Skip to main content

Main menu

  • Home
  • Current issue
  • Early View
  • Archive
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

User menu

  • Log in
  • Subscribe
  • Contact Us
  • My Cart

Search

  • Advanced search
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

Login

European Respiratory Society

Advanced Search

  • Home
  • Current issue
  • Early View
  • Archive
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions

ERS International Congress, Madrid, 2019: highlights from the Respiratory Intensive Care Assembly

Celal Satici, Daniel López-Padilla, Annia Schreiber, Aileen Kharat, Ema Swingwood, Luigi Pisani, Maxime Patout, Lieuwe D. Bos, Raffaele Scala, Marcus J. Schultz, Leo Heunks
ERJ Open Research 2020 6: 00331-2019; DOI: 10.1183/23120541.00331-2019
Celal Satici
1Respiratory Medicine, Istanbul Gaziosmanpasa Training and Research Hospital, Health Science University, Istanbul, Turkey
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Daniel López-Padilla
2Respiratory Dept, Gregorio Marañón University Hospital, Spanish Sleep Network, Madrid, Spain
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Daniel López-Padilla
Annia Schreiber
3Interdepartmental Division of Critical Care, University of Toronto, Unity Health Toronto (St Michael's Hospital) and the Li Ka Shing Knowledge Institute, Toronto, Canada
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Aileen Kharat
4Pulmonology Dept, Hôpitaux Universitaires de Genève, Geneva, Switzerland
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Ema Swingwood
5University Hospitals Bristol NHS Foundation Trust, Adult Therapy Services, Bristol Royal Infirmary, Bristol, UK
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Luigi Pisani
6Intensive Care, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Maxime Patout
7Rouen University Hospital, Rouen, France
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Lieuwe D. Bos
6Intensive Care, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands
8Respiratory Medicine, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Lieuwe D. Bos
  • For correspondence: l.d.bos@amc.uva.nl
Raffaele Scala
9Pulmonology and Respiratory Intensive Care Unit, S. Donato Hospital, Arezzo, Italy
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Marcus J. Schultz
6Intensive Care, Amsterdam UMC, Location AMC, University of Amsterdam, Amsterdam, the Netherlands
10Mahidol-Oxford Tropical Medicine Research Unit (MORU), Mahidol University, Bangkok, Thailand
11Nuffield Dept of Medicine, University of Oxford, Oxford, UK
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Leo Heunks
12Intensive Care, Amsterdam UMC, Location VUmc, Amsterdam, the Netherlands
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Abstract

The Respiratory Intensive Care Assembly of the European Respiratory Society is delighted to present the highlights from the 2019 International Congress in Madrid, Spain. We have selected four sessions that discussed recent advances in a wide range of topics: from acute respiratory failure to cough augmentation in neuromuscular disorders and from extra-corporeal life support to difficult ventilator weaning. The subjects are summarised by early career members in close collaboration with the Assembly leadership. We aim to give the reader an update on the most important developments discussed at the conference. Each session is further summarised into a short list of take-home messages.

Abstract

The #ERSCongress in Madrid had some great sessions on respiratory intensive care. This article highlights the most important sessions. http://bit.ly/2GtT0qL

Hot topic: acute respiratory failure

A European Respiratory Society statement on chest imaging in acute respiratory failure

Paolo Navalesi summarised the main findings of a European Respiratory Society (ERS) Task Force, that was recently published as an ERS statement on chest imaging in acute respiratory failure in the European Respiratory Journal [1]. The statement highlights the characteristics, clinical indications and limitations of five imaging techniques: chest radiography, chest computed tomography (CT), lung ultrasound (LUS), positron emission tomography (PET), and electrical impedance tomography.

The accuracy of the portable chest radiograph to detect pulmonary abnormalities consistent with acute respiratory distress syndrome (ARDS) is severely limited [2]. The gold standard in diagnosing ARDS is the chest CT, which can reveal typical abnormalities like parenchymal distortions, reticular opacities, ground-glass opacifications and consolidations [1]. More recently, LUS has been evaluated for the diagnosis of ARDS. The typical LUS pattern of ARDS is characterised by multiple B-lines usually coalescent and not well separated; this is different from the B-lines seen with cardiogenic pulmonary oedema. LUS may also encompass pleural line and subpleural abnormalities, consolidations and spared areas in ARDS [3]. Positron emission tomography has a very limited role in bedside management of ARDS [1].

The correlation between changes in lung water and changes on chest radiography, e.g. in the context of cardiac failure, is poor [4]. However, absence of multiple bilateral B-lines on LUS, a sign of increased extravascular lung water, excludes cardiogenic pulmonary oedema with a very high negative-predictive value [5]. Therefore, LUS may be more sensitive for detecting increased extravascular lung water than chest radiography.

Since CT is more sensitive than chest radiography in detecting pulmonary infiltrates in patients with a clinical suspicion of pneumonia, CT modifies the likelihood of diagnosing community-acquired pneumonia (CAP) in almost two-third of cases [6]. The pooled sensitivity and specificity of LUS for pneumonia are very high [7]. Therefore, it may seem timely to include LUS and/or chest CT in the diagnostic processes of CAP.

Both LUS and chest radiography are highly specific for detection of a pneumothorax. Additionally, while the specificity of LUS and CXR for pneumothorax is quite comparable, the sensitivity of LUS is much higher than that of CXR [8]. CT remains the gold standard, but it requires transportation to the scanner and risks associated with radiation exposure. While LUS is very useful for detecting pneumothorax [9], there is discussion about the reliability of LUS to determine the extension and exact location. LUS seems superior to chest radiography when compared to CT, but it remains unclear when LUS examination is sufficient to withhold CT examination for this purpose [10, 11].

Take-home messages

  • LUS and chest CT are increasingly taking a prominent role in the diagnostic process of ARDS and pneumonia;

  • LUS is more sensitive for the detection of pneumothorax than chest radiography, but cannot determine the extent of the pneumothorax requiring additional investigation with chest CT.

A worldwide perspective of ventilator management

Marcus Schultz summarised the findings of three recent large service reviews of ventilator management in intensive care unit (ICU) patients: 1) the “Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure” (LUNG SAFE) [12]; 2) the “PRactice of VENTilation in patients without ARDS” (PRoVENT) study [13]; and 3) the recently finished “PRactice of VENTilation in Middle-income Countries” (PRoVENT-iMiC) study [14].

There is convincing evidence for benefit of ventilation with a low tidal volume (VT) in patients with ARDS [15]. Ventilation with a low VT may also benefit patients without ARDS, especially when a low VT is compared to a high VT [16]. A recent randomised controlled trial of ventilation with a low VT versus ventilation with an intermediate VT showed no benefit of VT reduction in patients without ARDS [17]. It should be noted, though, that most patients in this study were receiving spontaneous ventilation during which setting the support to achieve a target VT is difficult if not impossible, attenuating the gap between the two study groups [18]. Thus, caution should be used when extrapolating the findings of this study concerning the potential clinical impact of larger VT differences. Overall, the evidence favours the use of ventilation with a low VT to improve outcomes in invasive mechanically ventilated patients who have a variety of diseases other than ARDS [19].

While high positive end-expiratory pressure (PEEP) may protect patients with moderate-to-severe ARDS [20], this may not be the case in patients with mild ARDS in whom it could actually be harmful. Evidence for benefit of high PEEP, and actually of PEEP at any level, is currently lacking for patients not having ARDS [21].

Approximately half of patients with ARDS in LUNG SAFE [22] and patients without ARDS in PRoVENT [23] received lung protective ventilation with a low VT and PEEP. While awaiting a detailed report on PRoVENT–iMiC [14], it can already be concluded that lung protective ventilation is also used in ICUs where resources are low.

There is increasing interest in driving pressure, the difference between the end-inspiratory plateau pressure and PEEP, as this parameter has a strong association with mortality and morbidity in patients with [22, 24], as well as in patients without, ARDS [23].

One recently published post hoc analysis of LUNG SAFE revealed that female ARDS patients are at a higher risk of receiving ventilation with a too high a VT than male ARDS patients (figure 1) [25]. One of the reasons for this alarming sex difference could be the use of a (too large) fixed VT in men and women, but also the difference in height between males and females could play a role [26]. Most strikingly, compared to males the mortality rates were significantly higher in females when ARDS was severe, and it could very well be that VT settings play a role.

FIGURE 1
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 1

Results from a recent post hoc analysis of LUNG SAFE. a) Cumulative frequency distribution of tidal volume in males and females. b) Odds ratios (OR) for intensive care unit (ICU) and hospital mortality of males versus females by ARDS severity at day 2 (resolved, mild, moderate and severe). #: male (ref. female). Reproduced from [25] with permission.

Take-home messages

  • Low VT ventilation is likely to benefit all patients, not only those with ARDS;

  • It is uncertain if a high PEEP strategy in patients without ARDS is beneficial;

  • Female patients with ARDS are possibly harmed by too high a VT due to fixed VT settings on mechanical ventilators.

A worldwide perspective on weaning from mechanical ventilation

Leo Heunks presented a preliminary analysis of the “Worldwide Assessment of Separation of Patients from Ventilatory Assistance” (WEAN SAFE) study, which is currently being analysed.

Longer duration of ventilation after the first separation attempt is associated with increased mortality and longer length of ICU stay [27, 28]. Weaning is a costly and critical process that comprises numerous hurdles [29–32], and there is a remarkable lack of standardisation in definitions or evidence-based practices of what should be the best course to take [27, 32, 34].

The WEAN SAFE study will answer several questions regarding weaning practices. The WEAN SAFE study ran in up to 500 centres worldwide, more than half of them located in Europe, and enrolled over 6000 patients receiving invasive ventilation for >2 days. The WEAN SAFE study collected detailed information regarding ventilation, the weaning process, presence of comorbidities and previous health status in terms of frailty. Barbara Johnson, representative for the European Lung Foundation and co-presenter with Leo Heunks, emphasised the importance of the patients' perspective in this type of study, including patient relevant outcome measures.

Take-home messages

  • There is variable practice in weaning due to a lack of standardisation;

  • The WEAN-SAFE study will provide insights into the common practices. This information is important to inform future intervention studies.

A bridge to lung transplantation in end-stage right-sided heart failure

Olaf Mercier summarised the current evidence for the benefit of extracorporeal life support (ECLS) as a bridge to lung transplantation for pulmonary arterial hypertension (PAH) leading to refractory right-sided heart failure (RHF).

Lung transplantation is the gold standard treatment for refractory RHF caused by PAH. Candidate selection should be performed by centres with extensive expertise, given the complexity of decisions and the demanding surgical procedure [35]. PAH triggers right ventricle remodelling to which some patients adapt worse than others [36]. Thus, ECLS should be initiated when secondary organ failures and/or terminal RHF is imminent despite optimised medical therapy [37]. Lung transplantation presents as a definitive solution for unloading the RV [38]. Timely decisions are crucial. Lower stroke volumes and higher right atrial pressures are associated with worse outcomes. Biomarkers are not useful to enlist a patient for lung transplantation [39].

Veno-arterial extracorporeal membrane oxygenation (ECMO) is the most commonly used type of ECLS as a bridge to lung transplantation for PAH patients [40]. Other ECLS techniques, such as pulmonary artery-left atrium communications, are also used, though much less often. The logical case is to propose ECLS as bridge to lung transplantation and activate an emergency organ allocation, which has been a successful formula for long-term survival [40–43]. Adequate time under ECLS prior to lung transplantation is still a matter of ongoing debate [44].

Take-home messages

  • Lung transplantation is the only treatment for refractory RHF due to PAH;

  • Veno-arterial ECMO can be initiated as a bridge to transplantation, but timing remains an important issue.

State-of-the-art session: respiratory critical care

Non-pharmacological strategies to prevent hospitalisation in advanced stable COPD

Annalisa Carlucci first addressed the topic of preventing readmission after a first exacerbation and then talked about how to prevent hospitalisation, independently of a previous exacerbation.

Preventing the readmission of COPD patients after a first exacerbation

Some factors can have a role in preventing patient's readmission following a COPD exacerbation.

Peri-exacerbation pulmonary rehabilitation

According to the European COPD Audit, a previous hospital admission is the strongest risk factor for readmission [45] and has a greater impact than age and comorbidities. The reason of this can be found in several insults occurring during the hospitalisation itself, including immobility, systemic inflammation, treatment with corticosteroids, reduced dietary intake, and catabolic/anabolic imbalance, which generate sarcopenia, rapid deconditioning and increased disability. Pulmonary rehabilitation seems to be crucial to contrasting these factors and has proven to significantly reduce hospital readmission and mortality [46]. Unfortunately, the majority of patients who could benefit from a rehabilitative treatment after an exacerbation are not referred to a rehabilitation centre [47]. Furthermore, almost 60% of them are non-adherent to rehabilitation, mainly because they are not interested or they feel too sick/frail [48].

Home noninvasive ventilation

Home noninvasive ventilation (NIV) after an acute COPD exacerbation, in case of persistent hypercapnia (arterial carbon dioxide tension >53 mmHg) 2–4 weeks after resolution of respiratory acidaemia, can improve admission-free survival as compared to home oxygen alone, according to Murphy et al. [49]. In contrast, Struik et al. [50] found no difference in terms of exacerbation rate and survival between patients randomised to NIV and patients randomised to standard treatment. However, the two studies differ in the time of starting NIV as in the latter study NIV was started 48 h after recovery from the acute event, which could explain the discordant results.

Treatment of concomitant obstructive sleep apnea

The incidence of obstructive sleep apnoea (OSA) in patients with pre-existing COPD hospitalised for pulmonary rehabilitation was found to reach 45% in patients screened with a polysomnography [51]. Concomitant OSA is an important risk factor for the need for invasive or noninvasive mechanical ventilation and longer hospital stays in hospitalised patients with COPD [52]. Furthermore, patients with both OSA and COPD showed a higher exacerbation rate (15% versus 8%, p=0.04) and lower survival (p<0.001) compared to COPD only patients with the same severity of obstruction and medical treatment [53]. Continuous positive airway pressure treatment was able to reduce the risk of exacerbation and improve survival to the level of that of patients with COPD alone.

Care bundles

Care bundles are a set of interventions and evidence-based practices that, when used together, significantly improve the process of care and patient outcomes (www.ihi.org).

A recent systematic review found that the use of care bundles reduced the risk of hospital readmissions compared to usual care [54]. In a randomised study [55] health coaching significantly reduced the rate of re-hospitalisation at 1, 3 and 6 months compared to usual care.

In summary, a suggested flowchart after an acute exacerbation requiring mechanical ventilation could be as follows. 1) Check for residual functional activity and consider rehabilitation. 2) Perform polygraphic/polysomnographic screening once the patient is stable to exclude the presence of OSA that can be treated with continuous positive airway pressure as a first level of treatment. 3) In cases of persistent hypercapnia (≥53 mmHg) wait 2–4 weeks and re-perform an arterial blood gas analysis and, if hypercapnia persists, treat with home NIV. 4) Care bundles have the potential to reduce the risk of hospital readmissions.

Prevention of exacerbation and hospitalisation in severe COPD, irrespective of a previous exacerbation

Although supported by less evidence, there are factors that can contribute to exacerbations and be modified.

The ability to use inhalers

In a recent study, a considerable percentage of patients made critical errors while using inhalers and in these patients the risk of exacerbation was significantly higher than in patients taking the drug correctly [56]. Therefore, training patients and regularly verifying their proficiency in the use of inhaler devices appears crucial to reducing the risk of exacerbations and hospitalisation.

Role of high-flow nasal cannula

In patients with chronic hypoxemic respiratory failure secondary to COPD, when used for at least 8 h·day−1, high-flow nasal cannula (HFNC) significantly reduced the risk of exacerbation and hospitalisation, as compared to standard oxygen therapy. This result was mainly ascribed to the effect of HFNC on improving clearance of secretions [57].

Preventing pneumonia

More than 30% of COPD exacerbations were found to be related to pneumonia [58]. These pneumonic exacerbations were associated with higher 30-day mortality as compared to non-pneumonic exacerbations (12% versus 8%, equivalent to an adjusted HR of 1.21).

The following factors may increase the risk of pneumonia. 1) The use of inhaled corticosteroids [59]. In fact, a recent panel expert recommendation paper [60] in patients with no exacerbations in the last 3 months and a normal blood eosinophil count, recommended inhaled corticosteroid withdrawal. 2) The presence of swallowing dysfunction. Its prevalence was found to correlate with the level of obstruction [61] reaching a higher rate in patients with more severe obstruction and with the frequency of exacerbation [62].

Role of tele-assistance

The use of telemedicine was found to prevent hospitalisation in COPD patients [63]. However, data are still controversial as in another randomised controlled trial [64] telemedicine did not prevent admissions compared to the control group.

Take-home messages

  • Education training in inhaler device use is crucial;

  • HFNC for >8 h a day may help to reduce exacerbations;

  • Assess possible withdrawal of ICS in patients with no exacerbations in the last 3 months and the risk of swallowing dysfunction, especially in patients with frequent exacerbations and more severe obstruction;

  • Further studies are needed to establish which patients can really benefit from telemedicine.

Non-invasive respiratory assistance to prevent intubation in acute respiratory failure

Professor Stefano Nava outlined the evidence on noninvasive respiratory support strategies for acute respiratory failure, which include supplementary oxygen, HFNC and NIV. Invasive tools comprise invasive ventilation and extracorporeal carbon dioxide removal (ECCO2R).

Hypercapnic respiratory failure

Supplemental oxygen must be used with caution in COPD patients, ideally targeting an oxygen saturation measured pulse oximetry of 88–92% [65]. High levels of oxygen are potentially dangerous especially in out of hospital settings [66], while abrupt withdrawal may induce a dangerous rebound hypoxaemia [67].

HFNC can reduce dead space fraction and as such reduce work of breathing in patients with COPD, although less effectively compared to NIV [68, 69]. Other potential beneficial effects of HFNC include humidification resulting in improved airway clearance. In addition, high inspiratory oxygen fraction can be delivered, although it is often not necessary in patients with acute exacerbation of COPD (AECOPD).

The only randomised controlled trial comparing HFNC with NIV in COPD with acute moderate hypercapnic failure showed that both strategies are equally effective [70], but trials are ongoing (e.g. ClinicalTrials.gov NCT03370666). Of note, HFNC has been used between NIV sessions, resulting in reduced dyspnoea sensation, although no reduction in total time on NIV [71].

The use of NIV in COPD patients with acute or acute on chronic respiratory failure with acidosis (pH<7.35 with no lower limit) remains the best practice [72], except for patients immediately meeting criteria for endotracheal intubation.

ECCO2R, or lung dialysis, is a technique that allows removal of arterial carbon dioxide, using a low flow veno-venous device [73]. It has been proposed in patients with COPD at high risk of failing NIV, or to expedite extubation in hypercapnic patients. Meta-analysis of pioneer studies suggest that the combined use of ECCO2R and NIV reduces arterial carbon dioxide tension, increases pH and lowers respiratory rate, but adverse events such as haemorrhage, thrombocytopenia, circuit clotting and pump malfunctions are relatively frequent [74]. ECCO2R was further discussed in the symposium on extra-corporeal support, which is summarised below.

Hypoxic respiratory failure

The role of NIV is limited, irrespective of the underlying disease and the oxygenation defect in ARDS [75], as the risk of NIV failure is high and delayed intubation increases the risk of death [76]. Importantly, higher VT are associated with NIV failure [77].

HFNC is superior to oxygen therapy for re-intubation prevention in low-risk patients [78] and is equivalent to NIV in patients at high risk [79] and in cardiothoracic surgery patients [80]. In CAP patients there was no difference between treatments in the primary analysis but benefits of HFNC versus NIV or standard oxygen were seen in a post hoc analysis in patients with arterial oxygen tension (PaO2)/inspiratory oxygen fraction (FIO2) <200 mmHg [81]. Jean-Pierre Frat discussed the current evidence for HFNC in another symposium, which is summarised below.

Take-home messages

  • Noninvasive mechanical ventilation has the best evidence for acute hypercapnic respiratory failure. In moderate hypercapnia, HFNC may be an alternative;

  • For acute hypoxemic respiratory failure, HFNC is generally preferred over NIV.

Strategies to prevent diaphragm and lung injury in ventilated patients during partially supported ventilation

After reviewing the physiology of respiratory drive [82], Leo Heunks addressed the topic of partially supported modes of ventilation and the risk of lung injury in patients with ARDS. According to data from the LUNG SAFE observational study [83], around 70% of patients with mild ARDS are ventilated using a partially supported mode, and almost 50% of patients with severe ARDS (PaO2/FIO2 ratio <100) exhibit a spontaneous breathing effort.

It is known that the match between severe lung injury and spontaneous breathing with high breathing effort is injurious. In a study by Yoshida et al. [84] rabbits were divided into four different groups according to the level of lung injury (mild or severe) and to the ventilator mode used (assisted or controlled). After 4 h of ventilation in rabbits with mild lung injury there were no differences in the mode used. While in those with severe lung injury, the presence of spontaneous breathing efforts dramatically increased the severity of lung injury.

Four mechanisms play a role in lung injury related to spontaneous breathing efforts: 1) transpulmonary pressure [85]; 2) transvascular pressure [86]; 3) patient ventilator asynchronies; and 4) pendelluft.

Leo Heunks then discussed the concept of patient self-inflicted lung injury (P-SILI) [87] as a mechanism of lung injury related to spontaneous breathing effort and explained how increased pressure swings caused by the patient's increased respiratory drive generate this injury.

Diaphragm injury

It is already well known that excessive unloading of the diaphragm by mechanical ventilation with no (or too low) residual effort by the patient leads to disuse atrophy, loss of muscle mass and weakness [88]. Only 3–4 days of mechanical ventilation were enough to determine a decrease in pressure generating capacity of the diaphragm of 25% [89]. Furthermore, disuse atrophy was evident after 2–3 days of controlled mechanical ventilation in brain dead patients [90]. It is less recognised that also insufficient loading by the ventilator (too low support) causes injury of the diaphragm and weakness. In a study by Hooijman et al. [91] biopsies of the diaphragm were performed in patients ventilated for a few days and who underwent thoracic surgery. The biopsies revealed fibre atrophy with tissue injury and inflammation and sarcomeric disruption, consistent with load-induced injury. Therefore, in patients with high respiratory drive, partially supported modes may result in both patient P-SILI and patient self-inflicted respiratory muscle injury.

How do we protect the diaphragm and lung in in those patients? How could we control the respiratory drive?

Modulation of drive: change assist

Reducing the level of pressure support may not change tidal volume, as the patient will increase the effort and the respiratory drive [92]. Therefore, the transpulmonary pressure will remain unchanged, as will the damage to the lung.

Modulation of drive: sedation with propofol and the use of neuromuscular blockers

Sedation with propofol can reduce VT and respiratory drive [93]. While, remifentanil (or any other opioid) is only able to change the respiratory rate and not modulate the respiratory drive [94]. If we are not able to control the respiratory drive with high doses of propofol, the introduction of neuromuscular blockers is probably useful. In fact, the use of neuromuscular blockers in the early stages of ARDS was found to reduce mortality in one study [92], although this was disputed in a larger and more recent randomised controlled trial [95].

Modulation of drive: partial relaxation

By titrating rocuronium we can probably modulate the respiratory drive. This would lead to a reduction of the VT to a safe range and the work of breathing to a physiological range.

Modulation of drive: ECCO2R

This could be a further experimental way to modulate the respiratory drive. In fact, in patients with ARDS, increasing ECMO flow can decrease VT and the pressure generated by the respiratory muscles [96].

To summarise, in a patient with high respiratory drive, a reasonable approach could be: 1) to reduce the level of pressure support, monitoring the VT; 2) if the VT does not change, increase the level of sedation; and 3) if the respiratory drive is not controlled with sedation, introduce neuromuscular blockers, being aware that by inducing muscle inactivity they potentially increase the risk of respiratory muscle dysfunction. However, excessive activity of the diaphragm is probably more damaging than inactivity.

Improving outcomes in interstitial lung disease patients mechanically ventilated in the ICU

Alexandre Demoule focused on outcomes and treatment strategies for interstitial lung disease (ILD) patients in the ICU. “We can only improve” was the take home message as the mortality of ILD patients exceeds 50% [97], with mechanical ventilation as a primary risk factor [98]. NIV and HFNC are scarcely explored and should not delay intubation. NIV probably retains more risks than benefits [99], and P-SILI (see above) is possible also with HFNC.

How to ventilate our ILD patient?

The decision to “not intubate” should be considered if there is no plan for recovery or transplantation. If intubation is performed, we are still lacking guidelines on ventilation settings and strategies. Translation from ARDS literature may not be feasible as we face similarities (bilateral lung injury, hypoxaemia, low compliance) but also key differences (lung recruitment and poorer reversibility). Lung protective ventilation with low PEEP may lead the way [100] as the potential for recruitability is probably low. ECMO is an option in candidates for lung transplantation [101]. Diagnostic workout must be aggressive in order to recognise and treat exacerbation factors for idiopathic pulmonary fibrosis/ILD.

Take-home messages

  • Patients with ILD undergoing mechanical ventilation are at a very high likelihood of mortality;

  • Advance care directives should be set for patients in whom there is no chance of recovery and no possibility for transplantation;

  • Mechanical ventilation in patients with pre-existent ILD should not aim at recruitment of lung with high PEEP.

Integrated strategies for acute NIV

Bronchoscopy during NIV

Raffaele Scala presented the current evidence for bronchoscopy as a diagnostic tool in patients undergoing NIV, especially in immunocompromised patients or in patients with ILD or in patients with hospital-acquired pneumonia [102]. Bronchoscopy is also used as a therapeutic tool to treat atelectasis or to perform airway clearance. However, bronchoscopy increases airway resistance by reducing tracheal lumen by 20% and by inducing bronchospasm. That results in an increased work of breathing that may affect the patient up to 2 h following the bronchoscopy [103]. Respiratory deterioration can occur in up to 35% of patients [102]. It has been shown that bronchoscopy in immunocompromised patients may worsen their outcome probably because it was performed after intubation during invasive ventilation in 61% of the cases [104].

As NIV decreases the work of breathing, its use during bronchoscopy may improve patients' outcome. It has been shown that the use of NIV during bronchoalveolar lavage in patients with acute respiratory failure improved its diagnostic yield [105]. However, there is still a lack of data to support such management. Performing bronchoscopy in patients with acute respiratory failure under NIV needs to be discussed and the risk–benefit balance assessed. If bronchoscopy is decided, the ventilator settings should be adjusted, as well as the interface [106]. The bronchoscopy needs to be performed by an experienced team regarding bronchoscopy and NIV. If necessary, the patient can be sedated using propofol during the procedure [107].

Take-home messages

  • Bronchoscopy during NIV can be used for diagnostic and therapeutic purposes and the two are complementary under specific circumstances;

  • There is sparse data on the safety and added value of bronchoscopy during NIV specifically;

  • Studies in immunocompromised ICU patients show that bronchoscopy may not be as safe as once thought especially if performed after intubation.

Acute respiratory failure: high-flow nasal oxygen and NIV

Jeanne-Pierre Frat presented the current approach to acute respiratory failure using NIV and HFNC. In patients with acute hypoxaemic respiratory failure, there is no recommendation for or against the use of NIV [72]. It has been suggested that the use of NIV may contribute to P-SILI [87]. Indeed, some patients with hypoxaemic respiratory failure exhibit a high respiratory drive and therefore have a high VT during NIV [108].

HFNC has predictable effects on end-expiratory pressure [109], reduces the anatomical dead space [110] and so decreases the work of breathing [111] in patients with acute hypoxaemic failure. It's use in these patients has been evaluated in a prospective randomised controlled trial that showed an improvement in survival with the use of HFNC [80]. In this study, intubation rate was not statistically different with the use of HFNC in the all population. However, subgroup analysis showed a benefit in the cohort of patients with the most severe hypoxaemic failure (PaO2/FIO2 ratio<200 mmHg). In immunocompromised patients, no benefit was shown for the use of HFNC on intubation rate or mortality [112]. However, a meta-analysis does suggest a benefit in this group of patients [113].

Take-home messages

  • NIV is not recommended in acute hypoxaemic respiratory failure;

  • HFNC is a safe alternative to standard oxygen in hypoxaemic acute respiratory failure;

  • There is conflicting evidence regarding the benefit of HFNC, especially in immunocompromised patients.

Mechanical insufflation–exsufflation devices and NIV

Miguel Goncalves explored the benefits and implementation options of using mechanical insufflation–exsufflation (MI-E) as a combined treatment option. It is well documented that NIV is the optimal treatment choice for hypercapnic respiratory failure (see summary of previous symposium). In this vulnerable patient group, secretion encumbrance is often present due to either an ineffective cough, or a defect to the muco-ciliary escalator. As a result, a comprehensive cough assessment in this specific population may be warranted and beneficial to informing timely treatment interventions.

Cough is as essential defence mechanism and previous research has highlighted critical thresholds where treatment is indicated. In a patient with a peak cough flow of ≤270 L·min−1 prophylactic cough augmentation is recommended due to the impact of a chest infection resulting in a further reduction in cough strength to ≤180 L·min−1 when no effective airway clearance will occur. In this situation a patient is at increased risk of retained secretions, ineffective secretion clearance and, therefore, repeated chest infections.

MI-E is a device that aids secretion clearance. This device augments inspiratory and expiratory flow to improve secretion mobilisation, through rapidly alternating positive and negative pressure, approximating normal cough [114]. Its possible benefits are clearing retained secretions and managing secretion load. These overlap with the contra-indications for NIV, giving rise to the question: could MI-E augment NIV?

The evidence base for MI-E is growing but is predominantly based in a neuromuscular population at present. It is known whether this device augments peak cough flow [114, 115]. Complications during home use are rare and include abdominal distension, pneumothoraxes, bradycardia and nausea [116–119].

More recently the safety of MI-E has been examined in endotracheally intubated patients. An observational study [120] reported no adverse events during MI-E use in these patients. The study authors concluded that MI-E may be safe and effective in the intubated population, but further work is required [120]. There are some commonly accepted contra-indications for the use of MI-E (table 1).

View this table:
  • View inline
  • View popup
TABLE 1

Relative and absolute contraindications to the use of mechanical insufflation–exsufflation

Miguel Goncalves went on to explore the wider application of MI-E in four main clinical situations. It requires emphasis that there is a very small evidence base for the application of MI-E in any of these situations at this moment in time: 1) early application to prevent intubation in the emergency department; 2) following early extubation and to facilitate rapid weaning; 3) the prevention/resolution of post-extubation failure; 4) in patients with chronic home mechanical ventilation to prevent hospitalisation.

Early MI-E application to prevent intubation in the emergency department

NIV is often used in the emergency department. Miguel Goncalves speculated that this is an opportunity for MI-E use with the aim of preventing intubation. Servera et al. [121] demonstrated the ability of NIV and MI-E to avoid the need for intubation in a group of neuromuscular patients with acute respiratory failure. A cohort prospective study completed in 17 patients (24 care episodes) reported that the noninvasive management was successful in preventing intubation in 79% of the episodes. Severe bulbar impairment was also found to be a limiting factor. An important limitation of the study was the small sample size and the lack of a randomised control group.

MI-E use following early extubation to facilitate rapid weaning and prevent post-extubation failure

A definition of “readiness to wean” as part of an extubation criteria often includes a manageable secretion load [122]. Early extubation may be challenging if there is a remaining secretion load. The need to await normalisation of secretions was very much challenged during this talk and a pro-active approach was championed. In those patients with secretions it was questioned whether they ever meet the criteria of a true manageable secretion load, thus making them “unweanable”. Miguel Goncalves hypothesised that there is a role for MI-E under these circumstances, especially in conjunction with NIV [123].

A randomised controlled trial examined the added value of MI-E in 75 critically ill adults intubated for >48 h [124]. They found significant reductions in re-intubation rate (48% versus 17%), mechanical ventilation duration and ICU length of stay. More recent trials demonstrate the superiority of MI-E in aspirated sputum weight, static lung compliance, airway resistance and work of breathing [125, 126]. Limitations of these studies impact their applicability. There is a general lack of long-term follow-up, and no investigation concerning patient and clinician perceived barriers and facilitators to use of MI-E in ventilated patients.

A recent Cochrane review [127] of cough augmentation techniques for extubation/weaning from mechanical ventilation identified only three trials for inclusion. The authors concluded that the role of cough augmentation techniques in prevention of extubation failure is unclear and additional robust research, including understanding intervention safety and intensity, is essential. Furthermore, despite emerging evidence in the intubated population a recent UK survey has highlighted limited adoption of this device in the intubated population [128].

Take-home messages

  • MI-E seems to be a safe intervention for home use in patients with neuromuscular disease;

  • There is less evidence for the use of MI-E in conjunction with invasive or noninvasive mechanical ventilation;

  • Future applications of MI-E might be to prevent intubation in patients with otherwise unmanageable secretions by allowing NIV or to facilitate early extubation and mediate weaning failure.

Analgo-sedation and NIV

Lara Pisani provided a clear overview of the available medications and the role they should play to facilitate NIV.

Sedation may sometimes be necessary but we have to ensure the respiratory drive is not abolished. Furthermore, the right drug needs to be used for the right patient. The key features of “the right” drug in combination with NIV are to: 1) improve comfort, reduce anxiety and increase tolerance; 2) perform procedures; 3) alleviate dyspnoea and achieve comfort in the palliative care setting.

Ideally, clinicians are looking for a drug that is short-acting, has a constant half-life, no accumulation in case of renal or liver failure, no impact on respiratory drive or haemodynamic status and has both anxiolytic and analgesic properties. Brochard et al. [129] reviewed common analgesics used in the ICU (table 2). Treatment effects should be monitored using the Richmond Agitation Sedation Scale or the Ramsay Sedation Scale.

View this table:
  • View inline
  • View popup
TABLE 2

Common analgesics used in the intensive care unit

A survey of sedation practices during NIV was performed more than a decade ago [130] with the aim of establishing what was the current practice towards sedation use during NIV. Authors reported that clinicians were using sedation and analgesic therapy infrequently but also highlighted that clinical practice was found to vary depending on clinical specialty and geographical area. There were seldom protocols in place and there was no assessment of outcomes to guide ongoing prescription titrations. It should be noted that this survey is now over 10 years old and so may not accurately reflect the practice of today.

Take-home messages

  • Sedation is not always required during NIV;

  • There is not a single drug of choice and the drug should be matched with the patient;

  • Analgesic sedation may reduce agitation due to NIV and improve tolerability;

  • Once analgesic sedation is started, the effect should be monitored using validated sedation scales and this should guide subsequent treatment decisions.

ECMO

ECMO in ARDS

Benjamin Seeliger started this symposium by outlining the evidence for veno-venous ECMO in severe ARDS. As discussed previously in this highlight paper, ARDS is a common cause of acute respiratory failure with a high mortality and, currently, only strategies that limit ventilator induced lung injury have shown to improve outcomes [12].

The emergence of severe ARDS with severe refractory hypoxaemia such as seen in the H1N1 pandemic was accompanied with an increased use of veno-venous ECMO. With this, the CESAR trial was published comparing ECMO versus conventional management in severe ARDS [131]. The results showed no significant difference in the survival between the treatments. The primary end-point was a composite end-point considering survival at 6 months without disability. It is important to underline a particularity in the design of the study: only one centre in the UK provided the ECMO technique which may have induced a centre-effect bias.

The high mortality of ARDS and questioning surrounding the positive effect of ECMO use led to the conception of the EOLIA trial [132]. This multicentre randomised clinical trial with a rescue therapy cross-over possibility compared early initiation of ECMO therapy to standard therapy in patients with severe ARDS. 68 centres across France participated, with a total of 249 patients undergoing randomisation. The inclusion criteria were patients with severe ARDS on mechanical ventilation for <7 days, persistent low PaO2/FIO2 despite standard ARDS treatment (e.g. protective ventilation, prone position, neuromuscular blocker use). The randomisation was stratified by centre and on the duration of the ventilation (cut-off 72 h). Patients in the control group were allowed to cross over to ECMO therapy (rescue therapy) if they had persistent severe hypoxaemia and on the discretion of the physician in charge. The primary end-point of mortality at 60 days was not statistically significant (−11% absolute risk) based on an estimated mortality of 60% in the conventional group and a power of 80%. It is important to specify that 35 patients underwent rescue ECMO therapy, which corresponds to 28% of the control group. These patients can account for a possible dilution effect of ECMO therapy in this intention to treat trial. The expected mortality of these patients without cross-over to ECMO therapy would probably be higher than the mortality of 60% presented for the statistical analysis. The secondary end-points, among which were treatment failure at 60 days, length of stay and days free of mechanical ventilation, were significantly better in the ECMO group. The safety profile of ECMO use was good and there were no significant differences between groups on bleedings. The trial was also stopped prematurely (the sample size needed was 75%) as the effect of ECMO could not be achieved. This could be due to the ambitious estimated effect size of 20% on the mortality due to treatment with ECMO. A Bayesian re-analyses of this trial showed that there is a likely positive effect of ECMO under a broad set of assumptions [133]. In clinical practice, this translates to the adoption of ECMO for very severe ARDS in expert centres.

Take-home messages

  •  Veno-venous ECMO is an accepted rescue treatment for ARDS patients with persistent severe hypoxaemia;

  •  The currently available evidence suggests a reduction in mortality in patients treated with veno-venous ECMO.

ECCO2R: a method for the future?

Vito Fanelli talked about the potential indications regarding ECCO2R. These include: AECOPD, ARDS and acute kidney failure requiring renal substitution therapy. The mechanism of ECCO2R is to clear the arterial carbon dioxide through a venous canula with a blood flow of 350–1000 mL·min−1. Importantly, it has no significant effect on oxygenation.

The aim of ECCO2R in ARDS is to provide carbon dioxide control in order to reduce the need for a larger VT to minimise ventilator-induced lung injury. As discussed in the previous sections of this article, ventilator-induced lung injury prevention is the most important treatment in ARDS. The SUPERNOVA trial assessed the feasibility and efficacy of the association of ECCO2R to ultra-protective ventilation in patients with moderate ARDS and an expected mechanical ventilation >24 h [134]. The use of ECCO2R facilitated the achievement of ultra-protective ventilation. The VT, plateau pressure and driving pressure were diminished while maintaining the same level of arterial carbon dioxide. Complications described with ECCO2R were canula haemorrhage requiring incidental blood transfusion.

AECOPD is a frequent complication that is typically associated with hypercapnia. In recent years, NIV has become a cornerstone in the treatment of hypercapnic exacerbation (see previous sections) with a positive effect on mortality. With the development of ECCO2R, its role in AECOPD treatment was questioned, especially considering the existing high rate of NIV failure [135]. In 2014, Del Sorbo et al. [136] studied the use of ECCO2R in AECOPD patients at risk of NIV failure to avoid oro-tracheal intubation. This match–control cohort study established that ECCO2R seemed to be safe and efficient in this group of patients. These observations need to be confirmed with future randomised control trials.

Recently, the place of ECCO2R in acute kidney failure requiring continuous renal replacement therapy has been studied. Acute kidney failure can be associated with multiple organ dysfunction syndrome and need for mechanical ventilation. All these elements lead to inflammation, cell apoptosis and humoral mediators release. In an open-label interventional clinical trial, Fanelli et al. [137] showed that there could be an improvement in renal function and lower levels of inflammatory mediators using ECCO2R and continuous renal replacement therapy in patients with ARDS and acute kidney failure. The hypothesis is a possible “cross-talk” between the lung and kidney leading to reduced mechanical stress and, therefore, less inflammatory response.

Take-home messages

  • ECCO2R can reduce the risk of ventilator-induced lung injury in moderate ARDS allowing achievement of protective mechanical ventilation by clearing the arterial carbon dioxide tension;

  • It may diminish the need for mechanical ventilation in patients with hypercapnic exacerbation of COPD if associated to NIV;

  • ECCO2R may interrupt the cross-talk lung/kidney interaction in patients with acute kidney failure which could result in a lower level of inflammation;

  • All these findings are preliminary and require validation in larger randomised controlled trials.

Mechanical ventilation in ECMO

Christoph Fisser spoke on how to set the ventilator during ECMO in ARDS. The standard care for all patients with ARDS involves the concept of “baby lung”. Protective ventilation is considered protective when a VT of 6 mL·kg−1 (ideal weight)/min and a plateau pressure <30 cmH20 are used. In real life it can be difficult to achieve this, as shown in a large observational international study (LUNG SAFE) [12] and as discussed in the talk by Marcus Schultz (see previous section in this article).

Gattinoni et al. [138] developed an equation called mechanical power which can be a surrogate for lung stress and, therefore, ventilator-related lung injury:Embedded Image where ΔV is the tidal volume, RR is the respiratory rate, ELrs is the elastance of the respiratory system, I:E is the inspiratory-to-expiratory time ratio, and Raw is the airway resistance. In theory, at least different variables of this equation can be adapted and improved with optimal ventilatory settings. For example, we know that VT reduction effectively limits lung injury [15]. Data suggest that ventilation with very low VT (3 mL·kg−1 predicted body weight) during ECMO [139] could be effective in the reduction of the inflammatory response. The respiratory rate is also a variable in the equation. Based on the data available in the LUNG SAFE study, patients with a lower respiratory rate had better survival [12]. Taking these two variables together, animal data indeed suggest that near apnoeic ventilation would have a reductive effect on lung inflammation [140].

With the limited evidence available for VT and respiratory rate it seems that the lower is the better. But it is important to bear in mind that the lowest is not the best. There are some side-effects of very low driving pressure and respiratory rate such as de-recruitment, which may result in oxygenation disturbances requiring a higher ECMO blood flow.

As discussed in the lecture by Leo Heunks in a previous sections, Christoph Fisser further emphasised the importance of navigating the balance between P-SILI and minimisation of sedation and muscle relaxation. The weaning of patients on ECMO and mechanical ventilation should be anticipated and discussed at the moment of cannulation. There are various algorithms available produced by different centres, but there are no evidence-based guidelines.

Take-home messages

  • Veno-venous ECMO could facilitate more protective mechanical ventilation and hereby limit lung injury and improve outcomes;

  • Calculation of mechanical power is an attractive method to estimate the damage that is potentially done by mechanical ventilation and provides a rationale for decreasing VT and respiratory rate;

  • More evidence is needed regarding the optimal ventilator settings during ECMO.

Neuro-prognostication in ECMO

Mirko Belliato discussed the prognostication of neurological outcome during ECMO. It is widely accepted that ECMO with arterio-venous cannulation is associated with 15% of neurological complications. In ECMO with veno-venous cannulation, the possible neurological complication can be linked to a reduced cerebral flow secondary to a rapid carbon dioxide level correction. With the increasing use of veno-venous ECMO in acute respiratory failure, there is more and more attention focused on the neurocognitive (dys)function of patients receiving ECMO and much can be learned from studies in a post-cardiac arrest indication. Different predictors of survival and neurological outcome are developed that aim is to help identify patients at risk of neurological complication and determinate level of impairment.

Electroencephalogram

In the first 24 h of ECMO, the presence of crisis, micro-voltage and reduced cerebral activity or micro-burst suppression contributes to early prediction of poor outcome [141].

Near-infrared-spectroscopy

This noninvasive technique measures the change in brain oxygenation. It can suggest a difference in the cerebral perfusion. A low near-infrared-spectroscopy is associated with a rapid onset poor outcome (risk of cerebral oedema development) and might be used to guide treatment in patients undergoing ECMO [142].

Biomarkers

The evidence for biomarkers in prognostication of neurological outcomes is premature. One biomarker that is frequently studied is neuron specific enolases. Levels of this molecule >75 μg·L−1 in the first 24–72 h is a sign of severe neuronal lesion [143]. Another molecule that was studied is the S-100 protein, but it has a low sensitivity which limits the potential application.

To date, none of these markers can be used clinically and should be used in a research setting.

Take-home messages

  • Prognostication of neurological outcomes during ECMO is difficult and most evidence comes from post-cardiac arrest veno-arterial ECMO;

  • Electroencephalogram, near-infrared-spectroscopy and biomarkers are being developed as prognostic tests but have not been validated sufficiently to allow for clinical application;

  • The findings in post-cardiac arrest patients are not directly applicable to ARDS patients undergoing veno-venous ECMO.

Closing remarks

This highlight paper discussed the most important sessions of the ERS Respiratory Intensive Care Assembly at the 2019 International Congress in Madrid. We summarised the recent advances in several topics that are highly relevant for pulmonologists, intensivists, nurses and researchers. We hope to see you next year at the International Congress in Vienna, Austria, and in the meantime follow us on Twitter @ERSAssembly2 or the ERS website.

Footnotes

  • Conflict of interest: C. Satici has nothing to disclose.

  • Conflict of interest: D. Lopez-Padilla has nothing to disclose.

  • Conflict of interest: A. Schreiber has nothing to disclose.

  • Conflict of interest: A. Kharat has nothing to disclose.

  • Conflict of interest: E. Swingwood has nothing to disclose.

  • Conflict of interest: L. Pisani has nothing to disclose.

  • Conflict of interest: M. Patout has nothing to disclose.

  • Conflict of interest: L.D. Bos reports grants from the Dutch lung foundation (Young Investigator grant and Public-Private Partnership grant), personal fees from Bayer (for consultancy), grants from the ERS (short-term fellowship) and grants from the Dutch Lung Foundation (Dirkje Postma Award), outside the submitted work.

  • Conflict of interest: R. Scala has nothing to disclose.

  • Conflict of interest: M. Schultz has nothing to disclose.

  • Conflict of interest: L. Heunks has nothing to disclose.

  • Received November 26, 2019.
  • Accepted January 23, 2020.
  • Copyright ©ERS 2020
http://creativecommons.org/licenses/by-nc/4.0/

This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.

References

  1. ↵
    1. Chiumello D,
    2. Sferrazza Papa GF,
    3. Artigas A, et al.
    ERS statement on chest imaging in acute respiratory failure. Eur Respir J 2019; 54: 1900435. doi:10.1183/13993003.00435-2019
    OpenUrlAbstract/FREE Full Text
  2. ↵
    1. Figueroa-Casas JB,
    2. Brunner N,
    3. Dwivedi AK, et al.
    Accuracy of the chest radiograph to identify bilateral pulmonary infiltrates consistent with the diagnosis of acute respiratory distress syndrome using computed tomography as reference standard. J Crit Care 2013; 28: 352–357. doi:10.1016/j.jcrc.2012.12.002
    OpenUrlCrossRefPubMed
  3. ↵
    1. Copetti R,
    2. Soldati G,
    3. Copetti P
    . Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome. Cardiovasc Ultrasound 2008; 6: 1–10. doi:10.1186/1476-7120-6-16
    OpenUrlCrossRefPubMed
  4. ↵
    1. Halperin BD,
    2. Feeley TW,
    3. Mihm FG, et al.
    Evaluation of the portable chest roentgenogram for quantitating extravascular lung water in critically ill adults. Chest 1985; 88: 649–652. doi:10.1378/chest.88.5.649
    OpenUrlCrossRefPubMed
  5. ↵
    1. Neskovic AN,
    2. Edvardsen T,
    3. Galderisi M, et al.
    Focus cardiac ultrasound: the European Association of Cardiovascular Imaging viewpoint. Eur Heart J Cardiovasc Imaging 2014; 15: 956–960. doi:10.1093/ehjci/jeu081
    OpenUrlCrossRefPubMed
  6. ↵
    1. Claessens YE,
    2. Debray MP,
    3. Tubach F, et al.
    Early chest computed tomography scan to assist diagnosis and guide treatment decision for suspected community-acquired pneumonia. Am J Respir Crit Care Med 2015; 192: 974–982. doi:10.1164/rccm.201501-0017OC
    OpenUrlCrossRefPubMed
  7. ↵
    1. Long L,
    2. Zhao HT,
    3. Zhang ZY, et al.
    Lung ultrasound for the diagnosis of pneumonia in adults: a meta-analysis. Med (Baltimore) 2017; 96: 1–6. doi:10.1097/MD.0000000000005713
    OpenUrl
  8. ↵
    1. Alrajhi K,
    2. Woo MY,
    3. Vaillancourt C
    . Test characteristics of ultrasonography for the detection of pneumothorax: a systematic review and meta-analysis. Chest 2012; 141: 703–708. doi:10.1378/chest.11-0131
    OpenUrlCrossRefPubMed
  9. ↵
    1. Volpicelli G,
    2. Boero E,
    3. Sverzellati N, et al.
    Semi-quantification of pneumothorax volume by lung ultrasound. Intensive Care Med 2014; 40: 1460–1467. doi:10.1007/s00134-014-3402-9
    OpenUrlCrossRefPubMed
  10. ↵
    1. Oveland NP,
    2. Lossius HM,
    3. Wemmelund K, et al.
    Using thoracic ultrasonography to accurately assess pneumothorax progression during positive pressure ventilation: a comparison with CT scanning. Chest 2013; 143: 415–422. doi:10.1378/chest.12-1445
    OpenUrlCrossRefPubMed
  11. ↵
    1. Soldati G,
    2. Testa A,
    3. Sher S, et al.
    Occult traumatic pneumothorax: diagnostic accuracy of lung ultrasonography in the emergency department. Chest 2008; 133: 204–211. doi:10.1378/chest.07-1595
    OpenUrlCrossRefPubMed
  12. ↵
    1. Bellani G,
    2. Laffey JG,
    3. Pham T, et al.
    Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA 2016; 315: 788–800. doi:10.1001/jama.2016.0291
    OpenUrlCrossRefPubMed
  13. ↵
    1. Neto AS,
    2. Barbas CS V,
    3. Simonis FD, et al.
    Epidemiological characteristics, practice of ventilation, and clinical outcome in patients at risk of acute respiratory distress syndrome in intensive care units from 16 countries (PRoVENT): an international, multicentre, prospective study. Lancet Respir Med 2016; 4: 882–893. doi:10.1016/S2213-2600(16)30305-8
    OpenUrl
  14. ↵
    1. Pisani L,
    2. Algera AG,
    3. Serpa Neto A, et al.
    PRactice of VENTilation in Middle-Income Countries (PRoVENT-iMIC): rationale and protocol for a prospective international multicentre observational study in intensive care units in Asia. BMJ Open 2018; 8: 1–9. doi:10.1136/bmjopen-2017-020841
    OpenUrlCrossRef
  15. ↵
    1. Brower RG,
    2. Matthay MA, et al.
    Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301–1308. doi:10.1056/NEJM200005043421801
    OpenUrlCrossRefPubMed
  16. ↵
    1. Serpa Neto A,
    2. Hemmes SNT,
    3. Barbas CS V, et al.
    Protective versus conventional ventilation for surgery. Anesthesiology 2015; 123: 66–78. doi:10.1097/ALN.0000000000000706
    OpenUrlCrossRefPubMed
  17. ↵
    1. Simonis FD,
    2. Serpa Neto A,
    3. Binnekade JM, et al.
    Effect of a low vs intermediate tidal volume strategy on ventilator-free days in intensive care unit patients without ARDS: a randomized clinical trial. JAMA 2018; 320: 1872–1880. doi:10.1001/jama.2018.14280
    OpenUrl
  18. ↵
    1. Simonis FD,
    2. Neto AS,
    3. Schultz MJ
    . The tidal volume fix and more… J Thorac Dis 2019; 11: E117–E122. doi:10.21037/jtd.2019.08.39
    OpenUrl
  19. ↵
    1. Rackley CR,
    2. MacIntyre NR
    . Low tidal volumes for everyone? Chest 2019; 156: 783–791. doi:10.1016/j.chest.2019.06.007
    OpenUrl
  20. ↵
    1. Briel M,
    2. Meade M,
    3. Mercat A, et al.
    Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA 2010; 303: 865–873. doi:10.1001/jama.2010.218
    OpenUrlCrossRefPubMed
  21. ↵
    1. Serpa Neto A,
    2. Filho RR,
    3. Cherpanath T, et al.
    Associations between positive end-expiratory pressure and outcome of patients without ARDS at onset of ventilation: a systematic review and meta-analysis of randomized controlled trials. Ann Intensive Care 2016; 6: 109. doi:10.1186/s13613-016-0208-7
    OpenUrl
  22. ↵
    1. Laffey JG,
    2. Bellani G,
    3. Pham TT, et al.
    Potentially modifiable factors contributing to outcome from acute respiratory distress syndrome: the LUNG SAFE study. Intensive Care Med 2016; 42: 1865–1876. doi:10.1007/s00134-016-4571-5
    OpenUrl
  23. ↵
    1. Simonis FD,
    2. Barbas CSV,
    3. Artigas-Raventós A, et al.
    Potentially modifiable respiratory variables contributing to outcome in ICU patients without ARDS: a secondary analysis of PRoVENT. Ann Intensive Care 2018; 8: 39. doi:10.1186/s13613-018-0385-7
    OpenUrl
  24. ↵
    1. Amato MBP,
    2. Meade MO,
    3. Slutsky AS, et al.
    Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med 2015; 372: 747–755. doi:10.1056/NEJMsa1410639
    OpenUrlCrossRefPubMed
  25. ↵
    1. McNicholas BA,
    2. Madotto F,
    3. Pham T, et al.
    Demographics, management and outcome of females and males with acute respiratory distress syndrome in the LUNG SAFE prospective cohort study. Eur Respir J 2019; 54: 1900609. doi:10.1183/13993003.00609-2019
    OpenUrlAbstract/FREE Full Text
  26. ↵
    LAS VEGAS Investigators. Epidemiology, practice of ventilation and outcome for patients at increased risk of postoperative pulmonary complications: LAS VEGAS – an observational study in 29 countries. Eur J Anaesthesiol 2017; 34: 492–507. doi:10.1097/EJA.0000000000000646
    OpenUrlCrossRefPubMed
  27. ↵
    1. Beduneau G,
    2. Pham T,
    3. Schortgen F, et al.
    Epidemiology of weaning outcome according to a new definition the WIND study. Am J Respir Crit Care Med 2017; 195: 772–783. doi:10.1164/rccm.201602-0320OC
    OpenUrlCrossRefPubMed
  28. ↵
    1. Maggiore SM,
    2. Battilana M,
    3. Serano L, et al.
    Ventilatory support after extubation in critically ill patients. Lancet Respir Med 2018; 6: 948–962. doi:10.1016/S2213-2600(18)30375-8
    OpenUrl
  29. ↵
    1. Routsi C,
    2. Stanopoulos I,
    3. Kokkoris S, et al.
    Weaning failure of cardiovascular origin: how to suspect, detect and treat – a review of the literature. Ann Intensive Care 2019; 9: 11–15. doi:10.1186/s13613-019-0481-3
    OpenUrl
    1. Baptistella AR,
    2. Sarmento FJ,
    3. da Silva KR, et al.
    Predictive factors of weaning from mechanical ventilation and extubation outcome: a systematic review. J Crit Care 2018; 48: 56–62. doi:10.1016/j.jcrc.2018.08.023
    OpenUrl
    1. Pham T,
    2. Brochard LJ,
    3. Slutsky AS
    . Mechanical ventilation: state of the art. Mayo Clin Proc 2017; 92: 1382–1400. doi:10.1016/j.mayocp.2017.05.004
    OpenUrl
  30. ↵
    1. Sklar MC,
    2. Burns K,
    3. Rittayamai N, et al.
    Effort to breathe with various spontaneous breathing trial techniques. Am J Respir Crit Care Med 2017; 195: 1477–1485. doi:10.1164/rccm.201607-1338OC
    OpenUrl
    1. Burns KEA,
    2. Soliman I,
    3. Adhikari NKJ, et al.
    Trials directly comparing alternative spontaneous breathing trial techniques: a systematic review and meta-analysis. Crit Care 2017; 21: 1–11. doi:10.1186/s13054-017-1698-x
    OpenUrl
  31. ↵
    1. Subirà C,
    2. Hernández G,
    3. Vázquez A, et al.
    Effect of pressure support vs T-piece ventilation strategies during spontaneous breathing trials on successful extubation among patients receiving mechanical ventilation: a randomized clinical trial. JAMA 2019; 321: 2175–2182. doi:10.1001/jama.2019.7234
    OpenUrl
  32. ↵
    1. Yusen RD,
    2. Christie JD,
    3. Edwards LB, et al.
    The registry of the International Society for Heart And Lung Transplantation: thirtieth adult lung and heart-lung transplant report – 2013; focus theme: Age. J Hear Lung Transplant 2013; 32: 965–978. doi:10.1016/j.healun.2013.08.007
    OpenUrl
  33. ↵
    1. Vonk Noordegraaf A,
    2. Westerhof BE,
    3. Westerhof N
    . The relationship between the right ventricle and its load in pulmonary hypertension. J Am Coll Cardiol 2017; 69: 236–243. doi:10.1016/j.jacc.2016.10.047
    OpenUrlFREE Full Text
  34. ↵
    1. Hoeper MM,
    2. Benza RL,
    3. Corris P, et al.
    Intensive care, right ventricular support and lung transplantation in patients with pulmonary hypertension. Eur Respir J 2019; 53: 1–12. doi:10.1183/13993003.01906-2018
    OpenUrl
  35. ↵
    1. Abrams D,
    2. Brodie D,
    3. Arcasoy SM
    . Extracorporeal life support in lung transplantation. Clin Chest Med 2017; 38: 655–666. doi:10.1016/j.ccm.2017.07.006
    OpenUrl
  36. ↵
    1. Weatherald J,
    2. Boucly A,
    3. Chemla D, et al.
    Prognostic value of follow-up hemodynamic variables after initial management in pulmonary arterial hypertension. Circulation 2018; 137: 693–704. doi:10.1161/CIRCULATIONAHA.117.029254
    OpenUrlAbstract/FREE Full Text
  37. ↵
    1. Gottlieb J,
    2. Greer M
    . Recent advances in extracorporeal life support as a bridge to lung transplantation. Expert Rev Respir Med 2018; 12: 217–225. doi:10.1080/17476348.2018.1433035
    OpenUrl
    1. De Perrot M,
    2. Granton JT,
    3. McRae K, et al.
    Impact of extracorporeal life support on outcome in patients with idiopathic pulmonary arterial hypertension awaiting lung transplantation. J Heart Lung Transplant 2011; 30: 997–1002. doi:10.1016/j.healun.2011.03.002
    OpenUrlCrossRefPubMed
    1. Savale L,
    2. Le Pavec J,
    3. Mercier O, et al.
    Impact of high-priority allocation on lung and heart-lung transplantation for pulmonary hypertension. Ann Thorac Surg 2017; 104: 404–411. doi:10.1016/j.athoracsur.2017.02.034
    OpenUrl
  38. ↵
    1. Hoopes CW,
    2. Kukreja J,
    3. Golden J, et al.
    Extracorporeal membrane oxygenation as a bridge to pulmonary transplantation. J Thorac Cardiovasc Surg 2013; 145: 862–868. doi:10.1016/j.jtcvs.2012.12.022
    OpenUrlCrossRefPubMed
  39. ↵
    1. Crotti S,
    2. Iotti GA,
    3. Lissoni A, et al.
    Organ allocation waiting time during extracorporeal bridge to lung transplant affects outcomes. Chest 2013; 144: 1018–1025. doi:10.1378/chest.12-1141
    OpenUrlCrossRefPubMed
  40. ↵
    1. Hartl S,
    2. Lopez-Campos JL,
    3. Pozo-Rodriguez F, et al.
    Risk of death and readmission of hospital-admitted COPD exacerbations: European COPD Audit. Eur Respir J 2016; 47: 113–121. doi:10.1183/13993003.01391-2014
    OpenUrlAbstract/FREE Full Text
  41. ↵
    1. Ryrsø CK,
    2. Godtfredsen NS,
    3. Kofod LM, et al.
    Lower mortality after early supervised pulmonary rehabilitation following COPD-exacerbations: a systematic review and meta-analysis. BMC Pulm Med 2018; 18: 154. doi:10.1186/s12890-018-0718-1
    OpenUrlCrossRefPubMed
  42. ↵
    1. Jones SE,
    2. Green SA,
    3. Clark AL, et al.
    Pulmonary rehabilitation following hospitalisation for acute exacerbation of COPD: referrals, uptake and adherence. Thorax 2014; 69: 181–182. doi:10.1136/thoraxjnl-2013-204227
    OpenUrlAbstract/FREE Full Text
  43. ↵
    1. Benzo R,
    2. Wetzstein M,
    3. Neuenfeldt P, et al.
    Implementation of physical activity programs after COPD hospitalizations: lessons from a randomized study. Chron Respir Dis 2015; 12: 5–10. doi:10.1177/1479972314562208
    OpenUrlCrossRefPubMed
  44. ↵
    1. Murphy PB,
    2. Rehal S,
    3. Arbane G, et al.
    Effect of home noninvasive ventilation with oxygen therapy vs oxygen therapy alone on hospital readmission or death after an acute COPD exacerbation. JAMA 2017; 317: 2177–2186. doi:10.1001/jama.2017.4451
    OpenUrl
  45. ↵
    1. Struik FM,
    2. Sprooten RTM,
    3. Kerstjens HAM, et al.
    Nocturnal non-invasive ventilation in COPD patients with prolonged hypercapnia after ventilatory support for acute respiratory failure: a randomised, controlled, parallel-group study. Thorax 2014; 69: 826–834. doi:10.1136/thoraxjnl-2014-205126
    OpenUrlAbstract/FREE Full Text
  46. ↵
    1. Schreiber A,
    2. Cemmi F,
    3. Ambrosino N, et al.
    Prevalence and predictors of obstructive sleep apnea in patients with chronic obstructive pulmonary disease undergoing inpatient pulmonary rehabilitation. COPD 2018; 15: 265–270. doi:10.1080/15412555.2018.1500533
    OpenUrl
  47. ↵
    1. Hirayama A,
    2. Goto T,
    3. Faridi MK, et al.
    Association of obstructive sleep apnoea with acute severity of chronic obstructive pulmonary disease exacerbation: a population-based study. Intern Med J 2018; 48: 1150–1153. doi:10.1111/imj.14016
    OpenUrl
  48. ↵
    1. Marin JM,
    2. Soriano JB,
    3. Carrizo SJ, et al.
    Outcomes in patients with chronic obstructive pulmonary disease and obstructive sleep apnea: the overlap syndrome. Am J Respir Crit Care Med 2010; 182: 325–331. doi:10.1164/rccm.200912-1869OC
    OpenUrlCrossRefPubMed
  49. ↵
    1. Ospina MB,
    2. Mrklas K,
    3. Deuchar L, et al.
    A systematic review of the effectiveness of discharge care bundles for patients with COPD. Thorax 2017; 72: 31–39. doi:10.1136/thoraxjnl-2016-208820
    OpenUrlAbstract/FREE Full Text
  50. ↵
    1. Benzo R,
    2. Vickers K,
    3. Novotny PJ, et al.
    Health coaching and chronic obstructive pulmonary disease rehospitalization: a randomized study. Am J Respir Crit Care Med 2016; 194: 672–680. doi:10.1164/rccm.201512-2503OC
    OpenUrlCrossRefPubMed
  51. ↵
    1. Molimard M,
    2. Raherison C,
    3. Lignot S, et al.
    Chronic obstructive pulmonary disease exacerbation and inhaler device handling: real-life assessment of 2935 patients. Eur Respir J 2017; 49: 1601794. doi:10.1183/13993003.01794-2016
    OpenUrlAbstract/FREE Full Text
  52. ↵
    1. Storgaard LH,
    2. Hockey HU,
    3. Laursen BS, et al.
    Long-term effects of oxygen-enriched high-flow nasal cannula treatment in COPD patients with chronic hypoxemic respiratory failure. Int J Chron Obstruct Pulmon Dis 2018; 13: 1195–1205. doi:10.2147/COPD.S159666
    OpenUrl
  53. ↵
    1. Søgaard M,
    2. Madsen M,
    3. Løkke A, et al.
    Incidence and outcomes of patients hospitalized with COPD exacerbation with and without pneumonia. Int J Chron Obstruct Pulmon Dis 2016; 11: 455–465. doi:10.2147/COPD.S96179
    OpenUrl
  54. ↵
    1. Kew K,
    2. Seniukovich A
    . Inhaled steroids and risk of pneumonia for chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2014; 3: CD010115. doi:10.1002/14651858.CD010115.pub2
    OpenUrlPubMed
  55. ↵
    1. Avdeev S,
    2. Aisanov Z,
    3. Arkhipov V, et al.
    Withdrawal of inhaled corticosteroids in COPD patients: rationale and algorithms. Int J Chron Obstruct Pulmon Dis 2019; 14: 1267–1280. doi:10.2147/COPD.S207775
    OpenUrl
  56. ↵
    1. Lindh MG,
    2. Johansson MB,
    3. Jennische M, et al.
    Prevalence of swallowing dysfunction screened in Swedish cohort of COPD patients. Int J Chron Obstruct Pulmon Dis 2017; 12: 331–337. doi:10.2147/COPD.S120207
    OpenUrl
  57. ↵
    1. Terada K,
    2. Muro S,
    3. Ohara T, et al.
    Abnormal swallowing reflex and COPD exacerbations. Chest 2010; 137: 326–332. doi:10.1378/chest.09-0482
    OpenUrlCrossRefPubMed
  58. ↵
    1. Vitacca M,
    2. Bianchi L,
    3. Guerra A, et al.
    Tele-assistance in chronic respiratory failure patients: a randomised clinical trial. Eur Respir J 2009; 33: 411–418. doi:10.1183/09031936.00005608
    OpenUrlAbstract/FREE Full Text
  59. ↵
    1. Ringbæk T,
    2. Green A,
    3. Laursen LC, et al.
    Effect of tele health care on exacerbations and hospital admissions in patients with chronic obstructive pulmonary disease: a randomized clinical trial. Int J Chron Obstruct Pulmon Dis 2015; 10: 1801–1808. doi:10.2147/COPD.S85596
    OpenUrlPubMed
  60. ↵
    1. Davidson AC,
    2. Banham S,
    3. Elliott M, et al.
    BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults. Thorax 2016; 71: Suppl. 2, ii1–i35. doi:10.1136/thoraxjnl-2015-208209
    OpenUrlFREE Full Text
  61. ↵
    1. O'Driscoll BR,
    2. Beasley R
    . Avoidance of high concentration oxygen in chronic obstructive pulmonary disease. BMJ 2010; 341: c5549. doi:10.1136/bmj.c5549
    OpenUrlFREE Full Text
  62. ↵
    1. Kane B,
    2. Turkington PM,
    3. Howard LS, et al.
    Rebound hypoxaemia after administration of oxygen in an acute exacerbation of chronic obstructive pulmonary disease. BMJ 2011; 342: d1557. doi:10.1136/bmj.d1557
    OpenUrlFREE Full Text
  63. ↵
    1. Spoletini G,
    2. Alotaibi M,
    3. Blasi F, et al.
    Heated humidified high-flow nasal oxygen in adults: mechanisms of action and clinical implications. Chest 2015; 148: 253–261. doi:10.1378/chest.14-2871
    OpenUrlCrossRefPubMed
  64. ↵
    1. Pisani L,
    2. Fasano L,
    3. Corcione N, et al.
    Change in pulmonary mechanics and the effect on breathing pattern of high flow oxygen therapy in stable hypercapnic COPD. Thorax 2017; 72: 373–375. doi:10.1136/thoraxjnl-2016-209673
    OpenUrlAbstract/FREE Full Text
  65. ↵
    1. Lee MK,
    2. Choi J,
    3. Park B, et al.
    High flow nasal cannulae oxygen therapy in acute-moderate hypercapnic respiratory failure. Clin Respir J 2018; 12: 2046–2056. doi:10.1111/crj.12772
    OpenUrl
  66. ↵
    1. Spoletini G,
    2. Mega C,
    3. Pisani L, et al.
    High-flow nasal therapy vs standard oxygen during breaks off noninvasive ventilation for acute respiratory failure: a pilot randomized controlled trial. J Crit Care 2018; 48: 418–425. doi:10.1016/j.jcrc.2018.10.004
    OpenUrl
  67. ↵
    1. Rochwerg B,
    2. Brochard L,
    3. Elliott MW, et al.
    Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J 2017; 50: 1602426. doi:10.1183/13993003.02426-2016
    OpenUrlAbstract/FREE Full Text
  68. ↵
    1. Boyle AJ,
    2. Sklar MC,
    3. McNamee JJ, et al.
    Extracorporeal carbon dioxide removal for lowering the risk of mechanical ventilation: research questions and clinical potential for the future. Lancet Respir Med 2018; 6: 874–884. doi:10.1016/S2213-2600(18)30326-6
    OpenUrl
  69. ↵
    1. Sklar MC,
    2. Beloncle F,
    3. Katsios CM, et al.
    Extracorporeal carbon dioxide removal in patients with chronic obstructive pulmonary disease: a systematic review. Intensive Care Med 2015; 41: 1752–1762. doi:10.1007/s00134-015-3921-z
    OpenUrl
  70. ↵
    1. Ferrer M,
    2. Esquinas A,
    3. Leon M, et al.
    Noninvasive ventilation in severe hypoxemic respiratory failure. Am J Respir Crit Care Med 2003; 168: 1438–1444. doi:10.1164/rccm.200301-072OC
    OpenUrlCrossRefPubMed
  71. ↵
    1. Carrillo A,
    2. Gonzalez-Diaz G,
    3. Ferrer M, et al.
    Non-invasive ventilation in community-acquired pneumonia and severe acute respiratory failure. Intensive Care Med 2012; 38: 458–466. doi:10.1007/s00134-012-2475-6
    OpenUrlCrossRefPubMed
  72. ↵
    1. Carteaux G,
    2. Millán-Guilarte T,
    3. De Prost N, et al.
    Failure of noninvasive ventilation for de novo acute hypoxemic respiratory failure. Crit Care Med 2016; 44: 282–290. doi:10.1097/CCM.0000000000001379
    OpenUrl
  73. ↵
    1. Hernández G,
    2. Vaquero C,
    3. González P, et al.
    Effect of postextubation high-flow nasal cannula vs conventional oxygen therapy on reintubation in low-risk patients: a randomized clinical trial. JAMA 2016; 315: 1354–1361. doi:10.1001/jama.2016.2711
    OpenUrl
  74. ↵
    1. Hernández G,
    2. Vaquero C,
    3. Colinas L, et al.
    Effect of postextubation high-flow nasal cannula vs noninvasive ventilation on reintubation and postextubation respiratory failure in high-risk patients. JAMA 2016; 316: 1565–1574. doi:10.1001/jama.2016.14194
    OpenUrlCrossRefPubMed
  75. ↵
    1. Stéphan F,
    2. Barrucand B,
    3. Petit P, et al.
    High-flow nasal oxygen vs noninvasive positive airway pressure in hypoxemic patients after cardiothoracic surgery. JAMA 2015; 313: 2331. doi:10.1001/jama.2015.5213
    OpenUrlCrossRefPubMed
  76. ↵
    1. Frat J-P,
    2. Thille AW,
    3. Mercat A, et al.
    High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N Engl J Med 2015; 372: 2185–2196. doi:10.1056/NEJMoa1503326
    OpenUrlCrossRefPubMed
  77. ↵
    1. Feldman JL,
    2. Del Negro CA
    . Looking for inspiration: new perspectives on respiratory rhythm. Nat Rev Neurosci 2006; 7: 232–242. doi:10.1038/nrn1871
    OpenUrlCrossRefPubMed
  78. ↵
    1. Bellani G,
    2. Laffey JG,
    3. Pham T, et al.
    Noninvasive ventilation of patients with acute respiratory distress syndrome: insights from the LUNG SAFE study. Am J Respir Crit Care Med 2017; 195: 67–77. doi:10.1164/rccm.201606-1306OC
    OpenUrl
  79. ↵
    1. Yoshida T,
    2. Nakahashi S,
    3. Nakamura MAM, et al.
    Volume-controlled ventilation does not prevent injurious inflation during spontaneous effort. Am J Respir Crit Care Med 2017; 196: 590–601. doi:10.1164/rccm.201610-1972OC
    OpenUrl
  80. ↵
    1. Slutsky AS,
    2. Ranieri VM
    . Ventilator-induced lung injury. N Engl J Med 2013; 369: 2126–2136. doi:10.1056/NEJMra1208707
    OpenUrlCrossRefPubMed
  81. ↵
    1. Yoshida T,
    2. Fujino Y,
    3. Amato MBP, et al.
    Fifty years of research in ARDS spontaneous breathing during mechanical ventilation risks, mechanisms, and management. Am J Respir Crit Care Med 2017; 195: 985–992. doi:10.1164/rccm.201604-0748CP
    OpenUrl
  82. ↵
    1. Brochard L,
    2. Slutsky A,
    3. Pesenti A
    . Mechanical ventilation to minimize progression of lung injury in acute respiratory failure. Am J Respir Crit Care Med 2017; 195: 438–442. doi:10.1164/rccm.201605-1081CP
    OpenUrl
  83. ↵
    1. Dres M,
    2. Goligher EC,
    3. Heunks LMA, et al.
    Critical illness-associated diaphragm weakness. Intensive Care Med 2017; 43: 1441–1452. doi:10.1007/s00134-017-4928-4
    OpenUrl
  84. ↵
    1. Jaber S,
    2. Petrof BJ,
    3. Jung B, et al.
    Rapidly progressive diaphragmatic weakness and injury during mechanical ventilation in humans. Am J Respir Crit Care Med 2011; 183: 364–371. doi:10.1164/rccm.201004-0670OC
    OpenUrlCrossRefPubMed
  85. ↵
    1. Levine S,
    2. Nguyen T,
    3. Taylor N, et al.
    Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans. N Engl J Med 2008; 358: 1327–1335. doi:10.1056/NEJMoa070447
    OpenUrlCrossRefPubMed
  86. ↵
    1. Hooijman PE,
    2. Beishuizen A,
    3. Witt CC, et al.
    Diaphragm muscle fiber weakness and ubiquitin-proteasome activation in critically ill patients. Am J Respir Crit Care Med 2015; 191: 1126–1138. doi:10.1164/rccm.201412-2214OC
    OpenUrlCrossRefPubMed
  87. ↵
    1. Doorduin J,
    2. Nollet JL,
    3. Roesthuis LH, et al.
    Partial neuromuscular blockade during partial ventilatory support in sedated patients with high tidal volumes. Am J Respir Crit Care Med 2017; 195: 1033–1042. doi:10.1164/rccm.201605-1016OC
    OpenUrl
  88. ↵
    1. Vaschetto R,
    2. Cammarota G,
    3. Colombo D, et al.
    Effects of propofol on patient-ventilator synchrony and interaction during pressure support ventilation and neurally adjusted ventilatory assist. Crit Care Med 2014; 42: 74–82. doi:10.1097/CCM.0b013e31829e53dc
    OpenUrlCrossRefPubMed
  89. ↵
    1. Costa R,
    2. Navalesi P,
    3. Cammarota G, et al.
    Remifentanil effects on respiratory drive and timing during pressure support ventilation and neurally adjusted ventilatory assist. Respir Physiol Neurobiol 2017; 244: 10–16. doi:10.1016/j.resp.2017.06.007
    OpenUrl
  90. ↵
    1. Moss M,
    2. Huang DT, et al.
    National Heart Lung and Blood Institute PETAL Clinical Trials Network, Moss M, Huang DT, et al. Early neuromuscular blockade in the acute respiratory distress syndrome. N Engl J Med 2019; 380: 1997–2008. doi:10.1056/NEJMoa1901686
    OpenUrl
  91. ↵
    1. Mauri T,
    2. Grasselli G,
    3. Suriano G, et al.
    Control of respiratory drive and effort in extracorporeal severe acute respiratory distress syndrome. Crit Care Med 2016; 125: 159–167.
    OpenUrl
  92. ↵
    1. Huapaya JA,
    2. Wilfong EM,
    3. Harden CT, et al.
    Risk factors for mortality and mortality rates in interstitial lung disease patients in the intensive care unit. Eur Respir Rev 2018; 27: 180061. doi:10.1183/16000617.0061-2018
    OpenUrlAbstract/FREE Full Text
  93. ↵
    1. Durheim MT,
    2. Judy J,
    3. Bender S, et al.
    In-hospital mortality in patients with idiopathic pulmonary fibrosis: a US cohort study. Lung 2019; 197: 699–707. doi:10.1007/s00408-019-00270-z
    OpenUrl
  94. ↵
    1. Aliberti S,
    2. Messinesi G,
    3. Gamberini S, et al.
    Non-invasive mechanical ventilation in patients with diffuse interstitial lung diseases. BMC Pulm Med 2014; 14: 194. doi:10.1186/1471-2466-14-194
    OpenUrlCrossRefPubMed
  95. ↵
    1. Fernández-Pérez ER,
    2. Yilmaz M,
    3. Jenad H, et al.
    Ventilator settings and outcome of respiratory failure in chronic interstitial lung disease. Chest 2008; 133: 1113–1119. doi:10.1378/chest.07-1481
    OpenUrlCrossRefPubMed
  96. ↵
    1. Trudzinski FC,
    2. Kaestner F,
    3. Schäfers H-J, et al.
    Outcome of patients with interstitial lung disease treated with extracorporeal membrane oxygenation for acute respiratory failure. Am J Respir Crit Care Med 2016; 193: 527–533. doi:10.1164/rccm.201508-1701OC
    OpenUrl
  97. ↵
    1. Cracco C,
    2. Fartoukh M,
    3. Prodanovic H, et al.
    Safety of performing fiberoptic bronchoscopy in critically ill hypoxemic patients with acute respiratory failure. Intensive Care Med 2013; 39: 45–52. doi:10.1007/s00134-012-2687-9
    OpenUrlCrossRefPubMed
  98. ↵
    1. Scala R,
    2. Pisani L
    . Noninvasive ventilation in acute respiratory failure: which recipe for success? Eur Respir Rev 2018; 27: 180029. doi:10.1183/16000617.0029-2018
    OpenUrlAbstract/FREE Full Text
  99. ↵
    1. Bauer PR,
    2. Chevret S,
    3. Yadav H, et al.
    Diagnosis and outcome of acute respiratory failure in immunocompromised patients after bronchoscopy. Eur Respir J 2019; 54: 1802442. doi:10.1183/13993003.02442-2018
    OpenUrlAbstract/FREE Full Text
  100. ↵
    1. Agarwal R,
    2. Khan A,
    3. Aggarwal AN, et al.
    Bronchoscopic lung biopsy using noninvasive ventilatory support: case series and review of literature of NIV-assisted bronchoscopy. Respir Care 2012; 57: 1927–1936. doi:10.4187/respcare.01775
    OpenUrlAbstract/FREE Full Text
  101. ↵
    1. Ergan B,
    2. Nava S
    . The use of bronchoscopy in critically ill patients: considerations and complications. Expert Rev Respir Med 2018; 12: 651–663. doi:10.1080/17476348.2018.1494576
    OpenUrl
  102. ↵
    1. Clouzeau B,
    2. Bui H-N,
    3. Guilhon E, et al.
    Fiberoptic bronchoscopy under noninvasive ventilation and propofol target-controlled infusion in hypoxemic patients. Intensive Care Med 2011; 37: 1969–1975. doi:10.1007/s00134-011-2375-1
    OpenUrlPubMed
  103. ↵
    1. Frat J-P,
    2. Ragot S,
    3. Coudroy R, et al.
    Predictors of intubation in patients with acute hypoxemic respiratory failure treated with a noninvasive oxygenation strategy. Crit Care Med 2018; 46: 208–215. doi:10.1097/CCM.0000000000002818
    OpenUrl
  104. ↵
    1. Mauri T,
    2. Turrini C,
    3. Eronia N, et al.
    Physiologic effects of high-flow nasal cannula in acute hypoxemic respiratory failure. Am J Respir Crit Care Med 2017; 195: 1207–1215. doi:10.1164/rccm.201605-0916OC
    OpenUrl
  105. ↵
    1. Möller W,
    2. Celik G,
    3. Feng S, et al.
    Nasal high flow clears anatomical dead space in upper airway models. J Appl Physiol 2015; 118: 1525–1532. doi:10.1152/japplphysiol.00934.2014
    OpenUrlCrossRefPubMed
  106. ↵
    1. Delorme M,
    2. Bouchard PA,
    3. Simon M, et al.
    Effects of high-flow nasal cannula on the work of breathing in patients recovering from acute respiratory failure. Crit Care Med 2017; 45: 1981–1988. doi:10.1097/CCM.0000000000002693
    OpenUrl
  107. ↵
    1. Azoulay E,
    2. Lemiale V,
    3. Mokart D, et al.
    Effect of high-flow nasal oxygen vs standard oxygen on 28-day mortality in immunocompromised patients with acute respiratory failure. JAMA 2018; 320: 2099–2107. doi:10.1001/jama.2018.14282
    OpenUrl
  108. ↵
    1. Huang H-B,
    2. Peng J-M,
    3. Weng L, et al.
    High-flow oxygen therapy in immunocompromised patients with acute respiratory failure: a review and meta-analysis. J Crit Care 2018; 43: 300–305. doi:10.1016/j.jcrc.2017.09.176
    OpenUrl
  109. ↵
    1. Chatwin M,
    2. Toussaint M,
    3. Gonçalves MR, et al.
    Airway clearance techniques in neuromuscular disorders: a state of the art review. Respir Med 2018; 136: 98–110. doi:10.1016/j.rmed.2018.01.012
    OpenUrl
  110. ↵
    1. Lacombe M,
    2. Del Amo Castrillo L,
    3. Boré A, et al.
    Comparison of three cough-augmentation techniques in neuromuscular patients: mechanical insufflation combined with manually assisted cough, insufflation-exsufflation alone and insufflation-exsufflation combined with manually assisted cough. Respiration 2014; 88: 215–222. doi:10.1159/000364911
    OpenUrlPubMed
  111. ↵
    1. Homnick DN
    . Mechanical insufflation-exsufflation for airway mucus clearance. Respir Care 2007; 52: 1296–1305.
    OpenUrlAbstract/FREE Full Text
    1. Schmitt JK,
    2. Stiens S,
    3. Trincher R, et al.
    Survey of use of the insufflator-exsufflator in patients with spinal cord injury. J Spinal Cord Med 2007; 30: 127–130. doi:10.1080/10790268.2007.11753923
    OpenUrlPubMed
    1. Crew JD,
    2. Svircev JN,
    3. Burns SP
    . Mechanical insufflation-exsufflation device prescription for outpatients with tetraplegia. J Spinal Cord Med 2010; 33: 128–134. doi:10.1080/10790268.2010.11689687
    OpenUrlPubMed
  112. ↵
    1. Suri P,
    2. Burns SP,
    3. Bach JR
    . Pneumothorax associated with mechanical insufflation-exsufflation and related factors. Am J Phys Med Rehabil 2008; 87: 951–955. doi:10.1097/PHM.0b013e31817c181e
    OpenUrlCrossRefPubMed
  113. ↵
    1. Sánchez-García M,
    2. Santos P,
    3. Rodríguez-Trigo G, et al.
    Preliminary experience on the safety and tolerability of mechanical “insufflation-exsufflation” in subjects with artificial airway. Intensive Care Med Exp 2018; 6: 8. doi:10.1186/s40635-018-0173-6
    OpenUrl
  114. ↵
    1. Servera E,
    2. Sancho J,
    3. Zafra MJ, et al.
    Alternatives to endotracheal intubation for patients with neuromuscular diseases. Am J Phys Med Rehabil 2005; 84: 851–857. doi:10.1097/01.phm.0000184097.17189.93
    OpenUrlCrossRefPubMed
  115. ↵
    1. Mehta S
    . Neuromuscular disease causing acute respiratory failure. Respir Care 2006; 51: 1016–1021.
    OpenUrlAbstract/FREE Full Text
  116. ↵
    1. Terzi N,
    2. Lofaso F,
    3. Masson R, et al.
    Physiological predictors of respiratory and cough assistance needs after extubation. Ann Intensive Care 2018; 8: 18. doi:10.1186/s13613-018-0360-3
    OpenUrl
  117. ↵
    1. Gonçalves MR,
    2. Honrado T,
    3. Winck JC, et al.
    Effects of mechanical insufflation-exsufflation in preventing respiratory failure after extubation: a randomized controlled trial. Crit Care 2012; 16: R48. doi:10.1186/cc11249
    OpenUrlCrossRefPubMed
  118. ↵
    1. Bach JR,
    2. Sinquee DM,
    3. Saporito LR, et al.
    Efficacy of mechanical insufflation-exsufflation in extubating unweanable subjects with restrictive pulmonary disorders. Respir Care 2015; 60: 477–483. doi:10.4187/respcare.03584
    OpenUrlAbstract/FREE Full Text
  119. ↵
    1. de Camillis ML F,
    2. Savi A,
    3. Goulart Rosa R, et al.
    Effects of mechanical insufflation-exsufflation on airway mucus clearance among mechanically ventilated ICU subjects. Respir Care 2018; 63: 1471–1477. doi:10.4187/respcare.06253
    OpenUrlAbstract/FREE Full Text
  120. ↵
    1. Rose L,
    2. Adhikari NK,
    3. Leasa D, et al.
    Cough augmentation techniques for extubation or weaning critically ill patients from mechanical ventilation. Cochrane Database Syst Rev 2017; 1: CD011833. doi:10.1002/14651858.CD011833.pub2
    OpenUrl
  121. ↵
    1. Swingwood E,
    2. Tume L,
    3. Cramp F
    . A survey examining the use of mechanical insufflation-exsufflation on adult intensive care units across the UK. J Intensive Care Soc 2019https://doi.org/10.1177/1751143719870121.
  122. ↵
    1. Brochard L,
    2. Lefebvre J-C,
    3. Cordioli R, et al.
    Noninvasive ventilation for patients with hypoxemic acute respiratory failure. Semin Respir Crit Care Med 2014; 35: 492–500. doi:10.1055/s-0034-1383863
    OpenUrlCrossRefPubMed
  123. ↵
    1. Devlin JW,
    2. Nava S,
    3. Fong JJ, et al.
    Survey of sedation practices during noninvasive positive-pressure ventilation to treat acute respiratory failure. Crit Care Med 2007; 35: 2298–2302. doi:10.1097/01.CCM.0000284512.21942.F8
    OpenUrlCrossRefPubMed
  124. ↵
    1. Peek GJ,
    2. Mugford M,
    3. Tiruvoipati R, et al.
    Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet 2009; 374: 1351–1363. doi:10.1016/S0140-6736(09)61069-2
    OpenUrlCrossRefPubMed
  125. ↵
    1. Combes A,
    2. Hajage D,
    3. Capellier G, et al.
    Extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. N Engl J Med 2018; 378: 1965–1975. doi:10.1056/NEJMoa1800385
    OpenUrl
  126. ↵
    1. Goligher EC,
    2. Tomlinson G,
    3. Hajage D, et al.
    Extracorporeal membrane oxygenation for severe acute respiratory distress syndrome and posterior probability of mortality benefit in a post hoc Bayesian analysis of a randomized clinical trial. JAMA 2018; 320: 2251–2259. doi:10.1001/jama.2018.14276
    OpenUrl
  127. ↵
    1. Combes A,
    2. Fanelli V,
    3. Pham T, et al.
    Feasibility and safety of extracorporeal CO2 removal to enhance protective ventilation in acute respiratory distress syndrome: the SUPERNOVA study. Intensive Care Med 2019; 45: 592–600. doi:10.1007/s00134-019-05567-4
    OpenUrl
  128. ↵
    1. Chandra D,
    2. Stamm JA,
    3. Taylor B, et al.
    Outcomes of noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease in the United States, 1998–2008. Am J Respir Crit Care Med 2012; 185: 152–159. doi:10.1164/rccm.201106-1094OC
    OpenUrlCrossRefPubMed
  129. ↵
    1. Del Sorbo L,
    2. Cypel M,
    3. Fan E
    . Extracorporeal life support for adults with severe acute respiratory failure. Lancet Respir Med 2014; 2: 154–164. doi:10.1016/S2213-2600(13)70197-8
    OpenUrl
  130. ↵
    1. Fanelli V,
    2. Cantaluppi V,
    3. Alessandri F, et al.
    Extracorporeal CO2 removal may improve renal function of patients with acute respiratory distress syndrome and acute kidney injury: an open-label, interventional clinical trial. Am J Respir Crit Care Med 2018; 198: 687–690. doi:10.1164/rccm.201712-2575LE
    OpenUrl
  131. ↵
    1. Gattinoni L,
    2. Tonetti T,
    3. Cressoni M, et al.
    Ventilator-related causes of lung injury: the mechanical power. Intensive Care Med 2016; 42: 1567–1575. doi:10.1007/s00134-016-4505-2
    OpenUrl
  132. ↵
    1. Bein T,
    2. Weber-Carstens S,
    3. Goldmann A, et al.
    Lower tidal volume strategy (≈3 ml/kg) combined with extracorporeal CO2 removal versus ‘conventional’ protective ventilation (6 ml/kg) in severe ARDS. Intensive Care Med 2013; 39: 847–856. doi:10.1007/s00134-012-2787-6
    OpenUrlCrossRefPubMed
  133. ↵
    1. Araos J,
    2. Alegria L,
    3. Garcia P, et al.
    Near-apneic ventilation decreases lung injury and fibroproliferation in an acute respiratory distress syndrome model with extracorporeal membrane oxygenation. Am J Respir Crit Care Med 2019; 199: 603–612. doi:10.1164/rccm.201805-0869OC
    OpenUrl
  134. ↵
    1. Sondag L,
    2. Ruijter BJ,
    3. Tjepkema-Cloostermans MC, et al.
    Early EEG for outcome prediction of postanoxic coma: prospective cohort study with cost-minimization analysis. Crit Care 2017; 21: 111. doi:10.1186/s13054-017-1693-2
    OpenUrl
  135. ↵
    1. Pozzebon S,
    2. Ortiz AB,
    3. Franchi F, et al.
    Cerebral near-infrared spectroscopy in adult patients undergoing veno-arterial extracorporeal membrane oxygenation. Neurocrit Care 2018; 29: 94–104. doi:10.1007/s12028-018-0512-1
    OpenUrl
  136. ↵
    1. Schrage B,
    2. Rübsamen N,
    3. Becher PM, et al.
    Neuron-specific-enolase as a predictor of the neurologic outcome after cardiopulmonary resuscitation in patients on ECMO. Resuscitation 2019; 136: 14–20. doi:10.1016/j.resuscitation.2019.01.011
    OpenUrl
PreviousNext
Back to top
Vol 6 Issue 1 Table of Contents
ERJ Open Research: 6 (1)
  • Table of Contents
  • Index by author
Email

Thank you for your interest in spreading the word on European Respiratory Society .

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
ERS International Congress, Madrid, 2019: highlights from the Respiratory Intensive Care Assembly
(Your Name) has sent you a message from European Respiratory Society
(Your Name) thought you would like to see the European Respiratory Society web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
Citation Tools
ERS International Congress, Madrid, 2019: highlights from the Respiratory Intensive Care Assembly
Celal Satici, Daniel López-Padilla, Annia Schreiber, Aileen Kharat, Ema Swingwood, Luigi Pisani, Maxime Patout, Lieuwe D. Bos, Raffaele Scala, Marcus J. Schultz, Leo Heunks
ERJ Open Research Jan 2020, 6 (1) 00331-2019; DOI: 10.1183/23120541.00331-2019

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
ERS International Congress, Madrid, 2019: highlights from the Respiratory Intensive Care Assembly
Celal Satici, Daniel López-Padilla, Annia Schreiber, Aileen Kharat, Ema Swingwood, Luigi Pisani, Maxime Patout, Lieuwe D. Bos, Raffaele Scala, Marcus J. Schultz, Leo Heunks
ERJ Open Research Jan 2020, 6 (1) 00331-2019; DOI: 10.1183/23120541.00331-2019
del.icio.us logo Digg logo Reddit logo Technorati logo Twitter logo CiteULike logo Connotea logo Facebook logo Google logo Mendeley logo
Full Text (PDF)

Jump To

  • Article
    • Abstract
    • Abstract
    • Hot topic: acute respiratory failure
    • State-of-the-art session: respiratory critical care
    • Integrated strategies for acute NIV
    • ECMO
    • Closing remarks
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • PDF

Subjects

  • Acute lung injury and critical care
  • Tweet Widget
  • Facebook Like
  • Google Plus One

More in this TOC Section

  • Highlights from the Respiratory Infections Assembly
  • Highlights from the Allied Respiratory Professionals
  • Highlights from the Paediatric Assembly
Show more Congress Highlights

Related Articles

Navigate

  • Home
  • Current issue
  • Archive

About ERJ Open Research

  • Editorial board
  • Journal information
  • Press
  • Permissions and reprints
  • Advertising

The European Respiratory Society

  • Society home
  • myERS
  • Privacy policy
  • Accessibility

ERS publications

  • European Respiratory Journal
  • ERJ Open Research
  • European Respiratory Review
  • Breathe
  • ERS books online
  • ERS Bookshop

Help

  • Feedback

For authors

  • Instructions for authors
  • Publication ethics and malpractice
  • Submit a manuscript

For readers

  • Alerts
  • Subjects
  • RSS

Subscriptions

  • Accessing the ERS publications

Contact us

European Respiratory Society
442 Glossop Road
Sheffield S10 2PX
United Kingdom
Tel: +44 114 2672860
Email: journals@ersnet.org

ISSN

Online ISSN: 2312-0541

Copyright © 2023 by the European Respiratory Society