 355

Following the introduction of NHF oxygen therapy intoour ICU, we found that patients tolerated NHF well, thatNHF obviated NIV in some cases, and that NHF patientsremained well oxygenated, even with open-mouth breath-ing. Work by Wettstein and colleagues supports those ob-servations and suggests that the mouth may act as an an-atomical reservoir for oxygen in some cases.6 We alsobelieved that NHF has facilitated early ICU discharge,because it can be managed effectively in the postoperative

Rachael L Parke MHSc and Shay P McGuinness are affiliated with theCardiothoracic and Vascular Intensive Care Unit, Auckland City Hospi-tal, New Zealand. At the time of this research Michelle L Eccleston RNwas affiliated with the Cardiothoracic and Vascular Intensive Care Unit,Auckland City Hospital, New Zealand; she is now affiliated with Fisher& Paykel, Auckland, New Zealand.

The authors have disclosed a relationship with Fisher & Paykel, whichprovides funding to the Auckland District Health Board for the salary ofthe research nurse in the Cardiothoracic and Vascular Intensive CareUnit, Auckland City Hospital, Auckland, New Zealand.

Rachael L Parke MHSc presented a version of this paper at the 53rdInternational Respiratory Congress of the American Association for Re-spiratory Care, held December 1-4, 2007, in Orlando, Florida.

Correspondence: Rachael L Parke, MHSc, Cardiothoracic and VascularIntensive Care Unit, Auckland City Hospital, Private Bag 92024, Auck-land 1010, New Zealand. E-mail: [email protected].



ward. We hypothesized that NHF would also improve thesuccess of oxygen therapy and improve oxygenation.

Studies in healthy volunteers showed that NHF can de-liver an accurate FIO2

7,8 and generate positive nasopharyn-geal pressure, which increases with increased gas flow.7,9

This positive and linear relationship between flow andpressure was further substantiated in a cardiothoracic ICUpopulation.10,11

The objective of this clinical study was to evaluatewhether NHF would be better tolerated and with fewertreatment failures than HFFM in patients with mild tomoderate hypoxemia.

Methods

We conducted a prospective randomized comparativestudy in our 24-bed cardiothoracic and vascular ICU. Ourregional ethics committee approved this study. Fundingfor the study was provided by Fisher & Paykel: they sup-plied the Optiflow circuits used in this study, and theypaid for the statistical analysis. All 3 authors designed thestudy and were responsible for data collection, analysis,and writing the paper. The authors consulted employees ofFisher & Pakel Healthcare regarding study design and dataanalysis.

Sixty patients with mild to moderate hypoxemic respi-ratory failure (Table 1) were enrolled. Patients requiringimminent mechanical ventilation and patients under ordersnot to receive mechanical ventilation were excluded. Ran-domization was with a random-numbers table in spread-sheet software (Excel, Microsoft, Redmond, Washington).Patients were randomized in blocks of 4, to ensure evendistribution of sample size between the 2 study arms. Al-location concealment was maintained with opaque, sealedenvelopes.

We recorded demographic data, Acute Physiology andChronic Health Evaluation II score, Sequential Organ Fail-ure Assessment score, arterial blood gas values, SpO2

, re-spiratory rate, and heart rate at baseline, 30 min, 1 hour,

2 hours, and 4 hours after randomization, and then as perunit protocol.

Participants were randomly allocated to receive humid-ified high-flow oxygen via either NHF (Optiflow, withMR880 humidifier, RT241 heated delivery tube, RT033large/RT034 small, wide-bore nasal cannula, Fisher &Paykel Healthcare, Auckland, New Zealand) (Fig. 1) orHFFM (standard face mask, MR850 humidifier, RT308heated delivery tube and air entrainer, Fisher & PaykelHealthcare, Auckland, New Zealand) with an aerosol mask(Hudson RCI, TFX Medical, High Wycombe, United King-dom) (Fig. 2). The NHF group commenced therapy at aninitial flow of 35 L/min. Flow and FIO2

were titrated to anarterial oxygen saturation (SpO2

or arterial saturation viablood gas analysis [SaO2

]) of � 95%. The HFFM groupreceived humidified oxygen at 31°C and 32 mg H2O/L,also titrated to an SpO2

or SaO2� 95%.

We calculated NIV rate, PaO2/FIO2

, SpO2, and stay. Con-

tinuous SpO2data and instances of desaturation (SpO2

� 93%for more than 5 s) were collected with the BedMasterExsoftware (version 2.02, Excel Medical Electronics, Jupiter,Florida). We graphed the saturation data and highlightedthe desaturation episodes. All episodes were identified bytime point and cross referenced to screen shots of the SpO2

Table 1. Definition of Mild to Moderate Hypoxemic RespiratoryFailure

Receiving � 4 L/min O2 via nasal cannulafor more than 4 h and/orrespiratory rate � 25 breaths/min and/orincreased work of breathing, evidenced by clinical signs such asdyspnea, in-drawing, accessory-muscle use, and diaphoresis

ORReceiving � 6 L/min O2 via a face mask

for more than 2 h and/orrespiratory rate � 25 breaths/min and/orincreased work of breathing, evidenced by clinical signs such asdyspnea, in-drawing, accessory-muscle use, and diaphoresis.

Fig. 1. Optiflow high-flow nasal oxygen system.

Fig. 2. Standard high-flow face-mask oxygen system.

NASAL HIGH-FLOW OXYGEN IN INTENSIVE CARE PATIENTS


trace. Episodes were discounted if the SpO2trace indicated

signal interference or signal loss. Allocated therapy wasconsidered successful if the patients were maintained on orweaned from their assigned oxygen therapy within 24 hoursof enrollment. Failure of therapy was defined as worseningrespiratory failure that required a change in the respirato-ry-support device within 24 hours of study enrollment. Forexample, patients on HFFM requiring more respiratorysupport would be deemed to have failed at the point theywere escalated to NIV. Worsening respiratory failure wasdetermined by the treating clinician, based on evidence ofone or more of: increased dyspnea, respiratory fatigue,worsening gas exchange, or intolerance of allocated ther-apy. Patients who failed their allocated therapy were thentreated at the discretion of the treating clinician (Fig. 3).

Statistical analysis was carried out with statistics soft-ware (SAS 9.1, SAS Institute, Cary, North Carolina, andExcel, Microsoft, Redmond, Washington). PaO2

/FIO2was

calculated for the 4-hour period by simple averaging, ex-cluding baseline data because there was no evidence oftime trend, and compared with analysis of covariance ad-justed for baseline. Additional regression analysis of PaO2

/FIO2

was also conducted to account for age, sex, diagnosis,Acute Physiology and Chronic Health Evaluation II score,and Sequential Organ Failure Assessment score. We usedFisher’s exact test to compare differences in therapy suc-cess, number of patients who needed NIV, and number ofpatients with oxygen desaturations. Differences in desatu-

rations rate were tested assuming Poisson data. We usedanalysis of variance to analyze treatment differences intime from randomization to ICU discharge and hospitalstay, and the log rank statistic to analyze survival. P values� .05 were considered statistically significant.

Results

Sixty patients were enrolled, and data from 56 wereanalyzed. Four patients (one from the NHF group, and 3from the HFFM group) were excluded: 2 refused consentfor all data collection, and 2 failed the screening (seeFig. 3). Baseline demographics were similar (Table 2).

More NHF patients (26/29) than HFFM patients (15/27)succeeded on their allocated therapy (P � .006). Of the 12patients in the HFFM group who failed allocated therapy,7 received NIV, and 5 were switched to NHF, one ofwhom subsequently required NIV. The 3 patients in theNHF group who failed allocated therapy were all treatedwith NIV, and none of them were switched to HFFM.

The rate of NIV in the NHF group was 3/29 (10%),compared with 8/27 (30%) in the HFFM group (P � .10)(see Fig. 3).

Where continuous saturation data were successfully re-corded, the NHF group had significantly fewer desatura-tions (P � .009). Seventy-one percent (10/14) of the HFFMgroup had at least one desaturation, compared to 42%

Fig. 3. Consort diagram of patient flow through study.



(8/19) of the NHF group (P � .16) (Table 3). BaselineSpO2

was similar.We analyzed PaO2

/FIO2of patients who had complete

data available for the first 4 hours (28 NHF, 22 HFFM).PaO2

/FIO2did not differ significantly between the groups

(P � .08). However, an additional regression analysis withadjustment for other covariates showed a treatment effectin favor of NHF (P � .03).

Neither time from randomization to ICU discharge norhospital stay differed significantly (P � .20 and P � .11,respectively, via analysis of variance; note that the sur-vival analysis gave very similar results). Of the other mea-sured variables (arterial blood gas values, respiratory rate,heart rate, and SpO2

) only average pH over 4 hours showed

an effect, and only when adjusted for the covariates de-scribed above (P � .04).

Discussion

There are many options for delivering oxygen therapyto patients with hypoxemic respiratory failure. Cliniciansare tasked with selecting the most appropriate device tomeet the individual patient’s requirements. This study aidsthe clinician by adding to the limited body of evidenceabout high-flow oxygen devices used in the critical-careenvironment.

This study indicates that NHF may be more effectivethan HFFM for the treatment of mild to moderate hypox-

Table 2. Demographics and Baseline Measurements (n � 56)

HFFM NHF P

Male/female 23/4 21/8 .2Ethnicity .5

New Zealand European 18 14Other European 5 6New Zealand Maori 1 2Pacific Island 3 4Tahitian 0 1Other 0 2

Age (mean and range y) 64 (26–85) 64 (39–83) .9Primary Diagnosis .9

Vascular surgery 3 3Cardiac surgery 21 20Thoracic surgery 1 2Cardiology 1 2Respiratory 1 2

APACHE II score (mean and range) 12 (1–21) 12 (5–25) .4Arterial pH (mean � SD) 7.37 � 0.06 7.37 � 0.05 .7PaCO2

(mean � SD mm Hg) 42 � 7 43 � 7 .8PaO2

(mean � SD mm Hg) 73 � 16 77 � 14 .3SpO2

(mean � SD %) 92 � 6 94 � 2 .4Respiratory rate (mean � SD breaths/min) 18 � 8 21 � 7 .3Heart rate (mean � SD beats/min) 85 � 12 94 � 15 .01

HFFM � high-flow oxygen via face maskNHF � nasal high-flow oxygenAPACHE � Acute Physiology and Chronic Health Evaluation

Table 3. Desaturation Data

Patients(n)

Mean Desaturations(no.)

Mean DesaturationsPer Patient

Mean Hours onTreatment

Mean DesaturationsPer Hour

HFFM 14 26 1.86 55.3 0.47NHF 19 15 0.79 73.1 0.21

HFFM � high-flow oxygen via face maskNHF � nasal high-flow oxygen



emic respiratory failure. Prior to this study, Optiflow NHFhad been available in our ICU for 6 months, during whichtime our clinicians reported an increase in the use of NHFand an associated reduction in need for NIV. This studywas undertaken to quantitatively assess that trend.

We found a significant difference in therapy successbetween the NHF and HFFM groups. We believe that thisis because patients tolerated NHF better. The limited avail-able clinical literature identifies patient acceptability(comfort and tolerance) while maintaining oxygenation askey features of NHF that are likely to improve overalltreatment effectiveness.12-16 Studies that compared facemasks and nasal masks to nasopharyngeal oxygen de-livery devices found that patients described the latter asmore comfortable and more effective.13,17,18 Face maskmay cause discomfort, induce claustrophobia, and im-pede oral intake and communication.19 Nasal mask re-quires patent nasal passages and mouth closure to min-imize leak, and can cause pressure sores and tissuenecrosis over the nasal bridge.20 Collectively, these prob-lems may cause poor adherence to therapy17 and in-creased nursing time. In our ICU we heat and humidifyoxygen delivered via HFFM. It is possible that the treat-ment effect would have been greater if the HFFM grouphad received oxygen that was not heated and humidified.Chanques et al found fewer dryness symptoms in patientsusing HFFM with a heated humidifier than in those usinga bubble humidifier.5

NHF provides body-temperature-and-pressure-saturatedgas (37°C, 44 mg H2O/L), which is important for patientcomfort16 and improves mucociliary clearance.21 Long-term humidity therapy with NHF in patients with chronicrespiratory disease improved lung function and reducedexacerbation days.22 Rea and colleagues proposed that theseimproved clinical outcomes may be the result of enhancedlung mucociliary clearance.22 Improved secretion clear-ance might also be a possible mechanism of action in theacute-care environment.

A difference in NIV rates between the 2 groups wasfound in this study; however, it should be recognized thatthis study was not powered adequately to detect this treat-ment effect. When designing this preliminary study, therewere no data available to carry out a sample-size calcula-tion. A sample size of 60 patients was deemed feasible andpragmatic for this study.

There is evidence that high gas flow directly into thenares generates positive airway pressure,9-11 which mayimprove gas exchange and reduce respiratory effort. Na-sopharyngeal positive pressure may reduce nasopharyn-geal resistance during inspiration and provide expiratoryresistance, which appears to be transmitted down the air-ways, leading to improved lung volumes.23 Another pos-sible explanation for clinical benefit is washout of ana-tomical dead space.15,24,25 High incoming gas flow may

flush expired CO2-rich gas from the upper airways in ex-change for oxygen-enriched gas available for the patient’snext breath, simultaneously reducing rebreathing of CO2

and increasing the effective FIO2. Sim and colleagues as-

sessed inspired FIO2with NHF during simulated respira-

tory failure.8 The FIO2achieved with 100% oxygen via

NHF at 40 L/min was unaffected by simulated respiratoryfailure. This may well be explained by high incoming gasflow minimizing the variability of room-air entrainment asthe respiratory pattern changes.

During the study period clinicians began to see NHF asa preferred option for patients with hypoxemic respiratoryfailure. This explains the 5 patients who were switchedfrom their allocated HFFM to NHF during the course ofthe study. We presume that those patients would have beencommenced on NIV had NHF not been available. How-ever, in the context of this pragmatic study, the treatingclinician was allowed to select any therapy if the random-ized treatment failed. We deemed it unethical to withholdNHF if HFFM failed.

It was not practical to blind participants and staff to theallocated therapy—a problem inherent to many studies ofmedical devices and oxygen therapy systems. This prob-lem was mitigated by randomization techniques and thegroups being comparable at baseline. A limitation of thisstudy was the absence of documented guidelines or pro-tocols for escalating respiratory support therapy. Whenassessing respiratory function in the failing patient, staffreported using clinical judgment and indicators such asSpO2

, respiratory rate, and work of breathing in preferenceto arterial blood gas measurements. Stated criteria for es-calating therapy varied and included subjective decisionmaking a large proportion of the time.

These were interesting and unexpected findings of thisstudy and highlight the need for more informative studyguidelines to minimize bias when performing research inthe real world of intensive care medicine. Although a dif-ference was found in the number of desaturation episodesbetween the 2 groups, a major limitation of this study wasthe availability of data for analysis. The limited amount ofdata available was directly attributable to problems withthe software used to download data after hours when re-search staff were not in attendance. This has highlightedconsiderations for future studies that require continuousdata from bedside monitoring systems. This represents afailure in the execution of the study methodology andhighlights some of the challenges when conducting re-search in the real world. Because of the lack of detaileddata available we were unable to complete a comprehen-sive analysis to determine the degree of desaturation andtreatment required for each episode.

Despite the limitations of this study, NHF appears to bea promising new area of respiratory care that warrantsfurther investigation in large, well designed clinical trials.



Conclusions

NHF has a growing place in the repertoire of respiratorytherapies available in the intensive care environment. Inthis study NHF was more successful than HFFM in thetreatment of mild to moderate hypoxemic respiratory fail-ure. We hypothesize that the difference in NIV rate foundin this study is attributable to positive pressure deliveredby the Optiflow system. The results and lessons learnedfrom this preliminary randomized controlled trial will in-form the development of an appropriately powered studyinto the effect of NHF on respiratory therapy outcomes.

REFERENCES

1. Kallstrom, TJ; American Association for Respiratory Care. AARCClinical Practice Guideline. Oxygen therapy for adults in the acutecare facility: 2002 revision & update. Respir Care 2002;47(6):717-720.

2. O’Driscoll BR, Howard LS, Davison AG. BTS guideline for emer-gency oxygen use in adult patients. Thorax 2008;63(S6):vi1-vi68.

3. Ryan S, Rankin N, Meyer E, Williams R. Energy balance in theintubated human airway is an indicator of human gas conditioning.Crit Care Med 2002;30(2):355-361.

4. Williams R, Rankin N, Smith T, Galler D, Seakins P. Relationshipbetween the humidity and temperature of inspired gas and the func-tion of the airway mucosa. Crit Care Med 1996;24(11):1214-1216.

5. Chanques G, Constantin JM, Sauter M, Jung B, Sebbane M, VerzilliD, et al. Discomfort associated with underhumidified high-flow ox-ygen therapy in critically ill patients. Intensive Care Med 2009;35(6):996-1003.


7. Williams A, Ritchie J, Gerard C. Evaluation of a high flow nasaloxygenation system: gas analysis and pharyngeal pressures (abstract).Intensive Care Med 2006;32(S1):S219.

8. Sim MA, Dean P, Kinsella J, Black R, Carter R, Hughes M. Perfor-mance of oxygen delivery devices when the breathing pattern ofrespiratory failure is simulated. Anaesthesia 2008;63(9):938-940.

9. Groves N, Tobin A. High flow nasal oxygen generates positive air-way pressure in adult volunteers. Aust Crit Care 2007;20(4):126-131.

10. Parke R, McGuinness S, Eccleston M. Nasal high-flow therapy de-livers low level positive airway pressure. Br J Anaesth 2009;103(6):886-890.

11. Parke RL, Eccleston M, McGuinness S. Delivering nasal high flowoxygen therapy at increasing gas flow rates generates higher airwaypressure. Respir Care 2011; in press.

12. Price AM, Plowright C, Makowski A, Misztal B. Using a high-flowrespiratory system (Vapotherm) within a high dependency setting.Nurs Crit Care 2008;13(6):298-304.

13. Tiruvoipati R, Lewis D, Haji K, Botha J. High-flow nasal oxygen vs.high-flow face mask: A randomized crossover trial in extubatedpatients. J Crit Care 2010;25(3):463-468.

14. Turnbull B. High-flow humidified oxygen therapy used to alleviaterespiratory distress. Br J Nurs 2008;17(19):1226-1230.

15. Lomas C, Roca O, Alvarez A, Masclans J. Fibroscopy in patientswith hypoxemic respiratory insufficiency: utility of the high-flownasal cannula. Respir Med 2009;2(3):121-124.

16. Waugh JB, Granger WM. An evaluation of 2 new devices for nasalhigh-flow gas therapy. Respir Care 2004;49(8):902-906.

17. Eastwood G, Reeves J, Cowie B. Nasopharyngeal oxygen in adultintensive care-lower flows and increased comfort. Anaesth IntensiveCare 2004;32(5):670-671.

18. Eastwood G, Dennis M. Nasopharyngeal oxygen (NPO) as a safeand comfortable alternative to face mask oxygen therapy. Aust CritCare 2006;19(1):22-24.

19. Sasaki H, Yamakage M, Iwasaki S, Mizuuchi M, Namiki A. Designof oxygen delivery systems influences both effectiveness and com-fort in adult volunteers. Can J Anesth 2003;50(10):1052-1055.

20. Evans T, Albert R, Angus D, Bion J, Chiche J, Epstein S, et al.International consensus conferences in intensive care medicine: non-invasive positive pressure ventilation in acute respiratory failure.Am J Respir Crit Care Med 2001;163(1):283-291.

21. Hasani A, Chapman TH, McCool D, Smith RE, Dilworth JP, AgnewJE. Domiciliary humidification improves lung mucociliary clearancein patients with bronchiectasis. Chron Respir Dis 2008;5(2):81-86.

22. Rea H, McAuley S, Jayaram L, Garrett J, Hockey H, Storey L, et al.The clinical utility of long-term humidification therapy in chronicairway disease. Respir Med 2010;104(4):525-533.

23. Fraser JF, Corley A, Caruana LR, Tronstad O, Barnett AG. Nasalhigh flow oxygen increases end expiratory lung volumes, improvesoxygenation and reduces work of breathing: a study using electricalimpedance tomography (abstract). Am J Respir Crit Care Med 2010;181(Suppl):A1668.

24. Dysart K, Miller TL, Wolfson MR, Shaffer TH. Research in highflow therapy: Mechanisms of action. Respir Med 2009;103(10):1400-5.

25. Chatila W, Nugent T, Vance G, Gaughan J, Criner GJ. The effects ofhigh-flow vs low-flow oxygen on exercise in advanced obstructiveairways disease. Chest 2004;126(4):1108-1115.

This article is approved for Continuing Respiratory Care Educationcredit. For information and to obtain your CRCE

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Is Humidification Always NecessaryDuring Noninvasive Ventilation in the Hospital?

Richard D Branson MSc RRT FAARC and Michael A Gentile RRT FAARC

IntroductionNormal HumidificationHumidification During Invasive VentilationPro: Humidification Is Needed During Noninvasive Ventilation

Patient ComfortAirways ResistanceSecretion Retention and RemovalSuccess of Noninvasive Ventilation

Con: Humidification Is Not Needed During Noninvasive VentilationLong-Term Versus Short-Term Noninvasive VentilationAmbient Air Supplies Enough Humidity for Short-Term Noninvasive

VentilationCost Versus Benefit of Humidification During Noninvasive VentilationEvidence Is Strong to Eliminate the Heat-and-Moisture Exchanger

From the Noninvasive Ventilation CircuitSummary

Noninvasive ventilation (NIV) is a standard of care for the treatment of exacerbation of chronicobstructive pulmonary disease, to prevent intubation and reduce morbidity and mortality. The needfor humidification of NIV gas is controversial. Some unique aspects of NIV conspire to alter thedelivered humidity and airway function. In the presence of air leaks, unidirectional air flow driesthe airways and increases airway resistance. Patient comfort is also a critical issue, as tolerance ofNIV is often tied to patient comfort. This paper provides the arguments for and against routinehumidification during NIV in the hospital setting. Data from clinical research demonstrate theeffects of delivered humidification on relevant physiologic variables. The impact of humidificationon NIV success/failure remains speculative. Key words: mechanical ventilation; noninvasive ventila-tion; NIV; humidification; chronic obstructive pulmonary disease. [Respir Care 2010;55(2):209–216.© 2010 Daedalus Enterprises]

Richard D Branson MSc RRT FAARC is affiliated with the Departmentof Surgery, University of Cincinnati Medical Center, Cincinnati, Ohio.Michael A Gentile RRT FAARC is affiliated with the Division of Pul-monary and Critical Care Medicine, Duke University Medical Center,Durham, North Carolina.

Mr Branson and Mr Gentile presented a version of this paper at the 44thRESPIRATORY CARE Journal Conference, “Respiratory Care Controver-sies II,” held March 13-15, 2009, in Cancun, Mexico.

Mr Branson has disclosed relationships with Ikaria, Bayer, Newport,CareFusion, and Covidien. Mr Gentile has disclosed no conflicts of in-terest.

Correspondence: Richard D Branson MSc RRT FAARC is affiliated withthe Department of Surgery, University of Cincinnati Medical Center,PO Box 670558, 231 Albert Sabin Way, Cincinnati OH 45267-0558.E-mail: [email protected].


Introduction

Noninvasive ventilation (NIV) for the treatment of ex-acerbation of chronic obstructive pulmonary disease(COPD) to prevent endotracheal intubation reduces mor-bidity and mortality.1-3 Ancillary therapies, including bron-chodilator, fluid management, and secretion clearance, arepart of a successful NIV program.4 The appropriate appli-cation of humidification during NIV, however, is poorlyunderstood and not uniformly accomplished.5 This issuerequires further study, as humidification may play an im-portant role in the success of NIV, because it relates tosecretion removal and patient comfort.

We will address the points of contention regarding hu-midification during NIV, discuss the available evidence,and, where evidence is lacking, provide our opinions onbest practice, based on our experience. Data supportingboth sides of the argument will be presented, with a finalconsensus as a goal.

Normal Humidification

The respiratory tract heats and humidifies inspired gasso the gas entering the alveoli is warmed to body temper-ature and fully saturated with water vapor. This conditionis commonly referred to as body temperature, atmosphericpressure, and saturated with water vapor (BTPS).6 Duringnormal breathing through an intact upper airway, inspiredgas entering the trachea is warmed to 29–32°C and is fullysaturated with water vapor. In the mid-trachea, tempera-ture and absolute humidity reach approximately 34°C andabsolute humidity is 34–38 mg H2O/L.7-9 The point atwhich the gas reaches 37°C and 100% relative humidity(which corresponds to an absolute humidity of44 mg H2O/L) is known as the “isothermic saturation bound-ary,”6 which is located below the carina during quiet breath-ing, in the third to fifth generation of the bronchial tree.6,8

Humidity and temperature are constant below the isother-mic saturation boundary, while above the isothermic sat-uration boundary the airway acts as a counter-current heat-and-moisture exchanger.6 Heat and moisture exchangecontinues as long as there is a thermal and moisture dif-ference between the gas and the airway mucosa: the greaterthe difference, the greater the transfer of heat and water.During hyperventilation or when cold, dry air enters thetrachea; the isothermic saturation boundary moves furtherdown the bronchial tree, pressing the lower respiratorytract into assisting with heat and moisture exchange.10,11

Expiratory gas is cooled when traversing the airway abovethe isothermic saturation boundary, resulting in water con-densation. However, the upper airway recovers only a partof the added inspiratory heat and moisture. During normalbreathing, the temperature of expired air ranges from 32°Cto 34°C at 100% relative humidity.

Under normal conditions for room air (temperature 22°C,relative humidity 50%, ambient humidity 9 mg H2O/L)and with a minute ventilation (VE) of approximately 8 L/min, the respiratory tract evaporates about 400 g of waterduring inspiration each day, and approximately 150 g ofwater condenses during expiration, so the daily water needfor respiratory humidification is about 250 g.9,10

Humidification of inspired gas is typically provided byevaporation of water from tracheobronchial secretions. Thelatent heat of vaporization is the heat that must be added toa liquid to change its state to vapor at a given temperature(or the amount of heat released when vapor condenses toa liquid).11 The latent heat of vaporization of water isapproximately 540 kcal/kg. As liquid water evaporates,sensible heat in the liquid is converted to latent heat in thevapor leaving the liquid, and the temperature of the re-maining liquid falls. Evaporation cools the airway. Themore water evaporating from the airway surface, the greaterthe airway temperature drop in that airway surface area.12

However, in the airway this cooling effect is partially com-pensated for by heat and water provided by the bronchialblood flow. In a normal adult the daily respiratory evap-orative heat loss is approximately 250 kcal, 65–70 kcal ofwhich are recovered by condensation during expiration.12,13

The intensity of heat and moisture exchange increaseswith breathing dry and cold air, and with increasing VE.When ventilation is provided via face mask instead of viaendotracheal tube, the inspired gas is heated and humidi-fied by the upper airways. NIV is a special circumstance ofthe patient breathing a high VE of cool, dry gas. WhenNIV is supplied via an intensive-care ventilator, the gas istypically anhydrous wall air and/or oxygen. Devices thatuse room air provide a slightly higher humidity. The leakcompensation of many NIV devices creates high flowthroughout the respiratory cycle, which also contributes torespiratory heat and moisture loss.14 During NIV, patientsoften breathe mainly via the oral route, which is less ef-ficient than nasal breathing. Dry mouth is one of the mostfrequently reported adverse effects of NIV.

Humidification During Invasive Ventilation

Humidification during invasive mechanical ventilationis a standard of care.15,16 Delivery of cool, anhydrous gasfrom institutional compressed air and liquid oxygen sys-tems to a patient with an instrumented airway, bypassingthe normal mechanisms of heat and humidification, hasdire consequences, including alterations in tracheobron-chial structure and function, inspissated secretions, mucusplugging of airways, endotracheal-tube occlusion, ciliarydyskinesis, and epithelial desquamation.17-21

There is agreement among clinicians that heating andhumidifying inspired gas during invasive ventilation are

IS HUMIDIFICATION ALWAYS NECESSARY DURING NONINVASIVE VENTILATION IN THE HOSPITAL?


required. The 2 general approaches for supplying heat andhumidification are (1) “active” (heated humidifier that uti-lizes an external power source and water supply), and(2) “passive” (heat-and-moisture exchanger [HME], whichrecycles the patient’s own heat and humidity).

However, the amount of heat and moisture that shouldbe delivered, and the device used, remain an area of de-bate. Clinical decision making on humidification requiresan understanding of the patient’s pathophysiology and theavailable equipment. Clearly, device selection must bebased on the patient’s lung disease, ventilator settings,intended duration of use, and other factors (eg, presence ofleaks, body temperature). Recent changes in the practiceof mechanical ventilation, particularly the use of smalltidal volume (VT) (4–6 mL/kg predicted body weight)also impact the choice of humidifier.21,22

Though heat and humidification of inspired gas is aclear standard of care in invasive ventilation, there are noagreed upon goals, so it is no surprise that standards forhumidification during NIV remain controversial.

Pro: Humidification Is NeededDuring Noninvasive Ventilation

NIV encompasses a myriad of therapies, from continu-ous positive airway pressure (CPAP) for sleep apnea athome and for cardiogenic pulmonary edema in pre-hospi-tal care, to high levels of ventilatory support in the hos-pital. Extensive literature demonstrates the benefits of hu-midification to improve comfort and tolerance of nasalCPAP for sleep apnea.23-39 However, our debate concernshumidification during NIV for COPD exacerbation in thehospital.

Patient Comfort

Successful NIV is predicted by improved patient com-fort, because the work of breathing is reduced. This ismost noticeable as decrease in accessory muscle use andrespiratory rate. Oxygen saturation may increase, and dys-pnea is relieved.1,3,4 Mask fit and leak around the maskalso impact patient comfort.3

Humidification can also affect patient comfort and, there-fore, NIV tolerance. In 16 patients with chronic hypercap-nia, Nava et al compared patient adherence to long-termNIV, airway symptoms, adverse effects, and number ofsevere pulmonary exacerbations that required hospitaliza-tion. In a randomized, crossover fashion, all the patientsused heated humidification for 6 months, and an HME for6 months. The investigators followed adverse effects ofNIV and patient-reported severity scores for each adverseeffect. They found fewer adverse effects with heated hu-midification (Table 1), including fewer sinus infectionsand pneumonias, although that difference was not statis-

tically significant. Hospitalizations for exacerbations weretwice as frequent in the HME group, although the inci-dence was low in both groups and not significantly differ-ent.31 The study used 2 types of humidification and foundbetter comfort with the heated humidifier. Comparison tono humidification would probably lead to even more dis-parate findings.

Lellouche and co-workers recently evaluated humidifi-cation during NIV in normal volunteers. They comparedno humidification to heated humidification and HME.32

They used 2 different ventilators: one with a turbine thatdelivers room air, and one intensive-care ventilator thatuses compressed air and oxygen inputs, and altered in-spired oxygen settings. The normal volunteers breathed onCPAP without humidification, with heated humidification,and with HME, at normal (10 L/min) and elevated (21 L/min) VE, and with and without leaks around the mask. Thedelivered humidity was measured, and the subjects ratedtheir comfort with a mucosal dryness 0–10 scale. No hu-midification delivered an absolute humidity of around5 mg H2O/L. The HME provided nearly 30 mg H2O/L, butthat value fell 30% in the presence of mask leak. Theheated humidifier provided 30 mg H2O/L regardless ofmask leak. Interestingly, the comfort scores were similarfor humidity ranges from 15 to 30 mg H2O/L, but with nohumidification (5 mg H2O/L) the comfort scores were halfof those with HME or heated humidifier. With no humid-ification the volunteers reported severe discomfort relatedto mouth dryness. The observation period was only 1 hour,and the discomfort associated with longer periods of un-humidified NIV would probably be magnified.

These data are compelling in light of the experiencewith long-term nasal ventilation at home, where two thirdsof patients report upper airway drying and discomfort.Hospitalized patients are more likely to have elevated VE,

Table 1. Adverse Effects With Heated Humidifier and Heat-and-Moisture Exchanger*

SymptomsBaseline

(%)Heated Humidifier

(%)HME(%)

Dry nose 21 28 42Runny nose 7 14 14Postural drip 0 0 7Nasal congestion 21 21 28Epistaxis 0 0 0Reduced sense of smell 7 28 28Sinus infection 14 36 50Dry throat 7 7 14Sore throat 7 7 7Cough 43 36 43

* Percent of patients who reported these adverse effects before (baseline) and during 6 monthsof using heated humidifier and 6 months of using heat-and-moisture exchanger (HME).(Data from Reference 31.)



fever, and dehydration, and more likely to receive oxygenand to have large mask leaks, which all contribute to upperairway dryness and discomfort. There is little doubt thatfailure to humidify gas, even during short-term NIV, re-sults in patient discomfort. As patient comfort is importantto NIV success, humidification probably improves NIVsuccess (Fig. 1).

Airways Resistance

The cooling of airway mucosa results in heat and mois-ture loss and drying, which increases airway resistance.Richards and colleagues found that 40% of patients onnasal CPAP reported dry nose and throat and sore throatduring therapy, probably due to mouth leak and the result-ing unidirectional gas flow.37 With normal volunteers, Rich-ards and colleagues found that during CPAP with a mouthleak, nasal airway resistance increased by a factor of three,but heated humidification ameliorated that increase in air-way resistance. A cool pass-over humidifier did not reducenasal airway resistance.37

Tuggey and colleagues studied the effect of mouth leakduring nasal NIV on VT, nasal resistance, and comfort.38

Following a mouth leak of approximately 40 L/min, theyfound increased nasal resistance, which resulted in a small(12%) but significant reduction in expired VT during pres-sure-targeted NIV. Heated humidification attenuated boththe nasal-resistance and VT changes. Comfort was greaterwith heated humidification, which also reduced the in-creased discomfort that followed a period of mouth leak.The short duration of observation (5 min) suggests thatpatients admitted to the hospital requiring NIV will haveeven greater alterations in resistance. The leak in this study(40 L/min) was similar to the leaks seen during in-hospitalNIV.38

Fischer et al found that nasal CPAP without humidifi-cation significantly decreased nasal humidity, which is a

key factor in the development of increased nasal resis-tance.39

The issue of mask leak is critical and unique to NIV.The normal respiratory tract operates as a counter-currentHME. When gas flow becomes unidirectional, all the mois-ture is lost because there is no chance to reclaim moisture.This also explains the reduced efficacy of an HME duringNIV.

Secretion Retention and Removal

Secretion management in the ventilated patient is ac-complished with various common and exotic techniques.40

Preservation of the patient’s innate cough mechanism isone of the many advantages of NIV over endotrachealintubation. However, nasotracheal suctioning is more trau-matic than suctioning via the endotracheal tube. In theintubated patient the secretion-management techniques aresuctioning and humidification.

The efficiency of heated humidification during NIV canbe adversely affected by the type of ventilator, elevatedfraction of inspired oxygen (FIO2

), and leak around themask or through the mouth during nasal NIV.41-43 Giventhe high flow, low humidity, and complications of unidi-rectional flow associated with NIV, and the ever presentleaks, drying of the respiratory mucosa and secretions isinevitable. While this remains a critical issue for NIV, ithas not been often studied. In a recent presentation at themeeting of the American Thoracic Society, Esquinas andcolleagues introduced some insight into this problem.44

They conducted an international survey to determine hu-midification practices and the relationship of those prac-tices to untoward outcomes. Data from 15 hospitals and1,635 patients were analyzed. They found that in patientswho failed NIV, difficult intubation was encountered in 88(5.4%), and in that group, failure to use humidificationwas the leading factor in predicting difficult intubation.Approximately half of the difficult-intubation patients hadnever received humidification during NIV. Forty-sevenpercent of the patients used a heated-wire-circuit humidi-fier, and 15% used pass-over humidifiers. Forty percent ofthe hospitals reported no protocols for humidification dur-ing NIV.

The most likely cause of difficult intubation is mucosaldrying and secretion retention. The presence of thick mu-cus in the oropharynx, and fragile, dry mucosa clearlycreate a difficult environment for endotracheal tube place-ment.

Success of Noninvasive Ventilation

NIV represents one of the great paradigm shifts in me-chanical ventilation over the last decade. The data on out-come improvements in patients with COPD exacerbation

Fig. 1. Patient comfort before, during, and after air leak, with andwithout humidification during noninvasive ventilation. (From datain Reference 39.)



are compelling. Successful NIV includes the appropriateselection of the patient, the NIV interface, the ventilator,and the variables chosen to identify NIV success/failure.Patient comfort is both a goal of NIV therapy and predic-tor of NIV success. Early time commitment while estab-lishing NIV also pays dividends in patient tolerance andNIV success.

The role of humidification in NIV success has beenunderappreciated. Table 2 lists the factors related to hu-midification that impact NIV therapy. Humidification im-proves patient comfort and therefore tolerance, and en-hances airway function and secretion removal. This is onearea of NIV that deserves further study in the near future.

Con: Humidification Is Not Needed DuringNoninvasive Ventilation

The success of NIV in avoiding endotracheal intubationin patients with COPD and congestive heart failure is in-disputable.1-3 Numerous clinical randomized controlled tri-als and meta-analyses have concluded that, compared tostandard care, NIV reduces dyspnea and respiratory dis-tress, improves gas exchange, reduces the need for intu-bation by up to 50%, and decreases mortality.45-48 How-ever, evidence is lacking to support the routine use ofactive humidification during NIV. Similar to the debateabout HME versus active humidification in invasive ven-tilation, there is no published recommendation or guide-line concerning the type of humidification that should beprovided during NIV for acute respiratory failure.

Clinical trials that have examined various humidifica-tion methods in intubated patients cannot be extrapolatedto NIV applications. Without supplemental humidificationthe gas may be dryer when an intensive-care ventilator isused. But, in contrast with an intubated patient, the upper

airways are not bypassed during NIV. Additionally, nostudies of humidification during NIV have measured quan-tifiable clinical outcomes, so the question of whether hu-midification during NIV affects outcome remains unan-swered. However, this lack of data for any associationbetween supplemental humidification and NIV failure andtolerance does not indicate that patient comfort is not in-fluenced by the absence of humidification. Important ques-tions remain regarding how much humidification is re-quired during NIV, and if it affects clinical outcomes.

Long-Term Versus Short-Term NoninvasiveVentilation

The clinical application of NIV in the acute setting typ-ically serves a single purpose: to avoid endotracheal intu-bation. Numerous randomized controlled clinical trials havedescribed successful use of NIV to accomplish that goal.45-49

The amount of time patients remained on NIV was vari-able, but only a few clinical trials mention the use ofhumidification, instead focusing on the patient interfaceand positive-pressure devices/parameters. Also of note isthat the patients who failed NIV and required intubationusually did so within 12 hours. A systematic review byRam and colleagues49 included 8 studies and found that,compared to usual care, NIV was associated with greaterimprovements in pH (weighted mean difference 0.03,95% CI 0.02 to 0.04), PaCO2

(weighted mean difference–0.40 mm Hg, 95% CI –0.78 to –0.03), and respiratoryrate (weighted mean difference –3.08 breaths/min, 95% CI–4.26 to –1.89) after 1 hour of treatment. The major find-ing was that patients responded to NIV within 1 hour,which indicates that humidification is not required for pa-tients who require NIV for only a short period.

In theory it appears logical to humidify gas deliveredvia NIV. However, NIV has traditionally been deliveredwith just ambient air, and questions remain as to who willbenefit from NIV humidification. During NIV, humidifi-cation takes place in the upper airways. Typically, NIV isused in patients with hypoxia, hypercarbia, and resultingrespiratory acidosis. It is unclear if any of these gas-ex-change impairments would benefit from supplemental hu-midification during NIV. It is possible that humidified gassimply makes NIV more tolerable when the face and upperairways come in contact with humidified gas. Physiolog-ical humidification mechanisms are not bypassed duringNIV, as compared to during invasive ventilation via anartificial airway. It may be useful to add supplementalhumidification in patients who have thick, retained, ortenacious secretions, or if nasal dryness/congestion inter-feres with NIV patient adherence and/or tolerance. Patientdiscomfort could occur from inspiration of dry gas, but towhat extent this discomfort may lead to NIV failure is

Table 2. Factors Related to Humidification During NoninvasiveVentilation

Patient IssuesComfortAirway resistanceReduced tidal volumeIncreased work of breathingDead spaceSecretion retentionFailure of therapyDifficult intubation

Device IssuesMinute ventilationFraction of inspired oxygenMask leakMouth leak during nasal noninvasive ventilationVentilator driving system



unknown. Clinical studies are needed to determine thebenefits of humidifying NIV gas.

Ambient Air Supplies Enough Humidity for Short-Term Noninvasive Ventilation

Heated humidification is most often used during me-chanical ventilation via an artificial airway. There is gen-eral agreement that 30 mg H2O/L is the theoretical mini-mum humidity to ensure adequate gas conditioning duringinvasive ventilation,44 However, it is not known if30 mg H2O/L is also required for NIV, during which theupper airways heat and humidify the inspired gas. Dataprovided by Lellouche et al suggest that the minimumabsolute humidity required during NIV is 15 mg H2O/L.43

Admittedly, there is a dramatic reduction in absolute hu-midity, down to 5 mg H2O/L, during NIV without humid-ification.44 Is that low humidity relevant for short-termNIV, when the threshold for improvements is measured at1, 2, 4, or 12 hours? To date there are no published data toassist clinicians in addressing this issue.

Cost Versus Benefit of Humidification DuringNoninvasive Ventilation

The majority of clinical trials that have measured out-comes of NIV have concentrated on NIV failure, definedby intubation, intensive care unit stay, hospital stay, andmortality. Other measurements assessed have been com-fort, adherence, and tolerance. Cost considerations enterinto the conversation with all medical procedures, andNIV is no exception. With no decisive evidence providingguidance, the question is whether the potential benefits ofhumidification outweigh the cost. Studies of NIV financialcosts have evaluated numerous factors, including person-nel, training, capital equipment, and other costs.50-52 Tworecent surveys of academic medical center emergency de-partments and Veterans Affairs hospitals discussed tech-nical aspects of NIV, such as NIV interfaces and devices,but failed to address humidification.53,54 The additionalequipment required for NIV humidification (humidifier,sterile water, heating chamber, specialized circuit) addsconsiderably to the procedural costs.

Evidence Is Strong to Eliminate the Heat-and-Moisture Exchanger From the NoninvasiveVentilation Circuit

It is rare to place an HME into an NIV circuit. The firstconcern is the large amount of dead space added by theHME. Additionally, the gas flow associated with NIV ismostly unidirectional, due to inherent leaks in the gasdelivery path. Thus, the amount of heat and moisture thatcan be exchanged is dramatically decreased. Despite the

physiologic concerns about greater dead space and lowefficiency with an HME, 2 studies evaluated the physio-logic effects of HME versus heated humidification.43,55

The results demonstrated that HME increases the work ofbreathing and may decrease patient adherence to therapyand ultimately cause NIV failure. The greater dead spacewith an HME may create an intolerable situation becauseof flow resistance and work of breathing. It is important toremember that an HME can affect ventilator triggering,and caution needs to be exercised.

Summary

Controversy continues concerning whether supplemen-tal humidification is routinely required during NIV in theacute-care setting. Gas law principles and clinical experi-ence suggest humidification may be added as warranted bypatient comfort and duration of NIV. Evidence is lackingto support the routine use of active humidification duringNIV. Few data have been reported in the field of NIVregarding humidification devices.

Should humidification be used with all patients receiv-ing NIV? Currently, information is not available to answerthat question. Only a properly designed randomized con-trolled clinical trial comparing outcomes of NIV patientsreceiving humidification versus ambient air will answerthe question. Potential clinical variables to measure in-clude improvements in gas exchange, intubation rate, andsubjective improvement in patient symptoms while usinghumidified versus ambient gas. The answer will assist inthe development of future consensus statements and prac-tice guidelines.

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Discussion

Gay: Mike, I admire your tenacityin trying to support the con argument.I’m a little surprised that you didn’ttry to use the relatively low infectionrate associated with humidification.Regardless, I think you have to givecredence to the CPAP literature, withthe evidence review1 that shows com-pelling data that humidification in-creases patient adherence to and tol-erance of CPAP, to the extent that evenCMS [Centers for Medicare and Med-icaid Services] pays for it, and there isnot a single device being produced nowthat doesn’t have built in humidifica-tion.

1. Gay P, Weaver T, Loube D, Iber C; Pos-itive Airway Pressure Task Force; Stan-dards of Practice Committee; AmericanAcademy of Sleep Medicine. Evaluationof positive airway pressure treatment forsleep related breathing disorders in adults.Sleep 2006;29(3):381-401.

MacIntyre: Might that be a short-term versus long-term phenomenon?

Gay: It could be, and I accept thatargument, because in most of the NIVstudies the patients were only on NIVfor hours. To the extent that you prob-

ably can’t show a great difference be-tween those who do and do not gethumidification in a randomized con-trolled trial, it doesn’t necessarily saythat it wouldn’t be a reasonable thingto do, given the lack of problematicsituations that you get in by usingheated humidity. I will raise my handalready to say, “Yes, we use it on ev-erybody.”

Borg:* Many French studies havebeen shown—and now the French re-quire us, from an industry standpoint,to provide humidifiers to long-termNIV patients. There is no way youcould get away with not doing it.

Gentile: I agree that it must be pro-vided during long-term NIV. I knowseveral people who wear CPAP atnight, and they say humidification isessential. But in all patients, especiallyshort-term patients coming through theemergency department, I don’t thinkit’s worth it.

Branson: Three hours total NIV, or3 hours in the emergency department?

Gentile: Three hours total.

Branson: Sounds like you’re non-invasively ventilating people whodon’t need NIV.

Gentile: We’re just good. We’vebeen doing it a long time. There wereseveral that were outliers, but eitherthey got better or they got intubated.

Branson: This issue has taken on re-newed importance for me. Some of ournew attendings will have patients onNIV on 60% oxygen and PEEP of10 cm H2O, and they’re on NIV for 12to 18 hours, and I’m begging them tointubate, but they keep trying to con-vince me that NIV is going to work.And in some of these patients whohaven’t gotten humidification, whenwe’re trying to intubate them, the firstthing we encounter is a big clot of mu-cus in the back of the throat, so youcan’t even see the vocal cords. I thinkthe answer is, the higher the FIO2

, thesicker the patient; the higher the pres-sure, the more you have to use a hu-midifier during NIV.

Gentile: I totally agree. Hey, I didn’tpick the con side of this debate.* Ulf Borg, Covidien, Boulder, Colorado.



PRESIDENTEPRESIDENT AND FOUNDING MEMBER

MARTA LAZZERI

[email protected]

VICE PRESIDENTEVICE PRESIDENT AND FOUNDING MEMBER

GIOVANNI OLIVA

[email protected]

SEGRETERIASECRETARY

ANNA BRIVIO

[email protected]

TESORIERETREASORER

ALESSIA COLOMBO

CONSIGLIERIBOARD

EMILIA PRIVITERA

GIANCARLO PIAGGI

ELENA REPOSSINI

ANTONELLA SANNITI

MAURIZIO SOMMARIVA

SERGIO ZUFFO

CONSIGLIERI ONORARIHONORARY BOARD

ROBERTO ADONE

MONICA BASSI

ANDREA BELLONE

ITALO BRAMBILLA

DALLO STATUTO DELLA ASSOCIAZIONE

Art. 1: è costituita l’Associazione Riabilitatoridell’Insufficienza Respiratoria (A.R.I.R.).

Art. 3: l’Associazione non ha finalità di lucroe intende promuovere la prevenzione e lariabilitazione delle patologie respiratorie. Per il conseguimento dei suoi scopil’Associazione concorre a:• Diffondere in campo clinico terapeutico e home care, la pratica della fisioterapia e riabilitazione respiratoria.• Organizzare la formazione, l’aggiornamento,il coordinamento, la promozione dello sviluppoprofessionale dei fisioterapisti con specifichecompetenze in ambito respiratorio.• Sostenere in campo scientifico e socialel’educazione e l’igiene respiratoria.• Promuovere la ricerca scientifica nel campodella fisioterapia e della riabilitazionerespiratoria.

Art. 4: sono soci le persone e gli enti cheverranno ammessi dal Consiglio e cheverseranno la quota di Associazione.

Art. 5: i soci si dividono in quattro categorie:1. soci fondatori2. soci ordinari3. soci sostenitori4. soci onorariSono soci fondatori coloro che hanno sottoscrittol’atto Costitutivo dell’Associazione e coloro i qualipur non avendo sottoscritto l’atto costitutivo siaattribuita dal Consiglio tale qualifica.Sono soci ordinari i fisioterapisti accettati dalConsiglio direttivo e che versano annualmentela quota associativa stabilita Sono soci sostenitori persone fisiche egiuridiche che intendono sostenere gli scopiche l’Associazione si prefigge. Sono soci onorari le persone e gli enti ai qualiil Direttivo attribuisce tale qualifica, ritenendolein grado, per qualità, titoli o attività, di dareall’Associazione un contributo d’opera o di prestigio.

Art. 6: l’Associazione trae mezzi perconseguire i propri scopi dai contributi dei socie da ogni altro provento che le confluisca.

Art. 9: i soci hanno diritto:di partecipare alle assemblee e di usufruiredel materiale tecnico e didatticodell’Associazione, così come, in viaprioritaria, di beneficiare delle iniziativepromosse dall’Associazione,

FROM THE STATUTE OF THE ASSOCIATION:

Art.1: The Associazione Riabilitatoridell’Insufficienza Respiratoria (A.R.I.R.) wasestablished in Milan on October 25, 1989.

Art.3: PURPOSE OF THE ASSOCIATIONARIR is a no profit entity, promoting theprevention and rehabilitation of respiratorydisease. In order to do this ARIR strives to:• Promote the practice of respiratory therapyand pulmonary rehabilitation within the clinical and therapeutic fields;• Organize the training, continuing education,coordination, and the promotion and theprofessional development of physiotherapisthaving specific competencies in therespiratory fields;• Support respiratory care understanding thehygiene within the scientific and social realms;• Promote scientific research in the field ofphysiotherapy and respiratory rehabilitation.

Art. 4: All persons and entities that areaccepted by the Board of Directors and whopay the associational fee are consideredmembers.

Art. 5: There are four categories of membership:1. Founding members2. Regular members3. Sustaining members4. Honorary members.Those who have taken part in the signing of the associational statute and those whom,thought not having signed the statute, aredeemed valid candidates by the Board ofDirectors are founding members.Physiotherapists accepted by the Board of Directors and who pay the establishedyearly associational fee are considered regular members.Natural and juridical persons who wish tosupport the pre-established purpose of theassociation are considered sustainingmembers.Persons and entities to which the Board of Directors deems such status appropriate,for reasons of capabilities, qualities, titles or activities able to give the Association a contribution of work or prestige, areconsidered honorary members.

Art. 6: The Association obtains the means ofcarrying out its purpose from the contributionsof its members and from any other proceedsgoing towards it.

Art. 9: MEMBER RIGHTSThe members have the right to: participate at he assemblies, utilize the technical andteaching materials of the Association, as wellas enjoy, as privileged members, the benefitsof the activities promoted by the Association.

DIRETTORE RESPONSABILEEDITOR IN CHIEF

ANTONELLA SANNITI

[email protected]

REDAZIONEEDITORIAL STAFF

CINZIA CIGOLINI, STEFANIA BROGI

RESPONSABILE SCIENTIFICOSCIENTIFIC ACCOUNTEE

ENRICO CLINI

BOARD EDITORIALEEDITORIAL BOARD

ANNA BRIVIO,MARTA CORNACCHIA,EMILIA PRIVITERA,MARTA LAZZERI, GIANCARLO PIAGGI, MAURIZIO SOMMARIVA, SERGIO ZUFFO

ARIR: www.arirassociazione.org

AARC: www.aarc.org

EDITOREEDITOR

ARIR EDIZIONI

ASSOCIAZIONE RIABILITATORI

DELL’INSUFFICIENZA RESPIRATORIA

UNITÀ SPINALE

A.O. OSPEDALE NIGUARDA

CA’ GRANDA MILANO

PIAZZA OSPEDALE MAGGIORE 320162 MILANO

REG. TRIBUNALE DI MILANO N.967DEL 06-07-06

Il periodico “Selezione ARIR da RespiratoryCare e AARC Times” costituisce il secondoimpegno editoriale dell’AssociazioneRiabilitatori dell’Insufficienza Respiratoria(ARIR).Le motivazioni di questa realizzazione si delineano nell’ambito dell’attività di didattica e aggiornamento chel’associazione svolge ormai da 20 anni.È proprio realizzando corsi per Fisioterapisti in molti ospedali italiani che l’Associazione ha conosciuto direttamente quali sono i principali problemi ed ostacoli che il Fisioterapista incontra nel processo continuo di aggiornamento in materia di Fisioterapia e Riabilitazione Respiratoria.Uno degli aspetti cruciali per mantenersi“al passo con i tempi” ,oltre a partecipare a corsi specifici, è rappresentato dallapossibilità di entrare in contatto con esperienze e realtà più evolute ma al tempo stesso applicabili alla realtà italiana.I criteri di valutazione e monitoraggio,le tecniche operative, gli approcci e le metodiche sono ciò che il Fisioterapistadeve acquisire per incrementare l’efficacia del suo intervento.La realtà della Fisioterapia e RiabilitazioneRespiratoria è molto diversa da paese a paese ed in particolare rispetto alla realtàamericana e questo rende l’aggiornamentoun’operazione complessa e difficoltosa oltre che onerosa.L’ARIR dagli inizi della sua costituzione si è posta tra i vari obiettivi anche quello di ridurr e le difficoltà e facilitarel’aggiornamento dei Fisioterapisti Italianiorganizzando corsi e convegni a cui ha invitato e invita numerosi colleghi stranieri,esperti nei diversi ambiti della Fisioterapia e Riabilitazione Respiratoria, promuovendocosì lo scambio culturale e professionale tra le diverse realtà europee e anche extra-europee.Con la realizzazione di “Selezione ARIR da Respiratory Care e AARC Times” l’ARIR intende rispondere ulteriormente e in modo concreto ad una esigenza centrale della formazione: l’accesso alle pubblicazioni scientifiche. Questo periodico offre a chi si occupa di Fisioterapia e Riabilitazione Respiratoriala possibilità di accedere ad alcune dellepubblicazioni scientifiche della AmericanAssociation for Respiratory Care (AARC),selezionando quelle più vicine alla realtàitaliana.“Selezione ARIR da Respiratory Care e AARC Times” è un periodico semestrale che nasce dalla volontà congiunta di ARIR e AARC frutto dell’affiliazione delle dueAssociazioni e sarà distribuito gratuitamente ai soci ARIR e verrà pubblicato nel websitedell’Associazione www.arirassociazione.orgnello spazio riservato ai soci.

A nome del Direttivo ARIRIl Presidente ARIR

Ft Marta Lazzeri

The review "ARIR selection from RespiratoryCare and AARC Time" is the second editorialengagement of the Italian AssociazioneRiabilitatori della Insufficienza Respiratoria(ARIR)The reasons of this workmust be found in the educational and updating activity that the association has been developingfrom more than 20 years.The association has directly known, during its courses which are the principalproblems and obstacles in many italianhospitals. Above all, the necessity of acontinuous updating in physiotherapy and respiratory care.In addition to attend specific courses, one of the meaning aspect to bring up to date, is to meet more developedexperiences and reality suitable to the italian ones.The evaluation criteria and the operativetechniques are the elements that any physiotherapist must study to ameliorate the efficacy of his/her job.The reality of physiotherapy and respiratory care is very different from country to country, particularly from the US one, thus making the updating a very difficult and expensive operation.From the beginning, one of ARIR objectivehas been that of making easy the updating of the italian physiotherapists, thus organizing events on specific topics (courses and congress). So far, many foreign people, experts in physiotherapy and respiratory care, has been invited from ARIR with the goal of promoting the cultural and professional exchange from european and extra Europeanexperiences.With the realization of "ARIR selection from Respiratory Care and AARC Time",ARIR wants to answer in a concrete way to a principal exigence of the professionaleducation: the access to the scientificarticles.This review offers to people who areencharged in physiotherapy and respiratorycare the access to scientific articles of theAmerican Association for Respiratory Care(AARC), selecting the ones closer to theitalian reality."ARIR selection from Respiratory Care and AARC Time" is a six month review born from the ARIR and AARC agreement,and it will be distributed for free to the ARIR members and published in the ARIR website (www.ariassociazione.org)in the page reserved to its members.

From the Board of DirectorsThe President of Arir

Marta Lazzeri


INTERNATIONALAFFILIATE

• Numero 02

• Anno 4

• Dicembre 2009

Noninvasive Ventilation in Neuromuscular Disease:Equipment and Application

Dean R Hess PhD RRT FAARC

The Physiologic Effects of Noninvasive VentilationRichard H Kallet MSc RRT FAARC

and Janet V Diaz MD

Selezione ARIRda e AARC Times

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Documents

Numero 0 Anno 8 3 Selezione ARIR - arirassociazione.org · American Association for Respiratory Care Continuing Medical Education from International Experts AARC Educational Programs