Cardiorespiratory responses to incremental dynamic exercise were assessed across four different levels of lower-body positive pressure (LBPP) and, as a separate study, during constant load (i.e constant work rate) exercise below and above each subject's ventilatory threshold (VT), both with and without 45 torr of LBPP.

ABSTRACT Patients with respiratory failure secondary to acute asthma exacerbation (AAE) frequently present at emergency units. Some patients may develop respiratory muscle fatigue. Current guidelines for the treatment of an AAE center on pharmacological treatment and invasive mechanical ventilation. Noninvasive positive pressure ventilation (NPPV) has an established role in COPD exacerbations. The role it can play in an AAE remains unanswered although it is frequently used in the clinical setting. Aims: The present study proposed to investigate if the early use of NPPV in the forms of continuous positive airway pressure (CPAP) or bilevel positive pressure ventilation (BPPV) together with standard medical therapy in AAE can decrease time of response to therapy compared to standard medical therapy alone. We further tested the effect of BPPV against CPAP. Methods: Asthmatic patients who presented with a severe AAE (PEFR % predicted < 60 %) at the emergency unit were randomized to either standard medical therapy (ST), ST and CPAP or ST and BPPV. Thirty patients fulfilled the inclusion criteria for the study. Groups presented similar baseline characteristics. The mean age for the group was 42.1 ± 12.6 years. Mean baseline PEFR % predicted was 35.2 ± 10.7 % (ST), 30.5 ± 11.7 % (ST + CPAP) and 33.5 ±13.8 % (ST + BPPV). Results: Hourly improvement (Δ) in respiratory rate and sensation of breathlessness was significantly better in the BPPV intervention group. Improvement (Δ) from baseline to end of treatment in respiratory rate and sensation of breathlessness was significant for both CPAP and BPPV (p = 0.0463; p = 0.0132 respectively) compared to ST alone. Lung function was significantly improved in the CPAP intervention group hourly and from baseline to end of treatment (p = 0.0403 for PEFR and p = 0.0293 for PEFR % predicted) compared to ST + BPPV and ST alone. The mean shift (Δ) in PEFR from baseline to 3 hours of treatment was 67.4, 123.5 and 86.8 L/min (p = 0.0445) for ST, ST + CPAP and ST + BPPV respectively. This corresponded to a 38.1, 80.8 and 51.7 % improvement in lung function respectively. Discussion: The effect of BPPV on the reduction of respiratory rate and sensation of breathlessness could be related to the inspiratory assistance provided by BPPV. The significant improvement in lung function in the CPAP group could be related to its intrinsic effect on the airway smooth muscle and / or on the airway smooth muscle load. Conclusion: The present results suggest that adding NPPV to standard treatment for an AAE not only improves clinical signs faster but also improves lung function faster. CPAP seems to have an intrinsic effect on the airway smooth muscle so rendering it more effective in ameliorating lung function.

Doctor of Philosphy (PhD) / This thesis describes the work carried out during four treks, each over 10-11 days, from 1400m to 5000m in the Nepal Himalaya and further work performed during several two-night sojourns at the Barcroft Laboratory at 3800m on White Mountain in California, USA. Nineteen volunteers were studied during the treks in Nepal and seven volunteers were studied at White Mountain. All subjects were normal, healthy individuals who had not travelled to altitudes higher than 1000m in the previous twelve months. The aims of this research were to examine the effects on sleep, and the ventilatory patterns during sleep, of incremental increases in altitude by employing portable polysomnography to measure and record physiological signals. A further aim of this research was to examine the relationship between the ventilatory responses to hypoxia and hypercapnia, measured at sea level, and the development of periodic breathing during sleep at high altitude. In the final part of this thesis the possibility of preventing and treating Acute Mountain Sickness with non-invasive positive pressure ventilation while sleeping at high altitude was tested. Chapter 1 describes the background information on sleep, and breathing during sleep, at high altitudes. Most of these studies were performed in hypobaric chambers to simulate various high altitudes. One study measured sleep at high altitude after trekking, but there are no studies which systematically measure sleep and breathing throughout the whole trek. Breathing during sleep at high altitude and the physiological elements of the control of breathing (under normal/sea level conditions and under the hypobaric, hypoxic conditions present at high altitude) are described in this Chapter. The occurrence of Acute Mountain Sickness (AMS) in subjects who travel form near sea level to altitudes above 3000m is common but its pathophysiology not well understood. The background research into AMS and its treatment and prevention are also covered in Chapter 1. Chapter 2 describes the equipment and methods used in this research, including the polysomnographic equipment used to record sleep and breathing at sea level and the high altitude locations, the portable blood gas analyser used in Nepal and the equipment and methodology used to measure each individual’s ventilatory response to hypoxia and hypercapnia at sea level before ascent to the high altitude locations. Chapter 3 reports the findings on the changes to sleep at high altitude, with particular focus on changes in the amounts of total sleep, the duration of each sleep stage and its percentage of total sleep, and the number and causes of arousals from sleep that occurred during sleep at increasing altitudes. The lightest stage of sleep, Stage 1 non-rapid eye movement (NREM) sleep, was increased, as expected with increases in altitude, while the deeper stages of sleep (Stages 3 and 4 NREM sleep, also called slow wave sleep), were decreased. The increase in Stage 1 NREM in this research is in agreement with all previous findings. However, slow wave sleep, although decreased, was present in most of our subjects at all altitudes in Nepal; this finding is in contrast to most previous work, which has found a very marked reduction, even absence, of slow wave sleep at high altitude. Surprisingly, unlike experimental animal studies of chronic hypoxia, REM sleep was well maintained at all altitudes. Stage 2 NREM and REM sleep, total sleep time, sleep efficiency and spontaneous arousals were maintained at near sea level values. The total arousal index was increased with increasing altitude and this was due to the increasing severity of periodic breathing as altitude increased. An interesting finding of this research was that fewer than half the periodic breathing apneas and hypopneas resulted in arousal from sleep. There was a minor degree of upper airway obstruction in some subjects at sea level but this was almost resolved by 3500m. Chapter 4 reports the findings on the effects on breathing during sleep of the progressive increase of altitude, in particular the occurrence of periodic breathing. This Chapter also reports the results of changes to arterial blood gases as subjects ascended to higher altitudes. As expected, arterial blood gases were markedly altered at even the lowest altitude in Nepal (1400m) and this change became more pronounced at each new, higher altitude. Most subjects developed periodic breathing at high altitude but there was a wide variability between subjects as well as variability in the degree of periodic breathing that individual subjects developed at different altitudes. Some subjects developed periodic breathing at even the lowest altitude and this increased with increasing altitude; other subjects developed periodic breathing at one or two altitudes, while four subjects did not develop periodic breathing at any altitude. Ventilatory responses to hypoxia and hypercapnia, measured at sea level before departure to high altitude, was not significantly related to the development of periodic breathing when the group was analysed as a whole. However, when the subjects were grouped according to the steepness of their ventilatory response slopes, there was a pattern of higher amounts of periodic breathing in subjects with steeper ventilatory responses. Chapter 5 reports the findings of an experimental study carried out in the University of California, San Diego, Barcroft Laboratory on White Mountain in California. Seven subjects drove from sea level to 3800m in one day and stayed at this altitude for two nights. On one of the nights the subjects slept using a non-invasive positive pressure device via a face mask and this was found to significantly improve the sleeping oxyhemoglobin saturation. The use of the device was also found to eliminate the symptoms of Acute Mountain Sickness, as measured by the Lake Louise scoring system. This finding appears to confirm the hypothesis that lower oxygen saturation, particularly during sleep, is strongly correlated to the development of Acute Mountain Sickness and may represent a new treatment and prevention strategy for this very common high altitude disorder.

Orthostatic intolerance (OI), i.e., the inability to maintain stable arterial pressure during upright posture, is a major problem for astronauts after spaceflight. Therefore, one important goal of spaceflight-related research is the development of countermeasures to prevent post flight OI. Given the rarity and expense of spaceflight, countermeasure development requires ground-based simulations of partial gravity to induce appropriate orthostatic effects on the human body, and to test the efficacy of potential countermeasures. To test the efficacy of upright lower body positive pressure (LBPP) as a model for simulating cardiovascular responses to lunar and Martian gravities on Earth, cardiovascular responses to upright LBPP were compared with those of head-up tilt (HUT), a well-accepted simulation of partial gravity, in both ambulatory and cardiovascularly deconditioned subjects. Results indicate that upright LBPP and HUT induced similar changes in cardiovascular regulation, supporting the use of upright LBPP as a potential model for simulating cardiovascular responses to standing and moving in lunar and Martian gravities. To test the efficacy of a short exposure to artificial gravity (AG) as a countermeasure to spaceflight-induced OI, orthostatic tolerance limits (OTL) and cardiovascular responses to orthostatic stress were tested in cardiovascularly deconditioned subjects, using combined 70º head-up tilt and progressively increased lower body negative pressure, once following 90 minutes AG exposure and once following 90 minutes of -6º head-down bed rest (HDBR). Results indicate that a short AG exposure increased OTL of cardiovascularly deconditioned subjects, with increased baroreflex and sympathetic responsiveness, compared to those measured after HDBR exposure. To gain more insight into mechanisms of causal connectivity in cardiovascular and cardiorespiratory oscillations during orthostatic challenge in both ambulatory and cardiovascularly deconditioned subjects, couplings among R-R intervals (RRI), systolic blood pressure (SBP) and respiratory oscillations in response to graded HUT and dehydration were studied using a phase synchronization approach. Results indicate that increasing orthostatic stress disassociated interactions among RRI, SBP and respiration, and that dehydration exacerbated the disconnection. The loss of causality from SBP to RRI following dehydration suggests that dehydration also reduced involvement of baroreflex regulation, which may contribute to the increased occurrence of OI.

Doctor of Philosphy (PhD) / This thesis describes the work carried out during four treks, each over 10-11 days, from 1400m to 5000m in the Nepal Himalaya and further work performed during several two-night sojourns at the Barcroft Laboratory at 3800m on White Mountain in California, USA. Nineteen volunteers were studied during the treks in Nepal and seven volunteers were studied at White Mountain. All subjects were normal, healthy individuals who had not travelled to altitudes higher than 1000m in the previous twelve months. The aims of this research were to examine the effects on sleep, and the ventilatory patterns during sleep, of incremental increases in altitude by employing portable polysomnography to measure and record physiological signals. A further aim of this research was to examine the relationship between the ventilatory responses to hypoxia and hypercapnia, measured at sea level, and the development of periodic breathing during sleep at high altitude. In the final part of this thesis the possibility of preventing and treating Acute Mountain Sickness with non-invasive positive pressure ventilation while sleeping at high altitude was tested. Chapter 1 describes the background information on sleep, and breathing during sleep, at high altitudes. Most of these studies were performed in hypobaric chambers to simulate various high altitudes. One study measured sleep at high altitude after trekking, but there are no studies which systematically measure sleep and breathing throughout the whole trek. Breathing during sleep at high altitude and the physiological elements of the control of breathing (under normal/sea level conditions and under the hypobaric, hypoxic conditions present at high altitude) are described in this Chapter. The occurrence of Acute Mountain Sickness (AMS) in subjects who travel form near sea level to altitudes above 3000m is common but its pathophysiology not well understood. The background research into AMS and its treatment and prevention are also covered in Chapter 1. Chapter 2 describes the equipment and methods used in this research, including the polysomnographic equipment used to record sleep and breathing at sea level and the high altitude locations, the portable blood gas analyser used in Nepal and the equipment and methodology used to measure each individual’s ventilatory response to hypoxia and hypercapnia at sea level before ascent to the high altitude locations. Chapter 3 reports the findings on the changes to sleep at high altitude, with particular focus on changes in the amounts of total sleep, the duration of each sleep stage and its percentage of total sleep, and the number and causes of arousals from sleep that occurred during sleep at increasing altitudes. The lightest stage of sleep, Stage 1 non-rapid eye movement (NREM) sleep, was increased, as expected with increases in altitude, while the deeper stages of sleep (Stages 3 and 4 NREM sleep, also called slow wave sleep), were decreased. The increase in Stage 1 NREM in this research is in agreement with all previous findings. However, slow wave sleep, although decreased, was present in most of our subjects at all altitudes in Nepal; this finding is in contrast to most previous work, which has found a very marked reduction, even absence, of slow wave sleep at high altitude. Surprisingly, unlike experimental animal studies of chronic hypoxia, REM sleep was well maintained at all altitudes. Stage 2 NREM and REM sleep, total sleep time, sleep efficiency and spontaneous arousals were maintained at near sea level values. The total arousal index was increased with increasing altitude and this was due to the increasing severity of periodic breathing as altitude increased. An interesting finding of this research was that fewer than half the periodic breathing apneas and hypopneas resulted in arousal from sleep. There was a minor degree of upper airway obstruction in some subjects at sea level but this was almost resolved by 3500m. Chapter 4 reports the findings on the effects on breathing during sleep of the progressive increase of altitude, in particular the occurrence of periodic breathing. This Chapter also reports the results of changes to arterial blood gases as subjects ascended to higher altitudes. As expected, arterial blood gases were markedly altered at even the lowest altitude in Nepal (1400m) and this change became more pronounced at each new, higher altitude. Most subjects developed periodic breathing at high altitude but there was a wide variability between subjects as well as variability in the degree of periodic breathing that individual subjects developed at different altitudes. Some subjects developed periodic breathing at even the lowest altitude and this increased with increasing altitude; other subjects developed periodic breathing at one or two altitudes, while four subjects did not develop periodic breathing at any altitude. Ventilatory responses to hypoxia and hypercapnia, measured at sea level before departure to high altitude, was not significantly related to the development of periodic breathing when the group was analysed as a whole. However, when the subjects were grouped according to the steepness of their ventilatory response slopes, there was a pattern of higher amounts of periodic breathing in subjects with steeper ventilatory responses. Chapter 5 reports the findings of an experimental study carried out in the University of California, San Diego, Barcroft Laboratory on White Mountain in California. Seven subjects drove from sea level to 3800m in one day and stayed at this altitude for two nights. On one of the nights the subjects slept using a non-invasive positive pressure device via a face mask and this was found to significantly improve the sleeping oxyhemoglobin saturation. The use of the device was also found to eliminate the symptoms of Acute Mountain Sickness, as measured by the Lake Louise scoring system. This finding appears to confirm the hypothesis that lower oxygen saturation, particularly during sleep, is strongly correlated to the development of Acute Mountain Sickness and may represent a new treatment and prevention strategy for this very common high altitude disorder.

Submitted by RODRIGO LIMA CARNEIRO null (rodrigolimacarneiro27@gmail.com) on 2016-09-06T19:51:25Z No. of bitstreams: 1 TESE DEFINITIVA RODRIGO.pdf: 2892805 bytes, checksum: 57411cf60137e34f88cd0c8a35de3ba2 (MD5) / Approved for entry into archive by Juliano Benedito Ferreira (julianoferreira@reitoria.unesp.br) on 2016-09-08T14:35:38Z (GMT) No. of bitstreams: 1 carneiro_rl_dr_jabo.pdf: 2892805 bytes, checksum: 57411cf60137e34f88cd0c8a35de3ba2 (MD5) / Made available in DSpace on 2016-09-08T14:35:38Z (GMT). No. of bitstreams: 1 carneiro_rl_dr_jabo.pdf: 2892805 bytes, checksum: 57411cf60137e34f88cd0c8a35de3ba2 (MD5) Previous issue date: 2016-07-22 / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Avaliaram-se os efeitos de diferentes concentrações do óxido nitroso (N2O) e da fração inspirada de oxigênio (FiO2) sobre a hematose, os parâmetros cardiorrespiratórios, intracranianos e o índice biespectral, em suínos anestesiados com propofol e mantidos em ventilação controlada a pressão. Para tanto, foram utilizados 48 suínos da raça Large White, machos ou fêmeas, distribuídos aleatoriamente em seis grupos: GN10(FiO2 = 0,9 e N2O = 0,1), GA10 (FiO2 = 0,9 e ar comprimido = 0,1), GN30(FiO2 = 0,7 e N2O = 0,3), GA30(FiO2 = 0,7 e ar comprimido = 0,3), GN50(FiO2 = 0,5 e N2O= 0,5), GA50 (FiO2 = 0,5 e ar comprimido = 0,5). Para todos os suínos, empregou-se como medicação pré- anestésica azaperona (2 mg/Kg) administrada pela via intramuscular. O propofol foi utilizado para indução e manutenção anestésicas (0,5 mg/Kg/min). Após a intubação orotraqueal, a sonda de Magill foi acoplada ao aparelho de anestesia inalatória equipado com ventilador volumétrico/pressométrico, para o fornecimento das misturas gasosas nas concentrações preconizadas para cada grupo. Após 100 minutos da indução anestésica foi administrado bolus, por via intravenosa, de rocurônio (0,6 mg/Kg) seguido por infusão contínua do mesmo fármaco (0,6 mg/Kg/h). Continuamente, iniciou-se a ventilação controlada ciclada a pressão (15 cmH2O) ajustada de maneira a permitir leitura de capnometria entre 35 e 45 mmHg. As observações das variáveis foram realizadas 100 minutos após a indução da anestesia (M0) e em intervalos de 15 minutos (de M15 a M75). Os dados foram submetidos à análise de variância de duas (Two-way ANOVA) e de uma via (One-way ANOVA), seguidas pelo teste de Bonferroni (p<0,05). Os resultados mostraram que houve alterações nas variáveis hemogasométricas (PaO2, PaCO2, SaO2, pHa, PvCO2 e SvO2), nos parâmetros da mecânica ventilatória (Vt, Vm, Tins, AaDO2, CvO2, Qs/Qt, P(a-ET)CO2, IR, IO, VO2, IVO2, TeO2), nas variáveis cardiovasculares (PAD, PAM, PVC, DC, PAPm, RVP e IRVP), nos parâmetros intracranianos (PPC e TIC) e no índice biespectral (BIS, QS e TS), sendo registradas diferenças significativas intergrupais. Em todos os grupos, as correlações entre Qs/Qt e AaDO2, Qs/Qt e IR, Qs/Qt e a/A e por fim, Qs/Qt e IO, foram fortes, excetuando-se GN10 nas correlações Qs/Qt e IR, Qs/Qt e IO que apresentaram-se moderadas. Concluiu-se que as diferentes FiO2 e concentrações de N2O não alteram as variáveis hemodinâmicas, cardiovasculres e intracranianas, porém o houve dimininuição do BIS quando utiliza-se N2O na concentração de 50%. FiO2 de 0,9 principalmente se associada ao N2O, deve ser evitada por contribuir com o aumento do shunt e a FiO2 de 0,7 sem adição de óxido nitroso na mistura gasosa mostrou-se mais adequada para ser utilizada durante a ventilação controlada à pressão em suínos anestesiados com propofol. / The effects of different concentrations of nitrous oxide (N2O) and fraction of inspired oxygen (FiO2) on hematosis, cardiorespiratory and intracranial parameters and bispectral index were evaluated in pigs anesthetized with propofol and maintained with pressure-controlled ventilation. Forty-eight Large White pigs, male or female, were randomly assigned into six groups:GN10 (FiO2 = 0.9 and N2O = 0.1), GA10 (FiO2 = 0.9 and compressed air = 0.1), GN30 (FiO2 = 0.7 and N2O = 0.3), GA30 (FiO2 = 0.7 and compressed air = 0.3), GN50 (FiO2 = 0.5 and N2O = 0.5) GA50 (FiO2 = 0.5 and compressed air = 0.5). Azaperone (2 mg/Kg) was used as standard pre-anesthetic medication and Propofol was used to induce and maintain anesthetic state (0.5 mg/Kg/min). Following endotracheal intubation, the Magill tube was coupled to an anesthesial equipped with a special fan which was able to control pressure/ volume of the gas mixture for each studied group. After 100 minutes of anesthetic induction, an intravenous bolus of rocuronium (0.6 mg/Kg) was administered, followed by continuous infusion of the same drug (0.6 mg/Kg/h). Then mechanical ventilation using cycled pressure (15 cmH2O) was adjusted in order to allow capnometry readings in between 35 and 45 mmHg. The observations of the variables were performed 100 minutes after anesthetic induction (M0) and at 15 minute intervals (M15 to M75). Data were subjected to two-way and one-way analysis of variance (ANOVA) followed by Bonferroni correction (p<0.05).The results showed changes in several variables and also significant intergroup differences were noticed. Among the main changes were: blood gas variables (PaO2, PaCO2, SaO2, pHa, PvCO2 and SvO2); mechanical ventilation parameters (Vt, Vm, Tins, AaDO2, CvO2, Qs/Qt, P (a-ET) CO2 , IR, IO, VO2, IVO2, TeO2); cardiovascular variables (DAP, MAP, PVC, DC, mPAP, PVR and PVRI); intracranial parameters (PPC and ICT) and also in the bispectral index (BIS, QS and TS). In all groups, the correlations between Qs/Qt and AaDO2, Qs/Qt and IR, Qs/Qt and a/A and finally, Qs/Qt and IO, were strong, except for GN10 (correlations Qs/Qt and IR, Qs/Qt and IO) that were moderate. It was concluded that the different FiO2 and N2O concentrations did not change hemodynamic variables , and intracranial cardiovasculres , but there was BIS decrease when N2O is used at a concentration of 50% . FiO2 0.9 mainly associated with N2O should be avoided for contributing to the increase of the shunt and FiO2 of 0.7 without the addition of nitrous oxide in the gas mixture was more suitable to be used during pressure controlled ventilation in pigs anesthetized with propofol. / FAPESP: 2013/25655-0

CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / IntroduÃÃo: A VentilaÃÃo NÃo Invasiva (VNI) consiste na oferta de suporte ventilatÃrio sem uso de prÃtese traqueal, atravÃs de uma interface (usualmente uma mÃscara) adaptada entre o ventilador e o paciente. Embora a VNI apresente eficÃcia semelhante ao mÃtodo invasivo em otimizar a troca gasosa de pacientes com insuficiÃncia respiratÃria de vÃrias etiologias, ainda hà uma taxa de insucesso considerÃvel desta modalidade. A despeito do fato de que a intolerÃncia à interface à um importante fator associado à falha do procedimento, existem poucos trabalhos na literatura comparando diferentes dispositivos. Assim, estudos que avaliem a eficÃcia e a seguranÃa e que comparem diferentes interfaces sÃo necessÃrios. A utilizaÃÃo de voluntÃrios sadios exibe a vantagem de eliminar os sintomas da insuficiÃncia respiratÃria que podem prejudicar uma avaliaÃÃo mais especÃfica da interface. Objetivos: Avaliar e comparar trÃs tipos de mÃscaras para VNI, em voluntÃrios sadios, quanto à freqÃÃncia e tipos de efeitos adversos e quanto ao nÃvel de conforto. CasuÃstica e MÃtodo: O estudo consistiu em um ensaio clÃnico randomizado do tipo crossover comparando as mÃscaras nasal (N), facial (F) e facial total (FT), em ventilador gerador de fluxo com orifÃcio exalatÃrio no circuito. Cada voluntÃrio usava as trÃs interfaces em uma seqÃÃncia randomizada. A VNI era aplicada por tempo total de 10 minutos para cada interface. Durante este perÃodo, dois nÃveis de pressÃo inspiratÃria e expiratÃria (IPAP e EPAP) no modo de ventilaÃÃo bilevel eram aplicados, por 5 minutos, com cada mÃscara. Foi testado um nÃvel baixo de pressÃo (Pbx) com IPAP de 11cmH2O e EPAP de 6cmH2O e um nÃvel moderado a alto de pressÃo (Pma) com IPAP de 15cmH2O e EPAP de 10cmH2O. Ao final de cada perÃodo de 5 minutos, era aplicado ao voluntÃrio questionÃrio padronizado de efeitos adversos das interfaces, incluindo dor em vÃrios pontos de pressÃo das mÃscaras, percepÃÃo incÃmoda de vazamentos, sensaÃÃo de ressecamento nasal e oral e claustrofobia. O voluntÃrio tambÃm indicava seu nÃvel de conforto (em uso da interface) atravÃs de uma Escala AnalÃgica Visual de 10 cm (EAV) (sendo zero o mÃximo desconforto e dez a ausÃncia de desconforto). Havia um intervalo de 10 minutos em respiraÃÃo espontÃnea sem mÃscara entre cada perÃodo de VNI. Durante todo o protocolo, foram monitorizados freqÃÃncia respiratÃria (f), Volume Corrente (VC), Oximetria de pulso (SpO2) e Capnografia (EtCO2) instalada entre a mÃscara e o orifÃcio exalatÃrio. Para a anÃlise comparativa das variÃveis categorizadas, foram utilizados os testes qui-quadrado de Pearson, exato de Fisher e Mcnemar e para as variÃveis quantitativas foram utilizados os testes ANOVA e dos mÃnimos quadrados. Resultados: Foram avaliados 24 voluntÃrios sadios (12 mulheres) com idade entre 18 e 35 anos (mÃdia de 25,7). Quanto aos efeitos adversos e considerando o nÃvel de pressÃo mais baixo (Pbx) observou-se 1. A incidÃncia de pelo menos um efeito foi de 91,7% para N e FT e 95,8% para F. 2. A mÃscara N teve mÃdia de efeitos adversos por paciente menor do que a F (3,58 x 5,0 p=0,002) e do que a FT (3,58 x 4,71 p=0,03). 3. O efeito adverso com maior incidÃncia nas trÃs interfaces foi âpressÃo da mÃscaraâ (N=54,2% F=66,7% e FT=66,7%). 4. Dor nos pontos de pressÃo foi significativamente menor com a FT do que com a F (37,5% x 66,7% p=0,01), sem diferenÃa em relaÃÃo à N. 5. A incidÃncia de percepÃÃo incÃmoda de vazamentos (olhos/boca) foi menor com a FT do que com a N (41,7% x 75% p=0,03) e sem diferenÃa significativa entre a N e a F. 6. Queixas de ressecamentos (nasal/oral) foram bem menos freqÃentes com a interface nasal tanto em relaÃÃo à facial (25% x 62,5% p= 0,01) quanto à facial total (25% x 75% p<0,001). 7. Em relaÃÃo à claustrofobia, a mÃscara facial total apresentou uma tendÃncia maior do que a nasal (33,3% x 8,3% p= 0,07). Considerando as mesmas variÃveis, ao se incrementar a pressÃo, verificou-se que: 1. A incidÃncia de efeitos adversos permaneceu alta, sendo 95,8% para N e FT e 100% para F. 2. A mÃdia de efeitos adversos por voluntÃrio na mÃscara nasal permaneceu menor, sendo estatisticamente significativa em relaÃÃo à facial (4,75 x 6,04 p= 0,009). 3. âPressÃo da mÃscaraâ continuou sendo o efeito adverso mais freqÃente nas trÃs interfaces (N=62,5% F=70,8% FT=75%). 4. NÃo houve mais diferenÃa entre as mÃscaras com relaÃÃo à dor nos pontos de pressÃo. 5. Com relaÃÃo aos vazamentos incÃmodos, houve apenas tendÃncia de piora em F comparando-se com FT (83,3% x 54,2% p= 0,09). 6. Ressecamentos permaneceram menos freqÃentes na mÃscara nasal, sendo N (41,7%) x F (66,7%) p= 0,03 e N (41,7%) x FT (79,2%) p=0,02. 7. Maior tendÃncia à claustrofobia persistiu na mÃscara FT em relaÃÃo à N (33,3% x 8,3% p= 0,07). 8. O incremento da pressÃo aumentou a mÃdia de efeitos adversos nas trÃs interfaces, sendo estatisticamente significativo na mÃscara nasal (3,58 x 4,75 p=0,003) e na facial (5,0 x 6,04 p= 0,007) e exibindo tendÃncia na facial total (4,71 x 5,33 p=0,07). 9. Em relaÃÃo à EAV de conforto, foi observado menos conforto com Pma em relaÃÃo à Pbx nas trÃs interfaces, sendo N (7,54 x 7,13 p=0,01), F (7,50 x 6,54 p<0,001) e FT (7,25 x 6,50 p=0,001), sem diferenÃa significativa entre as mesmas. NÃo houve variaÃÃes significativas com relaÃÃo aos parÃmetros fisiolÃgicos que pudessem influenciar o estudo comparativo dos efeitos adversos e conforto das interfaces. NÃo houve detecÃÃo de curva pelo capnÃgrafo quando se utilizou a mÃscara facial total, evidenciando a completa eliminaÃÃo do CO2 pelos orifÃcios exalatÃrios desta interface. ConclusÃo: As trÃs interfaces apresentaram alta incidÃncia de efeitos adversos em voluntÃrios sadios. A mÃscara nasal apresentou mÃdia de efeitos adversos por voluntÃrio menor do que as outras duas interfaces, destacando-se menor incidÃncia de ressecamentos. A mÃscara facial total parece estar associada a menos queixas de dor e de percepÃÃo incÃmoda de vazamentos, porÃm exibe maior tendÃncia à claustrofobia em comparaÃÃo Ãs outras duas interfaces. As trÃs interfaces apresentaram um bom nÃvel de conforto, sem diferenÃa significativa entre elas. O aumento dos nÃveis de pressÃo no modo bilevel diminuiu o conforto e aumentou os efeitos adversos relatados pelos voluntÃrios sadios nas trÃs interfaces / Rationale: Non-invasive ventilation (NIV) is defined as a ventilatory support technique using an interface (usually a mask) instead of tracheal intubation to adapt the patientâs respiratory system to the ventilator. Although it is as efficacious as the invasive method in terms of improving gas exchange in patients with respiratory failure due to various etiologies, it remains associated with considerable failure rates. Despite the association between interface and low tolerance to NIV, few studies have been published evaluating the efficacy and safety of each type of interface. interfaces are best studied on healthy subjects avoiding the interference of confounding factors related to respiratory failure. Objective: To evaluate and compare three types of masks used as NIV interface on healthy volunteers with regard to frequency and type of adverse events and level of comfort. Method: A randomized, crossover clinical trial was conducted to evaluate and compare nasal (N), facial (F), and total face (TF) masks adapted to healthy volunteers using a flow generator ventilator with a circuit exhalation valve. The three masks were tested on all subjects in random sequence during 10 minutes each, equally divided between two levels of expiratory and inspiratory positive airway pressure (EPAP; IPAP) in bilevel ventilation: a low-pressure (LoP) setup (IPAP: 11cmH2O; EPAP: 6cmH2O) and a moderate to high-pressure (MoHiP) setup (IPAP=15cmH2O; EPAP=10cmH2O). At the end of each 5-min period, the subjects were given a standardized written questionnaire on adverse events including questions about uncomfortable pressure and pain at contact points between mask and face, unpleasant perception of air leaks, nasal and oral mucosal dryness and claustrophobia. They also recorded sensations of comfort on a 10-cm visual analogical scale (10=absence of discomfort; 0=maximum discomfort). A 10-min interval of spontaneous, mask-free breathing was allowed between each period of NIV. The respiratory rate (RR), tidal volume (TV), pulse oxymetry (SpO2) and end-tidal CO2 volume (EtCO2), measured between mask and exhalation valve, were monitored during the entire protocol. While categorized variables were analyzed with Pearsonâs Chi-square test, Fisherâs exact test and McNemarâs test, continuous variables were analyzed with ANOVA and least-squares regression. Results: The study included 24 healthy volunteers (12 women) aged 18 to 35 (mean age: 25.7 years). The following was observed with regard to adverse events while using the LoP setup: a) The incidence of one or more adverse events by subject was 91.7% for N and TF and 95.8% for F; b) The number of adverse events per subject was smaller for N than for F (3.58 vs. 5.0; p=0.002) or TF (3.58 vs. 4.71; p=0.03); c) The most frequently reported adverse event was âmask pressureâ (N=54.2%; F=66.7%; FT=66.7%); d) Pain at points of mask contact was less frequently reported for TF than for F (37.5% vs. 66.7%; p=0.01), but no significant difference was observed between TF and N; e) The incidence of unpleasant air leak perception around the eyes or mouth was lower for TF than for N (41.7% vs. 75%; p=0.03) but no significant difference was observed between N and F; f) Complaints of nasal or oral dryness were much less frequent for N than for F (25% vs. 62.5%; p=0.01) or TF (25% vs. 75%; p<0.001); g) Claustrophobia was more frequently reported for TF than for N (33.3% vs. 8.3%; p=0.07). The higher airway pressure of the MoHiP setup resulted in: a) The incidence of one or more adverse events per subject remained high (95.8% for both N and TF; 100% for F); b) On the average, N continued to be associated with the lowest number of adverse events per subject, the difference between N and F being statistically significant (4.75 vs. 6.04; p=0.009); c) Mask pressure remained the most common complaint (N=62.5%; F=70.8%; FT=75%); d) No significant difference was observed concerning pain; e) Reports of unpleasant air leak perception increased more for F than for TF (83.3% vs. 54.2%; p=0.09); f) N continued to be associated with the lowest incidence of dryness (N=41.7% vs. F=66.7%; p=0.03; and N=41.7% vs. TF=79.2%, p=0.02); g) The incidence of claustrophobia remained higher for TF than for N, though not statistically so (33.3% vs. 8.3%; p=0.07); h) On the average, pressure augmentation induced a higher number of adverse events per subject in all 3 mask types. The increase was statistically significant in the case of N (3.58 vs. 4.75; p=0.003) and F (5.0 vs. 6.04; p=0.007) and tended to be so for TF (4.71 vs. 5.33; p=0.07); i) No significant difference was observed between the masks with regard to comfort, but the MoHiP setup was reportedly less comfortable than the LoP setup for all mask types: N (7.54 vs. 7.1; p=0.01), F (7.50 vs. 6.54; p<0.001) and TF (7.25 vs. 6.50; p=0.001). Physiological variations observed during the protocol could not account for the adverse events or comfort sensation reported. Interestingly, the CO2 curve remained undetected by the capnograph while using TF, probably because the exhaled CO2 was completely eliminated through orifices in the mask. Conclusions: All three mask types presented a high incidence of adverse events in healthy volunteers. The nasal (N) mask was associated with a lower mean number of adverse events per subject, especially with regard to dryness. Although the total face (TF) mask seemed to be associated with fewer reports of pain and with a lower incidence of unpleasant air leak perception, claustrophobia was also more frequently reported. The masks were equally efficacious in terms of comfort. Higher pressure levels in the bilevel mode were associated with increased reports of discomfort and adverse events in healthy volunteers

The use of noninvasive positive pressure ventilation (NPPV) in acute care settings has drastically increased within the past 20 years. Research has indicated that NPPV is equally as effective as traditional mechanical ventilation(MV) in treating acute exacerbations of chronic pulmonary obstructive disease (COPD) and cardiogenic pulmonary edema. Furthermore, the risk of complication from NPPV is much lower than MV, in terms of ventilator-associated pneumonia and sepsis. It is imperative for the nurse to understand the various indications, interfaces, and potential complications associated with NPPV use. In addition to treating acute exacerbations of COPD and cardiogenic pulmonary edema, NPPV has been used for prevention of reintubation, palliative care, and status asthmaticus. Furthermore, NPPV could be delivered through various interfaces, such as nasal, facial, and helmet. Each of these interfaces could eventually cause complications for the patient, such as skin ulceration and sepsis. However, there is limited amount of research available discussing the role of the nurse in caring for the patient with NPPV. There are no standardized guidelines established to assist the nurse in this care, in terms of interface selection, prevention of complications, and staffing patterns. Several recommendations are presented at the end of this thesis to guide future nursing research, education, and clinical practice, such as exploring the role of oral care and education for NPPV patients.

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