Download PDF
  • Francesca Nori
  • Review

High flow nasal cannula therapy in emergency room: may it change the path for COPD patients with exacerbation?

  • 1/2018-Febbraio
  • ISSN 2532-1285
  • https://doi.org/10.23832/ITJEM.2018.008

Francesca Nori MD1, Sossio Serra MD1, Corrado Battaglini MD1, Patrizia Cuppini MD1

Emergency Department, M. Bufalini Hospital, Cesena, Italy

Introduction

High flow nasal cannula (HFNC) therapy is a relatively new device that have been proven to be safe and useful in many clinical situation, as well as in ED (1-3). In this case, we want to discuss a potential use of HFNC therapy when NIV is recommended but is neither feasible nor tolerated.

Case Description

An 82-years-old man was admitted to our ED for dyspnea. His past medical history included COPD and chronic atrial fibrillation in anticoagulant therapy. Four months before he presented another exacerbation of COPD. Physical examination showed bilateral wheezes in the lung. Bed-side US described rare B lines, so patient was treated with IV corticosteroids and inhalatory beta agonist and anticholinergics. His values were: pH 7.28, pCO2 81.7 mmHg, pO2 72 mmHg, HCO3 – 38 mmol/L, FiO2 45% and Lac 1.84 mmol/L. Chest X-ray was suggestive for COPD exacerbation. NIV was started with PSV 8 cmH20 and PEEP 7 cmH20, but quickly removed because of intolerance. Second assessment of gas exchange was performed after this short time of ventilation and resulted in pH 7.31, pCO2 77.1 mmHg, pO­2 101 mmHg, HCO3­- 38 mmol/L, Lac 1.55 mmol/L, FiO2 30%. Then, high flow nasal therapy (AIRVO 2 Fisher and Paykel) was administered to patient with the following settings: 37°C, 50 L/min and FiO2 33%. Patient reported great comfort and showed high tolerance to the device and settings. A third gas assessment after one hour of treatment revealed decreasing level of CO2 (pCO2 68.7 mmHg) with stable pH and oxygenation (pH 7.33, pO2 61.7 mmHg, HCO3­- 36.1 mmol/L and Lac 1.45 mmol/L). The reduction in CO2 was stable during the following three hours and after, and it allow us to transfer the patient in general ward and not in sub-ICU. 

Discussion

High-flow nasal oxygen therapy is provided by relatively new devices that deliver totally conditioned heated and humidified gas through a nasal cannula at very high flow (up to 60L/min). Although the use of HFNC is well known in pediatric setting, its use in adult with respiratory failure is still controversial (4). Acute dyspnea is one of the most common causes of presentation in Emergency Departments and HFNC can improve that by the reduction of work breathing. This is a result of many factors such as the PEEP provided by the device which counteract the intrinsic one (5), the washing out of oropharyngeal dead space (6) and the changes in the respiratory resistances. In fact, HFNC can attenuate inspiratory resistance while increasing the expiratory one (5). It also facilitates secretion clearance through humidified gas (1).
The use of HFNC is nowadays quite well established in stable COPD patients because it reduces respiratory rate and transcutaneous carbon dioxide (7) and improves the breathing pattern (8). On the contrary, in acute hypercapnic respiratory failure due to COPD exacerbation its role has been not yet defined, mainly because NIV is strongly recommended as first line treatment able to improve pH, reduce respiratory rate, prevent immediate intubation and improves survival (9). It’s also recommended a trial with NIV in patients at risk of intubation, unless the patient is immediately deteriorating (4).
 
Regarding the use of HFNC in ED, it plays a key role in treating dyspnea and hypoxemia. Rittayamai et al. postulated that HFNC improved dyspnea and comfort compared to standard oxygen therapy in subjects presenting in the ED (10), but there were no differences in hospital admission rates between the groups. Furthermore, HFNC used as a first line oxygen treatment decrease risk of requiring escalation to NIV or intubation (11). Makdee et al. studied HFNC versus conventional oxygen therapy in cardiogenic pulmonary edema in ED. High-flow nasal cannula therapy may reduce the severity of dyspnea during the first hour of treatment, with no significant differences in the admission rate, ED and hospital lengths of stay, need for NIV, rate of intubation or mortality (12).
 
As concerning the timing of HFNC, there is sparse information. In one retrospective analysis performed by Gaunt et al. in a heterogeneous population of medical and trauma patients, the early use of HFNC was associated with decreased ICU and post ICU lengths of stay and reduce incidence of adverse events (12).

Teaching Point

According to ERS/ATS guidelines, NIV should not be used in patients with COPD exacerbation without acidosis in favor of medical treatment and supportive oxygen therapy targeted to a saturation of 88-92% (1).
 
However, whenever we are presented with cases of acute hypercapnic respiratory failure due to COPD exacerbation with acidosis (pH 7.25-7.35), we have to treat them with bi-level NIV. Unfortunately, NIV is not always well tolerated and mild to moderate sedation is often necessary. Furthermore, the medical staff could not be well trained to use NIV, which have an important impact on nurse workload in ED more than in other settings.
 
Despite of the mild to moderate acidosis, these COPD patients are frequently elderly chronically ill and tolerate well enough these levels of pH and CO2, that NIV could be not the treatment of choice because in many cases does not impact on gas exchange and/or on natural history of exacerbation. Therefore, in elderly COPD patients we sometimes prefer medical treatment and supportive oxygen therapy over NIV.
 
Considering the fact that HFNC improves respiratory rate, oxygenation, comfort and dyspnea in many different situation, we suggest its use also in COPD patients in which NIV is not tolerated or feasible, even if recommended.

References

  1. Roca O et al, Crit Care. 2016 Apr 28;20(1):109. doi: 10.1186/s13054-016-1263-z.
  2. Makdee O et al, Ann Emerg Med. 2017 Oct;70(4):465-472.e2. doi: 10.1016/j.annemergmed.2017.03.028. Epub 2017 Jun 23.
  3. Jones PG et al, Respir Care. 2016 Mar;61(3):291-9. doi: 10.4187/respcare.04252. Epub 2015 Nov 17.
  4. Rochwerg B et al. Eur Respir J. 2017 Aug 31;50(2). pii: 1602426. doi: 10.1183/13993003.02426-2016. Print 2017 Aug.
  5. Groves N, Tobin A Aust Crit Care. 2007 Nov;20(4):126-31. Epub 2007 Oct 10.
  6. Dysart K et al, Respir Med. 2009 Oct;103(10):1400-5. doi: 10.1016/j.rmed.2009.04.007. Epub 2009 May 21. Review.
  7. Fraser JF et al. Thorax. 2016 Aug;71(8):759-61. doi: 10.1136/thoraxjnl-2015-207962. Epub 2016 Mar 25.
  8. Pisani L et al Thorax. 2017 Apr;72(4):373-375. doi: 10.1136/thoraxjnl-2016-209673. Epub 2017 Jan 19.
  9. Plant PK Thorax. 2001 Sep;56(9):708-12.
  10. Rittayamai et al. Respir Care. 2015 Oct;60(10):1377-82. doi: 10.4187/respcare.03837. Epub 2015 Jun 9.
  11. Bell N et al, Emerg Med Australas. 2015 Dec;27(6):537-541. doi: 10.1111/1742-6723.12490. Epub 2015 Sep 29.
  12. Gaunt KA et al Respir Care. 2015 Oct;60(10):1383-9. doi: 10.4187/respcare.04016. Epub 2015 Jun 9.