Open access peer-reviewed chapter

Mechanical Ventilation for Patients with COPD

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Ozlem Ediboglu

Submitted: October 8th, 2020 Reviewed: February 15th, 2021 Published: July 14th, 2021

DOI: 10.5772/intechopen.96633

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Abstract

Mechanical ventilation is a lifesaving therapy in patients who have acute respiratory failure due to chronic obstructive pulmonary disease (COPD). Mechanical ventilaton either invasive or non-invasive has an important role in the management of acute exacerbation of COPD (AECOPD). AECOPD required hospitalizaton had increased mortality and poor prognosis. Ventilatory management success related to understanding physiopathology of the disease. Clinicians must be aware of deterioration of clinical signs of COPD patients. The most appropriate treatment should be performed at optimal time. Some COPD patients are at high risk for prolonged mechanical ventilation due to COPD is a progressive disease.

Keywords

  • mechanical ventilation
  • COPD
  • respiratory failure

1. Introduction

Chronic obstructive pulmonary disease (COPD) is a major global health problem which has high morbidity and mortality [1]. COPD is characterized by chronic inflammation of the airways and lung parenchyma. The most important physiologic abnormality is worsening of expiratory airflow limitation due to increased airway resistance and decreased elastic recoil [2]. Patients who have fexpiratory airflow limitation cannot breath normally and due to dynamic hyperinflation increase work of breathing. These physiologic changes are deteriorated unless avoid risk factors because of COPD is a progressive disease and can be complicated with different severity of acute exacerbation [1, 2, 3, 4].

Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is described an acute worsening of the clinical condition of the COPD patient [5]. Clinical features are highly variable and AECOPD has a negative impact of patients’ health status and outcomes [1, 6, 7, 8]. The reported mortality associated with a AECOPD is variably at 11% to 32% [9]. The mortality rate and costs are much higher in some patients requiring mechanical ventilation [10, 11]. In severe AECOPD, it is crucial to recognise acute respiratory failure (ARF) immediately and to decide appropriate treatment. ARF is defined as the inability to maintain the delivery of oxygen and/or removal of carbon dioxide acutely. Worsening gas exchange and consequently hypercapnia and/or hypoxemia occur in arterial blood gas sample (ABG) analysis [12].

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2. Non-invasive ventilation

Mechanical ventilation either invasive or non- invasive is lifesaving treatment for acute respiratory failure. It is targeted by non - invasive ventilation (NIV) to minimize risks of mechanical ventilation and maximize patients’ safety and comfort. Hence NIV is successful to provide alveolar ventilation and gas exchange as invasive mechanical ventilation (IMV); NIV accepted widely as the first choice in treating AECOPD patients with ARF [13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24]. NIV therapy success is related to appropriate patient selection and early application [14, 25, 26, 27]. The appropriate patient means that is alert, co-operative, compliant and has no contraindications [28].

NIV is applied after initial treatment if the pH remains <7.30 and after exclusion of reversible precipitating causes such as a pneumothorax, the depressant effect of uncontrolled oxygen therapy, or the excessive use of sedatives [29, 30, 31]. According to GOLD guide, NIV is considered at least one of these conditions; respiratory acidosis, weakness of respiratory muscles, severe dyspnea, increased work of breathing, accessory muscle using, intercostal retraction, paradoxal breathing and persistant hypoxemia with oxygen therapy [32]. Main determinants are experience of the clinician, place of the NIV therapy, clinical condition and theurapeutic requirement of patient [33, 34].

NIV can be apply with all ventilators used in IMV support [35]. It’s important to known technical specialities and settings by clinician. Portable ventilators, intermediate ventilators and ICU ventilators has been used [33, 36]. Portable ventilators are named according to targeted parameter as volume and pressure ventilators. The synonim name is portable device is bilevel or BiPAP (Bilevel positive airway pressure) ventilator. Clinicians must be aware of difference between settings of the two devices: While adjusting IPAP (inspiratory positive airway pressure), EPAP (expiratory positive airway pressure) levels setting in BiPAP device, pressure support (PS = IPAP - EPAP) and EPAP levels in ICU ventilators [33, 37]. Bi-level pressure support ventilators are simpler to use, cheaper, and more flexible than other types of ventilator currently available. ICU ventilators have full monitoring and alarm capability and can be given up to 100% FiO2 when needed [30, 33]. Whole appropriate equipment must be ready to iniciate the NIV therapy as single/double lumen circuit, nasal/oronasal NIV mask by different size [38]. Mask selection is more important than ventilator. In acute setting, oronasal mask is well tolerated and preferred by many clinicians [14, 38, 39].

NIV is contraindicated in these situations; respiratory or cardiac arrest, hemodynamic instability, inability to use mask, excessive secretion, high risk for aspiration, and uncooperative patient.

Initially it is began with low pressure levels as IPAP 8–10 cm H2O and EPAP 4–5 cm H2O. According to patient’s clinical status, pressure levels can be increased. Monitorization of clinical signs, parameters of mechanical ventilation and gas exchange at the bedside are very important. Especially clinician must be follow and record subjective symptoms like anxiety, consciousness, delirium, agitation, sedation, analgesia, patient comfort, dyspnea, tolerance of mask. All the time NIV therapy, physiological response like respiratory rate (RR), using accessory muscle, heart rate (HR) and rhythm, blood pressure (BP) must be recorded. After the first 1–2 hours ABG must be done. We must consider intubation, if no improvement in ABG, deterioration in level of consciousness, NIV poorly tolerated, and inadequate secretion clearance [1, 7, 21, 40].

NIV failure is associated with hospital mortality, length of hospital and ICU stay [41]. NIV failure indicators are found as initial pH <7.25, Glascow Coma Scale (GCS) <10, Acute Physiology and Chronic Health Evaluation (APACHE) II score > 25, severe comorbidity, asynchrony, leaks [7, 42], existing pneumonia, and bad initial response (no change RR, pH and paCO2) [14, 43]. The potantial causes NIV failure are defined that poor patient selection, progression of the underlying disease, wrong interface, wrong ventilator, inappropriate ventilator settings and clinican’s inexperience [44]. In a study, HACOR scores (heart rate, acidosis, consciousness, oxygenation, respiratory rate) be defined as a potential tool for clinical physicians to identify NIV failure earlier [45]. Patient tolerance to NIV is a critical factor determining its success in avoiding endotracheal intubation [46]. The most important point of the tolerance to NIV is optimal synchrony between the patient’s spontaneous breathing activity and the ventilator’s set parameters, known as “patient–ventilator interaction” [47]. Clinician can detected an asynchrony index (AI) (%) via visual inspection of asynchrony events (ineffective triggering, auto-triggering, premature cycling, double triggering and delayed cycling). AI is identified as number of asynchrony events/total RR X 100% and above 10% was accepted as severe asynchrony [44]. In a multicenter study, severe asynchrony was found 43% [48]. The level of pressure support and the existing of leaks were found independent predictive factors of severe asynchronies and severe asynchronies were detected 30% of patients [49]. Patient-ventilator synchrony is related to better success of NIV. For this reason, in case of asynchrony, the most appropriate strategies should be followed to improve synchronization with NIV [44].

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3. Invasive mechanical ventilation

Endotracheal intubation should be done any one of the following criteria immediately: respiratory arrest, loss of consciousness, psychomotor agitation requiring sedation, hemodynamic instability with a systolic BP less than 70 or greater than 180 mmHg, HR less than 50 beats/minute with loss of alertness, gasping for air. These criteria are named major criteria. Intubation was suggested any two of the following criteria also named minor criteria; RR >35 breath/min, worsening acidemia or pH < 7.25, paO2 < 40 mmHg or paO2/FiO2 < 200 despite oxygen therapy, decreasing level of consciousness [50]. Before intubation pre-oxygenation is essential. Intubation with the rapid sequence induction and cricoid pressure to reduce the risk of aspiration should ideally be performed by an experienced clinician [51].

After intubation, its targeted to improve gas exchange abnormality and to avoid auto-PEEP (PEEPi) [7, 52]. Dynamic hyperinflation(DHI) may exist before intubation or induced by mechanical ventilation. The minute volume (MV) should be adjusted to pH and not to the PaCO2 levels. Clinicians should be avoid overventilation and paCO2 levels should decreased gradually. It is important to provide lower MV (RR x tidal volume (TV)) and higher inspiratory flow rate which has allow longer expiratory time. Any mode can be used, either assist control (AC), synchronized intermittent mandatory ventilation with either volume or pressure target (SIMV-VS, SIMV-PS), or pressure support ventilation(PSV). Clinician’s experience is the most important determinant of mode selection. Initial ventilator settings are recommended like that; TV: 6–10 ml/kg, FiO2: 1.0, RR: 10–14 breaths/minute, no PEEP, inspiratory flow rate: 80–100 liter/minute with square waveform [1, 2, 4]. Monitoring the lung mechanics on ventilator graphic screen continously and detecting any sign of DHI or PEEPi are very important. The clinicians should be followed existing any clinical signs to avoid the complications of DHI. The most important complications of DHI are hypotension, hemodynamic collaps, barotrauma and increased work of breathing (WOB) [51, 53]. Therefore, that strategies must be applied by clinicians to reduce auto-PEEP; providing the longest expiratory phase that is possible, reducing patient ventilatory demand and MV, and reducing airflow resistance by bronchodilators and steroids [1].

Barotrauma is an important risk at the COPD patients. Elevated peak inspiratory pressure (PIP) does not reflect the alveolar pressure in patients with bronchospasm. Alveolar pressure can be detected with plateau pressure (Pplat) and suggested PIP < 50 cmH2O, Pplat < 30 cmH2O to avoid barotrauma [1].

Quantifying PEEPi is a difficult and favored process. PEEPi amount of proportionated with degree of bronchial obstruction. Different techniques can be used to calculate PEEPi. Clinicians can directly measure by occluding the expiratory port for 1–3 seconds at end expiration or by using expiratory hold maneuver on new ventilators. Static PEEPi can be measured in this way only in sedatized patients without active respiratory effort. The PEEPi can then be calculated by subtracting the external PEEP from the total PEEP. If there is spontan respiratory effort of the patient, dynamic PEEPi can be determined by simultanously recording esophageal pressure and airflow tracings. It is measured at end expiration as the negative deflection of esophageal pressure to the point of zero flow. The dynamic PEEPi is usually measured lower than static PEEPi by reason of different longer of time constant [1, 2, 4, 53, 54]. While PEEPi is determined extrinsic PEEP (PEEPe) at 80% of PEEPi should be added to reduce patient triggering effort. Ventilator trigger sensitivity must be justify minimal [1, 4, 6, 51, 55, 56].

Weaning should begin once the cause of the exacerbation is adequately treated and the patient is hemodynamically stable. Physiologic parameters must be followed intensively. It’s targeted MV < 15 L, RR < 30 breaths/minute, TV > 325 ml, rapid shallow breathing index (RSBI) <105, maximum inspiratory pressure (MIP) < −15. Although the superiority did not found among each other, different strategies were used to weaning. Daily spontaneous breathing trail (SBT) is one way of identifying patients stable to wean and it may reduce the number of ICU days. While decreasing gradually of PS has not been shown to be superior to SBT, PSV is preferable by many clinicians. Using NIV to facilitate weaning is accepted by multiple RCT [14, 15, 52, 57, 58].

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4. High flow oxygen therapy

Long term oxygen therapy (LTOT), is used mainly in COPD patients with chronic hypoxemia [32]. High flow oxygen therapy (HFOT) is a new technique for delivering oxygen. There are many studies using HFOT instead of conventional oxygen therapy (COT) recently. HFOT was well tolerated and was sensed as comfortable. By using this system, oxygen delivery trends provided to be lower, and paCO2 levels could be measured significant decreased. HFOT could be accepted as an alternative treatment to NIV due to it generates a modest degree of positive pressure almost 5–6 cmH2O. It provides a more physiological humidification and heating of the airways. In this settings, HFOT has been used with different aims, as an alternative to COT, and NIV [59, 60, 61, 62].

References

  1. 1. Reddy RM, Guntupalli KK. Review of ventilatory techniques to optimize mechanical ventilation in acute exacerbation of chronic obstructive pulmonary disease. Int J COPD 2007;2(4):441-452
  2. 2. Mowery NT. Ventilator Strategies for Chronic Obstructive Pulmonary Disease and Acute Respiratory Syndrome. Surg Clin N Am 2017;97:1381-1397
  3. 3. Levi MO. Structure and function of the respiratory muscles in patients with COPD: impairment or adaptation? Eur Respir J 2003; 22(Suppl 46):41-51s
  4. 4. Ediboglu O. Hasta Tiplerine Gore Mekanik Ventilasyon. Ed. Kunter E, Kıraklı C, Koşar F. Mekanik Ventilasyon. S: 75-89, TÜSAD Eğitim Kitapları Serisi, Probiz Ltd Şti, İstanbul 2013
  5. 5. Vogelmeier CF, Criner GJ, Martinez FJ, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2017 report: gold executive summary. Eur Respir J 2017;49: 1700214
  6. 6. O’Donnell DE, Hernandez P, Kaplan A, et al. Canadian Thoracic Society recommendations for management of chronic obstructive pulmonary disease - 2008 update - highlights for primary care. Can Respir J 2008;15 Suppl A:1A-8A
  7. 7. Kosar F. Kronik Obstruktif Akciğer Hastalığında Akut Solunum Yetmezliği ve Mekanik Ventilasyon. Turk Klin J Pulm Med Spec Topics 2010; 3 (2):20-28
  8. 8. Ambrosino N, Simonds A. The clinical management in extremely severe COPD. Respir Med 2007; 101 (8):1613-24
  9. 9. Gadre SK, Duggal A, Mireles-Cabodevila E, et al. Acute respiratory failure requiring mechanical ventilation in severe chronic obstructive pulmonary disease (COPD). Medicine (2018) 97:17 (e0487)
  10. 10. Alaithan AM, Memon JI, Rehmani RS, et al. Chronic obstructive pulmonary disease: hospital and intensive care unit outcomes in the Kingdom of Saudi Arabia. Int J Chron Obstruct Pulmon Dis 2012;7:819-823
  11. 11. Raurich JM, Perez J, Ibanez J, et al. In-hospital and 2-year survival of patients treated with mechanical ventilation for acute exacerbation of COPD. Arch Bronconeumol 2004;40:295-300
  12. 12. Breen D, Churches T, Hawker F, et al. Acute respiratory failure secondary to chronic obstructive pulmonary disease treated in the intensive care unit: a long term follow up study. Thorax 2002;57:29-33
  13. 13. Rochwerg B, Brochard L, Elliott MW, Hess D, et al. Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J 2017; 50: 1602426
  14. 14. Lieshhing T, Kwok H, Hill N. Acute applications of noninvasive positive pressure ventilation. Chest 2003:124; 699-713
  15. 15. Garpestad E, Brennan J, Hill N. Noninvasive ventilation for critical care. Chest 2007;132: 711-720
  16. 16. Scala R, Pisani L. Noninvasive ventilation in acute respiratory failure: which recipe for success? Eur Respir Rev 2018;27:180029
  17. 17. Hess D. Noninvasive ventilation for acute respiratory failure. Respir Care 2013;58(6):950-969
  18. 18. Evans TW. International Consensus Conferences in Intensive Care Medicine: noninvasive positive pressure ventilation in acute respiratory failure. Organised jointly by the American Thoracic Society, the European Respiratory Society, the 1394 Mowery European Society of Intensive Care Medicine, and the Societe de Reanimation de Langue Francaise, and approved by the ATS Board of Directors, December 2000. Intensive Care Med 2001;27(1):166-178
  19. 19. Girou E, Brun-Buisson C, Taillé S, et al. Secular trends in nosocomial infections and mortality associated with noninvasive ventilation in patients with exacerbation of COPD and pulmonary edema. JAMA 2003;290(22):2985-2991
  20. 20. Scala R, Naldi M. Ventilators for Noninvasive Ventilation to Treat Acute Respiratory Failure. Respir Care 2008;53(8):1054-1080
  21. 21. Brochard L. Mechanical ventilation: invasive versus noninvasive. Eur Respir J 2003;22: Suppl. 47. 31s–37s
  22. 22. International Consensus Conferences in Intensive Care Medicine: Noninvasive Positive Pressure Ventilation in Acute Respiratory Failure. Am J Respir Crit Care Med. 2001; 163: 283-291
  23. 23. Crimi C, Noto A. A European Survey of Noninvasive Ventilation Practices. Eur Respir J 2010;36:362-369
  24. 24. Schönhofer B, Sortor- Leger S. Equipment needs for noninvasive mechanical ventilation. Eur Respir J 2002;20:1029-1036
  25. 25. Plant PK, Owen JL, Elliott MW. Non-invasive ventilation in acute exacerbations of chronic obstructive pulmonary disease: long term survival and predictors of in-hospital outcome. Thorax 2001;56:708-712
  26. 26. Celikel T, Sungur M, Ceyhan B, et al. Comparison of noninvasive positive pressure ventilation with standard medical therapy in hypercapnic acute respiratory failure. Chest 1998; 114: 1636-1642
  27. 27. Yıldırım F. Kronik Obstrüktif Akciğer Hastalığı Akut Alevlenmede Noninvaziv Mekanik Ventilasyon Kullanımı. Noninvazif Mekanik Ventilasyon Uygulamaları. Ed Ocal S. TÜSAD Eğitim Kitapları Serisi Ekim 2017:119-127
  28. 28. Scala R, Naldi M, Archinucci I, et al. Noninvasive positive pressure ventilation in patients with acute exacerbations of COPD and varying levels of consciousness. Chest 2005; 128(3): 1657-1666
  29. 29. Plant P, Owen J, Elliott M. A multi centre randomised control trial of the early use of non invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. Lancet 2000;355:1931-1935
  30. 30. British Thoracic Society Standards of Care Subcommittee. Non-invasive ventilation in acute respiratory failure. Thorax 2002;57:192-211
  31. 31. Brochard L. Non invasive ventilation for acute exacerbations of COPD: a new standard of care. Thorax 2000;55:817-818
  32. 32. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease GOLD 2019 Report
  33. 33. Ediboglu O. Noninvazif Mekanik Ventilasyonda Cihazlar, Noninvazif Mekanik Ventilasyonda Modlar. Z. Karakurt (Ed) Organizasyondan Tedaviye Yoğun Bakım. Türk Toraks Derneği Toraks Kitapları Bölüm 6, 7, 2014
  34. 34. Penuelas O, Frutos Vivar F, Esteban A. Noninvasive positive pressure ventilation in acute respiratory failure. CMAJ 2007;177(10):1211-1218
  35. 35. Hess DR. The Evidence for Noninvasive Positive-Pressure Ventilation in the Care of Patients in Acute Respiratory Failure. A Systematic Review of the Literature. Respir Care 2004;49(7):810-829
  36. 36. Scala R, Naldi M. Ventilators for Noninvasive Ventilation to Treat Acute Respiratory Failure. Respir Care 2008;53(8):1054-1080
  37. 37. Kaya A, Ciledag A. Yoğun Bakım Ventilatörü ve BiPAP İle Noninvaziv Mekanik Ventilasyon Uygulamalarındaki Farklılıklar. Noninvazif Mekanik Ventilasyon Uygulamaları. Ed Ocal S. TÜSAD Eğitim Kitapları Serisi Ekim 2017
  38. 38. Navalesi P, Fanfulla F, Frigerio P, et al. Physiologic evaluation of noninvasive mechanical ventilation delivered with three types of masks in patients with chronic hypercapnic respiratory failure. Crit Care Med 2000; 28:1785-1790
  39. 39. Uğurlu AO, Ergan B, Takır HB, İn E, Ozyılmaz E, Edipoğlu O,et al. Approach of pulmonologists in Turkey to noninvasive mechanical ventilation use in acute respiratory failure. Tuberk Toraks 2015;63(4):213-225
  40. 40. Ediboglu O. Yoğun Bakımda Akut Solunum Yetmezliği Olan Hastanın Değerlendirilmesi ve Tedavi İlkeleri. Yoğun Bakim Protokolleri. N. Şenoğlu (Ed). Tepecik Hastanesi Yayınları/2017, İzmir
  41. 41. Shah NM, D’Cruz RF, Murphy PB. Update: non-invasive ventilation in chronic obstructive pulmonary disease. T Thorac Dis 2018;10(Suppl 1):S71-S79
  42. 42. Yıldırım F. Noninvaziv Mekanik Ventilasyon Başarısını Etkileyen Fizyolojik Parametreler. Noninvazif Mekanik Ventilasyon Uygulamaları. Ed Ocal S. TÜSAD Eğitim Kitapları Serisi Ekim 2017:28-38
  43. 43. Soo Hoo GW, Santiago S, Williams AJ. Nasal mechanical ventilation for hypercapnic respiratory failure in chronic obstructive pulmonary disease: determinants of success and failure. Crit Care Med 1994; 22:1253-1261
  44. 44. Hess DR. Patient-ventilator interaction during noninvasive ventilation. Respir Care 2011;56(2):153-165
  45. 45. Duan J, Wang S, Liu P, et al. Early prediction of noninvasive ventilation failure in COPD patients: derivation, internal validation, and external validation of a simple risk score. Ann. Intensive Care 2019; 9:108
  46. 46. Carlucci A, Richard J, Wysocki M, et al. Noninvasive versus conventional mechanical ventilation. An epidemiologic survey. Am J Respir Crit Care Med 2001; 163:874-880
  47. 47. Tobin M, Jubran A, Laghi F. Patient-ventilator interaction. Am J Respir Crit Care Med 2001; 163:1059-1063
  48. 48. Vignaux L, Vargas F, Roeseler J, et al. Patient–ventilator asynchrony during non-invasive ventilation for acute respiratory failure: a multicenter study. Intensive Care Med 2009; 35:840-846
  49. 49. Carlucci A, Pisani L, Malovini A, Nava S. Patient- ventilator asynchronies: may the respiratory mechanics play a role? Crit Care 2013; 17: R54
  50. 50. Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med 1995; 333(13): 817-822
  51. 51. Blanch L, Bernabe F. Measurement of air trapping, Intrinsic Positive End Expiratory Pressure and Dynamic Hyperinflation in Mechanically Ventilated Patients. Respir Care 2005;50(1):110-123
  52. 52. Gladwin MT, Pierson DJ. Mechanical ventilation of the patient with severe chronic obstructive pulmonary disease. Intensive Care Med (1998) 24:898-910
  53. 53. Davidson AC. The pulmonary physician in critical care. Critical care management of respiratory failure resulting from COPD. Thorax 2002;57:1079-1084
  54. 54. Ward NS, Dushay KM. Clinical concise review: Mechanical ventilation of patients with chronic obstructive pulmonary disease. Crit Care Med 2008 Vol. 36, No. 5: 1614-1619
  55. 55. Köhnlein T, Welte T. Ventilation in Obstructive Lung Disease Chapter 3. Eur Respir Mon 2006;36:34-48
  56. 56. Guerin C, Milic-Emili J, Fournier G: Effect of PEEP on work of breathing in mechanically ventilated COPD patients. Intensive Care Med 2000; 26:1207-1214
  57. 57. Esteban A, Frutos F, Tobin NJ, et al. A comparison of four methods of weaning patients from mechanical ventilation. N Eng J Med 1995; 332:345
  58. 58. Brochard L, Rauss A, Benito S, et al. Comparison of three methods of gradual withdrawal from ventilatory support during weaning from mechanical ventilation. Am J Respir Crit Care Med 1994;150:896
  59. 59. Vogelsinger H, Kaehler CM. Hihg-flow oxygen therapy in COPD patients: Optimised oxygen delivery. European Respiratory Society Annual Congress 2013, Noninvasive Ventilatory Support, 386: 347
  60. 60. Pisani L, Fasano L, 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; 51: 373-375
  61. 61. Longhini F, Pisani L, Lungu R, et al. High-flow oxygen therapy after noninvasive ventilation interruption in patients recovering from hypercapnic acute respiratory failure: A physiological Crossover trial. Crit Care Med 2019; 47: e506- e511
  62. 62. Pisani L, Astuto M, Prediletto I, Longhini F. High flow through nasal cannula in exacerbated COPD patients: a systematic review. Pulmonol 2019;25(6):348-354

Written By

Ozlem Ediboglu

Submitted: October 8th, 2020 Reviewed: February 15th, 2021 Published: July 14th, 2021