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 Table of Contents  
REVIEW ARTICLE
Year : 2016  |  Volume : 4  |  Issue : 2  |  Page : 50-55

Noninvasive ventilation in hypoxemic respiratory failure


1 Department of Pulmonary and Critical Care Medicine, Fortis Hospital, Kolkata, West Bengal, India
2 Department of Respiratory Medicine, Sleep and Non Invasive Ventilation Services, St. James's University Hospital, Leeds, United Kingdom

Date of Web Publication10-Jun-2016

Correspondence Address:
Raja Dhar
Department of Pulmonary and Critical Care Medicine, Fortis Hospital, Kolkata, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2320-8775.183841

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  Abstract 

Noninvasive ventilation (NIV) refers to positive pressure ventilation delivered through a noninvasive interface (nasal mask, facemask, or nasal plugs) etc. Over the past decade its use has become more common as its benefits are increasingly recognized. This review will focus on the evidence supporting the use of NIV in various conditions resulting in acute hypoxemic respiratory failure (AHRF), that is, non-hypercapnic patients having acute respiratory failure in the absence of a cardiac origin or underlying chronic pulmonary disease. Outcomes depend on the patient's diagnosis and clinical characteristics. Patients should be monitored closely for signs of noninvasive ventilation failure and promptly intubated before a crisis develops. The application of noninvasive ventilation by a trained and experienced team, with careful patient selection, should optimize patient outcomes.

Keywords: Bilevel positive airway pressure, continuous positive airway pressure, hypoxemic respiratory failure, noninvasive ventilation


How to cite this article:
Dhar R, Ghosh D, Krishnan S. Noninvasive ventilation in hypoxemic respiratory failure. J Assoc Chest Physicians 2016;4:50-5

How to cite this URL:
Dhar R, Ghosh D, Krishnan S. Noninvasive ventilation in hypoxemic respiratory failure. J Assoc Chest Physicians [serial online] 2016 [cited 2023 Mar 25];4:50-5. Available from: https://www.jacpjournal.org/text.asp?2016/4/2/50/183841


  Introduction Top


Over the past two decades, there has been increasing use of noninvasive ventilation (NIV). NIV has revolutionized the management of diverse causes of acute respiratory failure (ARF). NIV has demonstrated its mettle in reducing intubation rates and mortality rates in patients with severe acute exacerbation of chronic obstructive pulmonary disease (COPD)[1],[2] or cardiogenic pulmonary edema.[3]

The terms continuous positive airway pressure (CPAP) and NIV are sometimes used interchangeably. They are however distinctly different. With noninvasive CPAP, a face mask or other interface is used to apply a pressure greater than atmospheric to the proximal airway. The result is splinting open the upper airway, an increase in lung volume, and an increase in intrathoracic pressure. With CPAP, there is no inspiratory muscle unloading in fact, tidal ventilation is completely dependent on the respiratory muscles with CPAP. In NIV, two different pressures are used (an inspiratory pressure and an expiratory pressure), whereas continuous pressure maintains one constant pressure throughout the respiratory cycle. Theoretically, NIV may confer an advantage over CPAP, by reducing the work of breathing (WOB) during inspiration, and by providing additional inspiratory pressure.

The beneficial effects of NIV remain unclear in patients with acute hypoxemic respiratory failure (AHRF), that is, nonhypercapnic patients having ARF in the absence of a cardiogenic pulmonary edema or underlying chronic pulmonary disease.

There is a strong rationale for the use of NIV to treat AHRF. In fact, NIV achieves two important goals of mechanical ventilation in AHRF:

(a) Improvement of oxygenation due to Ventilation/Perfusion – V/Q mismatch and shunt through alveolar recruitment; (b) unloading of respiratory muscles. Moreover, in case of coexisting congestive heart failure, NIV can increase cardiac performance by reducing both preload and afterload of the left ventricle.

Despite its advantages over invasive ventilation (can be applied intermittently, avoids sedation, oral feeds can be given, and lower rates of nosocomial infections, etc.) NIV is not without concerns. Apart from claustrophobia, facial skin necrosis and gastric distention, a concern which cannot be dismissed is the delay in intubation leading to a worse outcome. Hence, the ability to predict those likely to fail with NIV is important. Patients in whom there is a high likelihood of failure would be spared the discomfort of a trial of NIV and intubation would not be delayed.


  Hypoxemic Respiratory Failure Top


Respiratory failure is defined as a failure to maintain adequate gas exchange and is characterized by abnormalities of arterial blood gas tensions. Type 1 or hypoxemic respiratory failure is defined by a PaO2 of <8 kPa with a normal or low PaCO2. Type 2 failure is defined by a PaO2 of <8 kPa and a PaCO2 of >6 kPa.

Hypoxemic failure most commonly presents acutely in conditions where there is an interference of gas transfer including acute pulmonary edema, pneumonia, interstitial lung disease, or lobar collapse. It might also be due to lack of oxygen delivery to the alveoli due to bronchoconstriction such as asthma or COPD.

Hypoxemic respiratory failure happens due to V/Q mismatch and/or shunt, which lead to a widening of alveolar–arterial oxygen (A–a) gradient. There is a mixture of low and high V/Q units within every lung depending on the underlying condition. The low units contributing to hypoxemia could be secondary to decrease in ventilation due to airway or interstitial disease. It could also be due to excess perfusion in normally ventilated areas due to diverted blood from areas affected by a pulmonary embolus. The high V/Q units indicate wasted ventilation but do not usually contribute to hypoxemia unless very severe. Increasing FiO2 to 100% will eliminate all low V/Q units thus improving hypoxemia. However, failure to improve hypoxemia by oxygen would mean presence of a shunt. Deoxygenated blood bypasses the ventilated alveoli leading to reduction in arterial blood oxygen content. Such shunts can occur where the alveoli are filled with fluid such as pneumonia, collapse, or pulmonary edema.


  Pathophysiological Effects of Noninvasive Ventilation Top


Effects on the respiratory system

Extrinsically applied positive end-expiratory pressure (PEEP) increases alveolar size and recruitment. This expands the area available for gas exchange, reduces intrapulmonary shunt, improves lung compliance, and decreases the WOB. NIV uniformly decreased inspiratory effort and WOB in patients with diverse etiologies and severity of pulmonary disease. At maximum inspiratory support (15 cmH2O), WOB and patient effort were reduced approximately 60%. NIV also acts to negate the effects of intrinsic PEEP, which is the cause of dynamic airway compression and gas trapping. Ventilation had beneficial effects on the A-a gradient, hypercarbia and hypoxia. Pressure support (alone or as part of bilevel ventilation) further augments alveolar ventilation and allows some respiratory muscle rest during the inspiratory phase.[4],[5]

Effects on the cardiovascular system

PEEP reduces venous return to the right side of the heart. Left ventricular preload, transmural pressure, and relative afterload are all decreased without altering myocardial contractility. Thus, the ejection fraction improves without an increase in myocardial oxygen consumption. It appears that those with worst ventricular dysfunction show the most significant improvement in stroke volume index with CPAP. In healthy subjects, nasal CPAP of 15 cmH2O decreased cardiac output 20–30%. In patients with stable COPD, high (10–20 cmH2O) pressure support with low (3–5 cmH2O), PEEP decreased cardiac output approximately by 20%. In patients with acute lung injury (ALI), those NIV levels had negligible effects on cardiac output. In patients with congestive heart failure, NIV often increased cardiac output by decreasing inspiratory effort and left ventricular afterload.

Overall, CPAP leads to a decrease in arterial pressure, heart rate, and rate-pressure product within 10 min, without exacerbation of hypotension.[4],[5]

Effects on other systems

Intracranial pressure (ICP) – in patients with raised ICP, there may be an increase in ICP by at least the same degree as the PEEP applied.

Renal – PEEP causes decreased sodium excretion and urine output, possibly due to raised vena caval pressure reducing cortical blood flow.[4]

Common causes of acute hypoxemic respiratory failure in where NIV might be considered:

  • Acute respiratory distress syndrome (ARDS)/ALI
  • Pneumonia
  • Asthma
  • Interstitial lung disease
  • Postoperative AHRF
  • Cardiopulmonary procedures
  • AHRF after thoracic trauma.


Noninvasive ventilation in acute respiratory distress syndrome/acute lung injury

Studies on NIV to treat ALI and ARDS have reported failure rates ranging from 50% to >80%, but no randomized controlled trials (RCTs) have focused on ALI/ARDS exclusively.[6],[7]

A meta-analysis by Agarwal et al. which included 13 studies with a total of 540 subjects found that the pooled intubation rate was 48%, and the pooled mortality rate was 35%. They had concluded that application of NIV in patients with ARDS does not decrease the rate of endotracheal intubation (ETI) or Intensive Care Unit (ICU) survival.[8] However, few of the studies analyzed were randomized, and the subjects had heterogeneous underlying pathologies (e.g., community-acquired pneumonia [CAP], sepsis, and near-drowning), which makes it difficult to draw conclusions related to ARDS. An observational study by Thille et al. showed that the milder is the degree of ARDS, the higher is the chance of success of NIV in avoiding ETI with a reduced ICU mortality.[9] They recommended that in patients with moderate ARDS, NIV may be worth attempting in those having a PaO2/FiO2 ratio >150 in the absence of hemodynamic instability or altered consciousness. The selection of patients is extremely crucial.

Other independent risk factors for NIV failure include severe hypoxemia, active cancer, shock, moderate/severe ARDS, lower Glasgow coma score, lower positive end-expiratory pressure level at NIV initiation shock, and metabolic acidosis were predictors of NIV failure.[10] A recent prospective multicenter survey found that when NIV was used as first-line therapy for selected ALI/ARDS patients (those with >2 organ failures, hemodynamic instability, or encephalopathy were excluded), 54% avoided intubation and had excellent outcomes.[11] Predictors of NIV failure were Simplified Acute Physiology Score II >34 and Pao2/FiO2 ≤175 after the 1st h of therapy.

Hence, the use of NIV as an alternative to invasive ventilation in severely hypoxemic patients with ARDS (i.e., PaO2/FiO2 200) is not generally recommended and should be limited to highly selected hemodynamically stable patients who can be closely monitored in an intensive care setting by highly skilled staff with a readiness to promptlyintubate if oxygenation fails to improve sufficiently within the 1st h.

Noninvasive ventilation in community-acquired pneumonia

Pneumonia has been a challenge to treat noninvasively and has been identified as a risk factor for NIV failure. An RCT by Confalonieri et al. showed that in selected patients with ARF caused by severe CAP, NIV was associated with a significant reduction in the rate of ETI and (21% vs. 50%; P = 0.03) and duration of ICU stay (1.8 vs. 6.6 days, P = 0.04). Subgroup of patients with COPD had a survival advantage at 2 months (88.9% vs. 37.5%; P = 0.05).[12] Another RCT on patients with hypoxemic respiratory failure showed that NIV reduced the need for intubation among patients with pneumonia (26% vs. 73% in the conventional therapy group).[7]

However, a more recent RCT [13] testing NIV as an alternative to invasive ventilation in patients with various types of ARF found that the subgroup with pneumonia did very poorly, with all eight patients randomized to NIV requiring intubation. The severity of hypoxemia and the co-existence of other acute organ failure are strong predictors of the outcome of NIV in CAP.

A study by Carrillo et al. showed that worsening radiographic infiltrate 24 h after admission, maximum sepsis-related (or sequential) organ failure assessment (SOFA) score and after 1 h of NIV, higher heart rate and lower PaO2/FiO2, and bicarbonate independently predicted NIV failure. SOFA, NIV failure, and older age independently predicted hospital mortality. Successful NIV was strongly associated with better survival. If predictors for NIV failure are present, avoiding delayed intubation of patients with “de novo” ARF would potentially minimize mortality.[14] A recent single-center study has suggested that in patients who fail on NIV and subsequently, ventilated have poorer outcomes and more complications.[15]

However, NIV might be beneficial in certain subgroups of patients. Use of NIV in recipients of solid organ transplantation with AHRF showed NIV was associated with a significant reduction in intubation rate (20% vs. 70%; P = 0.002), fatal complications (20% vs. 50%; P = 0.05), length of ICU stay (5.5 vs. 9; P = 0.03), and ICU mortality (20% vs. 50%; P = 0.05). Hospital mortality was similar in both groups.[16] In immunocompromised patients including hematological malignancies with evidence of pulmonary infiltrates on CXR, the early use of NIV in respiratory failure resulted in fewer intubations, complications and improved the likelihood of survival.[17]

Hence, NIV can be trialed cautiously in selected patients, and routine use of NIV in patients with severe pneumonia is not supported. They need careful monitoring due a high-risk of failure with a preparedness to intubate without delay in such situations.

Noninvasive ventilation in asthma

An acute asthmatic attack is accompanied by both an increase in inspiratory and expiratory indexes of airway obstruction accompanied by a significant dynamic hyperinflation and generation of a large negative pleural pressure that is needed to overcome the increased end-expiratory intrathoracic pressure and airway resistance.[18],[19],[20],[21] The progressive decline in forced expiratory volume in 1s, during an asthmatic attack, is associated with a proportional increase in the inspiratory WOB, contributing to inspiratory muscle fatigue.[18] Together with increased physiologic dead space and ventilation-perfusion mismatch,[22] the attack may culminate in a worsening hypoxemia with hypercarbia and respiratory failure.

The evidence is weak for the use of NIV in asthma patients with ARF. An uncontrolled study [23] observed improved gas exchange and avoidance of intubation in 15 of 17 patients with status asthmaticus, and all patients survived. A subsequent randomized pilot study in 33 patients with acute asthma, but not ARF showed improved flow rates and decreased hospitalizations with NIV versus sham NIV.[24] However, a Cochrane analysis [25] by Ram et al. concluded that large RCTs are needed before recommending NIV use in status asthmaticus. A trial of NIV can be considered in asthmatics who fail to respond adequately to initial bronchodilator therapy in an intensive care setting where they can be monitored closely and intubated promptly if there is no improvement in the 1st hr as these patients can deteriorate very rapidly.

Noninvasive ventilation in idiopathic pulmonary fibrosis exacerbations

An increasing number of patients with idiopathic pulmonary fibrosis (IPF) were admitted to ICU for the management of an episode of AHRF. Patients with IPF who develop AHRF have extremely poor prognosis. Invasive ventilation does not impact outcomes and is almost universally fatal.[26],[27] If it is following an operation, it is slightly more positive.[28] There are no large prospective studies looking at the impact of NIV on IPF with AHRF. A recent retrospective study by Vianello et al. showed the overall poor outcome of NIV, with more than 50% needing intubation and all they died in hospital. Those who survived had a lower admission respiratory rate, C-reactive protein, and pro-brain natriuretic peptide.[29] A small study showed just <50% of patients avoided intubation and survived more than 3 months. All patients who were intubated died.[30] We cannot draw any firm conclusion from such small studies but given invasive ventilation carries 100% mortality, NIV might be considered in highly selected patients with IPF exacerbations.

Noninvasive ventilation in postoperative acute hypoxemic respiratory failure

Anesthesia and postoperative pain cause changes in the respiratory system leading to hypoxemia, reduction in tidal volume, and atelectasis associated with a restrictive syndrome and a diaphragmatic dysfunction.[31],[32] Hypoxemia is known to complicate the recovery of 30–50% of patients after abdominal surgery; ETI and mechanical ventilation may be required in 8–10% of cases, increasing morbidity and mortality, and prolonging ICU and hospital stay.[33] Both CPAP and NIV have shown benefit in the postoperative period. When used prophylactically after major abdominal surgery [33] or thoracoabdominal aneurysm repair,[34] CPAP (10 cmH2O) reduces the incidence of hypoxemia, pneumonia, atelectasis, and intubations compared with standard treatment. Potential goals of NIV in the postoperative period include: Prevention of ARF (prophylactic treatment) and/or treat ARF and avoid reintubation (curative treatment).[35]

In the only RCT of NIV in the postoperative setting by Auriant et al., patients with hypoxemic respiratory failure after lung resection had reduced intubation and mortality rates if treated with NIV when compared with standard management.[36] In bariatric surgery when NIV is applied during the first 24 h, there is a significant improvement of forced vital capacity.[37] Because of these studies have examined different techniques following diverse surgeries, definite recommendations cannot be made. However, the data lend support to the use of CPAP or NIV in the peri- and post-operative situations, either prophylactically in high-risk patients or as an early therapy of respiratory insufficiency.

Noninvasive ventilation during Interventional cardiopulmonary procedures

Cardiopulmonary interventions such as fiberoptic bronchoscopy (FOB), transesophageal echocardiography may worsen oxygenation and clinical status in severely hypoxemic patients. An RCT by Maitre et al. has shown that CPAP alone (up to 7.5 cmH2O) improves oxygenation and reduces postprocedural respiratory failure in patients with severe hypoxemia undergoing bronchoscopy.[38] A prospective trial by the French assessing the feasibility and safety of noninvasive positive pressure ventilation through a face mask to performing FOB in patients with COPD contraindicating FOB in spontaneous ventilation concluded that NIV is safe for maintaining adequate gas exchange in hypoxemic and hypercapnic COPD patients, not in ARF.[39]

Evidence supports the use of NIV during FOB, especially with high risks of ETI, such as in immunocompromised patients. During transesophageal echocardiography, as well as in interventional cardiology and pulmonology, NIV can reduce the need for deep sedation or general anesthesia and prevent respiratory depression induced by deep sedation. Moreover, NIV is more effective than usual mask preoxygenation in improving oxygenation before ETI in high-risk patients in ICU.[40]

Noninvasive ventilation after thoracic trauma

Previous studies showed that posttraumatic respiratory failure was caused by an increased amount of interstitial and intra-alveolar fluids and described the concept of the so-called “traumatic wet lung,” and recommend positive airway pressure by mask to ensure adequate ventilation.[41],[42] More recently, trauma management has been guided according to the mechanism of injury, its anatomic involvement and the staging of the injury. Its main aims include pulmonary toilet, control of chest wall pain, surgical stabilization, and fluid management. However, ventilator management has received little attention [43] and this is reflected by a low-grade recommendation for the use of NIV in trauma patients by the British Thoracic Society guidelines.[44]

In an RCT conducted in 50 patients with severe hypoxemia complicating chest trauma, Hernandez et al. demonstrated that the application of NIV was associated with a significant reduction of the need for intubation as compared to only standard oxygen therapy.[45]


  Conclusion Top


The effectiveness of NIV in AHRF varies widely depending on the underlying conditions.

In severe CAP and mild ARDS without shock and multiple organ dysfunctions syndromes, especially in immunocompromised host cautious attempt of early NIV may be tried but only in high-intensity of care settings where facilities for intubation are quickly available. Its use in peri- and post-operative setting is on the rise with increasing awareness of the benefits of NIV in general. Use of NIV in other settings remain controversial and would remain so in the absence of large trials.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Brochard L, Mancebo J, Wysocki M, Lofaso F, Conti G, Rauss A, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med 1995 Sep 28;333:817-22.  Back to cited text no. 1
    
2.
Lightowler JV, Wedzicha JA, Elliott MW, Ram FSF. Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis. BMJ 2003 Jan 25;326:185.  Back to cited text no. 2
    
3.
Masip J, Roque M, Sánchez B, Fernández R, Subirana M, Expósito JA. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA 2005;294:31240-30.   Back to cited text no. 3
    
4.
Cross AM. Review of the role of non-invasive ventilation in the emergency department. J Accid Emerg Med 2000;17:79-85.   Back to cited text no. 4
    
5.
Kallet RH, Diaz JV. The physiologic effects of noninvasive ventilation. Respir Care 2009;54:102-15.   Back to cited text no. 5
    
6.
Antonelli M, Conti G, Moro ML, Esquinas A, Gonzalez-Diaz G, Confalonieri M, et al. Predictors of failure of noninvasive positive pressure ventilation in patients with acute hypoxemic respiratory failure: A multi-center study. Intensive Care Med 2001;27:1718-28.   Back to cited text no. 6
    
7.
Ferrer M, Esquinas A, Leon M, Gonzalez G, Alarcon A, Torres A. Noninvasive ventilation in severe hypoxemic respiratory failure: A randomized clinical trial. Am J Respir Crit Care Med 2003;15;168:1438-44.   Back to cited text no. 7
    
8.
Agarwal R, Gupta R, Aggarwal AN, Gupta D. Noninvasive positive pressure ventilation in acute respiratory failure due to COPD vs other causes: Effectiveness and predictors of failure in a respiratory ICU in North India. Int J Chron Obstruct Pulmon Dis 2008;3:737-43.   Back to cited text no. 8
    
9.
Thille AW, Contou D, Fragnoli C, Córdoba-Izquierdo A, Boissier F, Brun-Buisson C. Non-invasive ventilation for acute hypoxemic respiratory failure: Intubation rate and risk factors. Crit Care 2013;17:R269.  Back to cited text no. 9
    
10.
Rana S, Jenad H, Gay PC, Buck CF, Hubmayr RD, Gajic O. Failure of non-invasive ventilation in patients with acute lung injury: Observational cohort study. Crit Care Lond Engl 2006;10:R79.   Back to cited text no. 10
    
11.
Antonelli M, Conti G, Esquinas A, Montini L, Maggiore SM, Bello G, et al. A multiple-center survey on the use in clinical practice of noninvasive ventilation as a first-line intervention for acute respiratory distress syndrome. Crit Care Med 2007;35:18-25.   Back to cited text no. 11
    
12.
Confalonieri M, Potena A, Carbone G, Porta RD, Tolley EA, Umberto Meduri G. Acute respiratory failure in patients with severe community-acquired pneumonia. A prospective randomized evaluation of noninvasive ventilation. Am J Respir Crit Care Med 1999;160(5 Pt 1):1585-91.   Back to cited text no. 12
    
13.
Honrubia T, García López FJ, Franco N, Mas M, Guevara M, Daguerre M, et al. Noninvasive vs conventional mechanical ventilation in acute respiratory failure: A multicenter, randomized controlled trial. Chest 2005;128:3916-24.   Back to cited text no. 13
    
14.
Carrillo A, Gonzalez-Diaz G, Ferrer M, Martinez-Quintana ME, Lopez-Martinez A, Llamas N, et al. Non-invasive ventilation in community-acquired pneumonia and severe acute respiratory failure. Intensive Care Med 2012;38:458-66.   Back to cited text no. 14
    
15.
Mosier JM, Sakles JC, Whitmore SP, Hypes CD, Hallett DK, Hawbaker KE, et al. Failed noninvasive positive-pressure ventilation is associated with an increased risk of intubation-related complications. Ann Intensive Care 2015;5:4.   Back to cited text no. 15
    
16.
Antonelli M, Conti G, Bufi M, Costa MG, Lappa A, Rocco M, et al. Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: A randomized trial. JAMA 2000;283:235-41.   Back to cited text no. 16
    
17.
Hilbert G, Gruson D, Vargas F, Valentino R, Gbikpi-Benissan G, Dupon M, et al. Noninvasive ventilation in immunosuppressed patients with pulmonary infiltrates, fever, and acute respiratory failure. N Engl J Med 2001;344:481-7.   Back to cited text no. 17
    
18.
Martin JG, Shore SA, Engel LA. Mechanical load and inspiratory muscle action during induced asthma. Am Rev Respir Dis 1983;128:455–60.   Back to cited text no. 18
    
19.
Cormier Y, Lecours R, Legris C. Mechanisms of hyperinflation in asthma. Eur Respir J 1990;3:619-24.   Back to cited text no. 19
    
20.
Martin J, Powell E, Shore S, Emrich J, Engel LA. The role of respiratory muscles in the hyperinflation of bronchial asthma. Am Rev Respir Dis 1980;121:441-7.   Back to cited text no. 20
    
21.
Buda AJ, Pinsky MR, Ingels NB, Daughters GT, Stinson EB, Alderman EL. Effect of intrathoracic pressure on left ventricular performance. N Engl J Med 1979;301:453-9.   Back to cited text no. 21
    
22.
Wagner PD, Hedenstierna G, Bylin G. Ventilation-perfusion inequality in chronic asthma. Am Rev Respir Dis 1987;136:605-12.   Back to cited text no. 22
    
23.
Meduri GU, Cook TR, Turner RE, Cohen M, Leeper KV. Noninvasive positive pressure ventilation in status asthmaticus. Chest 1996;110:767-74.   Back to cited text no. 23
    
24.
Soroksky A, Stav D, Shpirer I. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest 2003;123:1018-25.   Back to cited text no. 24
    
25.
Ram FSF, Wellington S, Rowe B, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev 2005;3:CD004360.   Back to cited text no. 25
    
26.
Blivet S, Philit F, Sab JM, Langevin B, Paret M, Guérin C, et al. Outcome of patients with idiopathic pulmonary fibrosis admitted to the ICU for respiratory failure. Chest 2001;120:209-12.   Back to cited text no. 26
    
27.
Fumeaux T, Rothmeier C, Jolliet P. Outcome of mechanical ventilation for acute respiratory failure in patients with pulmonary fibrosis. Intensive Care Med 2001;27:1868-74.   Back to cited text no. 27
    
28.
Fernández-Pérez ER, Yilmaz M, Jenad H, Daniels CE, Ryu JH, Hubmayr RD, et al. Ventilator settings and outcome of respiratory failure in chronic interstitial lung disease. Chest 2008 May;133:1113-9.   Back to cited text no. 28
    
29.
Vianello A, Arcaro G, Battistella L, Pipitone E, Vio S, Concas A, et al. Noninvasive ventilation in the event of acute respiratory failure in patients with idiopathic pulmonary fibrosis. J Crit Care 2014;29:562-7.   Back to cited text no. 29
    
30.
Yokoyama T, Kondoh Y, Taniguchi H, Kataoka K, Kato K, Nishiyama O, et al. Noninvasive ventilation in acute exacerbation of idiopathic pulmonary fibrosis. Intern Med Tokyo Jpn 2010;49:1509-14.   Back to cited text no. 30
    
31.
Simonneau G, Vivien A, Sartene R, Kunstlinger F, Samii K, Noviant Y, et al. Diaphragm dysfunction induced by upper abdominal surgery. Role of postoperative pain. Am Rev Respir Dis 1983;128:899-903.   Back to cited text no. 31
    
32.
Warner DO. Preventing postoperative pulmonary complications: The role of the anesthesiologist. Anesthesiology 2000;92:1467-72.   Back to cited text no. 32
    
33.
Squadrone V, Coha M, Cerutti E, Schellino MM, Biolino P, Occella P, et al. Continuous positive airway pressure for treatment of postoperative hypoxemia: A randomized controlled trial. JAMA 2005;293:589-95.   Back to cited text no. 33
    
34.
Kindgen-Milles D, Müller E, Buhl R, Böhner H, Ritter D, Sandmann W, et al. Nasal-continuous positive airway pressure reduces pulmonary morbidity and length of hospital stay following thoracoabdominal aortic surgery. Chest 2005;128:821-8.   Back to cited text no. 34
    
35.
Jaber S, De Jong A, Castagnoli A, Futier E, Chanques G. Non-invasive ventilation after surgery. Ann Fr Anesthèsie Rèanimation 2014;33:487-91.   Back to cited text no. 35
    
36.
Auriant I, Jallot A, Hervé P, Cerrina J, Le Roy Ladurie F, Fournier JL, et al. Noninvasive ventilation reduces mortality in acute respiratory failure following lung resection. Am J Respir Crit Care Med 2001;164:1231-5.   Back to cited text no. 36
    
37.
Joris JL, Sottiaux TM, Chiche JD, Desaive CJ, Lamy ML. Effect of bi-level positive airway pressure (BiPAP) nasal ventilation on the postoperative pulmonary restrictive syndrome in obese patients undergoing gastroplasty. Chest 1997;111:665-70.   Back to cited text no. 37
    
38.
Maitre B, Jaber S, Maggiore SM, Bergot E, Richard JC, Bakthiari H, et al. Continuous positive airway pressure during fiberoptic bronchoscopy in hypoxemic patients. A randomized double-blind study using a new device. Am J Respir Crit Care Med 2000;162(3 Pt 1):1063-7.   Back to cited text no. 38
    
39.
Da Conceiçao M, Genco G, Favier JC, Bidallier I, Pitti R. [Fiberoptic bronchoscopy during noninvasive positive-pressure ventilation in patients with chronic obstructive lung disease with hypoxemia and hypercapnia]. Ann Fr Anesthèsie Rèanimation. 2000;19:231–6.   Back to cited text no. 39
    
40.
Baillard C, Fosse J-P, Sebbane M, Chanques G, Vincent F, Courouble P, et al. Noninvasive ventilation improves preoxygenation before intubation of hypoxic patients. Am J Respir Crit Care Med 2006;174:171-7.   Back to cited text no. 40
    
41.
Burford TH, Burbank B. Traumatic wet lung; observations on certain physiologic fundamentals of thoracic trauma. J Thorac Surg 1945;14:415-24.   Back to cited text no. 41
    
42.
Jensen NK. Recovery of pulmonary function after crushing injuries of the chest. Dis Chest 1952;22:319-46.   Back to cited text no. 42
    
43.
Vidhani K, Kause J, Parr M. Should we follow ATLS guidelines for the management of traumatic pulmonary contusion: the role of non-invasive ventilatory support. Resuscitation 2002;52:265-8.   Back to cited text no. 43
    
44.
British Thoracic Society Standards of Care Committee. Non-invasive ventilation in acute respiratory failure. Thorax 2002;57:192-211.   Back to cited text no. 44
    
45.
Hernandez G, Fernandez R, Lopez-Reina P, Cuena R, Pedrosa A, Ortiz R, et al. Noninvasive ventilation reduces intubation in chest trauma-related hypoxemia: a randomized clinical trial. Chest 2010;137:74-80.  Back to cited text no. 45
    




 

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