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Delclaux C, L'Her E, Alberti C, et al. Treatment of Acute Hypoxemic Nonhypercapnic Respiratory Insufficiency With Continuous Positive Airway Pressure Delivered by a Face Mask: A Randomized Controlled Trial. JAMA. 2000;284(18):2352–2360. doi:10.1001/jama.284.18.2352
Context Continuous positive airway pressure (CPAP) is widely used in the belief
that it may reduce the need for intubation and mechanical ventilation in patients
with acute hypoxemic respiratory insufficiency.
Objective To compare the physiologic effects and the clinical efficacy of CPAP
vs standard oxygen therapy in patients with acute hypoxemic, nonhypercapnic
Design, Setting, and Patients Randomized, concealed, and unblinded trial of 123 consecutive adult
patients who were admitted to 6 intensive care units between September 1997
and January 1999 with a PaO2/FIO2 ratio of 300 mm Hg
or less due to bilateral pulmonary edema (n = 102 with acute lung injury and
n = 21 with cardiac disease).
Interventions Patients were randomly assigned to receive oxygen therapy alone (n =
61) or oxygen therapy plus CPAP (n = 62).
Main Outcome Measures Improvement in PaO2/FIO2 ratio, rate of endotracheal
intubation at any time during the study, adverse events, length of hospital
stay, mortality, and duration of ventilatory assistance, compared between
the CPAP and standard treatment groups.
Results Among the CPAP vs standard therapy groups, respectively, causes of respiratory
failure (pneumonia, 54% and 55%), presence of cardiac disease (33% and 35%),
severity at admission, and hypoxemia (median [5th-95th percentile] PaO2/FIO2 ratio, 140 [59-288] mm Hg vs 148 [62-283] mm Hg; P = .43) were similarly distributed. After 1 hour of treatment,
subjective responses to treatment (P<.001) and
median (5th-95th percentile) PaO2/FIO2 ratios were greater
with CPAP (203 [45-431] mm Hg vs 151 [73-482] mm Hg; P
= .02). No further difference in respiratory indices was observed between
the groups. Treatment with CPAP failed to reduce the endotracheal intubation
rate (21 [34%] vs 24 [39%] in the standard therapy group; P = .53), hospital mortality (19 [31%] vs 18 [30%]; P = .89), or median (5th-95th percentile) intensive care unit length
of stay (6.5 [1-57] days vs 6.0 [1-36] days; P =
.43). A higher number of adverse events occurred with CPAP treatment (18 vs
6; P = .01).
Conclusion In this study, despite early physiologic improvement, CPAP neither reduced
the need for intubation nor improved outcomes in patients with acute hypoxemic,
nonhypercapnic respiratory insufficiency primarily due to acute lung injury.
Patients with severe hypoxemic acute respiratory insufficiency often
require life-supporting mechanical ventilation (MV). The placement of an endotracheal
tube to allow for MV is associated with a significant risk of local airway
injury and ventilator-associated pneumonia. Several studies found that noninvasive
ventilation (NIV) reduced the need for endotracheal intubation in patients
with acute exacerbations of chronic obstructive pulmonary disease (COPD).1,2
In addition, reports published over many years have suggested that patients
with cardiogenic pulmonary edema (CPE) or non-CPE may benefit from continuous
positive airway pressure (CPAP) delivered by a face mask.3-16
Most of these studies were nonrandomized, and in the few randomized studies,
the primary end point was often based on gas exchange criteria after a predetermined
duration of CPAP treatment.7,13
These studies demonstrated the ability of CPAP to improve hypoxemia but not
its ability to reduce the need for intubation and MV. However, one single-center,
randomized study found strong evidence that CPAP use reduced the need for
endotracheal intubation in patients with severe hypercapnic CPE.10
In patients with acute lung injury (ALI), applying positive pressure
to the airway opening has been shown to lessen the reduction in functional
residual capacity and to improve respiratory mechanics and gas exchange.17 These data have led intensive care unit (ICU) physicians
to widely use CPAP to prevent subsequent clinical deterioration and to reduce
the need for endotracheal intubation.5,6,8,9,11
However, the efficacy of this practice has not been evaluated. In particular,
uncertainty continues to surround the potential clinical benefits of CPAP
delivered by a face mask to patients with acute hypoxemic, nonhypercapnic,
respiratory insufficiency due to bilateral pulmonary edema, with or without
underlying cardiac disease.
We conducted a multicenter, prospective, randomized trial to compare
the efficacy of CPAP delivered through a full face mask with standard oxygen
therapy in ICU patients admitted with ALI with or without underlying cardiac
Between September 28, 1997, and January 19, 1999, 123 consecutive adults
admitted with acute respiratory insufficiency secondary to pulmonary edema
were recruited prospectively at the medical ICUs of 6 hospitals (Henri Mondor,
Créteil, France; La Cavalle Blanche, Brest, France; Croix Rousse, Lyon,
France; Sant Pau, Barcelona, Spain; Monastir Hospital, Monastir, Tunisia;
and La Sapienza University, Rome, Italy), which previously had participated
in NIV studies and had experience with the various NIV techniques.1,16,19,20 The
study protocol was approved by the appropriate institutional review boards.
Informed consent was obtained from all the patients.
Inclusion criteria were as follows: (1) acute respiratory insufficiency,
defined as the PaO2/FIO2 ratio of 300 mm Hg or less
after breathing oxygen at 10 L/min or more for 15 minutes, with the inspired
fraction of oxygen determined by a portable oxygen analyzer (MiniOX I; Mine
Safety Appliances Co, Pittsburgh, Pa); (2) the presence of bilateral lung
infiltrates on a posteroanterior chest radiograph; and (3) randomization within
3 hours after the criteria were first fulfilled.
Exclusion criteria were patients younger than 18 years; intubation was
refused or contraindicated; history of COPD; acute respiratory acidosis (defined
as a pH <7.30 and a PaCO2 >50 mm Hg); systolic blood pressure
less than 90 mm Hg under optimal therapy (fluid repletion); ventricular arrhythmias;
coma or seizures; life-threatening hypoxemia (defined as an SaO2
<80% with an oxygen mask); use of epinephrine or norepinephrine; and the
inability to clear copious airway secretions.
The precipitating cause of acute respiratory insufficiency and the presence
of a chronic or acute cardiac disease were recorded at admission. Patients
were randomly assigned to standard treatment (oxygen alone) or standard treatment
plus CPAP delivered by a face mask. Patients with ALI and no history of chronic
lung disease constituted the primary group of interest. Since increased pulmonary
permeability may coexist with left atrial or pulmonary capillary hypertension,18 patients with a history of cardiac disease also were
included. The coronary care unit (CCU), independent from the medical ICU,
treated patients with ischemic myocardial disease and those with heart failure
deemed unlikely to require MV. Patients with obvious cardiac disease were
primarily treated in the CCU, however, the only ones who were considered for
the study were those patients with cardiac disease who had a possible superimposed
noncardiac cause of respiratory failure, patients with extreme severity and
no response to treatment, or patients in whom cardiac insufficiency previously
was not known.
Because a cardiogenic mechanism contributing to the pulmonary edema
might have had a substantial influence on the study results, the randomization
was stratified based on whether there was an underlying cardiac disease (chronic
cardiac disease with class II, III, or IV of the New York Heart Association
functional classification or acute de novo cardiac disease). The stratification
was not based on whether it was CPE or non-CPE because in severely ill patients
with chronic cardiac disease admitted for acute respiratory insufficiency,
it is sometimes difficult to determine on admission whether decompensated
heart failure is the only cause of the episode of respiratory insufficiency.
Including patients with a history of cardiac disease, it was likely that using
clinical examination and simple biological criteria a proportion of these
patients would be eventually diagnosed as having cardiac disease. The stratification
was to ensure that patients with an underlying cardiac disease were equally
distributed between the 2 study groups. Sealed envelopes were used to randomly
assign patients to their treatment group.
Patients assigned to the standard treatment group (n = 61) received
oxygen delivered through a face mask. The FIO2 was measured using
the same oxygen analyzer in each center: the tip of the oxygen analyzer was
introduced via a small hole in the face mask. The goal was to achieve a pulse
oximetry SaO2 greater than 90%. Oxygen was delivered until endotracheal
intubation, death, or fulfillment of oxygen delivery cessation criteria (an
SaO2 ≥ 92% without oxygen and a respiratory rate < 30/min).
All patients with suspected cardiac insufficiency received diuretics
as required. Infectious causes were treated with antibiotics. Gastrointestinal
tract prophylaxis was administered to patients who were intubated with MV
or in patients with a history of gastrointestinal tract ulcer.21
Patients did not receive systematic ulcer prophylaxis under CPAP therapy.
Patients assigned to the CPAP plus oxygen group (n = 62) received periods
of CPAP in addition to the standard treatment. All study centers used a Vital
Signs, Inc (Totowa, NJ) device.22 The device
included (1) a Vital Flow 100 CPAP Flow Generator that delivered a flow (rate
0-130 L/min) that could be adjusted to the patient's inspiratory flow requirement,
with an adjustable FIO2 within the 34% to 100% range; (2) a spring-loaded,
positive end-expiratory pressure (PEEP) valve that provided a fixed end-expiratory
pressure (5, 7.5, or 10 cm H2O) with minimal resistance to airflow;
(3) a full face mask composed of a transparent mask and a soft inflatable
cushion; and (4) a dedicated headstrap. Airway humidification was achieved
by using a heated humidifier (MR640; Fisher & Paykel, Auckland, NZ).
For at least the first 6 to 12 hours, CPAP was given continuously and
then discontinuously as indicated based on patient tolerance and on whether
the pulse oximetry SaO2 was greater than 90% under oxygen alone.
For all patients, CPAP was started at 7.5 cm H2O. The level
could be decreased to 5 cm H2O or increased to 10 cm H2O
as needed based on the clinical response and tolerance. Continuous positive
airway pressure was delivered for at least 6 h/d and was continued until endotracheal
intubation, death, or fulfillment of the following cessation criteria: PaO2/FIO2 ratio greater than 300 mm Hg, or SaO2 between
95% and 100% and FIO2 of 40% or less without CPAP, or CPAP duration
less than 6 h/d. The criteria for oxygen delivery cessation were the same
as in the standard therapy group.
Endotracheal intubation was performed in patients with any of the following:
decreased alertness or major agitation requiring sedation, clinical signs
of exhaustion (active contraction of the accessory muscles of respiration
with paradoxical abdominal or thoracic motion), hemodynamic instability, cardiac
arrest, or refractory hypoxemia (SaO2 <85% with FIO2
Arterial blood gas values, respiratory rate, systolic blood pressure,
and pulse rate were collected at baseline, after 1 hour, and between the 6th
and 12th hours; the worst value of each of these variables was recorded once
a day. The response to treatment was recorded 1 hour after the initiation
of CPAP or oxygen treatment by asking patients to grade the effect of treatment
on their dyspnea: + 2, marked improvement; + 1, slight improvement; 0, no
change; − 1, slight deterioration; and − 2, marked deterioration.
The Simplified Acute Physiologic Score II23
(SAPS II) and the Logistic Organ Dysfunction score24
were calculated 24 hours after ICU admission and 24 hours after study inclusion.
Since CPAP use is assigned a specific weight in both scoring systems, the
treatment assigned by randomization could in itself modify the scores; consequently,
both scores were calculated without including the points for respiratory failure.
The following adverse events were recorded during spontaneous ventilation:
facial skin necrosis, conjunctivitis, sinusitis, gastric distension, aspiration,
pneumothorax, nosocomial pneumonia (based on clinical criteria), stress gastrointestinal
tract ulcer and bleeding, and cardiac arrest; and during MV: cardiac arrest
at endotracheal intubation, tracheal injury, pneumothorax, sinusitis, nosocomial
pneumonia (based on clinical criteria and quantitative cultures of protected
bacteriological sampling of the lungs), and stress gastrointestinal tract
ulcer and bleeding. Among these events, only adverse events not present at
admission were counted as those that occurred during the ICU stay.
The primary outcome variable was endotracheal intubation and MV at any
time during the study. The patient was used as the randomization unit. The
randomization protocol, computer-generated by the Department of Biostatistics
of Henri Mondor Hospital, was stratified based both on the study center and
the presence or absence of an underlying cardiac disease. Based on a preliminary
retrospective evaluation of medical charts of patients fulfilling the inclusion
criteria, the predicted intubation rate was approximately 40%. Sixty patients
per group were required to demonstrate a difference in the rate of endotracheal
intubation from 40% to 15% between the 2 groups, with a type I risk of error
of 5% and a power of 80%. The 15% rate of intubation was chosen because previous
studies had shown that 0% to 6% of patients receiving CPAP to treat CPE were
eventually intubated, but that a lower efficacy could be expected in non-CPE.10,13 Secondary outcome variables were
the length of ICU and hospital stays, number of adverse events during spontaneous
ventilation or MV (not present at admission; see above), duration of ventilatory
assistance, and hospital mortality rate.
Values are reported as medians with the 5th to 95th percentiles. All
statistical analyses were performed on an intention-to-treat basis, that is,
including all randomized patients. χ2 Tests or Fisher exact
tests were used to compare categorical variables between the 2 treatment groups.
Continuous variables were compared using the Wilcoxon rank sum test or Wilcoxon
matched pairs signed rank test when appropriate. P
values for all statistical tests were 2-tailed.
The Kaplan-Meier curve for intubation rates was plotted during the entire
follow-up. The log-rank test was used to compare the 2 randomized groups.
Independent factors associated with endotracheal intubation were analyzed
using a Cox regression model and then used to adjust treatment comparisons
considering both a stratified model based on the preexistence of cardiac disease
and a nonstratified model. In the nonstratified model, the interaction between
the treatment group and the cardiac disease group was formally tested by entering
an indicator interaction in the Cox regression model and by using a test for
heterogeneity.25 In the multivariate analysis,
in addition to baseline data, the persistence of respiratory failure (defined
as a PaO2/FIO2 ratio ≤200 mm Hg at 1 hour of treatment)
also was evaluated as an index of respiratory severity. This index was determined
at admission and at 1 hour, since most patients with fluid overload are already
improved at 1 hour, whereas patients with nonhydrostatic lung edema are still
hypoxemic. All computations were done using SAS software (SAS Institute, Cary,
The individuals responsible for assessing and recording the outcomes
(E.L'H., J.M., F.A., G.C., C.G., F.S., Y.L., and M.A.) only had access to
patient medical charts; biostatisticians (C.A. and E.L.) were responsible
for the computer database; and patient data were collected by the other investigators
(C.D., F.L., and L.B.).
The baseline characteristics of the 123 patients included in this study
are shown in Table 1. Patients
with an underlying cardiac disease were equally distributed between the 2
treatment groups (11 for oxygen alone and 11 for oxygen plus CPAP). The follow-up
was complete for all patients (Figure 1).
At study entry, all 123 patients had acute respiratory insufficiency
(defined as a PaO2/FIO2 ratio ≤300 mm Hg and the
presence of bilateral infiltrates on chest radiograph). Of these 123 patients,
21 (17%) eventually were classified as having pure cardiac decompensation;
102 patients (83%) had ALI (PaO2/FIO2 ratio ≤300
mm Hg due to increased lung permeability), among whom 74 (60%; 59 patients
without cardiac disease plus 15 with associated cardiac disease) had a PaO2/FIO2 ratio of 200 mm Hg or lower, indicating acute respiratory
distress syndrome (ARDS). Precipitating causes of pulmonary edema were equally
distributed between the 2 treatment groups (Table 2). Infectious causes represented 37 (61%) of the 61 patients
treated with oxygen alone and 42 (68%) of the 62 patients treated with oxygen
plus CPAP; direct lung injury due to pneumonia was the most frequent cause
(55% and 54%, respectively).
After 1 hour of treatment, patients receiving oxygen plus CPAP had a
significantly greater PaO2/FIO2 ratio increase (P = .02) and a significantly greater subjective response
to treatment than patients receiving oxygen alone (P<.001)
(Table 3 and Figure 2). Compared with baseline values at entry, CPAP also was
associated with a significant reduction in respiratory rate (P<.001) and a significant increase in pH levels (P = .01) at the end of the first treatment hour. During the remainder
of the study, however, these indices showed no significant differences between
the 2 treatment groups.
Nine of the 62 patients (14%) were unable to tolerate CPAP treatment:
2 of the 9 tolerated CPAP for less than 10 minutes and 7 for longer than 6
hours. Three of the 9 patients eventually required intubation.
The median percent SaO2 over time was consistently above
90% in both treatment groups (Figure 3).
In the oxygen plus CPAP group, the median daily duration of CPAP was significantly
longer in patients who eventually required intubation than in those who did
not (P = .03 at day 2, P
= .048 at day 3, and P = .02 at day 4) (Figure 4).
No significant differences were found between the 2 treatment groups
for any of the clinical outcome variables studied, including rate of endotracheal
intubation, length of hospital stay, and hospital mortality (Table 4 and Figure 5).
The indications for endotracheal intubation were similar in the 2 treatment
groups (Table 5). Four patients
randomized to the oxygen alone group subsequently were given oxygen plus CPAP
treatment, and another patient received NIV pressure support. Two patients
(1 in each group) were found a posteriori to meet an exclusion criterion (contraindication
to endotracheal intubation); neither patient was intubated and both died in
the ICU. Excluding these patients or switching them to the other group had
no significant effects on outcomes.
A multivariate analysis demonstrated that the SAPS II score (hazard
ratio [HR] per 1 SAPS II point, 1.05; 95% confidence interval, [1.03-1.07]),
absence of a cardiac disease (HR, 2.27 [1.08-4.75]), and PaO2/FIO2 ratio 200 mm Hg or less at 1 hour of treatment (HR, 2.35 [1.20-4.60])
were independently associated with endotracheal intubation. Treatment group
assignment as well as a PaO2/FIO2 ratio of 200 mm Hg
or less on admission were not associated with endotracheal intubation. The
absence of treatment effect remained unchanged when the stratified analysis
on preexistence of cardiac disease was performed. Moreover, there was no interaction
between the treatment and the cardiac disease groups.
When patients with and without an underlying cardiac disease were analyzed
separately, no significant benefits of oxygen plus CPAP treatment were found
for the need for endotracheal intubation, length of hospital stay, or hospital
mortality (Table 4).
Adverse events that occurred during spontaneous and MV were significantly
more common in the CPAP group (P = .01) (Table 6).
This multicenter, randomized, concealed, but unblinded trial of 123
patients showed that, despite early physiologic benefits, treatment with oxygen
plus CPAP delivered by a face mask did not reduce the need for intubation
in patients with acute, hypoxemic, and nonhypercapnic respiratory insufficiency,
among whom a majority had ALI, and it did not impact the length of hospital
stay or hospital mortality. A higher number of adverse events occurred with
the use of CPAP.
All centers were experienced in the delivery of face-mask ventilation
and had previously participated in NIV studies.1,16,19,20
Analysis of daily CPAP treatment duration data showed that CPAP was used for
at least 6 h/d, as required by the study protocol. Use of intubation in patients
in the oxygen plus CPAP group was not explained by a low compliance with CPAP
treatment. On the contrary, patients who eventually required intubation had
significantly longer daily CPAP treatment durations (Figure 3). In addition, SaO2 goals were achieved in both
groups (Figure 2). The fact that
a longer duration of CPAP use per day was associated with intubation could
raise the hypothesis that additional respiratory load due to CPAP use may
favor intubation. To minimize this problem, we used a continuous flow system
with adequate airway humidification and minimal loads imposed by the circuit.
Because the CPAP device was an adjustable-flow venturi, when high FIO2 is used, a slight reduction in total outflow may occur.22
Thus, it is possible that the CPAP system was less efficient for the most
severe patients needing the highest FIO2 and the highest flow.
Nevertheless, the multivariate analysis demonstrated that a PaO2/FIO2 ratio at 1 hour of 200 mm Hg or lower was an independent risk factor
for intubation whatever the treatment type. This index was taken at 1 hour
to more accurately identify patients with ARDS, since most patients with fluid
overload are already improved at 1 hour. This parameter was a marker of severity,
and this could not be reversed by CPAP treatment despite increasing its use.
Oxygen plus CPAP therapy was associated with a significantly greater
improvement of PaO2/FIO2 ratio within the first hour
than oxygen alone therapy. As a result, oxygenation was improved after 1 hour
in the CPAP group and of patient dyspnea. Similar results were obtained with
CPAP treatment in patients with cardiac disease or in the short-term studies
in patients with ALI.7,13,17
During the remainder of the study, no differences in oxygenation were demonstrated.
The leading cause of acute respiratory insufficiency in our study was
nonhydrostatic edema, that is, ALI (101 [82%] of the patients). The large
proportion of these patients with criteria for ARDS is representative of the
relative distribution of these 2 degrees of severity found in previous studies
(ALI [with no criteria for ARDS]: 1.8% vs ARDS: 6.9%, among all ICU admissions
in a recent multicenter prevalence survey).26
Our population included patients with cardiac dysfunction, a factor that may
have influenced the efficacy of CPAP treatment. Results were similar in patients
with and without cardiac disease (Table
4). Our study was not powered to determine the efficacy of oxygen
plus CPAP treatment in the subgroup of patients with pure CPE nor in specific
subsets of patients with non-CPE.
Bersten et al10 reported that oxygen
plus CPAP treatment in patients with severe hypercapnic CPE resulted in early
physiologic improvement and significantly reduced the need for intubation;
the PaO2/FIO2 ratio improvement with CPAP use was significant
only at 30 minutes, as compared with oxygen alone. The prompt improvement
with CPAP use was probably because the patients had rapidly resolving conditions:
mean (SD) CPAP duration of use was only 9.3 (4.9) hours and mean (SD) ICU
stay length was 1.2 (0.4) days. These results suggest that the patients had
extremely acute conditions in which CPAP treatment was beneficial because
the rapid improvement it afforded, although transient, lasted long enough
to give drug therapy time to act. Similar benefits were suggested by L'Her
et al.16 In these studies, most patients had
hypercapnic CPE, indicating frank ventilatory failure (patients with hypercapnia
were not included in our study). Hypoxemic nonhypercapnic pulmonary edema
in cardiac patients seems to respond to CPAP treatment differently for 2 possible
reasons: because the evolution may be spontaneously favorable under medical
therapy alone in patients with pure CPE or because the evolution may become
similar to ALI when the disease is triggered by a noncardiac event in cardiac
patients. The existence of ventilatory failure, with hypercapnia and respiratory
acidosis, indicates that the immediate prognosis depends on the ability of
the ventilatory function to cope with the loads. This can be obtained by reducing
the loads on the system (medications) or by assisting the respiratory muscle
function (CPAP or NIV therapy). The absence of frank ventilatory failure may
explain why these patients do not clearly benefit from CPAP therapy. Therefore,
CPAP may be beneficial in patients with a poorly tolerated but transient hypercapnic
episode of CPE but may be less advisable in patients with longer-lasting hypoxemia.
Confalonieri and colleagues27 recently
reported beneficial effects of NIV in patients with severe community-acquired
pneumonia, but this result was essentially explained by the subgroup of patients
with COPD. In a study by Wysocki et al28 of
NIV in patients without COPD admitted for acute respiratory failure, the need
for endotracheal intubation and the time from study entry to endotracheal
intubation affected were not decreased by NIV. In addition, the results suggested
that benefits occurred only in the subgroup of patients with hypercapnia.
Antonelli et al20 recently reported the
beneficial effects of NIV in selected patients with hypoxemia and acute respiratory
failure deemed to require intubation. They used pressure support ventilation
in addition to PEEP (mean [SD], 5.1 [1.4] cm H2O) and found that
this treatment improved gas exchange and was less likely to cause adverse
effects compared with conventional MV. Mean (SD) duration of NIV was only
2 (1) days in the patients who did not require intubation. It remains unclear
whether the higher level of support provided by the concomitant use of pressure
support and PEEP may explain the better results in the study by Antonelli
et al20 as compared with our study. Differences
in selection criteria also may have contributed to the differences in results
between these 2 studies.
If CPAP therapy does not reduce the need for endotracheal intubation,
then it may carry its own risks. Oxygen plus CPAP treatment was accepted by
86% of our patients, initially produced few adverse effects, and improved
subjective response compared with oxygen therapy. Nevertheless, of 8 patients
treated with CPAP, 4 experienced cardiac arrest and 4 who were treated with
CPAP experienced upper gastrointestinal tract bleeding. Continuous positive
airway pressure was not associated with a significant increase in adverse
events during spontaneous ventilation (7 vs 1, P
= .06). However, it may be difficult to ensure that the adverse effects occurring
during MV may not be explained by the period of spontaneous ventilation, for
instance, for gastrointestinal tract bleeding (4 patients in the oxygen plus
CPAP group and 0 in the oxygen alone group). In some cases, CPAP may prolong
the stressful period of spontaneous breathing, which could have been reduced
by MV, allowing to rest the patient. Although this study was not powered enough
to detect small benefits of CPAP therapy, it found a significantly higher
number of adverse events in centers well trained in the NIV technique.
In conclusion, CPAP provided rapid but transient improvements in oxygenation
and dyspnea compared with standard therapy but did not decrease endotracheal
intubation in patients with acute, nonhypercapnic respiratory insufficiency.
However, we found significantly more adverse events with CPAP.
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