Anestezjologia. Intensywna Terapia 1/2016-Cut-off point for switching from non-invasive ventilation to intubation in severe ARDS. Fifty shades of grey?

LISTY DO REDAKCJI

Cut-off point for switching from non-invasive ventilation to intubation in severe ARDS. Fifty shades of grey?

Luc Quintin

Department of Physiology, University of Lyon, Lyon, France

Key words: acute respiratory distress syndrome, severe ARDS, non-invasive ventilation

Należy cytować wersję:

Quintin L: Cut-off point for switching from non-invasive ventilation to intubation in severe ARDS. Fifty shades of grey? Anaesthesiol Intensive Ther 2016; 48: 62–64. doi: 10.5603/AIT.2016.0011.

Sir, I would like to thank Drs Skoczyński and Esquinas for their comments. Firstly, let us turn to their secondary points:

  1. The initial intention was to pre-oxygenate a severely hypoxic patient before tracheal intubation [1] with a Respironics ventilator in the emergency department (ED), not to manage the whole case under non-invasive ventilation (NIV) with an Evita 4 XL ventilator in the Critical Care Unit (CCU). Nevertheless, the ventilatory discoordination disappeared almost immediately following the initiation of NIV, calling for an iterative re-assessment of preconceived strategy.
  2. This case was not acute respiratory distress syndrome (ARDS), but acute hypoxemic non-hypercapnic respiratory failure: the opacities required by the Berlin definition could not be seen on the chest x-ray taken minutes after admission to the ED.
  3. Although the patient was conscious, cooperative and drowsy (Glasgow 14), he was fully able to answer questions, and denied repeatedly having inhaled heroin. Esquinas [2] reported intubation with Glasgow ≤ 11. Thus, unconsciousness is irrelevant.
  4. The arrhythmia was not sinus tachycardia, but supraventricular arrhythmia: no P waves were observed on the oscilloscope using a high-speed display. Nevertheless, arrhythmia was, presumably, a consequence of hypoxia, a trivial issue not further discussed in the report [3]. Magnesium followed by amiodarone was aimed at isolating, as early as possible upon presentation, a «pure» ventilatory distress vs. a combined ventilatory and circulatory distress. Lung toxicity of a single dose of 450 mg of amiodarone awaits documentation.
  5. The interface was a standard oro-nasal mask.
  6. High PEEP (up to 20 cm H2O) generated neither leak nor clinical gastric overdistension, in this patient. I recently handled acute hypoxia (SaO2 = 39%) due to postoperative atelectasis, with PEEP increased over 2 h from 5 to 24 cm H2O (Drager Evita 4XL, low pressure support: PS to Pplat < 30 cm H2O, FiO2 = 1), allowing the pneumologist to perform a bronchoscopy under spontaneous ventilation (SaO2 = 100% when beginning bronchoscopy), without leaks or gastric distension. The reader will decide whether this is again deliberate malpractice or careful, minute by minute, observation.
  7. A high tidal volume (Vt) under PS is no trivial issue [4]. At variance with high PS in the setting of chronic obstructive pulmonary disease (COPD) [5], minimal PS (≤ 8 cm) to compensate for the valves and tubing [6] will generate a low Vt: following the setting up of a high PEEP the lung operates on the highest slope of the pressure-volume curve [7].The observed Vt was 250–500 mL (not 800–1200 mL as stated by Skoczynski), compatible with permissive hypercapnia (46–69 mm Hg) in a quiet patient with respiratory drive depressed by heroin. This technique was delineated earlier [8]. Guldner proposed similar analysis in animals [9]: see note added in proof [3].
  8. Skoczynski and Esquinas question the use of excessively high FiO2 (FiO2 = 1). However, the definition of excessive use of O2 is an FiO2 > 0.5 when SaO2 is > 92%, for up to 12–30 h, and excluding the “first 6 h of shock” [10]. Given a P/F≈57, in the ED, the patient received FiO2 = 1, en route toward intubation and controlled mechanical ventilation. As SaO2 remained < 90% for at least ≈5 h, this does not fit with excessively high FiO2. Subsequently, FiO2 was reduced to 0.4 within ≈10 h. As severe hypoxia (PaO2 = 19–36 mm Hg) is compatible with life in elite climbers [11], the question may be posed whether benign neglect should be extended to an unstable patient presenting with acute cardio-ventilatory distress (P/F = 57 on zero PEEP, 30 L min-1 on high O2 concentration mask; P/F = 75 on PEEP = 15 after 2 h on NIV). Moreover, should SaO2 = 88–92% be aimed at in the present patient, as proposed in a fully stabilized patient [12]?

The modified NIH table [13] (tab. 1) uses high PEEP-low FiO2 in stabilized intubated mechanically ventilated patients (SaO2 ≈88–95%), at variance with the questionable combination of high FiO2-low PEEP [10, 12]:

Table 1. High PEEP group (after protocol change to use high PEEP; reproduced from [13])

FiO2 0.3 0.3 0.4 0.4 0.5 0.5 0.5–0.8 0.8 0.9 1.0
PEEP 12 14 14 16 16 18 20 22 22 22–24

Accordingly, in a non-intubated unstabilized patient, PEEP was increased up to 20 cm H2O over 4 h, while FiO2 was lowered to 0.4 over 8 h, after stabilization : “the practice of using higher FiO2 cannot be considered unreasonable under these settings[10].

The effect of O2 on the respiratory rate (RR) as a function of PaO2 under spontaneous ventilation-PS [14] in the setting of ARDS, is to be taken into account to lower the work of breathing, at variance with COPD. Therefore, setting a 88–92% goal in the setting of invasive controlled mechanical ventilation in ARDS in stabilized intubated patients [12] does not apply to the early use of high PEEP-spontaneous ventilation in an unstabilized patient under NIV.

As to the question whether high FiO2 acts synergistically with other insults to worsen alveolar damage, a “safe level and duration of O2 exposure has not been established even in normal humans” [12]. Accordingly, a cut-off point of FiO2 < 0.6 for 8 h 45 could not be retrieved from the reference [12] provided by Skoczynski and Esquinas. Avoiding the closing-opening of alveoli (atelectrauma) with high PEEP presumably avoided inflammation and terminated swiftly the disease. Any synergistic effect of high FiO2 and inflammation appears irrelevant, given the short time course of the disease.

Can 9 to 10 h be considered a swift recovery? To my surprise, the intensivist in charge on day 2 terminated the NIV at 08 h 30 am. In the setting of ARDS, P/F increases over 72 h or more [15, 16]. Thus, the reader may decide whether a recovery time over 10 h is swift or not (day 1, 10 pm : P/F≈57 on zero-PEEP, high O2 concentration mask; day 2, 08 45 am: P/F = 240, PEEP = 15, FiO2 = 0.4).

Secondly, how far should NIV go without being detrimental? Let’s consider Esquinas’ data: a) «in the NIV group, P/F and RR became significantly higher and lower 3–4 hours after randomization» (Fig. 3 in [2]). b) the avoidance of intubation is reported in 54% of the patients with a P/F = 116 ± 38 [17]: given the standard deviation, some of his patients had a low P/F ≈40–60, as in our report [3]. Indeed, Pichot [3] observed the phenomenon described by Esquinas [2, 17]. Nevertheless, the use of NIV in acute respiratory failure demands caution [18]. Firstly, in the setting of severe ARDS (P/F = 126), 84% of the patients needed intubation [19]. Does this imply that the remaining 16% should be intubated upfront or should they simply observed even more closely to proceed to intubation if appropriate? Secondly, following extubation after respiratory failure, NIV is associated with a 10 h delay re: re-intubation and a higher mortality (NIV: 38%; standard treatment + reintubation: 22%) [20]. Thus, NIV should not be used (except perhaps in COPD or immuno-compromised patients, or as a bridge to intubation). A sober interpretation only implies that patients presenting a second exacerbation of acute respiratory failure after extubation should be very closely re-assessed, e.g. at least hourly, and their trachea intubated early, as needed, should NIV fail. Individualized minute-by-minute observation in one considered patient (3) does not necessarily agree with epidemiologic findings [20]. Altogether, NIV is detrimental when extended too far. Indeed, one referee complimented our non-invasive management: “avoid tracheal tubes, minimize sedation, prevent ventilator-induced lung injury and nosocomial infections” [21]. Conversely, another referee considered this [3] management as malpractice (P 140, l 7). Again, the reader will decide whether our concluding insistence on minute by minute re-assessment in a highly restricted subset [3] was conservative enough.

ACKNOWLEDGEMENTS

Conflict of interest: Luc Quintin holds a US patent 8 703 697, April 22 2014: Method for treating early severe diffuse acute respiratory distress syndrome.

References:

  1. Baillard C, Fosse JP, Sebbane M et al.: Noninvasive ventilation improves preoxygenation before intubation of hypoxic patients. Am J Respir Crit Care Med 2006; 174: 171–177.
  2. 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: 1438–1444.
  3. Pichot C, Petitjeans F, Ghignone M, Quintin L: Swift recovery of severe acute hypoxemic respiratory failure under non-invasive ventilation. Anaesthesiol Intensive Ther 2015; 47: 138–142. doi: 10.5603/AIT. a2014.0053.
  4. Freebairn R, Hickling KG: Spontaneous breathing during mechanical ventilation in ARDS. Crit Care Shock 2005; 8: 61–66.
  5. Brochard L, Harf A, Lorino H, Lemaire F: Inspiratory pressure support prevents diaphragmatic fatigue during weaning from mechanical ventilation. Am Rev Respir Dis 1989; 139: 513–521.
  6. L’Her E, Deye N, Lellouche F et al.: Physiologic effects of noninvasive ventilation during acute lung injury. Am J Respir Crit Care Med 2005; 172: 1112–1128.
  7. Katz JA, Marks JD: Inspiratory work with and without continuous positive airway pressure in patients with acute respiratory failure. Anesthesiology 1985; 63: 598–607.
  8. Galland C, Ferrand FX, Cividjian A et al.: Swift recovery of severe hypoxemic pneumonia upon morbid obesity. Acta Anaesthesiol Belg 2014; 65: 109–117.
  9. Guldner A, PelosiP, Gama de Abreu M: Spontaneous breathing in mild and moderate versus severe acute respiratory distress syndrome. Curr Opin Crit Care 2014; 20: 69–76.
  10. Rachmale S, Li G, Wilson G, MalinchocM, Gajic O: Practice of excessive F(IO(2)) and effect on pulmonary outcomes in mechanically ventilated patients with acute lung injury. Respir Care 2012; 57: 1887–1893.
  11. Grocott MP, Martin DS, Levett DZ et al.: Arterial blood gases and oxygen content in climbers on Mount Everest. N Engl J Med 2009; 360: 140–149. doi: 10.1056/NEJMoa0801581.
  12. Aggarwal NR, Brower RG: Targeting normoxemia in acute respiratory distress syndrome may cause worse short-term outcomes because of oxygen toxicity. An Am Thorac Soc 2014; 11: 1449–1453. doi: 10.1513/AnnalsATS.201407–297PS.
  13. Brower RG, Lanken PN, MacIntyre N et al.: Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004; 351: 327–336.
  14. Pesenti A, Rossi N, Calori A, Foti G, Rossi GP: Effects of short-term oxygenation changes on acute lung injury patients undergoing pressure support ventilation. Chest 1993; 103: 1185–1189.
  15. Villar J, Perez-Mendez L, Lopez J et al.: An early PEEP/FIO2 trial identifies different degrees of lung injury in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2007; 176: 795–804.
  16. Talmor D, Sarge T, Malhotra A et al.: Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med 2008; 359: 2095–2104. doi: 10.1056/NEJMoa0708638.
  17. Antonelli M, Conti G, Esquinas A 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.
  18. Esteban A, Anzueto A, Frutos F et al. Characteristics and outcomes in adult patients receiving mechanical ventilation: a 28-day international study. JAMA 2002; 287: 345–355.
  19. Thille AW, Contou D, Fragnoli C, Cordoba-Izquierdo A, Boissier F, Brun-Buisson C: Non-invasive ventilation for acute hypoxemic respiratory failure: intubation rate and risk factors. Crit Care 2013; 17: R269.
  20. Esteban A, Frutos-Vivar F, Ferguson ND et al.: Noninvasive positive-pressure ventilation for respiratory failure after extubation. N Engl J Med 2004; 350: 2452–2460.
  21. Terragni PP, Birocco A, Faggiano C, Ranieri VM: Extracorporeal CO2 removal. Contrib Nephrol 2010; 165: 185–196. 10.1159/000313758.

Adres do korespondencji:
Luc Quintin MD, PhD
Physiologie
Campus de la Doua
8 Rue R Dubois
69 622 Villeurbanne, France
e-mail: lucquintin@yahoo.com

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