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Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema

  1. Flávia MR Vital1,*,
  2. Magdaline T Ladeira2,
  3. Álvaro N Atallah3

Editorial Group: Cochrane Heart Group

Published Online: 31 MAY 2013

Assessed as up-to-date: 5 APR 2011

DOI: 10.1002/14651858.CD005351.pub3


How to Cite

Vital FMR, Ladeira MT, Atallah ÁN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database of Systematic Reviews 2013, Issue 5. Art. No.: CD005351. DOI: 10.1002/14651858.CD005351.pub3.

Author Information

  1. 1

    Muriaé Cancer Hospital, Department of Physiotherapy, Muriaé, Minas Gerais, Brazil

  2. 2

    Escola Paulista de Medicina, Universidade Federal de São Paulo, Department of Internal and Therapeutic Medicine, São Paulo, São Paulo, Brazil

  3. 3

    Centro de Estudos de Medicina Baseada em Evidências e Avaliação Tecnológica em Saúde, Brazilian Cochrane Centre, São Paulo, São Paulo, Brazil

*Flávia MR Vital, Department of Physiotherapy, Muriaé Cancer Hospital, Cristiano Ferreira Varella, 555, Muriaé, Minas Gerais, Brazil. fvital@fcv.org.br. flaviavital@bol.com.br.

Publication History

  1. Publication Status: New search for studies and content updated (conclusions changed)
  2. Published Online: 31 MAY 2013

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Summary of findings    [Explanations]

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

 
Summary of findings for the main comparison. Non-invasive positive pressure ventilation (CPAP and bilevel NPPV) for cardiogenic pulmonary edema

Non-invasive positive pressure ventilation (CPAP and bilevel NPPV) for cardiogenic pulmonary oedema

Patient or population: patients with cardiogenic pulmonary oedema
Settings: Emergency Department or Intensive Care Unit
Intervention: Non-invasive positive pressure ventilation (CPAP and bilevel NPPV)

OutcomesIllustrative comparative risks* (95% CI)Relative effect
(95% CI)
No of Participants
(studies)
Quality of the evidence
(GRADE)
Comments

Assumed riskCorresponding risk

ControlNon-invasive positive pressure ventilation (CPAP and bilevel NPPV)

Hospital mortalityYStudy population1RR 0.66
(0.48 to 0.89)
1107
(20 studies)
⊕⊕⊕⊕
high2,3

204 per 1000135 per 1000
(98 to 182)

Moderate1

200 per 1000132 per 1000
(96 to 178)

Endotracheal intubation rateStudy populationRR 0.52
(0.36 to 0.75)
1261
(22 studies)
⊕⊕⊝⊝
low4,5

249 per 1000130 per 1000
(90 to 187)

Moderate

300 per 1000156 per 1000
(108 to 225)

Incidence of acute myocardial infarction (During intervention)Study populationRR 1.24
(0.79 to 1.95)
461
(8 studies)
⊕⊕⊕⊝
moderate5,6

153 per 1000190 per 1000
(121 to 299)

Moderate

169 per 1000210 per 1000
(134 to 330)

Incidence of acute myocardial infarction (After intervention)Study populationRR 0.7
(0.11 to 4.26)
154
(4 studies)
⊕⊝⊝⊝
very low5,7

26 per 100018 per 1000
(3 to 111)

Moderate

13 per 10009 per 1000
(1 to 55)

Intolerance to allocated treatmentStudy populationRR 0.47
(0.29 to 0.77)
1848
(13 studies)
⊕⊕⊕⊝
moderate8,9,10

234 per 1000110 per 1000
(68 to 180)

Moderate

350 per 1000165 per 1000
(101 to 269)

Hospital length of stayThe mean hospital length of stay in the intervention groups was
0.8 lower
(2.1 lower to 0.51 higher)
542
(10 studies)
⊕⊝⊝⊝
very low11,12

Intensive care unit length of stay (Copy)The mean intensive care unit length of stay (copy) in the intervention groups was
0.89 lower
(1.33 to 0.45 lower)
222
(6 studies)
⊕⊕⊝⊝
low5,13

*The basis for the assumed risk (e.g. the median control group risk across studies) is provided in footnotes. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI).
CI: Confidence interval; RR: Risk ratio;

GRADE Working Group grades of evidence
High quality: Further research is very unlikely to change our confidence in the estimate of effect.
Moderate quality: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
Low quality: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
Very low quality: We are very uncertain about the estimate.

 1 The most studies have mixed populations (with different levels of severity and co-morbidities).
2 Was included only two quasi-randomised trials, but sensitivity analysis with quasi-randomised studies exclusion (Bersten 1991; Weitz 2007), showed the results to remain statistically significant. L'Her 2004 was interrupted early due to a greater number in deaths and complications in the control group.
3 Although there is less 300 events in meta-analysis, when add Gray's study that analysed the mortality in 30 days, our meta-analysis of hospital mortality show that these study reinforce the favourable use of NPPV in ACPE with more 300 events.
4 Was included only two quasi-randomised trials, but sensitivity analysis with quasi-randomised studies exclusion (Bersten 1991; Weitz 2007), showed the results to remain statistically significant. Park 2004 was interrupted early due to a difference in the frequency of intubations. Lin 1991 lost 35 of the 80 (44%) randomised patients for having fulfilled the criteria of exclusion or having presented failures on the received intervention.
5 There is less 300 events in meta-analysis.
6 Although two studies (Sharon 2000; Thys 2002) were interrupted early due to the incidence of acute myocardial infarction and the second due to a batch of failures of treatment and clinical decline.
7 Was included one quasi-randomised trial (Weitz 2007). Lin 1991 lost 35 of the 80 (44%) randomised patients for having fulfilled the criteria of exclusion or having presented failures on the received intervention.
8 Was included two quasi-randomised trials (Bersten 1991; Weitz 2007). L'Her 2004 was interrupted early due to a greater number in deaths and complications in the control group and not present the results in relation to autonomy for the activities of daily living, patient comfort and some planned adverse effects to be observed. Lin 1991 lost 35 of the 80 (44%) randomised patients for having fulfilled the criteria of exclusion or having presented failures on the received intervention. Thys 2002 was interrupted early due to a batch of failures of treatment and clinical decline.
9 The grouping of the studies demonstrated relevant heterogeneity which was eliminated with the exclusion of Gray 2008 study, but we have not found plausible justification for this result
10 RR < 0.5
11 Was included two quasi-randomised trials (Bersten 1991; Weitz 2007). L'Her 2004 and Thys 2002 were interrupted early, the first due to a greater number in deaths and in the control group and the second due to a batch of failures of treatment and clinical decline. L'Her 2004 did not present the results in relation to autonomy for the activities of daily living, patient comfort and some planned adverse effects to be observed. Lin 1991 lost 35 of the 80 (44%) randomised patients for having fulfilled the criteria of exclusion or having presented failures on the received intervention.
12 The grouping of the studies demonstrated relevant heterogeneity.
13 Was included two quasi-randomised trials (Bersten 1991; Weitz 2007). Thys 2002 was interrupted early due to a batch of failures of treatment and clinical decline.

 

Background

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

This is an update of a systematic review previously published in 2008 about non-invasive positive pressure ventilation (NPPV) in acute cardiogenic pulmonary oedema (ACPE) (Vital 2008).

Recent publications showed that about 5.7 million Americans and 15 million Europeans have heart failure (HF) (AHA 2012; Dickstein 2008). In the United States, the estimate annual rates per 1000 population of new HF events for white men are 15.2 for those 65 to 74 years of age, 31.7 for those 75 to 84 years of age, and 65.2 for those 85 years of age. For white women in the same age groups, the rates are 8.2, 19.8, and 45.6, respectively. For black men, the rates are 16.9, 25.5, and 50.6, and for black women, the estimated rates are 14.2, 25.5, and 44.0, respectively (AHA 2012). Acute HF is defined as the rapid onset of signs and symptoms secondary to abnormal cardiac function. HF may occur in the presence or absence cardiac disease and may culminate in acute cardiogenic pulmonary oedema (ACPE) manifested by severe respiratory distress. The most common causes of ACPE are ischaemia, acute coronary syndromes, hypertensive crisis, valvular dysfunction, acute arrhythmias, pericardial disease, increased filling pressures or elevated systemic resistance and dilated cardiomyopathy (Dickstein 2008; Gibelin 2002; Guimarães 2004; Nieminen 2005; Williams 1995). ACPE typically presents with severe respiratory distress, tachypnoea,orthopnoea, crackles on auscultation, and oxygen desaturation (Dickstein 2008; Nieminen 2005). Patients with acute HF have a poor prognosis. The one-year mortality rate associated with acute myocardial infarction complicated by acute HF is nearly 30% (Nieminen 2005). Furthermore, the in-hospital and one-year mortality rates associated with ACPE are 12% and 40%, respectively (Nieminen 2005). The incidence and burden of illness imposed by acute HF and ACPE are substantial, underscoring the need for effective preventative and treatment strategies.

In ACPE, cardiac failure results in increased back pressure on the pulmonary circulation which in turn, precipitates extravasation of fluid into the alveoli. In addition to overwhelming the capacity of the lymphatics for fluid removal (Allison 1991), the oedema fluid dilutes surfactant and neutralises its lubricating properties. Consequently, the lungs become less compliant and the effort of breathing increases (Chadda 2002; Martínez 1995; Meyer 1998; Park 2001). In the upright patient, most oedema fluid collects at the lung bases. The oedema fluid causes intrapulmonary shunting and, consequently, ventilation-perfusion (V-Q) mismatch and redistribution of blood flow to the upper lobes. ACPE presents clinically with difficulty breathing, hypoxaemia and anxiety. The resulting sympathetic nervous system activation manifests clinically with tachycardia, hypertension, peripheral vasoconstriction and diaphoresis (Allison 1991).

Clinicians treat patients with ACPE with supplemental oxygen, diuretics, nitrates, nitroglycerin and morphine sulfate. Additional treatments may be required to address the etiology of ACPE and may include antihypertensive therapy, inotropic agents, thrombolysis or urgent surgery (Dickstein 2008; Guimarães 2004; Nieminen 2005; Remme 1997; Williams 1995). A subset of patients with ACPE may require endotracheal intubation and mechanical ventilation (Meyer 1998). Mechanical ventilation supports oxygenation by recruiting previously collapsed alveoli (Levitt 2001; Williams 1995) and thereby improves lung compliance. However, invasive ventilation increases the risk for complications including nosocomial infections (pneumonia, sinusitis) and tracheal injury (Gay 2009; Keenan 1997). Consequently, may prolong intensive care unit (ICU) and hospital stay (Pang 1998). Patients with ACPE can be supported with NPPV, which has been shown to improve mortality and endotracheal intubation rate (ETI) as an initial treatment for patients with acute exacerbations of chronic obstructive pulmonary disease (Ram 2004).

NPPV includes forms of ventilatory support applied without the use of an endotracheal tube, and is considered to include continuous positive airway pressure (CPAP), without or with inspiratory pressure support (bilevel NPPV or BiPAP® - Respironics, Inc, Murrysville, PA). The goals of NPPV use in the treatment of ACPE are to improve oxygenation, reduce the effort of breathing and increase cardiac output (Evans 2001). CPAP achieves these goals by maintaining positive airway pressure throughout the respiratory cycle thereby preventing alveolar collapse at end-expiration. CPAP increases lung compliance and decreases the effort of breathing, while decreasing cardiac preload and afterload (Allison 1991; Bersten 1991; Räsänen 1985). CPAP improves arterial oxygenation (PaO2) by increasing the functional residual capacity of the lungs and reducing intrapulmonary shunt (Räsänen 1985). With CPAP high mean airway pressures are avoided and lower mean intra-thoracic pressures develop during inspiration with favourable effects on venous return and a lower risk of barotrauma (Covelli 1982; Kelly 1997). Treatment with CPAP has beneficial effects on haemodynamics by ameliorating hypertension and tachycardia (Väisänen 1987). Unlike CPAP, bilevel NPPV combines inspiratory positive airway pressure with positive end-expiratory pressure. Consequently, bilevel NPPV differs from CPAP in providing inspiratory assistance to rest the muscles of respiration (Mehta 1997). CPAP and bilevel NPPV are applied with either a nasal or oronasal mask at the patient-ventilator interface (Chadda 2002; Keenan 1997). Complications associated with NPPV use include air leaks, mask discomfort, skin breakdown, eye irritation, sinus congestion, oronasal drying and patient-ventilator dyssynchrony. Pneumothoraces and pneumonias can occur with NPPV administration but are less frequent compared to invasive ventilation (Bach 1997; Gay 2009). NPPV may also delay endotracheal intubation with patient deterioration in the intervening time period (Wood 1998).

Over the past 30 years, numerous reports have appeared in the literature regarding the potential effectiveness of NPPV for patients with ACPE (Masip 2000; Park 2001; Räsänen 1985). The delay in uptake of the evidence may be due to the need for increased patient supervision, the experience of staff with NPPV, NPPV availability and concerns regarding potential adverse effects (Bersten 1991; Pang 1998). Evidence from at least one randomised trial supports that NPPV accelerates recovery of vital signs and blood gases while avoiding intubation (Park 2001). The role of bilevel NPPV in patients with ACPE remains controversial. In a comparison of CPAP with bilevel NPPV, the latter demonstrated more rapid recovery of respiratory and haemodynamic parameters (Lin 1991), but bilevel NPPV was also associated with an increased incidence of acute myocardial infarction (Mehta 1997).

In spite of the potential advantages of NPPV for the management of ACPE, there appears to be a lack of high quality clinical evidence to support use of these interventions. The purpose of this systematic review was to identify, critically appraise and summarise the evidence for NPPV use for ACPE.

 

Objectives

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

The primary objective of this review was to determine the effectiveness and safety of NPPV (CPAP and/or bilevel NPPV) plus standard medical care compared to standard medical care in adults with ACPE on hospital mortality and other clinically important outcomes. The second objective of this review was to directly compare the effects of CPAP and bilevel NPPV on clinically important outcomes.

 

Methods

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms
 

Criteria for considering studies for this review

 

Types of studies

We included blinded or unblinded randomised controlled trials (RCTs) or quasi-randomised controlled trials (QRCTs) in our review. We defined QRCTs as those in which the allocation procedure was unlikely to be adequately concealed (i.e. randomisation according to odd or even numbers, day of the week, social security number, or medical record number).

 

Types of participants

We included trials reporting on adult patients (>18 years) with acute or acute-on-chronic cardiogenic pulmonary oedema. We used the criteria of the American Heart Association (AHA) and/or the European Society of Cardiology (ESC) to define ACPE (Nieminen 2005; Williams 1995). Alternatively, a diagnosis of acute HF was based upon symptoms and clinical signs including dyspnoea, shortness of breath, nonproductive or cough productive of sputum), pallor, cyanosis, normal or elevated blood pressure, rales on auscultation and the presence of cold clammy skin. The diagnosis had to be supported by a chest radiograph, electrocardiograms, serum biomarkers of acute myocardial infarction or acute HF or echocardiography.

We excluded trials investigating NPPV for patients with a primary diagnosis of pneumonia, alternative etiologies of respiratory failure and its use as a weaning strategy.

 

Types of interventions

The control group included any form of standard medical care (SMC) provided for the management of cardiogenic pulmonary oedema (Nieminen 2005), excluding NPPV or alternative methods of ventilatory support.

The intervention group was standard medical care for the management of cardiogenic pulmonary oedema plus NPPV (CPAP and/or bilevel NPPV) applied through a nasal or facemask.

 

Types of outcome measures

 

Primary outcomes

  • Hospital mortality

 

Secondary outcomes

  • ETI
  • Incidence of acute myocardial infarction during and after intervention (during the hospital stay)
  • Intolerance to the allocated treatment (patients with criteria for intubation, but this situation did not happen, because they could get another type of ventilatory support)
  • Hospital length of stay (between admission to hospital up to death event or hospital leaving)
  • Intensive care unit (ICU) length of stay (time length in between admission to ICU up to death event or ICU leaving)
  • Arterial blood gases (PaCO2, PaO2) and pH one-hour post intervention
  • Vital signs: respiratory rate, heart rate, blood pressure 1-hour post intervention
  • Treatment failure (the combination of mortality and intubation and intolerance to the allocated treatment)
  • Adverse events

 

Search methods for identification of studies

 

Electronic searches

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) and the Database of Abstracts of Reviews Effectiveness (DARE) on The Cochrane Library (Issue 2, 2011), MEDLINE (Ovid, 1950 to 20 April 2011), EMBASE (Ovid, 1980 to 20 April 2011), Cumulative Index to Nursing and Allied Health Literature (CINAHL) (EBSCO, 1982 to 20 April 2011) and LILACS (1982 to 20 April 2011) . When the searches were run in 2009 we combined the search strategies with the highly sensitive search strategies to identify RCTs in MEDLINE (Dickersin 1994), EMBASE (Lefebvre 1996), and LILACS (Castro 1999). When the searches were re-run in 2011 the MEDLINE and EMBASE searches used the most current highly sensitive search filters for RCTs (Lefebvre 2011).

The search strategies for each database are presented in Appendix 1 (and Appendix 2 (2009 and 2011 searches, respectively).

 

Searching other resources

We reviewed the bibliographies of retrieved articles to identify related published and unpublished studies.
We contacted authors of included RCTs, experts in NPPV and ventilator manufacturers to obtain information on other published and unpublished studies. No language restrictions were applied.

 

Data collection and analysis

We followed the recommendations outlined in the Cochrane Handbook for Systematic Reviews of Interventions in preparing this review (Higgins 2011).

 

Selection of studies

Two authors (FV and ML) independently screened citations and selected trials meeting the inclusion criteria. Disagreements were resolved by a third author (AA).

 

Data extraction and management

Two authors (FV and ML) abstracted data using a standardised data collection form which highlighted characteristics of the study (design, methods of randomisation, withdrawals and dropouts, intention-to-treat analysis (ITT), informed consent, place and multicenter study), participants (age, gender, number, diagnostic criteria, inclusion and exclusion criteria) and interventions (type of NPPV, timing and duration of therapy, co-interventions, SMC (intervention and dose)) and the outcomes reported. We requested unpublished data from primary authors to supplement outcomes where needed. A third author (ANA) resolved disagreements. If consensus could not be reached, we contacted the author of the trial for additional information.

 

Assessment of risk of bias in included studies

We assessed the methodological quality of the included trials with emphasis on allocation concealment, generation of allocation sequence, detection bias, attrition bias, selective outcome reporting and adherence to ITT as follows (Higgins 2011; Schulz 1995):

 

Allocation concealment

  • Low risk of bias: randomisation method described that would not allow investigator/participant to know or influence intervention group before eligible participant entered in the study
  • Moderate risk of bias: randomisation stated but no information on method used is available
  • High risk of bias: method of randomisation used such as alternate medical record numbers or unsealed envelopes; any information in the study that indicated that investigators or participants could influence intervention group (quasi-randomised studies)

 

Generation of allocation sequence

  • Low risk of bias: adequate sequence generation
  • Moderate risk of bias: not reported in the paper or by contacting authors
  • High risk of bias: not adequate (quasi-randomised studies)

 

Detection bias

  • Low risk of bias: outcome assessors were independent from the individuals administering/supervising the assigned treatments
  • Moderate risk of bias: not reported in the paper or by contacting authors
  • High risk of bias: outcome assessors aware about the assigned treatments

 

Attrition bias

  • Low risk of bias: drop-outs without substantial (statistically significant) difference between the two comparison groups and/or a substantial drop-out rate within the sample as a whole
  • Moderate risk of bias: not reported in the paper or by contacting authors
  • High risk of bias: drop outs with substantial (statistically difference) between the two treatment groups and/or a substantial drop-out rate within the sample as a whole

 

Selective outcome reporting

  • Low risk of bias: reports of the study free of suggestion of selective outcome reporting
  • Moderate risk of bias: not reported in the paper or by contacting authors
  • High risk of bias: reports of the study with suggestion of selective outcome reporting

 

Adherence to the intention-to-treat principle

  • Yes: specifically reported by authors that intention-to-treat analysis was undertaken and this was confirmed on study assessment
  • No: not reported and lack of intention-to-treat analysis confirmed on study assessment (patients who were randomised were not included in the analysis because they did not receive the study intervention, they withdrew from the study or were not included because of protocol violation)

We also noted whether informed consent was obtained and whether the study was blinded.

 

Assessment of heterogeneity

We assessed the impact of heterogeneity using the I2 test (Higgins 2011). This test illustrates the percentage of variability in effect estimates resulting from heterogeneity, as opposed to sampling error. In the presence of the significant heterogeneity (>50%) and a sufficient number of studies reporting the outcome of interest, we conducted exploratory analyses to investigate potential sources of heterogeneity (e.g. participants, treatments and study quality). We hypothesised that age, gender and comorbidities may represent potential sources of heterogeneity among participants. Heterogeneity may be related to the initial treatment(s) used, the levels of pressure applied with NPPV or treatment duration. We considered P values < 0.10 to be statistically significant.

 

Data synthesis

We pooled dichotomous and continuous variables using relative risk (RR) and weighted mean difference (WMD), respectively, using random-effects models. We presented the number needed to treat (NNT) and risk difference (RD) for statistically significant results and assessed their robustness using a fixed-effect model. We report summary estimates of treatment effect with their associated 95% confidence intervals (CIs). All analyses were performed using the Cochrane Collaboration's statistical software, (Review Manager 2013). We considered P values < 0.05 to be statistically significant.

 

Sensitivity analysis

We decided a priori to conduct sensitivity analysis to assess the impact of excluding QRCTs on the outcomes of mortality and endotracheal intubation. Finally, we constructed funnel plots to assess for publication bias (Egger 1997).

 

Quality of the evidence

We used the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach to assess the overall quality of evidence (Guyatt 2008; Higgins 2011).

 

Results

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms
 

Description of studies

 

Study search

We identified 1248 citations from our electronic searches (250 in MEDLINE, 427 in EMBASE, 378 in CENTRAL, 137 in CINAHL, 37 in LILACS, and 19 in DARE). We identified two additional studies through searches in bibliographic references and through correspondence with authors. Two authors (FV, ML) pre-selected 35 references for more detailed review through abstract and title screening (see Figure 1 and Figure 2). All disagreements were resolved by a third reviewer (ANA). We have included 11 new studies with 21 previously included studies, totaling 32 studies involving 2,916 participants (Agmy 2008; Bautin 2005; Bellone 2004; Bellone 2005; Bersten 1991; Crane 2004; Delclaux 2000; Ferrari 2007; Ferrari 2010; Ferrer 2003; Fontanella 2010; Frontin 2010; Gray 2008; Kelly 2002; Levitt 2001; L'Her 2004; Liesching 2003; Lin 1991; Lin 1995; Martin-Bermudez 2002; Masip 2000; Mehta 1997; Moritz 2007; Nava 2003; Park 2001; Park 2004; Räsänen 1985; Sharon 2000; Takeda 1997; Takeda 1998; Thys 2002; Weitz 2007). This included 23 RCTs comparing NPPV plus standard medical care (CPAP and/or bilevel NPPV) to standard medical care and 14 RCTs comparing CPAP plus standard medical care and bilevel NPPV plus standard medical care directly. One of the studies was a mega trial (Gray 2008). Further details of the included studies are available in the section Characteristics of included studies and justifications for studies excluded are described in Characteristics of excluded studies.

 FigureFigure 1. QUOROM statement flow diagram of 2005
 FigureFigure 2. Figure 4. PRISMA statement flow diagram of 2011

 

Study design

Of the 32 parallel design studies, 30 were RCTs and 2 were QRCTs (Bersten 1991; Weitz 2007). Twenty seven studies were reported in full and five studies were reported in abstract form (Agmy 2008; Bautin 2005; Fontanella 2010; Liesching 2003; Martin-Bermudez 2002).

 

Population

The 32 studies were based in several countries including Finland, Australia, Taiwan, Japan, Spain, Israel, USA, Brazil, UK, Belgium, Egypt, Russian, Germany, France and Italy. Eight studies were multicentre studies (Crane 2004; Delclaux 2000; Ferrari 2010; Ferrer 2003; Gray 2008; L'Her 2004; Moritz 2007; Nava 2003). All studies reported on adult patients with acute or acute-on-chronic cardiogenic pulmonary oedema. The number of patients recruited in each study ranged from 8 to 1069 with similar numbers of patients in the intervention and control groups. We have included in the systematic review one mega trial (Gray 2008); however, only their adverse events and the outcome intolerance to the allocated treatment were recorded. The average age of participants was 74 years. The prevalence of cardiogenic pulmonary oedema for men and women was 47% and 53%, respectively.

While nine studies were conducted in the ICU (Agmy 2008; Bautin 2005; Delclaux 2000; Ferrer 2003; Fontanella 2010; Lin 1991; Räsänen 1985; Takeda 1997; Takeda 1998), four studies were undertaken in the emergency department and included patients referred to the ICU after being on a ward (Bersten 1991; Masip 2000; Mehta 1997; Thys 2002). Additionally, Park 2001 reported that it was conducted in the hospital without reference to a specific location, two studies did not report the venue (Liesching 2003; Martin-Bermudez 2002), and two other studies reported that the interventions were initiated in a mobile ICU and continued in the emergency department (Sharon 2000; Weitz 2007). Frontin 2010 reported that the interventions were initiated in a mobile ICU and continued in ICU. The remaining studies were solely undertaken in the emergency department.

 

Intervention

Of the studies identified, ten compared CPAP to SMC (Bersten 1991; Delclaux 2000; Frontin 2010; Kelly 2002; L'Her 2004; Lin 1991; Lin 1995; Räsänen 1985; Takeda 1997; Takeda 1998), and eight compared bilevel NPPV to SMC (Bautin 2005; Ferrer 2003; Levitt 2001; Masip 2000; Nava 2003; Sharon 2000; Thys 2002; Weitz 2007 ). Additionally, there were five three-arm studies comparing CPAP to bilevel NPPV and to SMC (Agmy 2008; Crane 2004; Gray 2008; Park 2001; Park 2004). Finally, nine studies directly compared CPAP with bilevel NPPV (Bellone 2004; Bellone 2005; Ferrari 2007; Ferrari 2010; Fontanella 2010; Liesching 2003; Martin-Bermudez 2002; Mehta 1997; Moritz 2007).

In  Table 1, we present, where reported, the different IPAP and EPAP levels used and the duration of NPPV administration. The choice of patient-ventilator interface for NPPV administration varied among the included studies with three studies using nasal masks exclusively (Mehta 1997; Takeda 1997; Takeda 1998). Two studies offered a choice between nasal and face masks based on patient effort (Ferrer 2003; Levitt 2001). One study used nasal masks for bilevel NPPV administration and face masks for CPAP administration (Park 2001). Four studies did not report the patient-ventilator interface used (Agmy 2008; Gray 2008; Liesching 2003; Sharon 2000). The remaining studies reported using face masks for NPPV administration.

In addition to supplemental oxygen, studies reported the use of pharmacologic treatments including furosemide, morphine, diamorphine, sodium nitroprusside, glyceryl trinitrate, nitrate, isosorbide dinitrate, nitroglycerin, digoxin, digitalis, dopamine, dobutamine, epinephrine, norepinephrine, diazepam, chlorpromazine and antibiotics. Generally the medical team was free to choose the type of medication and its dose for the management of pulmonary oedema. However, one study used high doses of isosorbide dinitrate in the control group (Sharon 2000).

 

Outcomes

Almost all studies reported hospital mortality, except for Frontin 2010, Gray 2008 and Liesching 2003. Frontin 2010 reported mortality after 30 days. Gray 2008 reported mortality after 7 and 30 days from the beginning of the intervention. In order to perform a meta-analysis taking into considering the weight of the mega-trial (which presented opposite results to the first version of this review), we included data on mortality in a separate meta-analysis. However, we were unable to consider the total number after randomisation by group in this meta-analysis since Gray 2008 did not provide this information, which precluded intention-to-treat analysis according to dichotomous outcomes expected. The remaining outcomes were variably reported by the included studies. All dichotomous outcomes were described in adherence with the intention-to-treat principle. All authors reported their studies using mean and standard deviations for continuous outcomes. We transformed units from kilo pascals to millimetres of mercury in pooling results reported for arterial blood gases in two studies (Crane 2004; Kelly 2002).

 

Risk of bias in included studies

The summary of risk of bias can be viewed illustratively in Figure 3 and Figure 4.

 FigureFigure 3. Risk of bias summary: review authors' judgements about each risk of bias item for each included study.
 FigureFigure 4. Risk of bias graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

 

Allocation

All studies included stated that treatment allocation was made randomly. The following studies, which adequately reported the method of allocation concealment, were classified as "low risk of bias": Bellone 2004; Bellone 2005; Crane 2004; Delclaux 2000; Ferrari 2007; Ferrari 2010; Frontin 2010; Gray 2008; Kelly 2002; L'Her 2004; Martin-Bermudez 2002; Masip 2000; Moritz 2007; Nava 2003; Park 2001; Park 2004; Räsänen 1985; Takeda 1998; Thys 2002. The following studies did not describe the method of allocation concealment and were classified as "moderate risk of bias": Agmy 2008; Bautin 2005; Ferrer 2003; Fontanella 2010; Levitt 2001; Liesching 2003; Lin 1991; Lin 1995; Mehta 1997; Sharon 2000; Takeda 1997. The following two studies had an inadequate (quasi-randomised) method and were classified as "high risk of bias": Bersten 1991; Weitz 2007.

In 19 studies sequence generation was described in an appropriate way (Bellone 2004; Bellone 2005; Crane 2004; Delclaux 2000; Ferrari 2007; Ferrari 2010; Ferrer 2003; Frontin 2010; Gray 2008; Levitt 2001; L'Her 2004; Martin-Bermudez 2002; Masip 2000; Mehta 1997; Moritz 2007; Nava 2003; Park 2001; Park 2004; Sharon 2000). Bersten 1991 and Weitz 2007 did not describe sequence generation.

 

Incomplete outcome data

Just two studies have presented significant losses during follow up: Mehta 1997 had lost 9 of the 36 (25%) randomised patients due to infections, exacerbation of COPD and delay in obtaining the informed permission or to initiate intervention; and Lin 1991 lost 35 of the 80 (44%) randomised patients for having fulfilled the exclusion criteria or having failed to receive the intervention.

 

Selective reporting

The majority of the studies planned and reported the outcomes analysed. Two studies omitted some information (Ferrari 2010; L'Her 2004). Ferrari 2010 planned to analyse the effect of NPPV on systemic blood pressure but did not report this outcome. L'Her 2004 did not present the results in relation to autonomy for activities of daily living, patient comfort and adverse effects.

 

Other potential sources of bias

Detection bias was the domain that generated more uncertainty in risk analysis of bias. The majority of studies did not report on blinding. Given the nature of the intervention, blinding of participants and personnel to the intervention was not feasible. Studies by Mehta and Thys were reported as being single-blinded, but in these instances the patient was reportedly blinded to his/her intervention (Mehta 1997; Thys 2002), which appears inconsistent with blinding. Only Delclaux 2000, Gray 2008, Martin-Bermudez 2002 and Moritz 2007 reported that the evaluators were independent.

Twenty-one studies performed analysis by ITT. For our analysis, we performed the analysis of all dichotomous variables by intention-to-treat.

Five studies were stopped early due to preliminary analysis which demonstrated significant differences between groups (L'Her 2004; Mehta 1997; Park 2004; Sharon 2000; Thys 2002). For examples, differences were seen in Mehta 1997 and Sharon 2000 due to the incidence of acute myocardial infarction, in Thys 2002 due to a batch of failures of treatment and clinical decline, in L'Her 2004 due to a greater number in deaths and complications in the control group and in Park 2004 due to a difference in the frequency of intubations. Seven studies did not explicitly report that informed consent was obtained (Agmy 2008; Bautin 2005; Fontanella 2010; Liesching 2003; Lin 1995; Martin-Bermudez 2002; Räsänen 1985).

Sharon's study used different doses of isosorbide dinitrate as standard treatment in the different randomised groups, which may have influenced its results.

The analysis of funnel plot for the outcome hospital mortality demonstrates the indicates asymmetry and the potential risk of publication bias (Figure 5).

 FigureFigure 5. Funnel plot of comparison: 1 Hospital Mortality, outcome: 1.1 NPPV (CPAP and BILEVEL) x SMC.

 

Quality of the evidence  

About 50% of the studies were considered as low risk of bias (Figure 3). The sole domain of quality that most studies did not report on was whether the analysis of outcomes was undertaken by the same person who applied the interventions (detection bias) (Figure 4). As such, we believe that the quality of the evidence included in this review is at moderate risk of bias.

More specifically, we defined seven relevant outcomes in order to assess the quality of evidence by GRADE (Guyatt 2008; Higgins 2011). The primary outcome (mortality) was supported by high quality evidence, two outcomes (incidence of acute myocardial infarction during intervention and intolerance to the allocated treatment) were considered to be supported by moderate quality evidence. Two outcomes (endotracheal intubation rate and ICU length of stay) were considered to be supported by low quality of evidence and for incidence of acute myocardial infarction after intervention and hospital length of stay were considered to be supported by very low quality evidence ( Summary of findings for the main comparison).

 

Effects of interventions

See:  Summary of findings for the main comparison Non-invasive positive pressure ventilation (CPAP and bilevel NPPV) for cardiogenic pulmonary edema

For studies comparing NPPV to SMC, we report our results as NPPV (CPAP and bilevel NPPV) versus SMC, CPAP alone versus SMC and bilevel NPPV alone versus SMC. In addition, we report results for studies directly comparing CPAP to bilevel NPPV. We report the pooled results for all primary and secondary analyses and sensitivity analyses conducted to explore potential sources of heterogeneity on the outcomes of hospital mortality and endotracheal intubation. The summary of our findings can be seen in  Summary of findings for the main comparison.

 

Hospital mortality

In 20 trials involving 1107 patients, we found a reduction in hospital mortality for patients treated with NPPV plus SMC compared with SMC care alone (RR 0.66, 95% CI 0.48 to 0.89). This translates into a RD of - 0.07 or 7% (95% CI -0.12 to -0.02) and NNT of 14 ( Analysis 1.1). Sensitivity analysis with the exclusion of quasi-randomised studies (Bersten 1991; Weitz 2007), did not change the results (RR 0.65, 95% CI 0.46 to 0.91;  Analysis 1.2). However if we consider Gray 2008 and Frontin 2010 that analysed the mortality in 7 and/or 30 days, our meta-analysis of hospital mortality indicates that these studies reinforce the favourable use of NPPV in ACPE (RR 0.72, 95% CI 0.55 to 0.94 and RR 0.75, 95% CI 0.60 to 0.95, respectively  Analysis 15.1 and  Analysis 16.1).This result could have been anticipated using cumulative meta-analysis techniques (Figure 6; MIX 2006).

 FigureFigure 6. Cumulative meta-analysis

Comparing CPAP plus SMC with SMC alone (13 trials, 699 patients) there was a lower hospital mortality rate in CPAP-treated patients (RR 0.60, 95% CI 0.39 to 0.94;  Analysis 1.6). The beneficial effect of CPAP translates into a RD of -11% (95% CI -0.18 to -0.04) and a NNT of 9. The effect of CPAP on hospital mortality remained significant after exclusion of a single QRCT (Bersten 1991) (RR 0.57, 95% CI 0.35 to 0.94;  Analysis 1.7).

However, we found no benefit of bilevel NPPV plus SMC compared with SMC care alone on hospital mortality (11 trials, 506 patients, RR 0.65, 95% CI 0.39 to 1.09;  Analysis 1.8), and after exclusion of quasi-randomised studies (Bersten 1991; Weitz 2007) ( Analysis 1.9). However, the similar effect size and wider confidence intervals for bilevel NPPV compared to the overall NPPV and CPAP-specific results is noted.

We found no differences in hospital mortality comparing CPAP plus SMC and bilevel NPPV plus SMC directly (12 trials, 694 patients, RR 1.10, 95% CI 0.61 to 1.97;  Analysis 1.12).

 

ETI rate

In 22 trials (1261 patients) we found a lower ETI rate for patients treated with NPPV plus SMC compared with SMC (RR 0.52, 95% CI 0.36 to 0.75;  Analysis 2.1). This translates into a RD of - 0.12 or 12% (95% CI -0.19 to -0.04) and a NNT of 8. Exclusion of two QRCTs (Bersten 1991; Weitz 2007) also revealed beneficial effect of NPPV compared to SMC (RR 0.53, 95% CI 0.37 to 0.78;  Analysis 2.2). This remained in Gray 2008 and Frontin 2010 that analysed the frequency intubation in seven days (RR 0.55, 95% CI 0.38 to 0.78;  Analysis 17.1).

When we compared CPAP plus SMC with SMC (14 trials, 825 patients) we found a significantly lower endotracheal intubation favouring CPAP-treated patients (RR 0.47, 95% CI 0.33 to 0.67, RD -15%, 95% CI -0.24 to -0.06, NNT 7;  Analysis 2.4). This result remained robust after exclusion of a single quasi-randomised trial (Bersten 1991) (RR 0.48, 95% CI 0.34 to 0.67;  Analysis 2.5).

We found no benefit of bilevel NPPV plus SMC compared with SMC alone on ETI rate (12 trials, 536 patients, RR 0.55, 95% CI 0.26 to 1.17;  Analysis 2.6). However with significant heterogeneity and after exclusion of the QRCT (Weitz 2007) and Sharon 2000 (whose patients received different doses of drugs) this altered the results: lower ETI favouring bilevel NPPV-treated patients (RR 0.45, 95% CI 0.26 to 0.80;  Analysis 2.7).

In 13 trials (721 patients) comparing CPAP plus SMC to bilevel NPPV plus SMC care, there did not appear to be any difference between the two techniques in reducing ETI (RR 1.04, 95% CI 0.55 to 1.97;  Analysis 2.10).

 

Incidence of acute myocardial infarction

In eight trials (461 patients) we found non-significant differences in the occurrence of acute myocardial infarction during treatment with NPPV plus SMC compared to SMC ( Analysis 3.1). A similar non-significant differences were found in comparisons of CPAP plus SMC compared to bilevel NPPV plus SMC ( Analysis 3.4), CPAP plus SMC care compared to SMC or bilevel NPPV plus SMC compared to SMC ( Analysis 3.2;  Analysis 3.3).

Only four studies (154 patients) comparing NPPV plus SMC to SMC alone reported no difference in the incidence of acute myocardial infarction after intervention ( Analysis 4.1); two studies reported no difference after CPAP plus SMC care compared to SMC (RR 1.08, 95% CI 0.11 to 10.23;  Analysis 4.2); three studies with bilevel NPPV plus SMC to SMC reported no difference in the incidence of acute myocardial infarction after intervention (RR 0.52, 95% CI 0.02 to 11.54;  Analysis 4.3); two studies compared CPAP plus SMC to bilevel NPPV plus SMC and demonstrated no difference (RR 1.57, 95% CI 0.57 to 4.32;  Analysis 4.4).

 

Intolerance to the allocated treatment

Thirteen studies (1848 patients) found a lower incidence of intolerance in the NPPV plus SMC (16%) compared to SMC (23%) (RR 0.47, 95% CI 0.29 to 0.77;  Analysis 5.1), The grouping of the studies demonstrated relevant heterogeneity, which was eliminated with the exclusion of Gray 2008 ( Analysis 5.2). We have not found plausible justification for this result. Nine studies (1304 patients) noted significantly lower intolerance with CPAP plus SMC compared to SMC (RR 0.55, 95% CI 0.36 to 0.85;  Analysis 5.3); seven studies (995 patients) found no difference related with intolerance to bilevel NPPV plus SMC care compared to SMC (RR 0.58, 95% CI 0.24 to 1.42;  Analysis 5.4). Three studies (894 patients) found no difference between CPAP plus SMC and bilevel NPPV plus SMC with respect to intolerance (RR 0.94, 95% CI 0.35 to 2.53;  Analysis 5.5).

 

Length of hospital and ICU stay

Ten trials (542 patients) demonstrated no significant difference in hospital length of stay between NPPV plus SMC compared to SMC (WMD -0.80 days, 95% CI -2.10 to 0.51;  Analysis 6.1). Though heterogeneity diminished after exclusion of one QRCT (Weitz 2007), it did not change the significance of our results ( Analysis 6.2). Five studies (337 patients) demonstrated no differences CPAP plus SMC compared to SMC (WMD -0.51 days, 95% CI -1.69 to 0.67;  Analysis 6.3). Seven studies (311 patients) showed no difference between bilevel plus SMC and SMC alone (WMD -1.38 days, 95% CI -3.38 to 0.62;  Analysis 6.4), and similar results were obtained between CPAP plus SMC and bilevel NPPV plus SMC (WMD -0.46 days, 95% CI -1.99 to 1.07;  Analysis 6.5).

Six studies (222 patients) comparing NPPV plus SMC to SMC alone demonstrated significantly shorter ICU stay favouring the NPPV group (WMD -0.89 days, 95% CI -1.33 to -0.45;  Analysis 7.1). Three studies (169 patients) indicated a significantly shorter ICU stay for patients treated with CPAP plus SMC (WMD -1.09 days, 95% CI -1.63 to -0.56;  Analysis 7.2). A further three studies (53 patients) showed no difference between bilevel NPPV plus SMC and SMC (WMD -0.65 days, 95% CI -1.37 to 0.06;  Analysis 7.3) while no difference was seen between CPAP plus SMC and bilevel NPPV plus SMC (WMD 0.31 days, 95% CI -0.78 to 1.40;  Analysis 7.4).

 

Vital signs one hour after intervention

 

Respiratory rate

Nine studies (438 patients) revealed significantly lower respiratory rates in patients on NPPV plus SMC in comparison with SMC (WMD -2.86 bpm, 95% CI -3.85 to -1.87;  Analysis 8.1). Seven studies (300 patients) had lower respiratory rate on CPAP plus SMC compared to SMC (WMD -2.39 bpm, 95% CI -3.70 to -1.07;  Analysis 8.2), while six studies (254 patients) showed lower respiratory rate in patients on bilevel NPPV plus SMC in comparison with those receiving SMC (WMD -3.52 bpm, 95% CI -4.80 to -2.23;  Analysis 8.3). Five studies (218 patients) did not show a significant difference between CPAP plus SMC and bilevel NPPV plus SMC (WMD 0.57 bpm, 95% CI -1.00 to 2.13;  Analysis 8.4).

 

Heart rate (HR)

Nine studies (438 patients) showed no significant difference between NPPV plus SMC and SMC in terms of heart rate (WMD -4.01 bpm, 95% CI -8.16 to 0.15;  Analysis 9.1). Seven studies (300 patients) found no difference between CPAP plus SMC and SMC (WMD -4.45 bpm, 95% CI -10.81 to 1.92;  Analysis 9.3). The grouping of the studies in these two analyses demonstrated heterogeneity, which was eliminated with the exclusion of Rasanen's and L'Her's studies and we have not found plausible justification for this result ( Analysis 9.2 and  Analysis 9.4). Six studies (254 patients) revealed lower heart rate in patients on bilevel NPPV plus SMC in comparison with SMC (WMD -4.21bpm, 95% CI -7.77 to -0.65;  Analysis 9.5) and no significant results were seen in four studies (182 patients) comparing CPAP plus SMC and bilevel NPPV plus SMC (WMD 0.56 bpm, 95 %CI -5.22 to 4.11;  Analysis 9.6).

 

Systolic blood pressure (SBP)

Six studies (182 patients) found no statistically significant difference between NPPV plus SMC and SMC groups in SBP (WMD -1.64 mmHg, 95% CI -7.83 to 4.56;  Analysis 10.1). Six studies (211 patients) found no statistically significant difference between CPAP plus SMC and SMC groups in SBP (WMD -0.12 mmHg, 95% CI -6.56 to 6.81;  Analysis 10.2). Similar non-significant differences were seen in comparison of bilevel NPPV plus and SMC (WMD 1.93 mmHg, 95% CI -7.94 to 11.80;  Analysis 10.3), and CPAP plus SMC versus bilevel NPPV plus SMC (WMD -1.17 mmHg, 95% CI -10.79 to 8.44;  Analysis 10.4). However, the last analysis showed significant heterogeneity, which was resolved after removing Bellone 2004, which showed higher baseline SBP value than other studies ( Analysis 10.5).

 

Diastolic blood pressure (DBP)

Five studies (138 patients) compared NPPV plus SMC and SMC care on DBP but found no difference (WMD -1.49 mmHg, 95% CI -6.43 to 3.45;  Analysis 11.1). Five studies (167 patients) compared CPAP plus SMC and SMC on DBP but found no difference (WMD -0.92 mmHg, 95% CI -9.10 to 7.27;  Analysis 11.2). However, heterogeneity was observed, which diminished after excluding studies Räsänen 1985 and Crane 2004 (there was a lower value for baseline DBP (mean and SD) in the latter studies in comparison with the others). After excluding those studies, the remaining three studies (107 patients) showed statistically significant lower DBP in patients on CPAP in comparison with those receiving SMC (WMD -7.32 mmHg, 95% CI -12.79 to -1.86;  Analysis 11.3). No difference was seen when bilevel NPPV plus SMC care was compared to SMC (four studies; 87 patients) (WMD -0.96 mmHg, 95% CI -6.09 to 4.16;  Analysis 11.4) or CPAP plus SMC vs bilevel NPPV plus SMC (WMD -2.60 mmHg, 95% CI -9.58 to 4.37;  Analysis 11.5). A change was observed when Crane 2004 and Martin-Bermudez 2002 were excluded, showing statistically significant better DBP in patients (n=62) on CPAP plus SMC in comparison with those receiving bilevel NPPV plus SMC, but we have not found plausible justification for this result (WMD -7.86 mmHg, 95% CI -13.03 to -2.70;  Analysis 11.6).

 

Mean blood pressure (MBP)

Three studies (256 patients) found no statistically significant difference between NPPV plus SMC compared to SMC (WMD -2.41 mmHg, 95% CI -8.27 to 3.45;  Analysis 12.1); similar non-significance was seen in comparison of CPAP plus SMC and SMC (one study, 89 patients) (WMD 3.00 mmHg, 95% CI -5.31 to 11.31;  Analysis 12.2), in bilevel NPPV plus SMC compared to SMC (two studies, 167 patients) (WMD -5.42 mmHg, 95%CI -11.60 to 0.76;  Analysis 12.3), and in comparison of CPAP plus SMC and Bilevel NPPV plus standard medical care (one study, 80 patients) (WMD -4.40 mmHg, 95% CI -13.25 to 4.45;  Analysis 12.4) .

 

Arterial blood gases and pH one hour after intervention

Four studies (140 patients) showed significantly higher PaO2 levels being found in NPPV plus SMC patients in comparison with those receiving SMC (WMD 10.04 mmHg, 95% CI 1.09 to 19.00;  Analysis 13.1 ). Five studies (177 patients) found no difference in arterial oxygen levels (PaO2) between CPAP plus SMC and SMC alone (WMD -2.64 mmHg, 95% CI -25.87 to 20.59;  Analysis 13.2). Pooling of these five studies showed significant heterogeneity. Exclusion of the Lin 1991 and Räsänen 1985 studies, which were conducted in ICU settings, showed significantly better PaO2 after one hour of intervention in SMC care patients in comparison with those receiving NPPV (WMD -22.09 mmHg, 95% CI -34.35 to -9.83;  Analysis 13.3). Three studies (79 patients) comparing bilevel NPPV plus SMC versus SMCe did not show any significant difference between the groups (WMD 4.79 mmHg, 95% CI -11.11 to 20.69;  Analysis 13.4). Three studies showed significantly higher PaO2 levels being found in bilevel NPPV plus SMC patients in comparison with those receiving CPAP plus SMCe (WMD -27.00 mmHg, 95% CI -44.75 to -9.25;  Analysis 13.5).

We did not pool PaCO2 and pH one hour after intervention as these outcomes require assessment with respect to baseline values (normal for each patient). Pooling of these parameters may not be meaningful.

 

Treatment failure

We defined treatment failure as a composite of mortality, endotracheal intubation and intolerance to the allocated treatment. No study in this review reported this outcome.

 

Adverse events

 Table 2 summarises the types and number of reported adverse events for both CPAP and bilevel NPPV, where they were reported, regardless of comparative intervention.

Fifteen studies reported adverse events with 232 events occurring in 1109 NPPV plus SMC treated patients and 154 events occurring in 751 SMC care treated patients. The adverse events reported were: skin damage, pneumothorax, pulmonary aspiration, gastric distension, vomiting, mask discomfort, hypotension, arrhythmia, progressive respiratory distress, gastrointestinal bleeding, asphyxia, conjunctivitis, sinusitis, eyes irritation, stroke, seizure, neurological failure (coma) and cardiorespiratory arrest. Participants receiving SMC had less skin damage and those treated with  NPPV had less progressive respiratory distress and neurological failure (coma). Confining the analysis to trials published after 2000 did not alter these results. A detailed description of these complications can be found in  Table 3,  Analysis 14.1 and  Analysis 14.2.

Ten studies reported adverse events with 88 events complications in the 544 CPAP plus SMC treated patients and 146 events in the 572 SMC treated patients. The adverse events reported were: skin damage, pneumonia, pulmonary aspiration, gastrointestinal bleeding, gastric distension, vomiting, asphyxia, pneumothorax, conjunctivitis, sinusitis, mask discomfort, hypotension, arrhythmia, progressive respiratory distress, cardiorespiratory arrest and neurological failure (coma). The CPAP group had fewer  progressive respiratory distress, cardiorespiratory arrest and neurological failure (coma). Details of adverse events in patients receiving CPAP and standard medical care are provided in  Table 4 and  Analysis 14.3.

Eight studies reported adverse events with 144 events occurring in 368 bilevel NPPV plus SMC care patients and 136 events occurring in 384 SMC. The adverse events reported were: skin damage, pneumonia, gastrointestinal bleeding, gastric distension, vomiting, pneumothorax, eyes irritation, sinusitis, mask discomfort, claustrophobia, cardiac arrest, stroke, seizure, gastric aspiration, hypotension, arrhythmia and progressive respiratory distress. Participants in the SMC group had a lower rate of skin damage  Details of the adverse events in people receiving bilevel NPPV plus SMC are provided in  Table 5 and  Analysis 14.4.

Five studies reported adverse events with 156 events occurring in 389 bilevel NPPV plus SMC treated patients and 126 events occurring in 376 CPAP plus SMC treated patients. The adverse events reported were: skin damage, pneumothorax, pulmonary aspiration, gastric distension, vomiting, mask discomfort, increased breathing discomfort, hypotension, arrhythmia, progressive respiratory distress, cardiorespiratory arrest, pharyngeal damage and cough. Patients treated with CPAP had fewer arrhythmias. A detailed description of the complications can be found in  Table 6 and  Analysis 14.5.

 

Discussion

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

The inclusion of eleven new studies in this review did not change significantly the results for the effectiveness of the use of NPPV compared with SMC, but it was possible to identify modest differences between CPAP and bilevel NPPV.

 

Summary of main results

Our meta-analysis demonstrates the effectiveness of NPPV and CPAP compared to SMC in reducing hospital mortality. Our results support that one death can be avoided for every 14 ACPE patients treated with NPPV. Similarly, one death can be prevented for every nine ACPE patients treated with CPAP. This means that 69 lives out of 1000 could be saved with the addition of NPPV to SMC. The reduction in mortality was supported by studies comparing CPAP to SMC but not by studies comparing bilevel NPPV to SMC or CPAP to bilevel NPPV. The effect size of bilevel NPPV was notably similar to CPAP compared to SMC, but these results were more imprecise. Potential reasons for these discordant findings may include the relatively small number of patients experiencing events in these studies leading to low power; incorporating more recent studies that may have led to reduced mortality from SMC; or a true difference between CPAP and bilevel NPPV, which is corroborated by the findings from studies that directly compare CPAP and bilevel NPPV in patients with ACPE. However, the mega trial published by Gray 2008 analysed mortality 7 and 30 days after the NPPV initiation in patients with ACPE and did not identify any important differences between the NPPV groups compared to the SMC. Nonetheless, when we include these data in a meta-analysis of our primary outcome (in-hospital mortality), we find a persistent benefit of NPPV in reducing mortality in patients with ACPE. We do identify limitations in Gray 2008 that may contribute with findings divergences. First, Gray 2008 reported that it used ITT analyses but its analysis did not include all randomised patients (follow-up bias). Second, the study did not report the total distribution of randomisation by group, which impeded the meta-analysis of various outcomes and could be considered as a potential source of heterogeneity (Higgins 2011). Third, the reporting of continuous variables included only mean value of the difference between zero and one hour after the intervention and not as mean and standard deviation. However, it has not been possible to obtain these data for our meta-analysis.

We also found that NPPV significantly reduced endotracheal intubation compared to SMC. Only eight patients need to be treated with NPPV to avoid 1 intubation. We noted similar results in studies comparing CPAP to SMC where the NNT was 7. Although NPPV has demonstrated to effectively reduce the intubation rate, it was not possible to assess if NPPV could postpone this outcome, as suggested in the study of Wood 1998. This randomised study reported significant delay in intubation and mechanical ventilation of acute respiratory distress syndrome (ARDS) patients treated with bilevel NPPV compared with SMC. The difference however was not found to be statistically significant (P=0.06), perhaps due to a low event rate (seven in the bilevel NPPV group and five in the SMC group). Likewise, the outcomes of mortality and intubation rate did not show statistically significant difference between the groups. In contrast to Confaloniere`s study of patients with pneumonia, although bilevel NPPV reduced the intubation rate, no difference in the time to intubate and initiate mechanical ventilation was observed (Confalonieri 1999).

An additional important finding of our review was that the incidence of acute myocardial infarction was not increased either during or after NPPV use. This is an important finding, as some studies (Mehta 1997; Rusterholtz 1999; Sharon 2000) had noted an increased incidence of acute myocardial infarction in patients treated with bilevel NPPV. To this end, few studies clearly distinguished between acute myocardial infarction at randomisation or evolving during or after NPPV initiation. Consistent with our results, Bellone and colleagues applied stringent criteria to detect acute myocardial infarction (Bellone 2004) and noted non-significant differences in acute myocardial infarction among CPAP and bilevel NPPV treated patients. Recent RCTs (Ferrari 2007; Moritz 2007; Gray 2008) have also shown no significant differences on the incidence of acute myocardial infarction and other relevant outcomes when compared CPAP to bilevel NPPV.

NPPV also appears to reduce the risk of progression of respiratory failure and neurological failure (coma) compared to SMC. These results were mainly influenced by studies conducted with CPAP, which additionally demonstrated a reduction in cardiovascular arrest and adverse events risk in general when compared to SMC. NPPV is associated with increased risk for skin damage, but this adverse event is not generally considered major. This adverse event outcome was primarily influenced by Nava's studies, which may be related to the particular time and use of NPPV mask in that study. CPAP demonstrated a lower risk of developing arrhythmias when compared to using bilevel NPPV. It is possible that this reduced risk of adverse events with the use of CPAP could be related to lower positive pressure levels than those used in the bilevel NPPV, which may influence haemodynamics and/or O2 consumption. Despite similar effect sizes between CPAP and bilevel NPPV in terms of our primary outcome, these safety data are notable.

Our review did not reveal a significant difference between NPPV and SMC in terms of hospital length of stay. However, our review supports about one-day reduction in ICU length of study with NPPV compared to SMC, and CPAP, in particular, compared to SMC. These differences were not supported in comparisons of bilevel NPPV to SMC and CPAP to bilevel NPPV. Some studies such as Holt 1994 have shown a reduction in hospital length of stay in ACPE patients using CPAP. We postulate that the reductions in ICU length of stay may be related to the reduction in intubation, as Wysocki 1995 related the smaller intubation rate to shorter hospital stay in a post-hoc analysis. Although our review found NPPV and CPAP to be better tolerated than SMC, future studies should assess whether a trade-off exists between treatment intolerance and other important outcomes such as mortality. In Crane 2004, while a large number of CPAP treated patients were intolerant of treatment, patients in this group also had lower mortality compared to bilevel NPPV and SMC.

NPPV was introduced to emergency departments in the early 1990s and became a relatively common place by approximately 2001 (Bersten 1991). In our review we noted similar reductions in mortality in patients treated with NPPV in the emergency department (RR 0.55, 95% CI 0.36 to 0.86;  Analysis 5.2) and in the ICU (RR 0.48, 95% CI 0.28 to 0.83;  Analysis 5.3). This finding supports initiation of NPPV in patients with ACPE in the emergency department. Additionally in our analysis, a cross-over RCTof 124 patients with out-of-hospital diagnosis of ACPE and use of CPAP demonstrated faster improvements in dyspnoea, faster improvements in PaO2, lower intubation rates, lower use of dobutamine, and lower hospital mortality (Plaisance 2007). These results reinforce the positive pressure concept considered as non-pharmacologic treatment and not a simple measure of support in ACPE cases.

We did find consistent effects of NPPV compared SMC and bilevel NPPV compared CPAP on PaO2 in patients with ACPE in first hour. However, it would be interesting if future studies analyse the existence of a direct relation among an early PaO2 improvements with outcomes such as mortality and need for intubation.

Some studies have postulated that patients with ACPE and hypercapnia (increased amount of carbon dioxide in the blood > 45 mmHg) may benefit to a greater extent from bilevel NPPV treatment (Hoffmann 1999; Rusterholtz 1999; Wysocki 1995; Wysocki 1999). In a post-hoc analysis, we pooled studies including ACPE patients with hypercapnia at admission (mean values of PaCO2) and compared NPPV to SMC on the outcomes of mortality and endotracheal intubation. Compared to all population with ACPE patients, we found significant reductions in mortality (RR 0.60, 95% CI 0.40 to 0.88;  Analysis 1.5 and ETI rate (RR 0.44, 95% CI 0.25 to 0.77;  Analysis 2.3) favouring hypercapnic patients although the between-group differences were not statistically significant. Similarly, we found favourable reductions in mortality and intubation in among patients treated with bilevel NPPV versus standard medical care (RR 0.59, 95% CI 0.34 to 1.02 and RR 0.47, 95% CI 0.22 to 0.97, respectively;  Analysis 1.10 and  Analysis 2.8) and no difference in mortality (RR 0.98, 95% CI 0.45 to 2.14;  Analysis 1.13 ) or intubation (RR 1.17, 95% CI 0.58 to 2.33;  Analysis 2.11) in hypercapnic patients compared with all population with ACPE patients treated with bilevel NPPV versus CPAP; although the between group differences are not statistically significant. These analysis are reinforced by the meta-analysis studies by Agmy 2008, Moritz 2007; Nava 2003 and Masip 2000 who realised the mortality analysis and/or endotracheal intubation rate in the subgroup of hypercapnics patients and the results were more favourable to the use of bilevel compared to SMC in mortality and intubation (RR 0.20, 95% CI 0.04 to 0.86 and RR 0.28, 95% CI 0.12 to 0.69, respectively;  Analysis 1.11 and  Analysis 2.9), but no significant differences between CPAP and bilevel (RR 1.06, 95% CI 0.33 to 3.37 and RR 0.92, 95% CI 0.26 to 3.21, respectively;  Analysis 1.14 and  Analysis 2.12). Though these comparisons didn't report significant difference to the meta-analysis results conducted in patients with ACPE in general. Our analyses have demonstrated that patients with ACPE and hypercapnia seem to benefit even more from the usage of NPPV, particularly from bilevel NPPV.

Once the benefits of NPPV have been demonstrated, cost-benefit analyses, like the one conducted by Newberry et al. showing that NPPV cost less than mechanical ventilation (Newberry 1995), are important. In another study, the cost of respiratory services were lower with NPPV compared with SMC, but total cost with NPPV was higher than in the SMC group (Kramer 1995).

 

Overall completeness and applicability of evidence

In this review, we pooled the results of 32 RCTs (27 comparing NPPV and SMC and 14 comparing CPAP and bilevel NPPV) in patients with ACPE on important clinical outcomes, or eleven studies additional than the first version of this systematic review. This update maintains the results of the previous version where both NPPV and CPAP reduce hospital mortality, endotracheal intubation, ICU length of stay and respiratory rate compared to SMC. We did not observe the same beneficial effects on important clinical outcomes among studies comparing bilevel NPPV to SMC and CPAP to bilevel NPPV, though these results were similar in their effect size yet more imprecise. We also found that NPPV, CPAP and bilevel NPPV were better tolerated than SMC alone. Importantly, compared to SMC, use of NPPV, bilevel NPPV and CPAP in patients with ACPE did not increase the incidence of acute myocardial infarction during or after intervention. However this update identified a lower incidence of important adverse events in patients receiving NPPV plus SMC, as lower risk of progression of respiratory failure and coma. If we consider only CPAP, also a lower risk of cardiorespiratory arrest is also demonstrated. Among the studies that made the direct comparison between CPAP and bilevel NPPV a significantly lower incidence of arrhythmias with CPAP was observed. The only adverse event significantly unfavourable to the use of NPPV identified was skin damage. Our results demonstrate the effectiveness and safety of NPPV, especially CPAP, as adjuvant therapy to SMC in patients with ACPE.

 

Quality of the evidence

We considered the quality of the evidence to be moderate, although there may be some potential for publication bias. We defined seven relevant outcomes in order to assess the quality of evidence by GRADE (Guyatt 2008; Higgins 2011), and the primary outcome of mortality was considered to supported by quality evidence, where incidence of acute myocardial infarction during intervention and intolerance to the allocated treatment were considered to supported by only moderate quality of evidence. The remaining (endotracheal intubation rate and ICU length of stay, incidence of acute myocardial infarction after intervention and hospital length of stay) were unsupported by adequate evidence.

 

Potential biases in the review process

The major weakness of our review is the comparatively small number of events within trials comparing bilevel NPPV to SMC and CPAP to bilevel NPPV, thus limiting the inferences that can be made from them. It is important to note that SMC varied widely among the studies and included different drugs at different dosages. This disparity may have influenced treatment effect across studies. For example, Sharon 2000 used high doses of isosorbide dinitrate, which was related to better results in important outcomes such as acute myocardial infarction incidence and need for intubations when compared with low doses of isosorbide. Another potential source of bias is the variable inclusion criteria across studies. Disparities in baseline characteristics may have influenced patient response to treatment. A final source of bias may be the different thresholds or criteria used for reintubation in the included studies.

Strengths of this review include methods to reduce bias (multimodal search strategy without language restrictions, duplicate independent screening and data abstraction and prespecified criteria for appraising methodologic quality) with the quantitative differential of the Cochrane reviews (Jadad 2000; McKibbon 2004). To this end, we obtained additional information from 17 authors (Agmy 2008; Bautin 2005; Bersten 1991; Bellone 2005; Crane 2004; Delclaux 2000; Ferrari 2007; Gray 2008; Kelly 2002; Martin-Bermudez 2002; Masip 2000; Nava 2003; Park 2004; Räsänen 1985; Takeda 1998; Thys 2002; Weitz 2007). As a result, our meta-analysis includes the largest number of trials exploring the role of NPPV in ACPE and consequently had increased power in pooling outcomes (Potts 2009). We analysed the impact of NPPV on a broad set of physiological and clinical outcomes. Although there was heterogeneity in some analyses, it was possible to observe that the exclusion of low quality studies did not influence the results (Bersten 1991; Weitz 2007). The generalisability of our findings is enhanced by the diverse nature of the trials included in our review, representing international experience with NPPV use for ACPE.

 

Agreements and disagreements with other studies or reviews

The first systematic review on the role of NPPV for ACPE reported a lower intubation rate with CPAP Pang 1998. Hess 2004 subsequently suggested that bilevel NPPV may benefit patients with ACPE with hypercapnia. Nadar 2005 then found that bilevel NPPV decreased intubation, improved oxygenation, and was better tolerated compared to CPAP in patients with ACPE. However, because of the concern regarding the potential for acute myocardial infarction, bilevel NPPV could not be recommended for treatment of ACPE. Our review supports the use of NPPV, and especially CPAP, in the treatment of ACPE. These findings are important as current ACPE management guidelines do not recommend NPPV use in the absence of A level of evidence (Nieminen 2005). The results of our review could make this recommendation possible.

However, newer meta-analyses have found results similar to ours (Collins 2006; Ho 2006; Masip 2005; Peter 2006;Weng 201O; Winck 2006), although with small differences in methodological and included studies, all conclude that NPPV is effective in reducing mortality in patients with ACPE. However, a mega-trial conducted in patients with ACPE was published and concluded that NPPV does not reduce mortality compared to SMC (Gray 2008); however, it is possible to observe several important differences in this study that differ from the others included in systematic reviews and meta-analysis as: mortality was evaluated after 7 or 30 days from the beginning of the intervention, while other studies have analysed mortality during the period of hospitalisation. Gray 2008 excluded patients who were more seriously ill. Approximately one in five patients in the SMC arm crossed over to NPPV within two hours of randomisation in Gray 2008, suggesting contamination that would attenuate the apparent effect of NPPV on mortality. Gray 2008 also had a 40% lower event rate than found in our meta-analysis, which may be due to differences in patient characteristics, SMC, or other unmeasured differences that could influence the size of the treatment effect of NPPV. The quality of the studies that had evaluated the primary outcome mortality was high, as of can be visualised in  Summary of findings for the main comparison, which strengthens our inference of the benefit of NPPV in reducing mortality in patients with ACPE.

 

Authors' conclusions

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

 

Implications for practice

Data from RCTs have demonstrated that NPPV (CPAP and bilevel NPPV) is effective in reducing hospital mortality, intubation rate and ICU length of stay. In addition, NPPV resulted in faster improvement and was better tolerated than SMC. Further, our meta-analysis did not demonstrate an increase in the incidence of acute myocardial infarction during and after NPPV application. We show a lower risk of progressive respiratory distress and neurological failure (coma) when compare NPPV to SMC and cardiorespiratory arrest when compare only CPAP to SMC as well as a lower risk of arrhythmia when comparing CPAP to bilevel NPPV. CPAP can be considered the first option in selection of NPPV due to more robust evidence for its effectiveness and safety and lower costs compared with bilevel NPPV.

 
Implications for research

Further studies are required to reduce uncertainty regarding length of hospital stay, long-term mortality, costs and the time required to manage NPPV. Additional research is required to elucidate if hypercapnic patients with ACPE may benefit to a greater extent than non-hypercapnic patients and if bilevel NPPV confers similar benefit or risks compared to CPAP.

 

Acknowledgements

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

We are grateful to the authors of the studies we reviewed and who kindly answered our e-mails or correspondence regarding additional data (Räsänen, Bersten, Kelly, Nava, Park, Takeda, Thys, Masip, Bellone, Crane, Delclaux, Ferrari, Bautin, Agmy, Gray and Weitz). We are also thankful for the critical evaluation of the professors Dr. Velasco IT, Dr. Scalabrini Neto A, Dr. Gonçalves AJ, Dr. Godoy MF and by the collaboration of the following co-authors in the first version of the publication of this systematic review: Burns K, Saconato H, Sen A, Hawkes CA and Soares B. We thank Joey Kwong by Chinese translation paper. Finally the Cochrane heart group for suggested improvements.

 

Data and analyses

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms
Download statistical data

 
Comparison 1. Hospital mortality

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) x SMC201107Risk Ratio (M-H, Random, 95% CI)0.66 [0.48, 0.89]

 2 NPPV (CPAP and BILEVEL) X SMC - sensitivity analysis181023Risk Ratio (M-H, Random, 95% CI)0.65 [0.46, 0.91]

 3 NPPV (CPAP and BILEVEL) X SMC- ED place9717Risk Ratio (M-H, Random, 95% CI)0.55 [0.36, 0.86]

 4 NPPV (CPAP and BILEVEL) X SMC - ICU place7365Risk Ratio (M-H, Random, 95% CI)0.48 [0.28, 0.83]

 5 NPPV (CPAP and BILEVEL) X SMC - in patients hypercanics - baseline9603Risk Ratio (M-H, Random, 95% CI)0.60 [0.40, 0.88]

 6 CPAP x SMC13699Risk Ratio (M-H, Random, 95% CI)0.60 [0.39, 0.94]

 7 CPAP X SMC - sensitivity analysis12659Risk Difference (M-H, Random, 95% CI)-0.12 [-0.19, -0.04]

 8 BILEVEL X SMC11506Risk Ratio (M-H, Random, 95% CI)0.65 [0.39, 1.09]

 9 BILEVEL X SMC - sensitivity analysis9458Risk Ratio (M-H, Random, 95% CI)0.63 [0.37, 1.09]

 10 BILEVEL X SMC - in patients hypercanics - baseline7401Risk Ratio (M-H, Random, 95% CI)0.59 [0.34, 1.02]

 11 BILEVEL X SMC - in patients hypercanics2104Risk Ratio (M-H, Random, 95% CI)0.20 [0.04, 0.86]

 12 CPAP X BILEVEL12694Risk Ratio (M-H, Random, 95% CI)1.10 [0.61, 1.97]

 13 CPAP X BILEVEL - in patients hypercanics - baseline9518Risk Ratio (M-H, Random, 95% CI)0.98 [0.45, 2.14]

 14 CPAP X BILEVEL - in patients hypercanics298Risk Ratio (M-H, Random, 95% CI)1.06 [0.33, 3.37]

 
Comparison 2. EETI rate

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC221261Risk Ratio (M-H, Random, 95% CI)0.52 [0.36, 0.75]

 2 NPPV (CPAP and BILEVEL) X SMC - sensitivity analysis201195Risk Ratio (M-H, Random, 95% CI)0.53 [0.37, 0.78]

 3 NPPV (CPAP and BILEVEL) X SMC - in patients hypercapnics - baseline9621Risk Ratio (M-H, Random, 95% CI)0.44 [0.25, 0.77]

 4 CPAP X SMC14825Risk Ratio (M-H, Random, 95% CI)0.47 [0.33, 0.67]

 5 CPAP X SMC - sensitivity analysis13785Risk Ratio (M-H, Random, 95% CI)0.48 [0.34, 0.67]

 6 BILEVEL X SMC12536Risk Ratio (M-H, Random, 95% CI)0.55 [0.26, 1.17]

 7 BILEVEL X SMC - sensitivity analysis10470Risk Ratio (M-H, Random, 95% CI)0.45 [0.26, 0.80]

 8 BILEVEL X SMC - in patients hypercapnics - baseline7401Risk Ratio (M-H, Random, 95% CI)0.47 [0.22, 0.97]

 9 BILEVEL X SMC - in patients hypercapnics3120Risk Ratio (M-H, Random, 95% CI)0.28 [0.12, 0.69]

 10 CPAP X BILEVEL13721Risk Ratio (M-H, Random, 95% CI)1.04 [0.55, 1.97]

 11 CPAP X BILEVEL - in patients hypercapnics - baseline9518Risk Ratio (M-H, Random, 95% CI)1.17 [0.58, 2.33]

 12 CPAP X BILEVEL - in patients hypercapnics298Risk Ratio (M-H, Random, 95% CI)0.92 [0.26, 3.21]

 
Comparison 3. Incidence of acute myocardial infarction (during intervention)

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC8461Risk Ratio (M-H, Random, 95% CI)1.24 [0.79, 1.95]

 2 CPAP X SMC3152Risk Ratio (M-H, Random, 95% CI)0.91 [0.37, 2.24]

 3 BILEVEL X SMC7356Risk Ratio (M-H, Random, 95% CI)1.40 [0.78, 2.49]

 4 CPAP X BILEVEL7409Risk Ratio (M-H, Random, 95% CI)0.66 [0.39, 1.10]

 5 BILEVEL X SMC - heterogeneity analysis6316Risk Ratio (M-H, Random, 95% CI)1.14 [0.69, 1.88]

 
Comparison 4. Incidence of acute myocardial infarction (after intervention)

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC4154Risk Ratio (M-H, Random, 95% CI)0.70 [0.11, 4.26]

 2 CPAP X SMC299Risk Ratio (M-H, Random, 95% CI)1.08 [0.11, 10.23]

 3 BILEVEL X SMC365Risk Ratio (M-H, Random, 95% CI)0.52 [0.02, 11.54]

 4 CPAP X BILEVEL268Risk Ratio (M-H, Random, 95% CI)1.57 [0.57, 4.32]

 
Comparison 5. Intolerance to allocated treatment

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC131848Risk Ratio (M-H, Random, 95% CI)0.47 [0.29, 0.77]

 2 NPPV (CPAP and BILEVEL) X SMC - heterogeneity analysis12692Risk Ratio (M-H, Random, 95% CI)0.42 [0.30, 0.58]

 3 CPAP X SMC91304Risk Ratio (M-H, Random, 95% CI)0.55 [0.36, 0.85]

 4 BILEVEL X SMC7995Risk Ratio (M-H, Random, 95% CI)0.58 [0.24, 1.42]

 5 CPAP X BILEVEL3894Risk Ratio (M-H, Random, 95% CI)0.94 [0.35, 2.53]

 
Comparison 6. Hospital length of stay

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC10542Mean Difference (IV, Random, 95% CI)-0.80 [-2.10, 0.51]

 2 NPPV (CPAP and BILEVEL) X SMC - heterogeneity analysis9519Mean Difference (IV, Random, 95% CI)-0.38 [-1.35, 0.58]

 3 CPAP X SMC5337Mean Difference (IV, Random, 95% CI)-0.51 [-1.69, 0.67]

 4 BILEVEL X SMC7311Mean Difference (IV, Random, 95% CI)-1.38 [-3.38, 0.62]

 5 CPAP X BILEVEL6402Mean Difference (IV, Random, 95% CI)-0.46 [-1.99, 1.07]

 
Comparison 7. ICU length of stay

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC6222Mean Difference (IV, Random, 95% CI)-0.89 [-1.33, -0.45]

 2 CPAP X SMC3169Mean Difference (IV, Random, 95% CI)-1.09 [-1.63, -0.56]

 3 BILEVEL X SMC353Std. Mean Difference (IV, Random, 95% CI)-0.65 [-1.37, 0.06]

 4 CPAP X BILEVEL3159Mean Difference (IV, Random, 95% CI)0.31 [-0.78, 1.40]

 
Comparison 8. Breath rate after one hour

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC9438Mean Difference (IV, Random, 95% CI)-2.86 [-3.85, -1.87]

 2 CPAP X SMC7300Mean Difference (IV, Random, 95% CI)-2.39 [-3.70, -1.07]

 3 BILEVEL X SMC6254Mean Difference (IV, Random, 95% CI)-3.52 [-4.80, -2.23]

 4 CPAP X BILEVEL5218Mean Difference (IV, Random, 95% CI)0.57 [1.00, 2.13]

 
Comparison 9. Heart rate after one hour

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC9438Mean Difference (IV, Random, 95% CI)-4.01 [-8.16, 0.15]

 2 NPPV (CPAP and BILEVEL) X SMC - heterogeneity analysis7329Mean Difference (IV, Random, 95% CI)-3.79 [-6.88, -0.70]

 3 CPAP X SMC7300Mean Difference (IV, Random, 95% CI)-4.45 [-10.81, 1.92]

 4 CPAP X SMC - heterogeneity analysis5191Mean Difference (IV, Random, 95% CI)-4.10 [-8.93, 0.72]

 5 BILEVEL X SMC6254Mean Difference (IV, Random, 95% CI)-4.21 [-7.77, -0.65]

 6 CPAP X BILEVEL4182Mean Difference (IV, Random, 95% CI)-0.56 [-5.22, 4.11]

 
Comparison 10. Sistolic blood pressure after one hour

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC6182Mean Difference (IV, Random, 95% CI)-1.64 [-7.83, 4.56]

 2 CPAP X SMC6211Mean Difference (IV, Random, 95% CI)0.12 [-6.56, 6.81]

 3 BILEVEL X SMC487Mean Difference (IV, Random, 95% CI)1.93 [-7.94, 11.80]

 4 CPAP X BILEVEL4182Mean Difference (IV, Random, 95% CI)-1.17 [-10.79, 8.44]

 5 CPAP X BILEVEL - heterogeneity analysis3136Mean Difference (IV, Random, 95% CI)2.57 [-4.30, 9.44]

 
Comparison 11. Diastolic blood pressure after one hour

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC5138Mean Difference (IV, Random, 95% CI)-1.49 [-6.43, 3.45]

 2 CPAP X SMC5167Mean Difference (IV, Random, 95% CI)-0.92 [-9.10, 7.27]

 3 CPAP X SMC - heterogeneity analysis3107Mean Difference (IV, Random, 95% CI)-7.32 [-12.79, -1.86]

 4 BILEVEL X SMC487Mean Difference (IV, Random, 95% CI)-0.96 [-6.09, 4.16]

 5 CPAP X BILEVEL4182Mean Difference (IV, Random, 95% CI)-2.60 [-9.58, 4.37]

 6 CPAP X BILEVEL - heterogeneity analysis262Mean Difference (IV, Random, 95% CI)-7.86 [-13.03, -2.70]

 
Comparison 12. Mean blood pressure after one hour

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC3256Mean Difference (IV, Random, 95% CI)-2.41 [-8.27, 3.45]

 2 CPAP X SMC189Mean Difference (IV, Random, 95% CI)3.00 [-5.31, 11.31]

 3 BILEVEL X SMC2167Mean Difference (IV, Random, 95% CI)-5.42 [-11.60, 0.76]

 4 CPAP X BILEVEL180Mean Difference (IV, Random, 95% CI)-4.40 [-13.25, 4.45]

 
Comparison 13. PaO2 (mmHg) after one hour

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC4140Mean Difference (IV, Random, 95% CI)10.04 [1.09, 19.00]

 2 CPAP X SMC5177Mean Difference (IV, Random, 95% CI)-2.64 [-25.87, 20.59]

 3 CPAP X SMC - heterogeneity analysis3117Mean Difference (IV, Random, 95% CI)-22.09 [-34.35, -9.83]

 4 BILEVEL X SMC379Mean Difference (IV, Random, 95% CI)4.79 [-11.11, 20.69]

 5 CPAP X BILEVEL3136Mean Difference (IV, Random, 95% CI)-27.00 [-44.75, -9.25]

 
Comparison 14. Adverse events

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC1511329Risk Ratio (M-H, Random, 95% CI)0.85 [0.63, 1.16]

    1.1 Skin damage
11594Risk Ratio (M-H, Random, 95% CI)6.62 [1.20, 36.55]

    1.2 Pneumonia
3232Risk Ratio (M-H, Random, 95% CI)0.35 [0.05, 2.20]

    1.3 Pulmonary aspiration
51255Risk Ratio (M-H, Random, 95% CI)1.58 [0.06, 38.61]

    1.4 Gastrointestinal Bleeding
3192Risk Ratio (M-H, Random, 95% CI)1.37 [0.27, 6.89]

    1.5 Gastric distention
8484Risk Ratio (M-H, Random, 95% CI)13.26 [0.82, 215.12]

    1.6 Vomiting
51229Risk Ratio (M-H, Random, 95% CI)1.06 [0.46, 2.47]

    1.7 Asphyxia
2170Risk Ratio (M-H, Random, 95% CI)3.0 [0.12, 72.31]

    1.8 Pneumothorax
61474Risk Ratio (M-H, Random, 95% CI)0.72 [0.08, 6.89]

    1.9 Conjunctivitis
2147Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    1.10 Sinusitis
2219Risk Ratio (M-H, Random, 95% CI)3.0 [0.12, 72.31]

    1.11 Disconfort with mask
7512Risk Ratio (M-H, Random, 95% CI)5.39 [0.97, 30.09]

    1.12 Hypotension
11030Risk Ratio (M-H, Random, 95% CI)0.82 [0.58, 1.16]

    1.13 Arrhythmia
11027Risk Ratio (M-H, Random, 95% CI)0.83 [0.50, 1.38]

    1.14 Progressive respiratory distress
21122Risk Ratio (M-H, Random, 95% CI)0.58 [0.37, 0.89]

    1.15 Cardiorespiratory arrest
31252Risk Ratio (M-H, Random, 95% CI)0.60 [0.29, 1.26]

    1.16 Neurological failure (coma)
190Risk Ratio (M-H, Random, 95% CI)0.10 [0.01, 0.71]

    1.17 Eye irritation
140Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    1.18 Stroke
1130Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    1.19 Seizures
1130Risk Ratio (M-H, Random, 95% CI)0.33 [0.01, 8.03]

 2 NPPV (CPAP and BILEVEL) X SMC - AFTER 20001110703Risk Ratio (M-H, Random, 95% CI)0.87 [0.63, 1.19]

    2.1 Skin damage
8492Risk Ratio (M-H, Random, 95% CI)6.62 [1.20, 36.55]

    2.2 Pneumonia
2152Risk Ratio (M-H, Random, 95% CI)0.35 [0.05, 2.20]

    2.3 Pulmonary aspiration
21095Risk Ratio (M-H, Random, 95% CI)1.58 [0.06, 38.61]

    2.4 Gastrointestinal Bleeding
2170Risk Ratio (M-H, Random, 95% CI)2.32 [0.35, 15.42]

    2.5 Gastric distention
4302Risk Ratio (M-H, Random, 95% CI)13.26 [0.82, 215.12]

    2.6 Vomiting
51229Risk Ratio (M-H, Random, 95% CI)1.06 [0.46, 2.47]

    2.7 Asphyxia
1130Risk Ratio (M-H, Random, 95% CI)3.0 [0.12, 72.31]

    2.8 Pneumothorax
51434Risk Ratio (M-H, Random, 95% CI)0.72 [0.08, 6.89]

    2.9 Conjunctivitis
2147Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    2.10 Sinusitis
2219Risk Ratio (M-H, Random, 95% CI)3.0 [0.12, 72.31]

    2.11 Disconfort with mask
7512Risk Ratio (M-H, Random, 95% CI)5.39 [0.97, 30.09]

    2.12 Hypotension
11030Risk Ratio (M-H, Random, 95% CI)0.82 [0.58, 1.16]

    2.13 Arrhythmia
11027Risk Ratio (M-H, Random, 95% CI)0.83 [0.50, 1.38]

    2.14 Progressive respiratory distress
21122Risk Ratio (M-H, Random, 95% CI)0.58 [0.37, 0.89]

    2.15 Cardiorespiratory arrest
31252Risk Ratio (M-H, Random, 95% CI)0.60 [0.29, 1.26]

    2.16 Neurological failure (coma)
190Risk Ratio (M-H, Random, 95% CI)0.10 [0.01, 0.71]

    2.17 Eye irritation
140Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    2.18 Stroke
1130Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    2.19 Seizures
1130Risk Ratio (M-H, Random, 95% CI)0.33 [0.01, 8.03]

 3 CPAP X SMC107133Risk Ratio (M-H, Random, 95% CI)0.63 [0.45, 0.87]

    3.1 Skin damage
7343Risk Ratio (M-H, Random, 95% CI)3.0 [0.13, 69.52]

    3.2 Pneumonia
180Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    3.3 Pulmonary aspiration
5908Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    3.4 Gastrointestinal Bleeding
122Risk Ratio (M-H, Random, 95% CI)0.33 [0.02, 7.39]

    3.5 Gastric distention
7447Risk Ratio (M-H, Random, 95% CI)11.00 [0.64, 189.65]

    3.6 Vomiting
3785Risk Ratio (M-H, Random, 95% CI)0.93 [0.34, 2.54]

    3.7 Asphyxia
140Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    3.8 Pneumothorax
5998Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    3.9 Conjunctivitis
2147Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    3.10 Sinusitis
189Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    3.11 Disconfort with mask
3265Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    3.12 Hypotension
1684Risk Ratio (M-H, Random, 95% CI)0.83 [0.55, 1.25]

    3.13 Arrhythmia
1682Risk Ratio (M-H, Random, 95% CI)0.55 [0.28, 1.09]

    3.14 Progressive respiratory distress
2776Risk Ratio (M-H, Random, 95% CI)0.53 [0.31, 0.92]

    3.15 Cardiorespiratory arrest
2777Risk Ratio (M-H, Random, 95% CI)0.41 [0.18, 0.91]

    3.16 Neurological failure (coma)
190Risk Ratio (M-H, Random, 95% CI)0.10 [0.01, 0.71]

 4 BILEVEL X SMC86823Risk Ratio (M-H, Random, 95% CI)1.05 [0.76, 1.46]

    4.1 Skin damage
6296Risk Ratio (M-H, Random, 95% CI)7.16 [1.27, 40.50]

    4.2 Nosocomial pneumonia
2152Risk Ratio (M-H, Random, 95% CI)0.35 [0.05, 2.20]

    4.3 Disconfort with mask
5274Risk Ratio (M-H, Random, 95% CI)5.39 [0.97, 30.09]

    4.4 Gastrointestinal bleeding
2170Risk Ratio (M-H, Random, 95% CI)2.32 [0.35, 15.42]

    4.5 Gastric dilatation
264Risk Ratio (M-H, Random, 95% CI)15.87 [0.96, 262.30]

    4.6 Vomiting
5848Risk Ratio (M-H, Random, 95% CI)1.21 [0.47, 3.11]

    4.7 Claustrophobia
1130Risk Ratio (M-H, Random, 95% CI)3.0 [0.12, 72.31]

    4.8 Pneumothorax
2832Risk Ratio (M-H, Random, 95% CI)1.01 [0.11, 9.63]

    4.9 Eye irritation
140Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    4.10 Sinusitis
1130Risk Ratio (M-H, Random, 95% CI)3.0 [0.12, 72.31]

    4.11 Cardiac arrest
2830Risk Ratio (M-H, Random, 95% CI)0.96 [0.25, 3.61]

    4.12 Stroke
1130Risk Ratio (M-H, Random, 95% CI)0.0 [0.0, 0.0]

    4.13 Seizures
1130Risk Ratio (M-H, Random, 95% CI)0.33 [0.01, 8.03]

    4.14 Gastric aspiration
1704Risk Ratio (M-H, Random, 95% CI)3.09 [0.13, 75.50]

    4.15 Hypotension
1698Risk Ratio (M-H, Random, 95% CI)0.82 [0.54, 1.23]

    4.16 Arrhythmia
1695Risk Ratio (M-H, Random, 95% CI)1.10 [0.64, 1.90]

    4.17 Progressive respiratory distress
1700Risk Ratio (M-H, Random, 95% CI)0.61 [0.36, 1.03]

 5 CPAP X BILEVEL57593Risk Ratio (M-H, Random, 95% CI)1.18 [0.94, 1.48]

    5.1 Skin damage
5790Risk Ratio (M-H, Random, 95% CI)0.64 [0.19, 2.16]

    5.2 Pneumothorax
2715Risk Ratio (M-H, Random, 95% CI)2.89 [0.12, 70.63]

    5.3 Pulmonary aspiration
3796Risk Ratio (M-H, Random, 95% CI)2.88 [0.12, 70.43]

    5.4 Gastric distension
3172Risk Ratio (M-H, Random, 95% CI)1.49 [0.56, 4.00]

    5.5 Vomiting
4857Risk Ratio (M-H, Random, 95% CI)0.97 [0.43, 2.19]

    5.6 Disconfort with mask
4735Risk Ratio (M-H, Random, 95% CI)1.03 [0.53, 2.00]

    5.7 Increased breathing discomfort
1576Risk Ratio (M-H, Random, 95% CI)1.42 [0.67, 3.02]

    5.8 Hypotension
2758Risk Ratio (M-H, Random, 95% CI)0.98 [0.65, 1.48]

    5.9 Arrhythmia
1677Risk Ratio (M-H, Random, 95% CI)2.00 [1.02, 3.92]

    5.10 Progressive respiratory distress
1679Risk Ratio (M-H, Random, 95% CI)1.19 [0.64, 2.21]

    5.11 Cardiorespiratory arrest
1678Risk Ratio (M-H, Random, 95% CI)1.61 [0.59, 4.38]

    5.12 Pharyngeal damage
180Risk Ratio (M-H, Random, 95% CI)0.95 [0.06, 14.69]

    5.13 Cough
180Risk Ratio (M-H, Random, 95% CI)0.32 [0.01, 7.57]

 
Comparison 15. Hospital or 7-day mortality

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC212263Risk Ratio (M-H, Random, 95% CI)0.72 [0.55, 0.94]

 
Comparison 16. Hospital or 30-day mortality

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC222387Risk Ratio (M-H, Random, 95% CI)0.75 [0.60, 0.95]

 
Comparison 17. General or 7-day ETI rate

Outcome or subgroup titleNo. of studiesNo. of participantsStatistical methodEffect size

 1 NPPV (CPAP and BILEVEL) X SMC232417Risk Ratio (M-H, Random, 95% CI)0.55 [0.38, 0.78]

 

Appendices

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms
 

Appendix 1. Search strategies 2009

 

MEDLINE (Ovid)

1 exp Heart Failure/ (66770)
2 exp Myocardial Infarction/ (126033)
3 cardiogenic oedema$.tw. (7)
4 cardiogenic edema$.tw. (39)
5 pulmonary oedema.tw. (2354)
6 pulmonary edema.tw. (9499)
7 cardiac failure.tw. (9005)
8 heart failure.tw. (73909)
9 cardiac insufficiency.tw. (3578)
10 Pulmonary Edema/ (13680)
11 heart insufficiency.tw. (672)
12 Ventricular Dysfunction, Left/ (14770)
13 wet lung.tw. (307)
14 or/1-13 (245334)
15 exp Respiration, Artificial/ (49052)
16 exp Ventilators, Mechanical/ (7535)
17 mechanical ventilation.tw. (17741)
18 artificial ventilation.tw. (2502)
19 assisted ventilation.tw. (1817)
20 artificial respiration.tw. (1465)
21 (respirator or respirators).tw. (3713)
22 bipap.tw. (366)
23 nippv.tw. (262)
24 nppv.tw. (290)
25 niv.tw. (750)
26 niav.tw. (0)
27 cpap.tw. (3643)
28 aprv.tw. (61)
29 ippb.tw. (267)
30 ippv.tw. (628)
31 peep.tw. (3253)
32 positive pressure ventilation.tw. (3426)
33 pulmonary ventilation.tw. (2151)
34 non invasive ventilation.tw. (573)
35 noninvasive ventilation.tw. (747)
36 pressure support ventilation.tw. (571)
37 positive end expiratory pressure.tw. (3381)
38 bi-level positive airway pressure.tw. (93)
39 bilevel positive airway pressure.tw. (169)
40 or/15-39 (69840)
41 14 and 40 (3618)
42 randomized controlled trial.pt. (283687)
43 controlled clinical trial.pt. (81002)
44 Randomized controlled trials/ (64251)
45 random allocation/ (66529)
46 double blind method/ (104848)
47 single-blind method/ (13580)
48 or/42-47 (478246)
49 exp animal/ not humans/ (3476457)
50 48 not 49 (445629)
51 clinical trial.pt. (461395)
52 exp Clinical Trials as Topic/ (224000)
53 (clin$ adj25 trial$).ti,ab. (168562)
54 ((singl$ or doubl$ or trebl$ or tripl$) adj (blind$ or mask$)).ti,ab. (101838)
55 placebos/ (28620)
56 placebo$.ti,ab. (120725)
57 random$.ti,ab. (467107)
58 research design/ (58374)
59 or/51-58 (1009730)
60 59 not 49 (935775)
61 50 or 60 (966076)
62 61 and 41 (369)
63 (2005$ or 2006$ or 2007$ or 2008$ or 2009$).em. (3387916)
64 63 and 62 (160)

 

CENTRAL (The Cochrane Library)

#1 MeSH descriptor Heart Failure explode all trees 4000
#2 MeSH descriptor Myocardial Infarction explode all trees 6778
#3 myocardial next infarction in All Text 12934
#4 (cardiogenic in All Text near/6 edema in All Text) 64
#5 (cardiogenic in All Text near/6 oedema in All Text) 24
#6 (pulmonary in All Text near/6 edema in All Text) 389
#7 (pulmonary in All Text near/6 oedema in All Text) 210
#8 heart next failure in All Text 8265
#9 cardiac next failure in All Text 768
#10 cardiac next insufficiency in All Text 187
#11 heart next insufficiency in All Text 27
#12 left next ventricular next insufficiency in All Text 8
#13 left next ventricular next dysfunction in All Text 764
#14 wet next lung in All Text 3
#15 (#1 or #2 or #3 or #4 or #5 or #6 or #7 or #8 or #9 or #10 or #11 or #12 or #13 or #14) 20230
#16 MeSH descriptor Respiration, Artificial explode all trees 3377
#17 MeSH descriptor Ventilators, Mechanical explode all trees 211
#18 mechanical next ventilation in All Text 3047
#19 artificial next ventilation in All Text 483
#20 assisted next ventilation in All Text 413
#21 artificial next respiration in All Text 52
#22 (positive in All Text near/6 pressure in All Text near/6 ventilation in All Text) 982
#23 (respirator in All Text or respirators in All Text) 8427
#24 pulmonary next ventilat* in All Text 782
#25 non next invasive next ventilation in All Text 164
#26 noninvasive next ventilation in All Text 127
#27 non-invasive next ventilation in All Text 164
#28 positive next airway next pressure in All Text 1088
#29 positive next pressure next respiration in All Text 1056
#30 pressure next support next ventilation in All Text 219
#31 mask next ventilation in All Text 120
#32 bipap in All Text 135
#33 nippv in All Text 66
#34 nppv in All Text 78
#35 niv in All Text 152
#36 cpap in All Text 1007
#37 niav in All Text 3
#38 aprv in All Text 11
#39 ippb in All Text 59
#40 ippv in All Text 133
#41 peep in All Text 375
#42 positive next end next expiratory next pressure in All Text 464
#43 (#16 or #17 or #18 or #19 or #20 or #21 or #22 or #23 or #24 or #25) 11353
#44 (#26 or #27 or #28 or #29 or #30 or #31 or #32 or #33 or #34 or #35) 2260
#45 (#36 or #37 or #38 or #39 or #40 or #41 or #42) 1632
#46 (#43 or #44 or #45) 12336
#47 (#15 and #46) 536

 

EMBASE (Ovid)

1 exp Congestive Heart Failure/ (29823)
2 exp Heart Infarction/ (124630)
3 cardiogenic oedema$.tw. (8)
4 cardiogenic edema$.tw. (29)
5 pulmonary oedema.tw. (1856)
6 pulmonary edema.tw. (7171)
7 cardiac failure.tw. (6888)
8 heart failure.tw. (66554)
9 cardiac insufficiency.tw. (1235)
10 Lung Edema/ (15202)
11 heart insufficiency.tw. (254)
12 heart left ventricle function/ (14936)
13 wet lung.tw. (246)
14 or/1-13 (220649)
15 exp Ventilator/ (5189)
16 exp Artificial Ventilation/ (56813)
17 mechanical ventilation.tw. (16434)
18 artificial ventilation.tw. (1731)
19 assisted ventilation.tw. (1491)
20 artificial respiration.tw. (477)
21 (respirator or respirators).tw. (2181)
22 bipap.tw. (343)
23 nippv.tw. (233)
24 nppv.tw. (282)
25 niv.tw. (653)
26 niav.tw. (0)
27 cpap.tw. (3121)
28 aprv.tw. (64)
29 ippb.tw. (138)
30 ippv.tw. (465)
31 peep.tw. (3010)
32 positive pressure ventilation.tw. (2867)
33 pulmonary ventilation.tw. (1053)
34 non invasive ventilation.tw. (571)
35 noninvasive ventilation.tw. (774)
36 pressure support ventilation.tw. (579)
37 positive end expiratory pressure.tw. (3039)
38 bi-level positive airway pressure.tw. (82)
39 bilevel positive airway pressure.tw. (180)
40 or/15-39 (68033)
41 14 and 40 (4482)
42 controlled clinical trial/ (67441)
43 random$.tw. (410939)
44 randomized controlled trial/ (174578)
45 follow-up.tw. (369197)
46 double blind procedure/ (74328)
47 placebo$.tw. (113396)
48 placebo/ (132301)
49 factorial$.ti,ab. (8626)
50 (crossover$ or cross-over$).ti,ab. (40537)
51 (double$ adj blind$).ti,ab. (86993)
52 (singl$ adj blind$).ti,ab. (7707)
53 assign$.ti,ab. (112821)
54 allocat$.ti,ab. (35785)
55 volunteer$.ti,ab. (101863)
56 Crossover Procedure/ (21843)
57 Single Blind Procedure/ (8587)
58 or/42-57 (1066875)
59 (exp animals/ or nonhuman/) not human/ (2748065)
60 58 not 59 (974762)
61 60 and 41 (561)
62 (2005$ or 2006$ or 2007$ or 2008$ or 2009$).em. (2870201)
63 61 and 62 (300)

 

CINAHL (EBCSO)

( (MH "Ventilators, Mechanical") or (MH "Positive Pressure Ventilation+") or ventilat* or CPAP or NPPV or bipap or nippv or aprv or ippb or ippv or peep ) and S4 and ( (MH "Clinical Trials+") or random$ or trial or clinical study or group$ or placebo$ )  

 

Appendix 2. Search strategies 2011

 

CENTRAL and DARE (The Cochrane Library)

#1 MeSH descriptor Heart Failure explode all trees
#2 MeSH descriptor Myocardial Infarction explode all trees
#3 myocardial next infarction in All Text
#4 (cardiogenic in All Text near/6 edema in All Text)
#5 (cardiogenic in All Text near/6 oedema in All Text)
#6 (pulmonary in All Text near/6 edema in All Text)
#7 (pulmonary in All Text near/6 oedema in All Text)
#8 heart next failure in All Text
#9 cardiac next failure in All Text
#10 cardiac next insufficiency in All Text
#11 heart next insufficiency in All Text
#12 left next ventricular next insufficiency in All Text
#13 left next ventricular next dysfunction in All Text
#14 wet next lung in All Text
#15 (#1 or #2 or #3 or #4 or #5 or #6 or #7 or #8 or #9 or #10 or #11 or #12 or #13 or #14)
#16 MeSH descriptor Respiration, Artificial explode all trees
#17 MeSH descriptor Ventilators, Mechanical explode all trees
#18 mechanical next ventilation in All Text
#19 artificial next ventilation in All Text
#20 assisted next ventilation in All Text
#21 artificial next respiration in All Text
#22 (positive in All Text near/6 pressure in All Text near/6 ventilation in All Text)
#23 (respirator in All Text or respirators in All Text)
#24 pulmonary next ventilat* in All Text
#25 non next invasive next ventilation in All Text
#26 noninvasive next ventilation in All Text
#27 non-invasive next ventilation in All Text
#28 positive next airway next pressure in All Text
#29 positive next pressure next respiration in All Text
#30 pressure next support next ventilation in All Text
#31 mask next ventilation in All Text
#32 bipap in All Text
#33 nippv in All Text
#34 nppv in All Text
#35 niv in All Text
#36 cpap in All Text
#37 niav in All Text
#38 aprv in All Text
#39 ippb in All Text
#40 ippv in All Text
#41 peep in All Text
#42 positive next end next expiratory next pressure in All Text
#43 (#16 or #17 or #18 or #19 or #20 or #21 or #22 or #23 or #24 or #25)
#44 (#26 or #27 or #28 or #29 or #30 or #31 or #32 or #33 or #34 or #35)
#45 (#36 or #37 or #38 or #39 or #40 or #41 or #42)
#46 (#43 or #44 or #45)
#47 (#15 and #46)

 

MEDLINE (Ovid)

1. exp Heart Failure/
2. exp Myocardial Infarction/
3. cardiogenic edema$.tw.
4. cardiogenic oedema$.tw.
5. pulmonary oedema.tw.
6. pulmonary edema.tw.
7. cardiac failure.tw.
8. heart failure.tw.
9. cardiac insufficiency.tw.
10. Pulmonary Edema/
11. heart insufficiency.tw.
12. Ventricular Dysfunction, Left/
13. wet lung.tw.
14. or/1-13
15. exp Respiration, Artificial/
16. exp Ventilators, Mechanical/
17. mechanical ventilation.tw.
18. artificial ventilation.tw.
19. assisted ventilation.tw.
20. artificial respiration.tw.
21. (respirator or respirators).tw.
22. bipap.tw.
23. nippv.tw.
24. nppv.tw.
25. niv.tw.
26. niav.tw.
27. cpap.tw.
28. aprv.tw.
29. ippb.tw.
30. ippv.tw.
31. peep.tw.
32. positive pressure ventilation.tw.
33. pulmonary ventilation.tw.
34. non invasive ventilation.tw.
35. noninvasive ventilation.tw.
36. pressure support ventilation.tw.
37. positive end expiratory pressure.tw.
38. bi-level positive airway pressure.tw.
39. bilevel positive airway pressure.tw.
40. or/15-39
41. 14 and 40
42. randomized controlled trial.pt.
43. controlled clinical trial.pt.
44. randomized.ab.
45. placebo.ab.
46. drug therapy.fs.
47. randomly.ab.
48. trial.ab.
49. groups.ab.
50. 42 or 43 or 44 or 45 or 46 or 47 or 48 or 49
51. exp animals/ not humans.sh.
52. 50 not 51
53. 41 and 52
54. ((2001009* or 201010* or 201011* or 201012* or 2011*) not ("20100921" or "20100922" or "20100923" or "20100924" or "20100925" or "20100926" or "20100927" or "20100928" or "20100929" or "20100930")).ed.
55. 53 and 54

 

EMBASE (Ovid)

1. exp Congestive Heart Failure/
2. exp Heart Infarction/
3. cardiogenic oedema$.tw.
4. cardiogenic edema$.tw.
5. pulmonary oedema.tw.
6. pulmonary edema.tw.
7. cardiac failure.tw.
8. heart failure.tw.
9. cardiac insufficiency.tw.
10. Lung Edema/
11. heart insufficiency.tw.
12. heart left ventricle function/
13. wet lung.tw.
14. or/1-13
15. exp Ventilator/
16. exp Artificial Ventilation/
17. mechanical ventilation.tw.
18. artificial ventilation.tw.
19. assisted ventilation.tw.
20. artificial respiration.tw.
21. (respirator or respirators).tw.
22. bipap.tw.
23. nippv.tw.
24. nppv.tw.
25. niv.tw.
26. niav.tw.
27. cpap.tw.
28. aprv.tw.
29. ippb.tw.
30. ippv.tw.
31. peep.tw.
32. positive pressure ventilation.tw.
33. pulmonary ventilation.tw.
34. non invasive ventilation.tw.
35. noninvasive ventilation.tw.
36. pressure support ventilation.tw.
37. positive end expiratory pressure.tw.
38. bi-level positive airway pressure.tw.
39. bilevel positive airway pressure.tw.
40. or/15-39
41. 14 and 40
42. random$.tw.
43. factorial$.tw.
44. crossover$.tw.
45. cross over$.tw.
46. cross-over$.tw.
47. placebo$.tw.
48. (doubl$ adj blind$).tw.
49. (singl$ adj blind$).tw.
50. assign$.tw.
51. allocat$.tw.
52. volunteer$.tw.
53. crossover procedure/
54. double blind procedure/
55. randomized controlled trial/
56. single blind procedure/
57. 42 or 43 or 44 or 45 or 46 or 47 or 48 or 49 or 50 or 51 or 52 or 53 or 54 or 55 or 56
58. (animal/ or nonhuman/) not human/
59. 57 not 58
60. 41 and 59
61. ("201038" or "201039" or "201040" or "201041" or "201042" or "201043" or "201044" or "201045" or "201046" or "201047" or "201048" or "201049" or "201050" or "201051" or "201052" or 2011*).em.
62. 60 and 61

 

CINAHL

S47 S43 and S46
S46 S44 or S45
S45 EM 2010
S44 EM 2009
S43 S14 and S39 and S42
S42 S40 or S41
S41 TI (random* or trial or clinical study or group* or placebo*) or AB (random* or trial or clinical study or group* or placebo*)
S40 (MH "Clinical Trials+")
S39 S15 or S16 or S17 or S18 or S19 or S20 or S21 or S22 or S23 or S24 or S25 or S26 or S27 or S28 or S29 or S30 or S31 or S32 or S33 or S34 or S35 or S36 or S37 or S38
S38 TI (bi-level positive airway pressure) or AB (bi-level positive airway pressure)
S37 TI (positive end expiratory pressure) or AB (positive end expiratory pressure)
S36 TI (pressure support ventilation) or AB (pressure support ventilation)
S35 TI (noninvasive ventilation) or AB (noninvasive ventilation)
S34 TI (non invasive ventilation) or AB (non invasive ventilation)
S33 TI (pulmonary ventilation) or AB (pulmonary ventilation)
S32 TI (positive pressure ventilation) or AB (positive pressure ventilation)
S31 TI (peep) or AB (peep)
S30 TI (ippv) or AB (ippv)
S29 TI (ippb) or AB (ippb)
S28 TI (aprv) or AB (aprv)
S27 TI (cpap) or AB (cpap)
S26 TI (niav) or AB (niav)
S25 TI (niv) or AB (niv)
S24 TI (nppv) or AB (nppv)
S23 TI (nippv) or AB (nippv)
S22 TI (bipap) or AB (bipap)
S21 TI (respirator or respirators) or AB (respirator or respirators)
S20 TI (artificial respiration) or AB (artificial respiration)
S19 TI (assisted ventilation) or AB (assisted ventilation)
S18 TI (artificial ventilation) or AB (artificial ventilation)
S17 TI (mechanical ventilation) or AB (mechanical ventilation)
S16 (MH "Ventilation, Mechanical, Differentiated")
S15 (MH "Ventilators, Mechanical")
S14 S1 or S2 or S3 or S4 or S5 or S6 or S7 or S8 or S9 or S10 or S11 or S12 or S13
S13 TI (wet lung) or AB (wet lung)
S12 (MH "Ventricular Dysfunction, Left")
S11 TI (heart insufficiency) or AB (heart insufficiency)
S10 (MH "Pulmonary Edema")
S9 TI (cardiac insufficiency) or AB (cardiac insufficiency)
S8 TI (heart failure) or AB (heart failure)
S7 TI (cardiac failure) or AB (cardiac failure)
S6 TI (pulmonary edema*) or AB (pulmonary edema*)
S5 TI (pulmonary oedema*) or AB (pulmonary oedema*)
S4 TI (cardiogenic edema*) or AB (cardiogenic edema*)
S3 TI (cardiogenic oedema*) or AB (cardiogenic oedema*)
S2 (MH "Myocardial Infarction+")
S1 (MH "Heart Failure, Congestive+")

 

What's new

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

Last assessed as up-to-date: 5 April 2011.


DateEventDescription

12 November 2012New search has been performedNew search in April 2011 found 11 new studies

1 December 2011New citation required and conclusions have changedEleven new studies have been included in this review update.

Background section has been updated.

No changes have been made to the methodology. The search strategies have been modified in MEDLINE and EMBASE, and the dates over which the databases were searched were updated.

The conclusions have been amended slightly. The use of CPAP produces fewer adverse events compared to the standard treatment or compared the Bilevel NPPV, but the main thrust of the review has not changed.



 

History

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

Protocol first published: Issue 3, 2005
Review first published: Issue 3, 2008


DateEventDescription

17 April 2008AmendedConverted to new review format.



 

Contributions of authors

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

Flávia Vital did the protocol conceiving, designing, coordinating and writing and did the following tasks: selection of studies, quality evaluation, extraction and analysis data, final report and completion of the Cochrane publication and updating.

Álvaro Atallah did the protocol writing and did the following tasks: data analysis, final report and completion of the Cochrane publication and updating. Expertise advice.

Magdaline Ladeira did the protocol writing and the following tasks: selection of studies, quality evaluation, completion of the Cochrane publication and updating.

 

Declarations of interest

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms

None known.

 

Sources of support

  1. Top of page
  2. Summary of findings    [Explanations]
  3. Background
  4. Objectives
  5. Methods
  6. Results
  7. Discussion
  8. Authors' conclusions
  9. Acknowledgements
  10. Data and analyses
  11. Appendices
  12. What's new
  13. History
  14. Contributions of authors
  15. Declarations of interest
  16. Sources of support
  17. Index terms
 

Internal sources

  • Department of Urgency Medicine, Universidade Federal de São Paulo, Brazil.
  • Brazilian Cochrane Centre, Brazil.

 

External sources

  • No sources of support supplied

* Indicates the major publication for the study

References

References to studies included in this review

  1. Top of page
  2. AbstractRésumé scientifiqueResumo摘要
  3. Summary of findings
  4. Background
  5. Objectives
  6. Methods
  7. Results
  8. Discussion
  9. Authors' conclusions
  10. Acknowledgements
  11. Data and analyses
  12. Appendices
  13. What's new
  14. History
  15. Contributions of authors
  16. Declarations of interest
  17. Sources of support
  18. Characteristics of studies
  19. References to studies included in this review
  20. References to studies excluded from this review
  21. References to ongoing studies
  22. Additional references
  23. References to other published versions of this review
Agmy 2008 {published and unpublished data}
  • Agmy G. The effect of CPAP and NPPV on acute pulmonary edema due to systolic diastolic or valvular heart failure [Abstract]. European Respiratory Journal 2007;30(Suppl 51):321.
  • Agmy G, Makhlouf H, Mohammed A, Ghanem M, Mohammed H. CPAP versus BiPAP in acute cardiogenic pulmonary edema experience with 129 patients [Abstract]. European Respiratory Society Annual Congress 2008;8:1937.
  • Agmy GM. The effect of CPAP and NPPV on acute cardiogenic pulmonary edema due to systolic, diastolic or valvular heart failure [Abstract]. American Thoracic Society International Conference 2007;1:A963.
Bautin 2005 {published and unpublished data}
  • Bautin A, Khubulava G, Naumov A, Garifzjanov A, Etin V. NPPV in the treatment of the cardiogenic edema (CPE) after heart surgery [Abstract]. European Respiratory Journal 2005;26(Suppl 49):3112.
Bellone 2004 {published data only}
  • Bellone A, Monari A, Cortellaro F, Vetorello M, Arlati S, Coen D. Myocardial infarction rate in acute pulmonary edema: noninvasive support ventilation versus continuous positive airway pressure. Critical Care Medicine 2004;32(9):1860-5.
Bellone 2005 {published data only}
  • Bellone A, Vettorello M, Monari A, Cortellaro F, Coen D. Noninvasive pressure support ventilation vs. continuous positive airway pressure in acute hypercapnic pulmonary edema. Intensive Care Medicine 2005;31:807-11.
Bersten 1991 {published and unpublished data}
  • Bersten AD, Holt AW, Vedig AE, Skowronski GA, Bagooley CJ. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. New England Journal of Medicine 1991;325(26):1825-30.
Crane 2004 {published and unpublished data}
  • Crane SD, Elliott MW, Gilligan P, Richards K, Gray AJ. Randomized controlled comparison of continuous positive airway pressure, bilevel non-invasive ventilation, and standard treatment in emergency department patients with acute cardiogenic pulmonary oedema. Emergency Medicine Journal 2004;21:155-61.
Delclaux 2000 {published data only}
  • Delclaux C, L'Her E, Alberti C, Mancebo J, Abroug F, Conti G, et al. Treatment of acute hypoxemic nonhypercapnic respiratory insufficiency with continuous positive airway pressure delivery by a face mask. JAMA 2000;284:2352-60.
Ferrari 2007 {published data only}
  • Ferrari G, Olliveri F, De Filippi G, Milan A, Apra F, Boccuzzi A, et al. Noninvasive positive airway pressure and risk of myocardial infarction in acute cardiogenic pulmonary edema: continuous positive airway pressure vs noninvasive positive pressure ventilation. Chest 2007;132(6):1804-9.
Ferrari 2010 {published data only}
  • Ferrari G, Groff P, De Filippi G, Giostra F, Mazzone M, Potale G, et al. Continuous positive airway pressure (CPAP) vs. noninvasive positive pressure ventilation (NIV) in acute cardiogenic pulmonary edema (ACPE): A prospective randomized multicentric study. Journal of Emergency Medicine 2006;30:246-7.
  • Ferrari G, Milan A, Groff P, Pagnozzi F, Mazzone M, Molino P, et al. Continuous positive airway pressure vs. Pressure support ventilation in acute cardiogenic pulmonary edema: a randomized trial. Journal of Emergency Medicine 2010;39(5):676-84.
Ferrer 2003 {published data only}
  • Ferrer M, Esquinas A, Leon M, Gonzalez G, Alarcon A, Torres A. Noninvasive Ventilation in Severe Hypoxemic Respiratory Failure: A Randomized Clinical Trial. American Journal of Respiratory and Critical Care Medicin 2003;168:1438-44.
  • Ferrer M, Esquinas A, Leon M, Gonzalez G, Alarcon A, Torres A. Non-vasive Ventilation in Severe Acute Hypoxemic Respiratory Failure. A Randomized Clinical Trial. Intensive Care Medicine 2002;28:S68.
Fontanella 2010 {published data only}
  • Bordonali T, Fontanella B, Affatato A, Saporetti A, Carubelli V, Ciccarese C, et al. Comparison of continuous positive airway pressure (CPAP) versus bilevel non invasive pressure support ventilation (NIPSV) in acute cardiogenic pulmonary edema. European Heart Journal 2009;30:369. [EMBASE: 797]
  • Fontanella B, Affatato A, Ciccarese C, Sacchini M, Volpini M, Bianchetti F, et al. Prospective comparison of continuous positive airway pressure (CPAP) versus bilevel non invasive pressure support ventilation (BPAP) in acute cardiogenic pulmonary edema. European Heart Journal Supplements 2010;12 (supplement F):F37-F38.
Frontin 2010 {published data only}
  • Frontin P, Bounes V, Houzé-Cerfon CH, Charpentier S, Houzé-Cerfon V, Ducassé JL. Continuous positive airway pressure for cardiogenic pulmonary edema: a randomized study. American Journal of Emergency Medicine 2011;29(7):775-81.
Gray 2008 {published data only}
  • Gray A, Goodacre S, Newby DE, Masson M, Sampson F, Nicholl J. Noninvasive Ventilation in AcuteCardiogenic Pulmonary Edema. New England Journal of Medicine 2008;359:142-51.
  • Gray AJ, Goodacre S, Newby DE, Masson MA, Sampson F, Dixon S, et al. A multicentre randomised controlled trial of the use of continuous positive airway pressure and non-invasive positive pressure ventilation in the early treatment of patients presenting to the emergency department with severe acute cardiogenic pulmonary oedema: the 3CPO trial. Health Technology Assessment 2009;13(33):1-106.
Kelly 2002 {published and unpublished data}
  • Kelly CA, Newby DE, McDonagh TA, MacKay TW, Barr J, Boon NA, et al. Randomised controlled trial of continuous positive airway pressure and standard oxygen therapy in acute pulmonary oedema. European Heart Journal 2002;23:1379-86.
L'Her 2004 {published data only}
  • L'Her E, Duquesne F, Girou E, Rosiere XD, Le Conte P, Renault S, et al. Noninvasive continuous positive airway pressure in elderly cardiogenic pulmonary edema patients. Intensive Care Medicine 2004;30:882-8.
Levitt 2001 {published data only}
Liesching 2003 {published data only}
  • Liesching TN, Cromier K, Nelson D, Short K, Sucov A, Hill NS. Bilevel noninvasive ventilation vs continuous positive airway pressure to treat acute pulmonary edema. American Journal of Respiratory and Critical Care Medicine 2003;167(Suppl 7):27.
Lin 1991 {published data only}
  • Lin M, Chiang H. The efficacy of early continuous positive airway pressure therapy in patients with acute cardiogenic pulmonary edema. Journal of the Formosan Medical Association 1991;90(8):736-43.
Lin 1995 {published data only}
Martin-Bermudez 2002 {published and unpublished data}
  • Martin-Bermudez R, Rodrı´guez-Portal J, Garcı´a-Garmendia J. Noninvasiveventilation in cardiogenic pulmonay edema. Preliminary results of a randomizedtrial [Abstract]. Intensive Care Medicine 2002;28:S68.
Masip 2000 {published data only}
  • Masip J, Betbesé AJ, Paéz J, Vecilla F, Cañizares R, Padró J, et al. Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomized trial. Lancet 2000;356:2126-32.
Mehta 1997 {published data only}
  • Mehta S, Jay GD, Woolard RH, Hipona RA, Connolly EM, Cimini DM, et al. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Critical Care Medicine 1997;25(4):620-8.
Moritz 2007 {published data only}
  • Moritz F, Brousse B, Gellee B, Chajara A, L'Her E, Hellot MF, et al. Continuous positive airway pressure versus bilevel noninvasive ventilation in acute cardiogenic pulmonary edema: a randomized multicenter trial. Annals of Emergency Medicine 2007;50(6):666-75.
Nava 2003 {published and unpublished data}
  • Carbone G, Di Battista N, Nava S. Noninvasive bilevel ventilation vs conventional therapy in the treatment of acute cardiogenic pulmonary edema: a randomized controlled study. European Respiratory Journal 2000;16:A3815.
  • Nava S. Bilevel ventilation reduces the rate of endotracheal intubation in the hypercapnic, but not in the hypoxemic patients during acute respiratory failure due to cardiogenic pulmonary edema: a multicenter randomized study vs standard medical therapy. European Respiratory Journal 2001;18:A184s.
  • Nava S, Carbone G, DiBattista N, Bellone A, Baiardi P, Cosentini R, et al. Noninvasive ventilation in cardiogenic pulmonary edema. American Journal of Respiratory and Critical Care Medicine 2003;168:1432-7.
Park 2001 {published and unpublished data}
  • Park M. Randomized prospective trial of oxygen, continuos and bilevel positive airway pressure in the treatment of cardiogenic acute pulmonary edema. American Journal of Respiratory and Critical Care Medicine 2002;165(Suppl 8):A27.
  • Park M, Lorenzi-Filho G, Feltrim MI, Viecili PRN, Sangean MC, Volpe M, et al. Oxygen therapy, continuous positive airway pressure, or noninvasive bilivel positive pressure ventilation in the treatment of acute cardiogenic pulmonary edema. Arquivos Brasileiros de Cardiologia 2001;76(3):226-30.
Park 2004 {published and unpublished data}
  • Park M, Sangean MC, Volpe MS, Feltrim MIZ, Nozawa E, Leite PF, et al. Randomized, prospective trial of oxygen, continuous positive airway pressure by face mask in acute cardiogenic pulmonary edema. Critical Care Medicine 2004;32(12):2407-15.
Räsänen 1985 {published data only}
  • Räsänen J, Heikkilä J, Downs J, Nikki P, Väisänen I, Viitanen A. Continuous positive airway pressure by face mask in acute cardiogenic pulmonary edema. American Journal of Cardiology 1985;55:296-300.
Sharon 2000 {published data only}
  • Sharon A, Shpirer I, Kaluski E, Moshkovitz Y, Milanov O, Polak R, et al. High-dose intravenous Isosorbide-dinitrate is safer and better than Bi-PAP ventilation for severe pulmonary edema. Journal of the American College of Cardiology 2000;36(3):832-7.
Takeda 1997 {published and unpublished data}
  • Takeda S, Takano T, Ogawa R. The effect of nasal continuous positive airway pressure on plasma endothelin-1 concentrations in patients with severe cardiogenic pulmonary edema. Anesthesia & Analgesia 1997;84:1091-6.
Takeda 1998 {published and unpublished data}
  • Takeda S, Neijima J, Takano T, Nakanishi K, Takayama M, Sakamoto A, et al. Effect of nasal continuous positive airway pressure on pulmonary edema complicating acute myocardial infarction. Circulation Journal 1998.;62:553-8.
Thys 2002 {published and unpublished data}
  • Thys F, Roeseler J, Reynaert M, Liistro G, Rodenstein DO. Noninvasive ventilation for acute respiratory failure: a prospective randomised placebo-controlled trial. European Respiratory Journal 2002;20:545-55.
Weitz 2007 {published and unpublished data}
  • Weitz G, Struck J, Zonak A, Balnus S, Perras B, Dodt C. Prehospital noninvasive pressure support ventilation for acute cardiogenic pulmonary edema. European Journal of Emergency Medicine 2007;14(5):276-9.

References to studies excluded from this review

  1. Top of page
  2. AbstractRésumé scientifiqueResumo摘要
  3. Summary of findings
  4. Background
  5. Objectives
  6. Methods
  7. Results
  8. Discussion
  9. Authors' conclusions
  10. Acknowledgements
  11. Data and analyses
  12. Appendices
  13. What's new
  14. History
  15. Contributions of authors
  16. Declarations of interest
  17. Sources of support
  18. Characteristics of studies
  19. References to studies included in this review
  20. References to studies excluded from this review
  21. References to ongoing studies
  22. Additional references
  23. References to other published versions of this review
Acosta 2000 {published data only}
  • Acosta B, DiBenedetto R, Rahimi A, Acosta MF, Cuadra O, Van Nguyen A, et al. Hemodynamic effects of noninvasive bilevel positive airway pressure on patients with chronic congestive heart failure with systolic dysfunction. Chest 2000;118(4):1004-9.
Albert 2000 {published data only}
Alper 2007 {published data only}
  • Alper BS. Evidence-based medicine. Noninvasive ventilation reduces mortality in cardiogenic pulmonary edema. Clinical Advisor for Nurse Practitioners 2007;10(5):158.
Alper 2008 {published data only}
  • Alper BS. Evidence-based medicine. Noninvasive ventilation may improve respiratory distress in acute heart failure. Clinical Advisor for Nurse Practitioners 2008;11(11):118.
Andrade 1998 {published data only}
  • Andrade CLV, Mendoza JN. Acute respiratory distress of the adult [Distress respiratorio agudo del adulto]. Boletín del Hospital San Juan de Dios 1998;45(1):13-9.
Antonelli 2001 {published data only}
  • 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 Medicine 2001;27(11):1718-28.
Aronow 2007 {published data only}
Barach 1938 {published data only}
  • Barach AL Martin J, Eckman M. Positive pressure respiration and its application to the treatment of acute pulmonary edema. Annals of Internal Medicine 1938;12:754-95.
Baratz 1992 {published data only}
  • Baratz DM, Westbrook PR, Shah PK, Mohsenifar Z. Effect of nasal continuous positive airway pressure on cardiac output and oaxygen delivery in patients with congestive heart failure. Chest 1992;102(5):1397-401.
Bavry 2008 {published data only}
  • Bavry AA. Effect of continuous positive airway pressure and noninvasive positive pressure ventilation in acute cardiogenic pulmonary oedema (3CPO). ACC Cardiosource Review Journal 2008;17(9):37.
Bellone 2002 {published data only}
  • Bellone A, Barbieri A, Ricci C, Iori E, Donateo M, Massobrio M, et al. Acute effects of non-invasive ventilatory support on functional mitral regurgitation in patients with exacerbation of congestive heart failure. Intensive Care Medicine 2002;28(9):1348-50.
Blomqvist 1991 {published data only}
  • Blomqvist H. Does PEEP facilitate the resolution of extravascular lung water after experimental hydrostatic pulmonary edema?. European Respiratory Journal 1991;4:1053-9.
Bollaert 2002 {published data only}
  • Bollaert PE, Sauder PH, Girard F, Rusterholtz TH, Feissel M, Harlay ML, et al. Continuous positive airway pressure (CPAP) VS proportional assist ventilation (PAV) for noninvasive ventilation in cardiogenic pulmonary edema. American Journal of Respiratory and Critical Care Medicine. 2002; Vol. 165, issue Suppl 8:A387.
Bouquin 1998 {published data only}
  • Bouquin V, L'Her E, Moriconi M, Jobic Y, Matheu B, Guillo P, et al. Spontaneous ventilation in positive expiratory pressure in cardiogenic pulmonary edema. Archives des maladies du Coeur et des Vaisseaux 1998;91(10):1243-8.
Bradley 2000 {published data only}
Brezins 1993 {published data only}
  • Brezins M, Benari B, Papo V, Cohen A, Bursztein S, Markiewicz W. Left ventricular function in patients with acute myocardial infarction, acute pulmonary edema, and mechanical ventilation: Relationship to prognosis. Critical Care Medicine 1993;21(3):380-5.
Brijker 1999 {published data only}
  • Brijker F, van den Elshout FJ, de Rijk A, Folgering HT, Bosch FH. Use of noninvasive mechanical ventilation to avoid intubation during acute respiratory insufficiency. Nederlands Tijdschrift voor Geneeskunde 1999;143(36):1819-23.
Brochard 1998 {published data only}
Chadda 2002 {published data only}
  • Chadda K, Annane D, Hart N, Gajdos P, Raphael JC, Lofaso F. Cardiac and respiratory effects of continuous positive airway pressure and noninvasive ventilation in acute cardiac pulmonary edema. Critical Care Medicine 2002;30(11):2457-61.
Chen 2008 {published data only}
Crane 2002 {published data only}
  • Crane SD. Epidemiology, treatment and outcome of acidotic, acute, cardiogenic pulmonary oedema presenting to and Emergency department. European Journal of Emergency Medicine 2002;9:320-4.
Craven 2000 {published data only}
Cross 2000 {published data only}
Cross 2003 {published data only}
  • Cross AM, Cameron P, Kierce M, Ragg M, Kelly AM. Non-invasive ventilation in acute respiratory failure: a randomized comparison of continuous positive airway pressure and bi-level positive airway pressure. Emergency Medicine Journal 2003;20(6):531-4.
Cydulka 2005 {published data only}
  • Cydulka RK. Noninvasive ventilation in cardiogenic pulmonary edema: A multicenter randomized trial. Annals of Emergency Medicine 2005;45(2):227-8.
Domenighetti 2002 {published data only}
  • Domenighetti G, Gayer R, Gentilini R. Noninvasive pressure support ventilation in non-COPD patients with acute cardiogenic pulmonary edema and severe community-acquired pneumonia: acute effects and outcome. Intensive Care Medicine 2002;28(9):1226-32.
Du Cailar 1975 {published data only}
  • Du Cailar J, Huguenard P, Kielen J, Griffe D. Justification, methods and indications for positive-pressure respiration in controlled and spontaneous ventilation in lesional pulmonary edeman. Annales de l'Anesthesiologie Francaise 1975;2:196-206.
Eaton 2002 {published data only}
Evans 2001 {published data only}
  • Evans TW, Albert RK, Angus DC, Bion JF, Chiche J, Epstein SK, et al. International Consensus conferences in intensive care medicine: noninvasive positive pressure ventilation in acute respiratory failure. American Journal of Respiratory and Critical Care Medicine 2001;163:283-91.
Fromm 1995 {published data only}
  • Fromm Jr RE, Varon J, Gibbs LR. Congestive heart failure and pulmonary edema for emergency physician. Journal of Emergency Medicine 1995;13(1):71-87.
Giacomini 2003 {published data only}
  • Giacomini M, Iapichino G, Cigada M, Minuto A, Facchini R, Noto A, et al. Short-term noninvasive pressure support ventilation prevents ICU admittance in patients with acute cardiogenic pulmonary edema. Chest 2003;123(6):2057-61.
Girou 2003 {published data only}
  • Girou E, Brun-Buisson C, Taille S, Lemaire F, Brochard L. Secular trends in nosocomial infections and mortality associated with noninvasive ventilation in patients with exacerbation of COPD and pulmonary edema. JAMA 2003;290(22):2985-91.
Gorbunova 2005 {published data only}
  • Gorbunova M, Babak S, Tatrskiy A. Effect of nasal continuous positive airway pressure on respiratory failure and left ventricular dysfunction complicating acute myocardial infarction [Abstract]. European Respiratory Journal 2005;26(Suppl 49):1.
Gray 2009 {published data only}
  • Gray AJ, Goodacre S, Newby DE, Masson MA, Sampson F, Dixon S. A multicentre randomised controlled trial of the use of continuous positive airway pressure and non-invasive positive pressure ventilation in the early treatment of patients presenting to the emergency department with severe acute cardiogenic pulmonary oedema: the 3CPO trial. Health Technology Assessment 2009;13(33):1-106.
Guerra 2005 {published data only}
  • Guerra JF. Noninvasive ventilation in acute cardiogenic pulmonary edema [Ventilación no invasiva en el edema pulmonar agudo cardiogénico: debe individualizarse?]. Medicina Clínica 2005;124(4):142-3.
Guntupalli 1984 {published data only}
  • Guntupalli KK. Acute pulmomnary edema. Cardiology Clinics 1984;2(2):183-200.
Gust 1998 {published data only}
  • Gust R, Bohrer H. Changes in crdiac output do not explain the higher rate of myocardial infarction associated with the use of bilevel compared with continuous positive airway pressure. Critical Care Medicine 1998;26(2):415-6.
Hao 2002 {published data only}
  • Hao CX, Luo XR, Liu YM. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure by nasal face mask. Acta Academiae Medicinae Jiangxi 2002;42(5):48-50.
Hess 2004 {published data only}
  • Hess DR. The evidence for noninvasive positive-pressure ventilation in the care of patients in acute respiratory failure: a systematic review of the literature. Respiratory Care 2004;49(7):810-29.
Hilberg 1997 {published data only}
Hipona 1996 {published data only}
Hoffman B 1999 {published data only}
  • Hoffmann B. Welte F. The use of noninvasive pressure support ventilation for severe respiratory insufficiency due to pulmonary oedema. Pneumologie 1999;53(6):316-21.
Hoffmann 1999 {published data only}
Holt 1994 {published data only}
  • Holt AW, Bersten AD, Fuller S, Piper RK, Worthley LI, Vedig AE. Intensive care costing methodology: cost benefit analysis of mask continuous positive airway pressure for severe cardiogenic pulmonary oedema. Anaesthesia and Intensive Care 1994;22(2):170-4.
Hotchkiss 1998 {published data only}
Hubble 2006 {published data only}
  • Hubble MW, Richards ME, Jarvis R, Millikan T, Young D. Effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema. Prehospital Emergency Care 2006;10(4):430-9.
Hughes 1999 {published data only}
  • Hughes CM. Review: continuous positive airway pressure support reduces the need for intubation in patients with cardiogenic pulmonary edema. ACP Journal Club 1999;130(3):58.
Iapichino 2004 {published data only}
  • Iapichino G, Giacomini M, Bassi G, Borotto E, Minuto A. Non invasive mechanical ventilation in acute cardiogenic pulmonary edema: is it all done?. Minerva Anestesiologica 2004;70(4):151-7.
Jackson 2000 {published data only}
  • Jackson P. Continuous positive airway pressure: the need for prehospital research and clinical trials. Australasian Journal of Emergency Care 2000;7(3):22-5.
Jackson 2001 {published data only}
Jackson R 2001 {published data only}
Kallio 2003 {published data only}
  • Kallio T, Kuisma M, Alaspaa A, Rosenberg PH. The use of prehospital continuous positive airway pressure treatment in presumed acute severe pulmonary edema. Prehospital Emergency Care 2003;7(2):209-13.
Keenan 2004 {published data only}
  • Keenan SP, Sinuff T, Cook DJ, Hill NS. Does noninvasive positive pressure ventilation improve outcome in acute hypoxemic respiratory failure? A systematic review. Critical Care Medicine 2004;32(12):2516-23.
Kelly 2001 {published data only}
Kiely 1998 {published data only}
  • Kiely JL, Deegan P, Buckley A, Shiels P, Maurer B, McNicholas WT. Efficacy of nasal continuous positive airway pressure therapy in chronic heart failure: Importance of underlying cardiac rhythm. Thorax 1998;53(11):957-62.
Kindgen-Milles 2000 {published data only}
  • Kindgen-Milles D, Buhl R, Gabriel A, Bohner H, Muller E. Nasal continuous positive airway pressure: A method to avoid endothracheal reintubation in postoperative high-risk patients with severe nonhypercapnic oxygenation failure. Chest 2000;117(4):1106-11.
Kosowsky 2000 {published data only}
  • Kosowsky JM, Storrow AB, Carleton SC. Continuous and bilevel positive airway pressure in the treatment of acute cardiogenic pulmonary edema. American Journal of Emergency Medicine 2000;18(1):91-5.
Kosowsky 2001 {published data only}
  • Kosowsky JM, Stephanides SL, Branson RD, Sayre MR. Prehospital use of continuous positive airway pressure (CPAP) for presumed pulmonary edema: a preliminary case series. Prehospital Emergency Care 2001;5(2):190-6.
Kramer 1995 {published data only}
  • Kramer N, Thomaas JM, Meharg J, Cece RD, Hill NS. Randomized, prospective trial of noninvasive positive pressure ventilation in acute respiratory failure. American Journal of Respiratory and Critical Care Medicine 1995;151:1799-806.
L'Her 1998 {published data only}
  • L'Her E, Duquesne F, Paris A, Mouline J, Renault A, Garo B, Boles JM. Spontaneous positive end-expiratory pressure ventilation in elderly patients with cardiogenic pulmonary edema. Presse Medicale 1998;27(22):1089-94.
L'Her E 1998 {published data only}
  • L'Her E, Moriconi M, Texier F, Bouquin V, Kaba L, Renault A, Garo B, Boles JM. Non-invasive continuous positive airway pressure in acute hypoxaemic respiratory failure--experience of an emergency department. European Journal of Emergency Medicine 1998;5(3):313-8.
Lal 1969 {published data only}
Lapinsky 1994 {published data only}
Leman 2005 {published data only}
  • Leman P, Greene S, Whelan K, Legassick T. Simple lightweight disposable continuous positive airways pressure mask to effectively treat acute pulmonary oedema: randomized controlled trial. Emergency Medicine Australasia 2005;17(3):224-30.
Lenique 1997 {published data only}
  • Lenique F, Habis M, Lofaso F, Dubois-Randé J, Harf A, Brochard L. Ventilatory and hemodynamic effects of continuous positive airway pressure in left heart failure. American Journal of Respiratory and Critical Care Medicine 1997;155:500-5.
Li 2004 {published data only}
  • Li XK, Zhao WH. The treatment of acute cardiogenic pulmonary edema with noninvasive positive pressure ventilation. Chongqing Medical Journal 2004;34(4):575-6.
Liesching T 2003 {published data only}
Lo Coco 1997 {published data only}
  • Lo Coco A, Vitali G, Marchese S, Bozzo P, Pesco C, Arena A. Treatment of acute respiratory failure secondary to pulmonary oedema with bi-level positive airway pressure by nasal mask. Monaldi Archives For Chest Disease 1997;52(5):444-6.
Mackay CA 2000 {published data only}
  • Mackay CA, Mackay TW, Barr J, Newby D, McDonagh T, Douglas NJ. Randomized controlled trial of CPAP vs conventional therapy in acute pulmonary edema. American Journal Respiratory Critical Care Medicine 2000;161:A416.
Masip 2008 {published data only}
Massaria 1976 {published data only}
  • Massaria E, De Liguori S, Castelli P, Cattani C, Merli M, Pratelli EM. Use of artificial respiration in complicated acute myocarial infarct. Critical evaluation. Minerva Anestesiologica 1976;42(5):391-5.
Meduri 1991 {published data only}
Mehta 2000 {published data only}
  • Mehta S, Liu PP, Fitzgerald FS, Allidina YK, Douglas Bradley T. Effects of continuous positive airway pressure on cardiac volumes in patients with ischemic and dilated cardiomyopathy. American Journal of Respiratory and Critical Care Medicine 2000;161(1):128-34.
Mehta 2004 {published data only}
Mehta 2005 {published data only}
Minuto 2003 {published data only}
  • Minuto A, Giacomini M, Giamundo B, Tartufari A, Denkewitz T, Marzorati S, et al. Non-invasive mechanical ventilation in patients with acute cardiogenic pulmonary edema. Minerva Anestesiologica 2003;69(11):835-40.
Mollica 2001 {published data only}
  • Mollica C, Brunetti G, Buscajoni M, Cecchini L, Maialetti E, Marazzi M, et al. Non-invasive pressure support ventilation in acute hypoxemic (non hypercapnic) respiratory failure. Observations in Respiratory Intermediate Intensive Care Unit. Minerva Anestesiologica 2001;67(3):107-15.
Moritz 2003 {published data only}
  • Moritz F, Benichou J, Vanhest M, Richard JC, Line S, Hellot MF, et al. Boussignac continuous positive airway pressure device in the emergency care of acute cardiogenic pulmonary oedema: a randomized pilot study. European Journal of Emergency Medicine 2003;10(3):204-8.
Murray 2002 {published data only}
  • Murray S. Bi-level positive airway pressure (BiPAP) and acute cardiogenic pulmonary oedema (ACPO) in the emergency department. Australian Critical Care 2002;15(2):51-63.
Murray 2003 {published data only}
  • Murray S. Bi-level positive airway pressure (BiPAP) and acute cardiogenic pulmonary oedema (ACPO) in emergency department. Australian Emergency Nursing Journal 2003;6(1):19-35.
Nadar 2005 {published data only}
  • Nadar S, Prasad N, Taylor RS, Lip GYH. Positive pressure ventilation in the management of acute and chronic cardiac failure: A systematic review and meta-analysis. International Journal of Cardiology 2005;99(2):171-85.
Nava 2002 {published data only}
  • Nava S, Carlucci A. Non-invasive pressure support ventilation in acute hypoxemic respiratory failure: Common strategy for differnet pathologies?. Intensive Care Medicine 2002;28(9):1205-7.
Newberry 1995 {published data only}
Newby 2007 {published data only}
  • Newby D. 3CPO. ACC Cardiosource Review Journal 2007;16(10):38-43.
Nikki 1982 {published data only}
  • Nikki P, Rasanen J, Tahvanainen J, Makelainen A. Ventilatory pattern in respiratory failure arising from acute myocardial infarction. I. Respiratory and hemodynamic effects of IMV4 vs IPPV12 and PEEP0 vs PEEP10. Critical Care Medicine 1982;10(2):75-8.
Niranjan 1998 {published data only}
Panacek 2002 {published data only}
  • Panacek EA, Kirk JD. Role of noninvasive ventilation in the managemnet of acutely descompensated heart failure. Reviews i Cardiovascular Medicine 2002;3(Suppl 4):S35-40.
Pang 1998 {published data only}
  • Pang D, Keena SP, Cook DJ, Sibald WJ. The effect of positive pressure airway support on mortality and the need for intubation i cardiogenic pulmonary edema: A systematic review. Chest 1998;114(4):1185-92.
Park 2005 {published data only}
  • Park M. Noninvasive ventilation in threatment of the acute pulmonary oedema. Where are we really?. Jornal do médico - Hospital Sírio Libanês 2005;38:10-1.
Park 2006 {published data only}
  • Lorenzi-Filho, Geraldo DB. Noninvasive mechanical ventilation in the treatment of acute cardiogenic pulmonary edema. Clinics 2006;61(3):247-252.
Perel 1983 {published data only}
Perkins 2006 {published data only}
  • Perkins GD, McAuley DF, Thickett DR, Gao F. From the authors. American Journal of Respiratory and Critical Care Medicine 2006;173(11):1291-Transcatheter valve implantation versus aortic valve replacement for aortic stenosis in high-risk patients2.
Philip-joet 1999 {published data only}
  • Philip-Joet FF, Paganelli FFF, Dutau HL. Hemodynamic effects of bilevel nasal positive airway pressure ventilation in patients with heart failure. Respiration 1999;66:136-43.
Plaisance 2007 {published data only}
  • Plaisance P, Pirracchio R, Berton C, Vicaut E, Payen D. A randomized study of out-of-hospital continuous positive airway pressure for acute cardiogenic pulmonary oedema. European Heart Journal 2007;28(23):2895-901.
Pollack 1996 {published data only}
  • Pollack CV Jr, Torres MT, Alexander L. Feasibility study of the use of bilevel positive airway pressure for respiratory support in the emergency department. Annals of Emergency Medicine 1996;27(2):189-92.
Poponick 1999 {published data only}
Popova 2010 {published data only}
  • Popova X, Avdeev S, Nekludova G, Chuchalin A. Effect of noninvasive ventilation (NIV) on exercise tolerance in patients with acute decompensated heart failure [Abstract]. Europe Respiratory Society Conference. 2010:E3918.
Poulton 1936 {published data only}
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Rabatin 1999 {published data only}
Rasanen J 1985 {published data only}
Rizk 1982 {published data only}
Roche 2003 {published data only}
Rusterholtz 1999 {published data only}
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Rutherholtz 2008 {published data only}
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Vaisanen 1987 {published data only}
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Werdan 1999 {published data only}
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Widger 2001 {published data only}
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Wood 1998 {published data only}
Wright 2001 {published data only}
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References to ongoing studies

  1. Top of page
  2. AbstractRésumé scientifiqueResumo摘要
  3. Summary of findings
  4. Background
  5. Objectives
  6. Methods
  7. Results
  8. Discussion
  9. Authors' conclusions
  10. Acknowledgements
  11. Data and analyses
  12. Appendices
  13. What's new
  14. History
  15. Contributions of authors
  16. Declarations of interest
  17. Sources of support
  18. Characteristics of studies
  19. References to studies included in this review
  20. References to studies excluded from this review
  21. References to ongoing studies
  22. Additional references
  23. References to other published versions of this review
NCT00554580 {published and unpublished data}
  • Effect of Continuous Positive Airway Pressure on Short Term Inhospital Prognosis for Acute Pulmonary Edema. Ongoing study November 6, 2007.
NCT00912158 {published data only}
  • Noninvasive Mechanical Ventilation in Acute Cardiogenic Pulmonary Edema. Ongoing study April 8, 2009.

Additional references

  1. Top of page
  2. AbstractRésumé scientifiqueResumo摘要
  3. Summary of findings
  4. Background
  5. Objectives
  6. Methods
  7. Results
  8. Discussion
  9. Authors' conclusions
  10. Acknowledgements
  11. Data and analyses
  12. Appendices
  13. What's new
  14. History
  15. Contributions of authors
  16. Declarations of interest
  17. Sources of support
  18. Characteristics of studies
  19. References to studies included in this review
  20. References to studies excluded from this review
  21. References to ongoing studies
  22. Additional references
  23. References to other published versions of this review
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