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NIV through the helmet can be used as first-line intervention for early mild and moderate ARDS: an unproven idea thinking out of the box

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The lunatic, the lover, and the poet, are of imagination all compact.

Are you sure/That we are awake? It seems to me/That yet we sleep, we dream

William Shakespeare, A Midsummer Night’s Dream

Debating data have been published as regards the beneficial or deleterious effect of spontaneous breathing (SB) in comparison to controlled mechanical ventilation (CMV) during acute respiratory failure [1, 2].

Spontaneous breathing (SB) has been shown having several beneficial effects such as improving ventilation-perfusion matching and decreasing muscle atrophy and ventilator-induced lung injury (VILI) [3, 4].

There are experimental evidences that SB can also cause or worsen lung injury during mechanical ventilation [5, 6].

The implicated mechanisms include negative intra-thoracic and increased trans-alveolar pressure with a lack of control of tidal volume (VT), ventilation inhomogeneity and cyclic and static overinflation [7].

In animals with severe lung injury, SB could worsen lung injury. Muscle paralysis might be more protective by preventing injuriously high transpulmonary pressure and high driving pressure [8].

One of the most important determinants of the ventilator-induced lung injury is considered the transpulmonary pressure, that is, calculated as PL = Pao − Ppl, where PL is the difference between the pressure at the airway opening and the pleural or oesophageal pressure (used as a surrogate of the pleural pressure).

During SB, the airway pressure (Paw) is lower than during CMV, but this does not always translate into a lower pressure across the lung (i.e. a lower PL).

Only the transalveolar pressure, which equals the product of lung elastance and volume, is dissipated across the alveolus and is usually considered to cause VILI.

Instead of the absolute value of transpulmonary pressures, some investigators identify the lung stress with the variation of the transpulmonary pressure between end inspiration and end expiration, obtained during occlusion manoeuvres. All these manoeuvres are quite complicated to be performed while patients’ breathing spontaneously, especially under pressure support ventilation (PSV) and their validity, is put in question.

However, obtaining reliable physiological measurements in patients during noninvasive ventilation (NIV) or/and in patients spontaneously breathing without an endotracheal tube is extremely difficult, and the measurement cannot be reliably achieved through the conventional manoeuvres.

The only study that reports some interesting physiological measurements was the one published by L’Her et al. who showed that noninvasive pressure support of 10–15 cm H2O above a positive end-expiratory pressure (PEEP) of 5–10 cm H2O was the best combinations to reduce the inspiratory muscle effort, oesophageal pressure and dyspnoea and improve oxygenation [9]. In addition, experiments conducted on trained marathon runners in the sixties and more recently in endurance-trained individual put in evidence that the mechanism of spontaneous breathing-induced lung damage is not really understood. Indeed, these individuals during the exercise develop potentially injurious tidal volumes (TV) > 3 l, minute volumes (MV) (exceeding the 160 l/min) and transpulmonary pressures (ranging from − 40 cm H2O up to + 60 cm H2O) without developing any lung damage [10, 11].

Consequently, the question whether the noninvasive ventilation preserving the spontaneous breathing can be safely used for moderate and mild ARDS remains substantially unanswered.

Noninvasive positive pressure ventilation has been convincingly shown to be safe and effective as first-line treatment in patients with acute hypercapnic respiratory failure and acute cardiogenic pulmonary oedema [12,13,14,15]. Despite some data suggest that NIV may also avoid intubation in heterogeneous categories of patients with acute hypoxemic respiratory failure [16,17,18,19,20,21,22], its safety and efficacy in such a context is still debated, given the high failure rate and the possible detrimental effect on the clinical outcome [22,23,24,25,26,27,28,29,30,31,32,33,34].

As patients’ comfort is crucial for NIV success, over the last years, a great effort has been made to optimize NIV tolerability. Different interfaces are available for noninvasive ventilation [35]: in spite of face masks being more commonly used, helmet has been shown to improve patients’ comfort, allowing patients’ interaction, speech and feeding and not limiting cough. Nonetheless, skin necrosis, gastric distension or eye irritation are seldom observed during helmet NIV, while these may be consequences of long-term treatments with face masks [36, 37].

Moreover, differently from face masks, helmets permit longer-term treatments and allow the setting of higher levels of PEEP without causing air leaks or important patient-ventilator asynchrony; this aspect may be crucial when treating severely hypoxemic patients with acute respiratory failure and the acute respiratory distress syndrome (ARDS) [38]. Interestingly, higher PEEP during fully controlled mechanical ventilation in the early phase of the disease improves mortality in ARDS patients, and raising evidence indicates that it may exert beneficial effects also if spontaneous breathing is maintained [38, 39]. As a general rule, more severe patients (those with lower FRC and a higher shunt mechanism) are more recruitable and most benefit from higher PEEP that can be assured through the helmet during NIV with minimal leaks.

Helmet may allow NIV to fully exert its beneficial effects. In this sense, a recent randomized controlled trial comparing continuous NIV delivered with helmet or face-mask in patients with ARDS showed a lower intubation rate and a lower 90-day mortality in patients in the helmet group who, accordingly, underwent treatments with higher PEEP and lower FiO2 [40]. In this study, however, pressure support (PSV) delivered with NIV and low-flow-continuous positive airway pressure (CPAP) were indifferently used in patients randomized to the helmet group, despite their mechanisms of action, efficacy and potential harmful effects are profoundly different, especially given the high relevance of the driving pressure in such a context [41].

No study has ever clarified whether first-line treatment with helmet NIV as compared to other forms of oxygen support or invasive ventilation may yield a significant benefit to critically ill patients with respiratory failure.

The unproven idea that captured my imagination, needing a specific trial aimed to confirm our observational data, was using the noninvasive ventilation through the helmet as a tool for the early treatment of a mild and moderate form of ARDS.

A human being should follow the inspiration.

References

  1. 1.

    Marini JJ. Spontaneously regulated vs. controlled ventilation of acute lung injury/acute respiratory distress syndrome. Curr Opin Crit Care. 2011;17(1):24–9.

  2. 2.

    Mascheroni D, Kolobow T, Fumagalli R, Moretti MP, Chen V, Buckhold D. Acute respiratory failure following pharmacologically induced hyperventilation: an experimental animal study. Intensive Care Med. 1988;15(1):8–14.

  3. 3.

    Grasso F, Engelberts D, Helm E, Frndova H, Jarvis S, Talakoub O, et al. Negative-pressure ventilation: better oxygenation and less lung injury. Am J Respir Crit Care Med. 2008;177(4):412–8.

  4. 4.

    Xia J, Zhang H, Sun B, Yang R, He H, Zhan Q. Spontaneous breathing with biphasic positive airway pressure attenuates lung injury in hydrochloric acid– induced acute respiratory distress syndrome. Anesthesiology. 2014;120(6):1441–9.

  5. 5.

    Yoshida T, Uchiyama A, Matsuura N, Mashimo T, Fujino Y. Spontaneous breathing during lung-protective ventilation in an experimental acute lung injury model: high transpulmonary pressure associated with strong spontaneous breathing effort may worsen lung injury. Crit Care Med. 2012;40(5):1578–85.

  6. 6.

    Yoshida T, Uchiyama A, Matsuura N, Mashimo T, Fujino Y. The comparison of spontaneous breathing and muscle paralysis in two different severities of experimental lung injury. Crit Care Med. 2013;41(2):536–45.

  7. 7.

    Dreyfuss D, Saumon G. Ventilator-induced lung injury. Am J Respir Crit Care Med. 1998;157(1):294–323.

  8. 8.

    Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med. 2014;370(10):980.

  9. 9.

    L'Her E, Deye N, Lellouche F, Taille S, Demoule A, Fraticelli A, Mancebo J, Brochard L. Physiologic effects of noninvasive ventilation during acute lung injury. Am J Respir Crit Care Med. 2005 Nov 1;172(9):1112–8.

  10. 10.

    Olafsson S, Hyatt RE. Ventilatory mechanics and expiratory flow limitation during exercise in normal subjects. J Clin Invest. 1969;48(3):564–73.

  11. 11.

    Guenette JA, Witt JD, McKenzie DC, Road JD, Sheel WA. Resiratory mechanics during exercise in endurance trained men and women. J Physiol. 2007;581(3):1309–22.

  12. 12.

    Brochard L, Mancebo J, Wysocki M, Lofaso F, Conti G, Rauss A, Simonneau G, Benito S, Gasparetto A, Lemaire F. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med. 1995;333:817–22.

  13. 13.

    Weng C-L, Zhao Y-T, Liu Q-H, Fu C-J, Sun F, Ma Y-L, Chen Y-W, He Q-Y. Meta-analysis: noninvasive ventilation in acute cardiogenic pulmonary edema. Ann Intern Med. 2010;152:590–600.

  14. 14.

    Masip J, Roque M, Sánchez B, Fernández R, Subirana M, Expósito JA. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA. 2005;294:3124–30.

  15. 15.

    Mariani J, MacChia A, Belziti C, Deabreu M, Gagliardi J, Doval H, Tognoni G, Tajer C. Noninvasive ventilation in acute cardiogenic pulmonary edema: a meta-analysis of randomized controlled trials. J Card Fail. 2011;17:850–9.

  16. 16.

    Antonelli M, Conti G, Rocco M, Bufi M, De Blasi RA, Vivino G, Gasparetto A, Meduri GU. A comparison of noninvasive positive-pressure ventilation and conventional mechanical ventilation in patients with acute respiratory failure. N Engl J Med. 1998;339:429–35.

  17. 17.

    Antonelli M, Conti G, Bufi M, Costa MG, Lappa A, Rocco M, Gasparetto A, Meduri GU. Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial. JAMA. 2000;283:235–41.

  18. 18.

    Gristina GR, Antonelli M, Conti G, Ciarlone A, Rogante S, Rossi C, Bertolini G. Noninvasive versus invasive ventilation for acute respiratory failure in patients with hematologic malignancies: a 5-year multicenter observational survey. Crit Care Med. 2011;39:2232–9.

  19. 19.

    Antonelli M, Conti G, Esquinas A, Montini L, Maggiore SM, Bello G, Rocco M, Maviglia R, Pennisi MA, Gonzalez-Diaz G, et al. A multiple-center survey on the use in clinical practice of noninvasive ventilation as a first-line intervention for acute respiratory distress syndrome. Crit Care Med. 2007;35:18–25.

  20. 20.

    Carrillo A, Gonzalez-Diaz G, Ferrer M, Martinez-Quintana ME, Lopez-Martinez A, Llamas N, Alcazar M, Torres A. Noninvasive ventilation in community-acquired pneumonia and severe acute respiratory failure. Intensive Care Med. 2012;38:458–66.

  21. 21.

    Hilbert G, Gruson D, Vargas F, Valentino R, Gbikpi-Benissan G, Dupon M, Reiffers J, Cardinaud JP. Noninvasive ventilation in immunosuppressed patients with pulmonary infiltrates, fever, and acute respiratory failure. N Engl J Med. 2001;344:481–7.

  22. 22.

    Ferrer M, Esquinas A, Leon M, Gonzalez G, Alarcon A, Torres A. Noninvasive ventilation in severe hypoxemic respiratory failure: a randomized clinical trial. Am J Respir Crit Care Med. 2003;168:1438–44.

  23. 23.

    Papazian L, Corley A, Hess D, Fraser JF, Frat J-P, Guitton C, Jaber S, Maggiore SM, Nava S, Rello J, et al. Use of high-flow nasal cannula oxygenation in ICU adults: a narrative review. Intensive Care Med. 2016. https://doi.org/10.1007/s00134-016-4277-8.

  24. 24.

    Carteaux G, Millán-Guilarte T, De Prost N, Razazi K, Abid S, Thille AW, Schortgen F, Brochard L, Brun-Buisson C, Mekontso Dessap A. Failure of noninvasive ventilation for de novo acute hypoxemic respiratory failure: role of tidal volume. Crit Care Med. 2016;44:282–90.

  25. 25.

    Demoule A, Chevret S, Carlucci A, Kouatchet A, Jaber S, Meziani F, Schmidt M, Schnell D, Clergue C, Aboab J, et al. Changing use of noninvasive ventilation in critically ill patients: trends over 15 years in francophone countries. Intensive Care Med. 2015. https://doi.org/10.1007/s00134-015-4087-4.

  26. 26.

    Demoule A, Girou E, Richard J-C, Taille S, Brochard L. Benefits and risks of success or failure of noninvasive ventilation. Intensive Care Med. 2006;32:1756–65.

  27. 27.

    Ferrer M, Esquinas A, Arancibia F, Bauer TT, Gonzalez G, Carrillo A, Rodriguez-Roisin R, Torres A. Noninvasive ventilation during persistent weaning failure: a randomized controlled trial. Am J Respir Crit Care Med. 2003;168:70–6.

  28. 28.

    Möller W, Celik G, Feng S, Bartenstein P, Meyer G, Eickelberg O, Schmid O, Tatkov S. Nasal high flow clears anatomical dead space in upper airway models. J Appl Physiol. 2015;118:1525–32.

  29. 29.

    Mündel T, Feng S, Tatkov S, Schneider H. Mechanisms of nasal high flow on ventilation during wakefulness and sleep. J Appl Physiol. 2013;114:1058–65.

  30. 30.

    Roca O, Riera J, Torres F, Masclans JR. High-flow oxygen therapy in acute respiratory failure. Respir Care. 2010;55:408–13.

  31. 31.

    Corley A, Caruana LR, Barnett AG, Tronstad O, Fraser JF. Oxygen delivery through high-flow nasal cannulae increase end-expiratory lung volume and reduce respiratory rate in post-cardiac surgical patients. Br J Anaesth. 2011;107:998–1004.

  32. 32.

    Parke RL, McGuinness SP. Pressures delivered by nasal high flow oxygen during all phases of the respiratory cycle. Respir Care. 2013;58:1621–4.

  33. 33.

    Maggiore SM, Idone FA, Vaschetto R, Festa R, Cataldo A, Antonicelli F, Montini L, De Gaetano A, Navalesi P, Antonelli M. Nasal high-flow vs Venturi mask oxygen therapy after extubation: effects on oxygenation, comfort and clinical outcome. Am J Respir Crit Care Med. 2014;190:282–8.

  34. 34.

    Hernández G, Vaquero C, González P, Subira C, Frutos-Vivar F, Rialp G, Laborda C, Colinas L, Cuena R, Fernández R. Effect of postextubation high-flow nasal cannula vs conventional oxygen therapy on reintubation in low-risk patients: a randomized clinical trial. JAMA. 2016;315:1354–61.

  35. 35.

    Nava S, Navalesi P, Gregoretti C. Interfaces and humidification for noninvasive mechanical ventilation. Respir Care. 2009;54:71–84.

  36. 36.

    Antonelli M, Conti G, Pelosi P, Gregoretti C, Pennisi MA, Costa R, Severgnini P, Chiaranda M, Proietti R. New treatment of acute hypoxemic respiratory failure: noninvasive pressure support ventilation delivered by helmet—a pilot controlled trial. Crit Care Med. 2002;30:602–8.

  37. 37.

    Antonelli M, Pennisi MA, Pelosi P, Gregoretti C, Squadrone V, Rocco M, Cecchini L, Chiumello D, Severgnini P, Proietti R, et al. Noninvasive positive pressure ventilation using a helmet in patients with acute exacerbation of chronic obstructive pulmonary disease: a feasibility study. Anesthesiology. 2004;100:16–24.

  38. 38.

    Briel M, Meade M, Mercat A, Brower RG, Talmor D, Walter SD, Slutsky AS, Pullenayegum E, Zhou Q, Cook D, 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;303:865–73.

  39. 39.

    Yoshida T, Roldan R, Beraldo MA, Torsani V, Gomes S, De Santis RR, Costa ELV, Tucci MR, Lima RG, Kavanagh BP, et al. Spontaneous effort during mechanical ventilation: maximal injury with less positive end-expiratory pressure. Crit Care Med. 2016. https://doi.org/10.1097/CCM.0000000000001649.

  40. 40.

    Patel BK, Wolfe KS, Pohlman AS, Hall JB, Kress JP. Effect of noninvasive ventilation delivered by helmet vs face mask on the rate of endotracheal intubation in patients with acute respiratory distress syndrome. JAMA. 2016;60637:1–7.

  41. 41.

    Amato MBP, Meade MO, Slutsky AS, Brochard L, Costa ELV, Schoenfeld DA, Stewart TE, Briel M, Talmor D, Mercat A, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372:747–55.

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Acknowledgements

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None was declared by the authors. Publication of this supplement was supported by Fresenius Kabi.

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About this supplement

This article has been published as part of Critical Care, Volume 23 Supplement 1, 2019: Future of Critical Care Medicine (FCCM) 2018. The full contents of the supplement are available at https://ccforum.biomedcentral.com/articles/supplements/volume-23-supplement-1.

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Correspondence to Massimo Antonelli.

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Keywords

  • ARDS
  • Hypoxemic respiratory failure
  • Helmet pressure support