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Noninvasive Positive-Pressure Ventilation To Treat Hypercapnic Coma Secondary to Respiratory Failure^*

^* From the Intensive Care Unit (Drs. Gónzalez Díaz, Carrillo Alcaraz, Pardo Talavera, Jara Pérez, Esquinas Rodriguez, and García Cordoba), Hospital JM Morales Meseguer, Murcia, Spain; and Pulmonary, Critical Care, and Sleep Division (Dr. Hill), Tufts-New England Medical Center, Boston, MA.

Correspondence to: Gumersindo Gónzalez Díaz, MD, Intensive Care Unit. Hospital Morales Meseguer, C/Marqués de los Velez s/n, 30008 Murcia, Spain; e-mail: gumersindoj.gonzalez{at}carm.es

	Abstract

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Introduction: Hypercapnic coma secondary to acute respiratory failure (ARF) is considered to be a contraindication to the use of treatment with noninvasive positive-pressure ventilation (NPPV). However, intubation exposes these patients to the risk of complications such as nosocomial pneumonia, sepsis, and even death.

Patients and methods: We performed a prospective, open, noncontrolled study to assess the outcomes of NPPV therapy in patients with a Glasgow coma scale (GCS) score of 8 points due to ARF. The primary goal of the study was to determine the success of NPPV therapy (defined as a response to therapy allowing the patient to avoid endotracheal intubation, and to survive a stay in the ICU and at least 24 h on a medical ward) in patients with hypercapnic coma, compared to those who started NPPV therapy while awake. The secondary goal of the study was to identify the variables that can predict a failure of NPPV therapy in these patients.

Results: A total of 76 coma patients (80%) responded to NPPV therapy, and 605 patients with GCS scores > 8 responded to therapy (70%; p = 0.04). A total of 25 coma patients died in the hospital (26.3%), and 287 noncoma patients died in the hospital (33.2%; p = 0.17). The variables related to the success of NPPV therapy were GCS score 1 h posttherapy (odds ratio [OR], 2.32; 95% confidence interval [CI], 1.53 to 3.53) and higher levels of multiorgan dysfunction, as measured by the maximum sequential organ failure assessment index score reached during NPPV therapy (OR, 0.72; 95% CI, 0.55 to 0.92).

Conclusions: We concluded that selected patients with hypercapnic coma secondary to ARF can be treated as successfully with NPPV as awake patients with ARF.

Key Words: acute respiratory failure • bilevel positive airway pressure • COPD • hypercapnic coma • noninvasive ventilation

	Introduction

TOP Abstract Introduction Materials and Methods Results Discussion References

 
In recent years, the use of therapy with noninvasive positive-pressure ventilation (NPPV) has become more widespread in ICUs for the treatment of acute respiratory failure (ARF).¹² In patients who experience acute exacerbations of COPD, NPPV therapy not only improves physiologic manifestations of respiratory failure, but also reduces the need for endotracheal intubation, the complications related to mechanical ventilation, the duration of hospitalization, and hospital mortality.^345678910 Furthermore, the treatment of these patients by NPPV may be more cost-effective than traditional therapies, including invasive mechanical ventilation.¹¹ Less evidence supports the use of NPPV to treat hypoxemic respiratory failure. The six randomized studies^121314151617 thus far published on this application have not provided definitive results, mainly because they have included small numbers of patients with ARF of diverse etiologies.¹⁸¹⁹

Of course, either acute hypoventilatory or hypoxemic respiratory failure can eventually lead to coma, which is usually related to increased PaCO₂ and other metabolic disturbances. Without exception, the randomized studies^{345678910111213141516171819} evaluating the use of NPPV to treat ARF have used neurologic deterioration as an exclusion criterion, based on the concern that a depressed sensorium would predispose the patient to aspiration. In two review articles, the deterioration of consciousness was considered to be a contraindication to NPPV therapy²⁰ and a criterion for its exclusion.²¹ An international consensus conference²² considered the presence of severe encephalopathy with a Glasgow coma scale (GCS) score < 10 to be a contraindication for NPPV therapy. Ordinarily, these patients are intubated for airway protection. However, the need to exclude patients with coma from consideration for NPPV therapy has never been evaluated prospectively. Furthermore, we have observed that some patients who have declined intubation have successful outcomes using NPPV therapy despite their initial presentation while in a coma. This experience has led us to reexamine our experience with such patients. The objective of the present study was to evaluate prospectively the effectiveness and safety of NPPV when applied using bilevel positive airway pressure to patients with ARF and severe neurologic deterioration (GCS score 8) compared to those who present a score > 8. A second objective was to determine the variables that predict the lack of response to NPPV therapy in patients presenting with coma.

	Materials and Methods

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This prospective, observational study was carried out between January 1, 1997, and May 31, 2002, in patients who were admitted to the ICU with ARF and a severe deterioration of consciousness (GCS score 8). The study was approved by the ethics committee at our institution, and written consent was obtained from patients or their next of kin.

Patients Included
Consecutive patients presenting with ARF were treated with NPPV for the following standard indications: moderate-to-severe respiratory distress accompanied by tachypnea (for hypoventilatory causes, > 24 breaths/min; for hypoxemic causes, > 29 breaths/min) and acute or acute-on-chronic CO₂ retention (PaCO₂, > 45 mm Hg; pH < 7.35); or severe hypoxemia coma (PaO₂/fraction of inspired oxygen [FIO₂] ratio, < 200). Patients with coma (GCS score, 8) and CO₂ retention formed one group, and those without coma served as a comparison group.

Patients Excluded
Contraindications to the use of NPPV therapy were agonal breathing and apnea, recent facial, esophageal, or upper airway surgery, uncontrolled GI hemorrhaging, excessive airway secretions, or a facial deformity preventing the application of the mask. Hemodynamic instability that is responsive to treatment with fluid resuscitation and vasoactive drugs was not considered to be a contraindication to NPPV therapy. Patients were excluded if another etiology of coma, such as a hypoglycemic, neurologic, or pharmacologic etiology, was identified by means of clinical history and laboratory analysis. A CT scan of the head was obtained if the patients remained comatose despite normalization of pH and PaCO₂.

Ventilator, Ventilation Mode, and Interface
NPPV therapy was administered using bilevel positive airway ventilation (BiPAP ST-D or VISION Ventilator Support Systems; Respironics, Inc; Murrysville, PA) via a properly fitted face mask (Respironics). The head of the bed was raised to 45° in order to minimize the risk of pulmonary aspiration. The face mask was attached by means of head straps and was tightened to minimize leaks, although care was taken to avoid excessive tightening. Artificial skin was applied over the bridge of the nose in the majority of patients. Some leaking occurred around the nasogastric catheters, but it was minimized by placing the catheter in the position that minimized leaking and, when necessary, using tape or gauze to reduce leaks. We monitored inspiratory pressure and made certain that leaks were not large enough to reduce delivered pressures.

Noninvasive Ventilation Protocol
On admission to the ICU, a nasogastric tube was placed in all patients to minimize the risk of gastric distension and vomiting. The ventilator was set in the spontaneous/timed mode, with a minimum respiratory rate (RR) of 20 to 25 breaths/min. The initial inspiratory positive airway pressure (IPAP) was set at 12 cm H₂O. IPAP levels were raised by 2 to 3 cm H₂O every 4 h as tolerated in order to keep pH at > 7.3 but did not exceed 30 cm H₂O.

Expiratory positive airway pressure (EPAP) was begun at a level of 5 cm H₂O, although this could also be raised if needed to counterbalance the intrinsic positive end-expiratory pressure level or to treat hypoxemia, or it could be lowered to enhance patient comfort. FIO₂ was adjusted to maintain an arterial oxygen saturation of > 92% with an FIO₂ of < 60%, if possible. Arterial blood gas samples were obtained from each patient before connection to the ventilator and at 1 h posttherapy. Subsequently, samples were obtained every 12 h or as clinically indicated.

All patients continued to receive mechanical ventilation until the GCS score rose to 15. When patients were being oxygenated adequately (ie, O₂ saturation, > 95%; FIO₂, < 40% or equivalent) and the RR was 24 breaths/min, we decreased the levels of IPAP and EPAP by 3 cm H₂O and 2 cm H₂O each hour, respectively, until pressures of 12 cm H₂O and 5 cm H₂O, respectively, were reached. If oxygenation and RR remained stable, we discontinued NPPV therapy and observed. If the RR rose to > 30 breaths/min, oxygen saturation fell to < 88%, or the patient became diaphoretic or manifested other evidence of excessive respiratory effort, we resumed NPPV therapy and intermittently discontinued it, as tolerated, until the patient could sustain unassisted breathing.

Criteria for Intubation
Patients who had not declined such a procedure were intubated endotracheally if any of the following conditions occurred: worsening respiratory distress despite NPPV therapy; respiratory arrest; unmanageable airway secretions; uncontrolled ventricular arrhythmias; hemodynamic instability that was unresponsive to therapy with fluid resuscitation and/or vasoactive drugs (with a maximum norepinephrine dose of 0.3 µg/kg/min); RR persistently > 40 breaths/min despite optimized interface and ventilation; failure of gas exchange to improve within the first 2 to 3 h of NPPV therapy; or lack of improvement in consciousness (ie, an increase of at least 2 points from the base GCS from the start of NPPV therapy). Patients who had declined intubation continued to receive NPPV therapy until they improved, declined further NPPV therapy, or died.

Effectiveness of the Technique
NPPV therapy was held to be successful when the patient avoided endotracheal intubation, completely recovered consciousness, was discharged from the ICU, and remained alive and conscious on a hospital ward for at least 24 h without requiring the resumption of NPPV therapy. Patients were considered to be intolerant to therapy if they were unable to cooperate with the technique, pulling the mask off and refusing to continue. Lack of response to NPPV therapy occurred if patients experienced a worsening of gas exchange or respiratory distress despite optimization of the technique, leading to intubation or death. Survivors were patients who were alive at hospital discharge.

Measurements
At the start of NPPV therapy, the following variables were also recorded: age; sex; indicators of severity with APACHE (acute physiologic and chronic health evaluation) II score and simplified acute physiologic score (SAPS) II; original location of the patient (ie, emergency department or hospital ward); underlying disease; and premorbid respiratory status. RR, heart rate, arterial BP, continuous arterial oxygen saturation, GCS score, temperature, and urine output were measured hourly. Also recorded were the total time of NPPV use in days and hours, as well as the ventilator parameters IPAP, EPAP, FIO₂, and air leakage.

In addition to the arterial blood gas samples, daily blood samples were also analyzed for levels of glucose, urea, creatinine, and hepatic enzymes, WBC count, and hemoglobin and platelet concentration. ICU patients underwent daily chest radiographs. During the patient’s hospital stay, these additional variables also were recorded. The appearance of multiorgan failure syndrome was measured by the sequential organ failure assessment (SOFA) index,²³ with the failure score in each organ being recorded daily, along with the appearance of ventilation-related complications (eg, skin lesions, mucous dryness, vomiting, pulmonary aspiration, and discomfort). In addition, the stay in the ICU and in the hospital, hospital survival or mortality, and the mortality expected according to the SAPS II system were recorded.

Statistical Analysis
Continuous variables were expressed as the mean ± SD, and categoric variables were recorded as percentages. The relationship between two qualitative variables was tested using the ² test or the Fisher exact test. The Kolmogorov-Smirnov test was used to identify variables with a normal distribution. In these cases, mean values were compared using the Student t test for independent data, while a paired t test was applied to compare the data of each patient before and after treatment. Variables without homogeneous variance and normal distribution were compared by nonparametric testing (Mann-Whitney). The relation between two qualitative variables was assessed by calculating Pearson correlation coefficients. All analyses were two-tailed, and significance was taken to be p 0.05. Finally, multivariate analysis was performed with logistic regression. Only variables with p 0.10 in univariate analysis were studied in the multivariate analysis. Statistical analysis was carried out using a statistical software package (SPSS, version 10.0; SPSS; Chicago, IL).

	Results

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During the period of the study, 2,865 ARF patients were admitted to the ICU, of whom 958 (33.4%) were treated with NPPV. Of these patients, 95 (10.1%) had GCS scores on ICU admission 8, and 863 had GCS scores > 8. The global success rate of NPPV therapy was slightly higher in coma patients than in patients with GCS scores > 8 (80.0% and 70.1%, respectively; p = 0.0434). Despite this, the hospital mortality rate was not significantly different between the two groups. The mortality rate of hypercapnic coma patients was 26.3%, compared to 33.2% for those patients who were not in a coma (p = 0.1706) [Table 1 ]. In the largest subgroup, patients with COPD, the success rate in those with severe encephalopathy was 86%, compared to 89% in other patients (p = 0.5430). Similarly, the hospital mortality rate was not significantly different between the groups (27% and 20%, respectively; p = 0.2411). On the other hand, coma patients with hypoxemic ARF caused by pneumonia or ARDS showed a lower NPPV success rate than those with higher levels of consciousness (25% vs 45%, respectively; p = 0.299), although the hospital mortality rates were similar (50% and 47%, respectively; p = 1.000).

Physiologic Measurements
At study entry, all comatose patients had severe respiratory failure. Most were hypercapnic, but some were hypoxemic initially, developed muscular fatigue, and became hypercapnic. The mean PaO₂/FIO₂ ratio on ICU admission was 139 ± 43, the mean PaCO₂ was 99 ± 19 mm Hg (range, 60 to 166 mm Hg), and the mean pH was 7.13 ± 0.06 (range, 6.93 to 7.23). Physiologic parameters, with the exception of RR and systolic BP, improved significantly after 1 h of NPPV therapy (Table 2 ).

A positive response to therapy (ie, success) was achieved in 76 of the comatose patients (80.0%). Thirteen patients (13.7%) were intubated, 10 because of shock that was unresponsive to therapy with fluids or vasoactive drugs and 3 for worsening respiratory failure. Six patients (6.3%), all of whom had DNI orders, died during NPPV therapy. The mean duration of stays in the ICU and hospital were 6.7 ± 16.8 days and 18.9 ± 19.9 days, respectively (Table 3 ). No patient was readmitted to the ICU after discharge to the ward. Ten patients (10.5%) died in the ICU (including the 6 who died while using NPPV), and 15 patients (15.8%) died while on hospital wards at least 24 h after ICU discharge, for a total of 25 deaths (Table 3). Of the 10 deaths that occurred in the ICU, 5 were caused by ARF and the others were caused by multiorgan failure. Of the 15 patients who died while on the ward, all had COPD, 11 died of ARF, 4 died of nosocomial infections, and 12 had DNI orders.

Complications
Complications attributable to NPPV were observed in 29 patients (30.5%) but did not lead to the lack of response to NPPV therapy (Table 3). The most frequent complication (affecting 23 patients [24.2%]) was skin ulceration on the nose or forehead. Gastric distension was observed in five patients, even though all patients had a nasogastric tube in place. In three of these patients, vomiting occurred, and one patient experienced pulmonary aspiration necessitating endotracheal intubation.

Factors Predicting Success of NPPV
A univariate analysis that was performed to identify factors that correlated with the response or lack of response to NPPV therapy demonstrated that neither gender nor age was related to a response to NPPV therapy (Table 4 ). Not surprisingly, lack of response was more likely among patients with higher acuity of illness and organ failure scores. GCS score, RR, pH, PaCO₂, and PaO₂/FIO₂ ratio on ICU admission did not correlate with response to therapy, but, with the exception of RR, improvements in these variables within the first hour of NPPV therapy did correlate with a response to therapy (Table 4). A response to NPPV therapy was also significantly related to the etiology for ARF (p = 0.013), with the vast majority of patients who responded to NPPV therapy having COPD and two having severe asthma. Two asthmatic patients were men, were 55 and 60 years old, had pH values of 7.05 and 6.96, respectively, PaCO₂ values of 98 and 110 mm Hg, respectively, GCS scores of 8 and 6, respectively, and durations of NPPV therapy of 8 and 6 h, respectively.

	Discussion

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Some earlier studies have found that higher levels of consciousness at the start and after the first hour of therapy correlate with a response to NPPV therapy.²⁴ Antón et al²⁵ evaluated 44 episodes of COPD exacerbation in 37 patients, and found that a better state of consciousness at initiation and greater improvement after the first hour of therapy predicted a response to NPPV therapy. Brochard et al⁴ have made similar observations, reporting that an improvement in encephalopathy during the first 12 h of NPPV use is associated with a response to NPPV. However, only a few reports have previously described the use of NPPV in the context of hypercapnic coma. In one study,²⁶ 3 of 30 patients with ARF were in comas with a GCS score of 3, 2 patients were successfully treated with NPPV, and the other patients did not respond to therapy. A second report²⁷ described the restoration of full consciousness in an elderly patient with hypercapnic coma after treatment with NPPV for 61 h. More recently, a 92-year-old woman with COPD who was in a hypercapnic coma (pH 7.06; PaCO₂, 185 mm Hg, GCS score, 3) was treated with NPPV via a face mask using bilevel airway pressure ventilation (inspiratory pressure, 30 cm H₂O; expiratory pressure, 5 cm H₂O). Her GCS score was 15 after receiving ventilation for 10 h, and she was discharged home from the hospital after 15 days.²⁸ In a retrospective series²⁹ that used the iron lung negative-pressure ventilator to treat 150 patients with coma secondary to hypercapnic respiratory failure, the mean hospital admission APACHE II score was 31, PaCO₂ was 112 mm Hg, and arterial pH was 7.13. Despite the severity of illness on presentation, 70% of patients avoided intubation and survived the hospitalization.

In view of these initial favorable experiences using NPPV in patients with blunted levels of consciousness, we instituted the present NPPV protocol to prospectively treat and follow-up patients with ARF that was associated with severe encephalopathy or coma. Using this protocol, we have observed few complications, with most consisting of adverse mask-related side effects (eg, nasal ulceration) or gastric insufflation (Table 3). The most important complications were vomiting in three patients, one of whom aspirated and required intubation despite the presence of a nasogastric tube. This experience raises questions about the effectiveness of routine nasogastric tube insertion, and, as a consequence, we no longer routinely place nasogastric tubes in these patients.

Our overall NPPV therapy response rate, measured by the avoidance of endotracheal intubation and discharge alive from the ICU, was 80% in this seriously ill patient population. The rate was highest in patients with airway obstruction and lowest in those with pneumonia or ARDS. The response rate for COPD patients in our study (86.4%) compares favorably with the range of response rates (75 to 100%) reported previously in controlled trials.⁴⁶⁷⁸⁹ The reported response rates for NPPV therapy in patients with pneumonia and/or ARDS have been variable, but usually are lower than those in COPD patients.³⁰

One surprise in our study was that the overall NPPV success rate was actually higher in comatose patients than in noncomatose patients (80.0% vs 70.1%, respectively; p = 0.043). However, this was related to the proportionately greater percentage of patients with COPD (69.5% vs 25.5%, respectively) and the lower percentage of patients with pneumonia and ARDS (8.4% vs 22.5%, respectively) in the comatose vs noncomatose groups of patients. Because of the relatively high (and comparable) success rates in the COPD subgroups (upper 80% range) and the lower success rates in the pneumonia/ARDS subgroups, this unequal distribution of subgroups favored a higher overall success rate in the comatose group. Thus, it is most accurate to conclude that success rates were comparable between the comatose and noncomatose groups. The important inference from our study is that NPPV therapy can be applied to patients with severe encephalopathy and to comatose patients (GCS scores 8) without increasing failure or mortality rates relative to noncomatose patients with similar diagnoses.

The mean APACHE II score and SAPS II among our patients were remarkably high, higher than in most previous controlled trials.⁴⁶⁷⁸⁹ Only the retrospective series of coma patients who were treated in the iron lung²⁹ included higher APACHE II scores, and even then only slightly. The very high acuity scores in our study are explained by the advanced age of the patients, and the severity of the neurologic and gas exchange derangements. In particular, a low mean pH (7.13) contributed to the high acuity scores, and such low pH values have been associated with lower success rates in prior studies.¹⁰²⁴ Nonetheless, our success rate is comparable to that reported in some prior studies and is even better than others, despite having a lower mean pH.²⁴ The similarity of our results and those of the study of comatose COPD patients²⁹ who were treated with iron lungs is remarkable (success rate, 80% vs 70%, respectively). The two studies also obtained similar results for the number of hours of ventilation that was necessary for the patient to recover consciousness, the total number of hours of ventilation, and, above all, the hospital mortality rate (26% vs 24%, respectively). One case-control study³¹ of COPD patients who were treated by noninvasive ventilation obtained similar success rates with the use of iron lungs and NPPV therapy.

Both the BiPAP ST-D and VISION ventilators (Respironics) were used in the current study. Although the VISION ventilator has an oxygen blender, graphic display, inspiratory time limit, and adjustable "rise time" that the BiPAP ST-D ventilator lacks, success rates were similar between the two devices. This may be related to the comatose state of the patients, which permitted excellent synchrony without sedation and negated the synchrony-enhancing features of the VISION ventilator. Also, most of our patients did not have severe hypoxemic respiratory failure, and the few who did were treated with the VISION ventilator. Of the eight patients with pneumonia, seven were treated with the VISION ventilator, including five patients who did not respond to therapy, whereas only one of the patients was treated with the BiPAP ST-D ventilator.

The improved survival rate over the last few years, because of patient selection and severity scores, did not change over time, and we believe that this was due to the increasing experience and enhanced skills of the doctors and nurses, as well as to improvements in ventilator and mask technology. The multivariate model identified the following two factors that were significantly related to NPPV success: an increase in the GCS 1 h after starting NPPV therapy; and a lower multiorgan failure score, as measured by the maximum SOFA index. Some prior studies³²³³³⁴ have identified age and APACHE II score as predictors of NPPV success or failure, but these were not significant predictors in our study. However, other studies^24253536 have also failed to find a significant relationship between success rate and APACHE II score. Lack of response to NPPV therapy has also been associated with a lower initial pH in some studies,⁴²⁴ but not in all.³² In our study, initial pH, RR, PaCO₂, and PaO₂/FIO₂ ratio were unrelated to the success of therapy. However, when these variables were measured 1 h posttherapy, PaCO₂, pH, and PaO₂/FIO₂ ratio were higher in successful cases, whereas RR was lower, which is consistent with the findings of prior studies.³⁴³⁴³⁵

Considering that death in the ICU or within the first 24 h after transfer to a regular hospital floor constituted NPPV failure, it is not surprising that predictors of mortality overlapped with predictors of NPPV failure in our study. For example, a higher SOFA index of multiorgan dysfunction was a strong predictor of both NPPV failure and mortality, which is consistent with the findings of prior studies.³⁷³⁸³⁹ At the initiation of therapy, RR and DNI status also predicted higher mortality rates. Not surprisingly, NPPV failure also was associated with a high risk of death. ICU and hospital mortality rates of NPPV-treated comatose patients presenting with ARF were 10% and 26%, respectively, and among COPD patients they were 4.5% and 27.3%, respectively. The hospital standardized mortality rate (the ratio between the mortality rate in our population and that predicted by the SAPS II system) was very low (0.49). While acknowledging that the uncontrolled nature of our study precludes firm conclusions being drawn about the effect of NPPV on survival, we believe that the low standardized mortality rate is highly suggestive of a survival benefit that is attributable to NPPV, which most likely is related to the avoidance of the complications of intubation.

The limitations of our study include its observational design and the lack of control subjects, which weaken the conclusions that we can draw. Also, many of our patients were very ill and may have died regardless of whether NPPV was used or not. Thus, the reliance on mortality rate alone as a way of assessing the effectiveness of the technique may be misleading, In addition, it is important to emphasize that these results were obtained in a center that was highly experienced to apply NPPV therapy. The results may not be so favorable in less experienced centers.

We conclude that patients with hypercapnic coma who are otherwise good candidates for NPPV therapy have outcomes after NPPV therapy that are as good as those of similar noncomatose patients. Patients with reversible causes for their ARF, such as COPD, asthma, or cardiogenic pulmonary edema, have the best outcomes, whereas those patients with ARDS or pneumonia are less likely to respond to therapy. Based on our findings, we think that coma should no longer be considered a contraindication to NPPV therapy. Rather, appropriate candidates for the NPPV modality who present while in a coma should be offered a trial of NPPV, with the expectation that intubation and mortality can be avoided in the majority of cases.

	Footnotes

 
Abbreviations: APACHE = acute physiologic and chronic health evaluation; ARF = acute respiratory failure; DNI = do not intubate; EPAP = expiratory positive airway pressure; FIO₂ = fraction of inspired oxygen; GCS = Glasgow coma scale; IPAP = inspiratory positive airway pressure; NPPV = noninvasive positive-pressure ventilation; RR = respiratory rate; SAPS = simplified acute physiology score; SOFA = sequential organ failure assessment

Drs. González Díaz and Carillo Alcarez belong to the Spanish Investigation Net in Acute Respiratory Failure (RED GIRA).

Received for publication May 6, 2004. Accepted for publication August 31, 2004.

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