Write a critical appraisal that demonstrates comprehension of two quantitative research studies. Use the “Research Critique Guidelines – Part II” document to organize your essay. Successful completion of this assignment requires that you provide a rationale, include examples, and reference content from the study in your responses.

Use the practice problem and two quantitative, peer-reviewed research articles you identified in the Topic 1 assignment to complete this assignment.

In a 1,000–1,250 word essay, summarize two quantitative studies, explain the ways in which the findings might be used in nursing practice, and address ethical considerations associated with the conduct of the study.

Prepare this assignment according to the guidelines found in the APA Style Guide, located in the Student Success Center. An abstract is not required.

This assignment uses a rubric. Please review the rubric prior to beginning the assignment to become familiar with the expectations for successful completion.

ResearchCritique Guidelines – Part II

Use this document to organize your essay. Successful completion of this assignment requires that you provide a rationale, include examples, and reference content from the studies in your responses.

Quantitative Studies

Background

1. Summary of studies. Include problem, significance to nursing, purpose, objective, and research question.

How do these two articles support the nurse practice issue you chose?

1. Discuss how these two articles will be used to answer your PICOT question.

2

. Describe how the interventions and comparison groups in the articles compare to those identified in your PICOT question.

Method of Study:

1. State the methods of the two articles you are comparing and describe how they are different.

2. Consider the methods you identified in your chosen articles and state one benefit and one limitation of each method.

Results of Study

1. Summarize the key findings of each study in one or two comprehensive paragraphs.

2. What are the implications of the two studies you chose in nursing practice?

Outcomes Comparison

1. What are the anticipated outcomes for your PICOT question?

2. How do the outcomes of your chosen articles compare to your anticipated outcomes?

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High-Flow Nasal Cannula in Early Emergency Department Management
of Acute Hypercapnic Respiratory Failure Due to Cardiogenic Pulmonary

Edema.

Authors: Nicolas Marjanovic, Alexandre Flacher, Loic Drouet, Aude Le Gouhinec, Hakim Said and Jean-Francois Vigneau
Date: Sept. 2020

From: Respiratory Care(Vol. 65, Issue 9)
Publisher: Daedalus Enterprises, Inc.

Document Type: Clinical report
Length: 5,282 words
DOI: http://dx.doi.org/10.4187/respcare.07278

Abstract:
BACKGROUND: Noninvasive ventilation (NIV) is the recommended ventilatory support for acute cardiogenic
pulmonary edema (CPE) associated with acute respiratory failure or hypercapnia. High-flow nasal cannula
(HFNC) has emerged as an alternative to NIV in acute hypoxemic respiratory failure. We aimed to assess the
efficacy of HFNC on early changes in [mathematical expression not reproducible] and respiratory parameters in
patients in the emergency department with acute hypercapnic CPE and to compare it to NIV. METHODS: We
conducted a prospective observational study in consecutive emergency department patients with acute
hypercapnic CPE. Subjects received either HFNCor NIV, according to the attending emergency physician’s
expertise in HFNC. The primary outcome was change in [mathematical expression not reproducible] after
treatment for 1 h. Secondary outcomes were change in pH, breathing frequency, signs of work of breathing, and
comparisons to NIV. RESULTS: Twenty-seven subjects with a discharge diagnosis of hypercapnic CPE were
analyzed. Subjects had a median age of 87 y (interquartile range [IQR] 78-93); 37% were male. Twelve (44%)
received HFNC, and 15 (56%) received NIV. Median of changes in [mathematical expression not reproducible]
from baseline to after 1 h of treatment were 7 mm Hg (IQR 4-11, P = .002) for HFNC and 3 mm Hg (IQR 1-8, P =
.02) for NIV, with no between-group difference. pH, breathing frequency and signs of work of breathing also
improved after both HFNC and NIV. CONCLUSIONS: This preliminary study suggests that HFNC treatment for 1
h improves [mathematical expression not reproducible] and respiratory parameters in subjects with hypercapnic
acute CPE in a manner that is comparable to NIV. Further studies are needed to assess HFNC as a possible
alternative to NIV in early management of acute hypercapnic respiratory failure of cardiogenic origin.
(ClinicalTrials.gov registration NCT03883555.) Key words: respiratory insufficiency; cardiogenic pulmonary
edema/heart failure; noninvasive ventilation; high-flow nasal cannula; emergency medicine. [Respir Care 2020;
65(9):1241-1249. [c] 2020 Daedalus Enterprises]

Introduction

Acute cardiogenic pulmonary edema (CPE) is one of the main diagnoses for patients admitted for dyspnea in emergency
departments. (1) Severe CPE is associated with respiratory failure and hypercapnia in about 40% of patients. (2-4)
Hypercapnia may lead to altered consciousness and central apnea, and it may be associated with higher intubation and in-
hospital mortality rates. (5-7)

http://dx.doi.org/10.4187/respcare.07278

Noninvasive ventilatory support, including noninvasive ventilation (NIV) or CPAP, is recommended as a first-line treatment for
acute hypoxic and hypercapnic respiratory failure associated with acute CPE, along with intravenous diuretics and a nitrate
derivative. (6,8,9) NIV improves alveoli recruitment, decreases work of breathing (WOB), and improves cardiac output.
Consequently, NIV allows rapid correction of respiratory and blood gas parameters in acute CPE and contributes to a reduced
intubation rate and improved in-hospital mortality compared to standard oxygen therapy. (10) However, NIV may be poorly
tolerated in certain patients, in whom it is associated with failure of treatment and poor outcomes. (11-13)

High-flow nasal cannula (HFNC) represents another strategy in the ventilatory management of patients with acute respiratory
failure. (6,14) HFNC delivers a heated and humidified air-oxygen blend through a nasal cannula. It achieves flows up to 60
L/min and [mathematical expression not reproducible] ranging from 0.21 to 1.0, both of which can be adapted to patient needs.
Its effects are mediated through the delivery of PEEP and dead space washout. (15-18) HFNC is usually easier to apply and is
better tolerated than NIV. (19) In adults, HFNC has beenevaluated in ICU and postoperative settings in comparison toNIV and
standard oxygen therapy for the treatment of hypoxemic respiratory failure. (20) Compared to conventional oxygen therapy,
HFNC may decrease the need for tracheal intubation. (21) Its benefits over NIV with regard to intubation rate and mortality still
require confirmation. (22-24) HFNC is emerging as an alternative strategy in the management of acute hypoxemic respiratory
failure of heterogeneous etiologies. However, it has scarcely been explored in the treatment of select hypercapnic respiratory
failure or in the context of early emergency department management. (25-28) In the emergency department setting, HFNC has
been reported to be noninferior to NIV in preventing endotracheal intubation in unselected emergency department subjects with
acute respiratory failure, as well as in the subgroup of subjects with acute decompensated heart failure. (29,30) HFNC has also
been reported to lower 60-min breathing frequency compared to standard oxygen therapy in a randomized controlled trial of
128 subjects with mild acute CPE in the emergency department. (31) Recent evidence from 2 retrospective studies and
secondary analysis of a randomized controlled trial suggest that HFNC may be effective in treating hypercapnia in subgroups
of subjects with hypercapnic respiratory failure of all causes. (29,32,33) To our knowledge, no prospective study to date has
examined the benefits of HFNC treatment in early management of acute hypercapnic respiratory failure in an emergency
department.

We aimed to evaluate HFNC as a possible alternative to NIV in emergency department patients with acute hypercapnic CPE,
assessing its efficacy with regard to early changes in [mathematical expression not reproducible], respiratory parameters, and
indirect signs of WOB and comparing it to NIV.

Methods

Study Design and Setting

We conducted a prospective, observational, and comparative study in the emergency department of Montpellier University
Hospital with an annual census of 82,000 patients. This study was conducted as a preliminary study to the randomized
controlled OPTICAP study (ClinicalTrials.gov: NCT02874339). Our institutional review board approved the study (IRB-
MTP-12-03) with a waiver of written informed consent because the procedures were all part of routine care. It was designed
and reported according to STROBE guidelines.

This study was intended as a study preliminary to a larger randomized controlled trial. Because of the novelty of the study and
the lack of available data on the effect of HFNC on [mathematical expression not reproducible] at the time of study design, the
sample size was calculated based on data available for NIV. We planned to include 16 subjects in each group so as to be able
to show a significant 5 mm Hg decrease in [mathematical expression not reproducible], with an alpha of 5% and a study power
of 80%.

Selection of Participants

Adult patients admitted to the emergency department for acute hypercapnic respiratory failure related to acute CPE from
February 2015 to September 2016 were enrolled. Inclusion criteria were: (1) signs of acute respiratory failure including
breathing frequency of at least 20 breaths/min, useof accessory respiratory muscles or paradoxical abdominal movement, or
associated high blood pressure; (2) clinical suspicion of acute CPE based on a history of acute CPE, bilateral crackles on chest
examination, or bilateral infiltrates compatible with pulmonary edema on chest radiograph; (3) and hypercapnia defined as
[mathematical expression not reproducible] > 45 mm Hg on arterial blood gas testing.

The main exclusion criteria were clinical suspicion of exacerbation of COPD, long-term oxygen therapy or ventilatory support
for chronic lung disease, clinical suspicion of sepsis at admission including fever > 38.5[degrees]C, contraindication to NIV
according to international guidelines (9) for NIV treatment including hemodynamic instability (mean arterial pressure < 65 mm Hg, use of vasopressors) or a Glasgow coma scale score [less than or equal to] 12 points, requirement for endotracheal intubation, and use of ventilatory support prior to inclusion, including CPAP or NIV administered before admission to the hospital.

Ventilatory Support Modalities

Subject management was performed according to our standard of care for the management of respiratory failure. A tour
emergency department, HFNC was used as an alternative ventilatory support to NIV in patients showing signs of respiratory
failure; NIV was applied with careful monitoring to prevent escalation to invasive ventilation. Subjects received either NIV or
HFNC according to the presence of an attending emergency physician with expertise in using HFNC. Standardized protocols
were implemented for both NIV and HFNC treatment.

HFNC was administered via large- or medium-bore binasal prongs, using an Airvo2 system (Fisher and Paykel Healthcare,
Courtabeuf, France). Flow was initially set at 60 L/min, temperature was set at 37[degrees]C, and [mathematical expression
not reproducible] was adjusted to maintain a target [mathematical expression not reproducible] of at least 92%. Flow,
[mathematical expression not reproducible], and temperature could be adjusted to patient tolerance, as recommended.

NIV was administered through a face mask or oronasal mask(Respironics, Philips Healthcare, France), in a pressure controlled
continuous spontaneous ventilation mode using a dedicated device (Monnal T60 and T75, Airliquide Medical Systems, Antony,
France). Initial settings were: PEEP 5-10 cm [H.sub.2]O, pressure support 6-10 cm [H.sub.2]O above PEEP, and
[mathematical expression not reproducible] adjusted to a target [S.sub.p][O.sub.2] of at least 92%. Both ventilatory treatments
were applied in 1-h sessions and resumed as needed, according to international guidelines for NIV treatment. (9) Subjects
were closely monitored, with repeat clinical evaluation every 15 min and serial blood gas testing every hour. Standard oxygen
therapy was administered as required to maintain a target [S.sub.p][O.sub.2] of at least 92% between sessions or at
termination. Oxygen was delivered by nasal cannula or nonrebreather mask. Ventilatory support sessions were ended if signs
of acute respiratoryfailure had resolved or when endotracheal intubation criteria had been met.

Prespecified criteria for endotracheal intubation were used to avoid the risk of delayed intubation: hemodynamic instability,
deterioration of neurologic status, or signs of persisting or worsening respiratory failure as defined by at least 2 of the following
criteria: breathing frequency > 40 breaths/min,lack of improvement in signs of high respiratory muscle work load, and
[S.sub.p][O.sub.2] < 90% despite high [mathematical expression not reproducible] (ie,[mathematical expression not reproducible] > 0.80). (14) All subjects received concomitant standard medical therapy for CPE, including intravenous diuretics
and nitrate derivative.

Outcome Measurements

This was a preliminary study aimed at exploring the value of HFNC in the setting of hypercapnia. We chose [mathematical
expression not reproducible], which is an objective measurement, as the primary outcome. We evaluated its change at an early
time point, ie, at 1 h after initiation of ventilatory support. Secondary outcomes were change in breathing frequency, signs of
increased WOB, results of blood gas analysis, and comparisons between HFNC and NIV. All outcome criteria were measured
via serial evaluation performed at baseline and at 5-10 min after the end of each 1-h ventilatory session, with the subject
receiving standard oxygen therapy as required to maintain a target [S.sub.p][O.sub.2] of at least 92%, according to our
standard of care and international guidelines. (9)

Arterial blood gas testing was carried out according to clinical routine testing. Blood (1 mL) was sampled by radial artery
puncture and collected in heparinized syringes. Blood gas analyses were performed at the central biochemistry laboratory
using the Omni-S COBAS B221 system (RocheDiagnostics, France). Normal ranges were as follow: pH = 7.35-7.45;
[mathematical expression not reproducible] = 35-45 mm Hg; [mathematical expression not reproducible] = 78-98 mm Hg;
HC[O.sub.3] = 22-26 mmol/L; base excess = -2 to +2 mmol/L. Hypercapnia was defined as [mathematical expression not
reproducible]> 45 mm Hg. Acidosis was defined as pH [less than or equal to] 7.34.

Clinical parameters including breathing frequency, signs of increased WOB, and vital signs were assessed serially by the
treating emergency physician. Breathing frequency was measured over 1 min. Signs of increased WOB were evaluated based
on the use of accessory respiratory muscles (intercostal and subcostal muscles) and paradoxical abdominal breathing. Each of
the 3 signs was graded from 1 (absent) to 5 (very high). Scores were subsequently added on a 15-point scale assessing the
overall severity of signs of increased WOB.

We also collected chest radiographs and laboratory data including NT-proBNP, hs-cTNT, C-reactive protein, and bloodcell
counts according to our standard of care to adjudicate discharge diagnosis. Discharge diagnosis was adjudicated
retrospectively upon review of subject medical records, secondary to all additional examinations, including hospitalization data,
by 2 independent emergency physicians. Diagnosis of acute CPE was established according to the ESC Guidelines for
diagnosis and treatment of acute heart failure. (8)

Statistical Analysis

Datawere collected prospectively by the attending emergency physicians or research assistants using a standardized form.
Data were recorded and stored in an Excel database before transfer to SPSS 23.0 software (IBM, Armonk, New York) for
analysis.

Quantitative data were analyzed as median (interquartile range [IQR]) and were compared at baseline between groups using a
Mann-Whitney U test. Qualitative data were analyzed as numbers and proportion and were compared between groups using a
chi-square test or a Fisher exact test. The primary outcome was reported as the median of differences (IQR) in [mathematical
expression not reproducible] between baseline values and values after 1 h of treatment. Changes in secondary outcomes
between baseline values and values after 1 h of treatment were reported as median of differences (IQR). Before- and after-
treatment comparisons were tested using the Wilcoxon signed-rank test. Between-group differences for frequency data were
reported as odds ratios and 95% CIs; CIs were calculated using the modified Wald method. Results were considered
statistically significantly different if P [less than or equal to] .05 or if the 95% CI did not include 1 for the odds ratio.

Results

We enrolled a total of 45 subjects who presented with hypercapnic respiratory failure suspected to be due to acute CPE over
the study period (Fig. 1). We excluded 5 patients who presented with prespecified exclusion criteria, including underlying
exacerbation of COPD or sepsis.

We secondarily excluded 8 subjects with a final diagnosis other than CPE at emergency department or hospital discharge,
leaving 27 subjects in the study analysis. Subjects were elderly with a median age of 87 y (IQR 78-93). They presented with
severe acute respiratory failure, as shown by a breathing frequency of 32 breaths/min (IQR 26-39) and indirectsigns of
increased WOB recorded in 22 (81%) subjects, and moderate respiratory acidosis (Table 1). Main precipitating factors for CPE
were atrial fibrillation (15%), hypertensive crisis (26%), and respiratory tract infection (22%). Fifteen (56%) subjects received
NIV, and 12 (44%) received HFNC as ventilatory support. Baseline characteristics were similar in both treatment groups (Table
1).

HFNC was administered for a median duration of 67 (IQR 60-90) min, with a median flow range of 50 (IQR 40-60) L/min and a
median [mathematical expression not reproducible] of 0.50 (IQR 0.40-0.57). NIV was administered for a median duration of 70
(IQR 60-90) min. NIV was provided in the pressure controlled continuous spontaneous ventilation mode, with median
[mathematical expression not reproducible] of 0.60 (IQR 0.34-0.62). HFNC was not terminated prematurely before the end of
the 1-h ventilatory session in any subject, whether because of worsening of respiratory failureor failure to tolerate the
treatment. Two (7%) subjects were transferred to ICU after emergency department management; both had been treated with
NIV. No subjects required escalation to invasive ventilation, whether in the emergency department or the ICU.

Compared to baseline, [mathematical expression not reproducible] significantly improved 1 h after initiation of treatment in both
treatment groups (Table 2, Fig. 2). The median change in [mathematical expression not reproducible] (mm Hg) between
baseline and after 1 h of treatment was 7 (IQR 4-11, P = .002) for HFNC and 3 (IQR 1-8, P = .02) for NIV.

pH improved 1 h after initiation of treatment in both treatment groups (Table 2, Fig. 3). The median change in pH was 0.08
(IQR 0.04-0.24, P = .005) for HFNC and 0.04(IQR 0.01-0.12, P = .005) for NIV. Breathing frequency and signs of increased
WOB also significantly improved 1 h after initiation of treatment in both treatment groups (Table 2, Fig. 3).

HFNC improved breathing frequency with a median change of 5 breaths/min (IQR 2-12, P = .028). HFNC also reduced the
severity of increased WOB with a median change of 3 (IQR 1-6, P = .005) on the 15-point scale, and the number of subjects
with signs of increased WOB by 73% (P = .008).

NIV improved breathing frequency with a median change of 8 breaths/min (IQR 2-12, P = .036), and signs of increased WOB
with a median change of 2 (IQR 0-4, P = .005) on the 15-point scale. The number of subjects with signs of increased WOB was
reduced by 54% (P = .031).

There was no between-group difference in changes in [mathematical expression not reproducible] at 1 h after initiation of
treatment (Table 2). There was nobetween-group difference in percent of subjects with normalized [mathematical expression
not reproducible] or in other blood gas or clinical parameters recorded at 1 h, except for breathing frequency(P = .02).

Discussion

Toour knowledge, this is the first prospective study specifically designed to assess the efficacy of HFNC treatment in the early
management of patients with respiratory failure due to hypercapnic acute CPE. This study also compares HFNCto NIV in the
treatment of hypercapnia in a population of subjects presenting with acute respiratory failure of homogenous etiology in the
setting of early emergency department management. There are limited data to date comparing the efficacy of HFNC to that of
NIV in hypercapnic respiratory failure. Our results indicate that 1 h of HFNC treatment effectively improves [mathematical
expression not reproducible] and pH, as well as respiratory parameters such as breathing frequency and signs of increased
WOB in this specific patient population. Furthermore, our results suggest that HFNC may be as effective as NIV in improving
[mathematical expression not reproducible] after a 1-h ventilatory session in this specific patient population.

Besides studies exploring the use of HFNC to treat COPD exacerbation, data in the literature regarding acute hypercapnic
respiratory failure are from subjects with unselected respiratory failure. Our results confirm the effect of HFNC on hypercapnia
reported previously in a subset of emergency department subjects with hypercapnic respiratory failure of all causes in 2
retrospective studies. (32,33) Our results are also in line with the decrease in [mathematical expression not reproducible]
reported by Doshi et al (29) in a randomized controlled trial of subjects in the emergency department with unselected acute
respiratory failure. Doshi et al (29) reported a reduction in [mathematical expression not reproducible] of > 5 mm Hg at 1 h after
both HFNC and NIV, and a further decrease at 4 h in their subgroup analysis of 121 hypercapnic subjects. (30)

Hypercapnia is a common complication in patients with . The causes are multiple and still poorly understood. An
undocumented underlying chronic lung disease that increases dead space could favor hypercapnia. (3,4) In addition, rib cage
stiffness and respiratory muscle fatigue caused by increased airway pressure and obstruction due to edema may lead to
alveolar hypoventilation and hypercapnia. In our study population, which excluded chronic lung diseases and sepsis, age, and
high body mass index may be associated factors.

The ability of HFNC to reduce [mathematical expression not reproducible] in hypercapnic CPE may be mediated by complex
mechanisms. Two main mechanisms have been identified in experimental and pilot studies. First, HFNC is able to provide
continuous wash out of dead space in the upper airways, preventing the rebreathing of C[O.sub.2]. (15,16) HFNC thereby
enables a functional reduction in dead space and reduces minute ventilation by slowing down the breathing frequency and
reducing WOB, as shown in subjects with COPD. (34) HFNC also provides a slight level of PEEP (ie, 2-5 cm [H.sub.2]O),
which improves alveolar recruitment and tidal volume, contributing to alveoli clearance and to [mathematical expression not
reproducible] reduction. The PEEP-like effect is dependent on air flow, as well as on a closed mouth. (35) It may be reduced to
0-2cm [H.sub.2]O in open-mouth patients, as observed in subjects after cardiac surgery. (18,20) The PEEP-like effect may be
lowered in patients with acute hypercapnic CPE, who are often unable to maintain a closed mouth during HFNC treatment due
to severe respiratory failure. However, a flow-mediated effect that optimizes alveolar ventilation and gas exchange could also
play a role in the rapid decrease in [mathematical expression not reproducible] observed in our study, where a high flow was
administered to subjects (ie, 50 L/min).

In addition to the improvement in [mathematical expression not reproducible] and pH, our results suggest that HFNC may be
effective in decreasing the breathing frequency and signs of increased WOB. The improved breathing frequency and reduced
signs of increased WOB obtained after 1 h of treatment in our study probably result from all of these mechanisms combined.
HFNC has been shown to confer effects similar to those of NIV on diaphragmatic WOB as estimated with diaphragm
ultrasound. Additional benefits of HFNC over NIV have been reported in adult subjects with cystic fibrosis who had been
stabilized after over median 3 days under NIV. Both breathing frequency and minute ventilation were reduced. (36) No effects
were observed on transcutaneous C[O.sub.2] in this physiologic study, which included 15 subjects ventilated with HFNC and
NIV for 30 min in a cross-over random order, which was probably due to the short duration of HFNC treatment. (37) NIV
seemed to have a greater effect on breathing frequency than HFNC in our subjects. We assumed that NIV combined the effect
of pressure support and high PEEP to improve breathing frequency more quickly than HFNC, for which PEEP is limited,
especially when suboptimal nasal flow was administered (ie, < 60 L/min) or when the mouth of the patient was open. (17-18)

Several limitations have to be acknowledged. The main limitationis the small sample recruited from a single emergency
department. The lack of a randomized study design and of blinding are 2 other major limitations. The choice of ventilatory
support was based on the presence of an attending emergency physician trained in the use HFNC. We cannot exclude the
possibility that emergency department physicians’ expertise may have biased our results. We cannot exclude selection bias,
with NIV administered to more severe patients. Indeed, there seems to be a trend toward a higher baseline [mathematical
expression not reproducible] level in the NIV group. The study sample and resulting power (68%) were lower than planned.
However, the effects of HFNC on [mathematical expression not reproducible] were higher than expected a priori, resulting in a
significant difference in the primary outcome. This study was intended as pilot study. Preliminary data were used to design a
well-powered, randomized controlled noninferiority trial comparing the efficacy of HFNC and NIV in subjects with hypercapnic
respiratory failure due to CPE treated in the emergency department (OPTICAP). Although a drop of 5-10 mm Hg in
[mathematical expression not reproducible] following 1 h of HFNC treatment may not be relevant clinically, especially in
patients with severe hypercapnia, it should be regarded as a sign of early response to HFNC. Absence of improvement in
[mathematical expression not reproducible], with no associated improvement in pH or signs of WOB, at1 h should prompt the
emergency physician to reconsider thetreatment pathway or to consider escalating treatment to NIV or invasive mechanical

ventilation.

Conclusions

Our results, although preliminary, support the use of HFNC as alternative support for the early emergency department
management of hypercapnia in patients with hypercapnic respiratory failure related to acute CPE. HFNC could be considered
as an alternative to NIV in patients in the emergency department who are intolerant to NIV or for whom NIV is contraindicated.
Further randomized controlled studies are needed to explore the efficacy of HFNC compared to that of NIV in terms of longer
duration and subject-centered outcomes in acute hypercapnic CPE.

ACKNOWLEDGMENTS

We thank Jeffrey Arsham for reviewing and editing our original English-language manuscript. We thank Denis Frasca and
Nicolas Molinari for their help with statistical analyses. We thank the emergency department staff, including physicians,
residents, and nurses, for their contribution to patient screening, enrollment, and management throughout the study.

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Nicolas Marjanovic, Alexandre Flacher, Loic Drouet, Aude Le Gouhinec, Hakim Said, Jean-Francois Vigneau, Barbara Chollet,
Sophie Lefebvre, and Mustapha Sebbane

The authors are affiliated with the Department of Emergency Medicine and Prehospital Care, Montpellier University Hospital,
Montpellier, France.

Dr Marjanovic presented a version of this paper at the annual conference of the French Society for Emergency Medicine
(Urgences 2019), on June 6, 2019, and Dr Lefebvre presented a version of this paper at the annual conference of the French
Society of Anesthesia and Intensive Care on September 19, 2019, in Paris, France.

Fisher and Paykel provided the Optiflow Airvo2 devices. The authors have disclosed no conflicts of interest.

Correspondence: Mustapha Sebbane MD PhD, Emergency Department, Montpellier University Hospital, Hopital Lapeyronie,
191 avenue du Doyen Gaston Giraud, 34295 Montpellier, Cedex 5, France. E-mail: m-sebbane@chu-montpellier.fr.

QUICK LOOK

Current knowledge

High-flownasal cannula (HFNC) therapy is an alternative strategy for the management of acute hypoxemic respiratory failure of
heterogeneous etiologies. Recent evidence from retrospective studies and subgroup analysis of patients with hypercapnic
respiratory failure of allcauses suggest that HFNC may be effective in treating hypercapnia.

Table 1. Subject Characteristics at Baseline

Overall

Age, y 87 (78-93)
Men 10 (37)
Women 17 (63)
History
Chronic lung disease 7 (26)
Cardiogenic heart failure 8 (30)
Hypertension 15 (56)
Diabetes 5 (18)
Clinical parameters
Temperature, [degrees]C 37.1 (36.5-37.5)
f, breaths/min 32 (26-39)
[mathematical expression not reproducible],% (*) 95 (91-98)
Oxygen flow at baseline, L/min 4 (1-9)
Heart rate, beats/min 86 (75-118)
SBP, mm Hg 148 (117-177)
DBP, mm Hg 72 (62-89)
Signs of increased WOB 22 (81)
Increased WOB score ([dagger]) 6 (4-10)
Biological parameters
[mathematical expression not reproducible], mm Hg 55 (49-64)
[mathematical expression not reproducible], mm Hg 102 (70-136)
pH 7.29 (7.22-7.35
HC[O.sub.3], mEq 27 (25-29)
NT-proBNP, ng/L 4,547 (1,821-8,929)
hs-cTNT, ng/L 41.6 (25.4-72.5)
Creatinine, mmol/L 98 (68-117)
White blood cell count, [10.sup.9]/L 9.1 (6.4-14)
Other therapeutics
Furosemide 27 (100)
Nitrate derivative 16 (59)
Antibiotics 3 (11)
[[beta].sub.2] agonist 6 (22)

HFNC

Age, y 91 (77-94)
Men 7 (58)
Women 5 (42)
History
Chronic lung disease 4 (33)
Cardiogenic heart failure 3 (25)
Hypertension 5 (51)
Diabetes 2 (17)
Clinical parameters
Temperature, [degrees]C 37.5 (36.5-37.7)
f, breaths/min 34 (27-41)
[mathematical expression not reproducible],% (*) 93 (90-98)
Oxygen flow at baseline, L/min 3 (1-8)
Heart rate, beats/min 97 (80-128)
SBP, mm Hg 156 (124-172)
DBP, mm Hg 80 (63-85)
Signs of increased WOB 11 (92)
Increased WOB score ([dagger]) 7 (4-9)

What this paper contributes to our knowledge

Treatment with HFNC for 1 h improved [mathematical expression not reproducible] and respiratory parameters, including pH,
breathing frequency, and signs of increased work of breathing in hypercapnic patients presenting in the emergency department
with respiratory failure due to acute cardiogenic pulmonary edema. HFNC might be considered as alternative support for early
management of acute hypercapnic cardiogenic pulmonary edema in the emergency department setting.

DOI: 10.4187/respcare.07278

Biological parameters
[mathematical expression not reproducible], mm Hg 50 (49-61)
[mathematical expression not reproducible], mm Hg 99 (61-155)
pH 7.30 (7.20-7.36)
HC[O.sub.3], mEq 27 (25-30)
NT-proBNP, ng/L 3,520 (1,579-11,585)
hs-cTNT, ng/L 38.9 (29.5-74.4)
Creatinine, mmol/L 91 (69.8-114.8)
White blood cell count, [10.sup.9]/L 9.7 (6.9-13.4)
Other therapeutics
Furosemide 12 (100)
Nitrate derivative 8 (67)
Antibiotics 2 (17)
[[beta].sub.2] agonist 3 (25)

NIV

Age, y 82 (79-92)
Men 3 (20)
Women 12 (80)
History
Chronic lung disease 3 (20)
Cardiogenic heart failure 5 (33)
Hypertension 10 (67)
Diabetes 3 (20)
Clinical parameters
Temperature, [degrees]C 37.1 (36.4-37.3)
f, breaths/min 29 (26-36)
[mathematical expression not reproducible],% (*) 96 (94-98)
Oxygen flow at baseline, L/min 5 (2-14)
Heart rate, beats/min 79 (68-98)
SBP, mm Hg 146 (111-184)
DBP, mm Hg 71 (61-92)
Signs of increased WOB 11 (73)
Increased WOB score ([dagger]) 6 (3-11)
Biological parameters
[mathematical expression not reproducible], mm Hg 60 (48-71)
[mathematical expression not reproducible], mm Hg 102 (72-125)
pH 7.29 (7.21-7.35)
HC[O.sub.3], mEq 27 (24-29)
NT-proBNP, ng/L 5,069 (1,970-8,369)
hs-cTNT, ng/L 44.9 (17.6-74.9)
Creatinine, mmol/L 110 (63-126)
White blood cell count, [10.sup.9]/L 8.2 (6-17.9)
Other therapeutics
Furosemide 15 (100)
Nitrate derivative 8 (53)
Antibiotics 1 (7)
[[beta].sub.2] agonist 3 (20)

P

Age, y .40
Men .057
Women
History
Chronic lung disease .66
Cardiogenic heart failure .17
Hypertension .26
Diabetes >.99
Clinical parameters
Temperature, [degrees]C .23
f, breaths/min .28
[mathematical expression not reproducible],% (*) .31
Oxygen flow at baseline, L/min .21
Heart rate, beats/min .058
SBP, mm Hg >.99
DBP, mm Hg .94
Signs of increased WOB .22

Increased WOB score ([dagger]) .72
Biological parameters
[mathematical expression not reproducible], mm Hg .45
[mathematical expression not reproducible], mm Hg .88
pH .98
HC[O.sub.3], mEq .49
NT-proBNP, ng/L .76
hs-cTNT, ng/L .67
Creatinine, mmol/L .58
White blood cell count, [10.sup.9]/L .46
Other therapeutics
Furosemide >.99
Nitrate derivative >.99
Antibiotics >.99
[[beta].sub.2] agonist >.99

Data are presented as median (interquartile range) or n (%). P values
refer to comparison between groups. Overall: n = 27 subjects; HFNC: n =
12 subjects; NIV: n = 15 subjects.
(*) [mathematical expression not reproducible] could be recorded with
or without standard oxygen therapy.
([dagger]) Work of breathing is scored on a 15-point scale.
HFNC = high-flow nasal cannula
NIV = noninvasive ventilation
f = breathing frequency
SBP = systolic blood pressure
DBP = diastolic blood pressure
WOB = work of breathing
NT-proBNP = N-terminal pro b-type natriuretic peptide
hs-cTNT = hypersensitive cardiac troponin-T

Table 2. Changes in Blood Gas Analysis and Other Parameters After
Treatment

Baseline

Blood gas analysis
[mathematical expression not reproducible], mm Hg 50 (49-61)
D[mathematical expression not reproducible], mm Hg NA
[mathematical expression not reproducible] normalization NA
pH 7.30
(7.20-7.36)
[mathematical expression not reproducible], mm Hg 99 (61-155)
Respiratory parameters
f, breaths/min 34 (27-41)
[mathematical expression not reproducible],% 93 (90-98)
Increased WOB 11 (92)
WOB score ([dagger]) 7 (4-9)
Vital signs
Heart rate, beats/min 97 (80-128)
SBP, mm Hg 156 (124-172)
DBP, mm Hg 80 (63-85)

HFNC
After 1 h HFNC

Blood gas analysis
[mathematical expression not reproducible], mm Hg 45 (42-49)
D[mathematical expression not reproducible], mm Hg 7 (4-11)
[mathematical expression not reproducible] normalization 7 (8)
pH 7.38
(7.36-7.42)
[mathematical expression not reproducible], mm Hg 89 (75-99)
Respiratory parameters
f, breaths/min 26 (25-29)
[mathematical expression not reproducible],% 95 (94-98)
Increased WOB 3 (25)

WOB score ([dagger]) 3 (3-4)
Vital signs
Heart rate, beats/min 81 (73-128)
SBP, mm Hg 143 (117-162)
DBP, mm Hg 70 (57-80)

P

Blood gas analysis
[mathematical expression not reproducible], mm Hg .002
D[mathematical expression not reproducible], mm Hg NA
[mathematical expression not reproducible] normalization NA
pH .005

[mathematical expression not reproducible], mm Hg .42
Respiratory parameters
f, breaths/min .03
[mathematical expression not reproducible],% .44
Increased WOB .008
WOB score ([dagger]) .005
Vital signs
Heart rate, beats/min .24
SBP, mm Hg .07
DBP, mm Hg .31

Baseline

Blood gas analysis
[mathematical expression not reproducible], mm Hg 60 (48-71)
D[mathematical expression not reproducible], mm Hg NA
[mathematical expression not reproducible] normalization NA
pH 7.29
(7.21-7.35)
[mathematical expression not reproducible], mm Hg 102 (72-125)
Respiratory parameters
f, breaths/min 29 (26-36)
[mathematical expression not reproducible],% 96 (94-98)
Increased WOB 11 (73)
WOB score ([dagger]) 6 (3-11)
Vital signs
Heart rate, beats/min 79 (68-98)
SBP, mm Hg 146 (111-184)
DBP, mm Hg 71 (61-92)

NIV
After 1 h NIV

Blood gas analysis
[mathematical expression not reproducible], mm Hg 52 (44-61)
D[mathematical expression not reproducible], mm Hg 3 (1-8)
[mathematical expression not reproducible] normalization 6 (5)
pH 7.34
(7.30-7.40)
[mathematical expression not reproducible], mm Hg 83 (72-126)
Respiratory parameters
f, breaths/min 21 (18-26)
[mathematical expression not reproducible],% 96 (95-97)
Increased WOB 5 (33)
WOB score ([dagger]) 3 (3-4)
Vital signs
Heart rate, beats/min 76 (63-93)
SBP, mm Hg 128 (109-142)
DBP, mm Hg 66 (58-71)

P

Blood gas analysis
[mathematical expression not reproducible], mm Hg .02
D[mathematical expression not reproducible], mm Hg NA
[mathematical expression not reproducible] normalization NA
pH .005

[mathematical expression not reproducible], mm Hg .86
Respiratory parameters
f, breaths/min .036
[mathematical expression not reproducible],% .16
Increased WOB .031
WOB score ([dagger]) .005
Vital signs
Heart rate, beats/min .036
SBP, mm Hg .02
DBP, mm Hg .13

P (*)

Blood gas analysis
[mathematical expression not reproducible], mm Hg .08
D[mathematical expression not reproducible], mm Hg .09
[mathematical expression not reproducible] normalization .43
pH .11

[mathematical expression not reproducible], mm Hg .7
Respiratory parameters
f, breaths/min .03
[mathematical expression not reproducible],% .56
Increased WOB .69
WOB score ([dagger]) .65
Vital signs
Heart rate, beats/min .14
SBP, mm Hg .11
DBP, mm Hg .42

Data are presented as median (interquartile range) or n (%). Changes in
[mathematical expression not reproducible] are reported as median of
differences (interquartile range). P values refer to comparison between
groups. (*) P values refer to comparisons between HFNC and NIV at 1 h.
P [less than or equal to] .05 is considered statistically significant.
([dagger]) Work of breathing is scored on a 15-point scale.
HFNC = high-flow nasal cannula
NIV = noninvasive ventilation
NA = not applicable
f = breathing frequency
WOB = work of breathing
SBP = systolic blood pressure
DBP = diastolic blood pressure

Copyright: COPYRIGHT 2020 Daedalus Enterprises, Inc.
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Source Citation
Marjanovic, Nicolas, et al. “High-Flow Nasal Cannula in Early Emergency Department Management of Acute Hypercapnic

Respiratory Failure Due to Cardiogenic Pulmonary Edema.” Respiratory Care, vol. 65, no. 9, Sept. 2020, p. 1241+. Gale
OneFile: Nursing and Allied Health, link.gale.com/apps/doc/A635192464/PPNU?u=canyonuniv&sid=PPNU&xid=94da256e.
Accessed 10 Mar. 2021.

Gale Document Number: GALE|A635192464

http://www.rcjournal.com/

HIGH FLOW NASAL CANNULA REFERENCES

Marjanovic, N., Flacher, A., Drouet, L., Gouhinec, A. L., Said, H., Vigneau, J.-F., Chollet, B., Lefebvre, S.,
& Sebbane, M. (2020, September). High-Flow Nasal Cannula in Early Emergency Department
Management of Acute Hypercapnic Respiratory Failure Due to Cardiogenic Pulmonary Edema.
Respiratory Care, 65(9), 1241+.
https://link.gale.com/apps/doc/A635192464/PPNU?u=canyonuniv&sid=PPNU&xid=94da256e

RESPIRATORY RESEARCH REFERENCES

Curley, M. A. (2011, September). Respiratory research in the critically ill pediatric patient: why is it so
difficult? Respiratory Care, 56(9), 1247+.
https://link.gale.com/apps/doc/A268405180/PPNU?u=canyonuniv&sid=PPNU&xid=ed3d0e64