0
Original Research: CRITICAL CARE MEDICINE |

Noninvasive Positive Airway Pressure and Risk of Myocardial Infarction in Acute Cardiogenic Pulmonary Edema*: Continuous Positive Airway Pressure vs Noninvasive Positive Pressure Ventilation FREE TO VIEW

Giovanni Ferrari, MD, FCCP; Federico Olliveri, MD; Giovanna De Filippi, MD; Alberto Milan, MD; Franco Aprà, MD; Adriana Boccuzzi, MD; Marcella Converso, MD; Paolo Navalesi, MD
Author and Funding Information

*From the High Dependency Unit (Drs. Ferrari, Olliveri, De Fillippi, Aprà, Converso, and Boccuzzi), Ospedale San Giovanni Bosco, Torino; Department of Medicine and Experimental Oncology (Dr. Milan), San Giovanni Battista Hospital, Torino; and Intensive Care Unit (Dr. Navalesi), SCDU Anestesia, Rianimazione e Terapia Intensiva-Azienda Ospedaliera “Maggiore della Carità,” Università “A. Avogadro” del Piemonte Orientale, Novara, Italy.

Correspondence to: Giovanni Ferrari, MD, FCCP, High Dependency Unit, Ospedale San Giovanni Bosco, Piazza Donatore del Sangue 3 10154 Torino, Italy; e-mail: giovanni_ferrari@fastwebnet.it



Chest. 2007;132(6):1804-1809. doi:10.1378/chest.07-1058
Text Size: A A A
Published online

Background: The addition of both noninvasive continuous positive airway pressure (n-CPAP) or noninvasive intermittent positive pressure ventilation (n-IPPV) to medical treatment has been shown to improve the outcome of patients with acute cardiogenic pulmonary edema (ACPE). Previous studies indicated a potential risk of new-onset acute myocardial infarction (AMI) associated with the use of n-IPPV. Although further studies did not confirm this observation, a few recent metaanalyses could not eliminate all the doubts at this regards because of the paucity of data available and the presence of confounding factors. This study aims to assess whether the application of n-IPPV, as opposed to n-CPAP, increases the rate of AMI in ACPE patients.

Methods: Fifty-two patients with severe hypoxemia consequent to ACPE were randomized to receive n-CPAP (n = 27) or n-IPPV (n = 25) in addition to medical therapy. Patients with signs of acute coronary syndrome on hospital admission were excluded from the study. Cardiac markers, ECG, and clinical/physiologic parameters were assessed at study entry, after 30 and 60 min, and every 6 h for the first 2 days.

Results: No significant difference was observed in the rate of AMI (26.9% and 16% with n-CPAP and n-IPPV, respectively, p = 0.244). Rate of intubation (p = 0.481), death (p = 0.662), and hospital stay (p = 0.529) were not different between the two groups. Both techniques were effective in improving gas exchange and vital signs in patients with ACPE.

Conclusions: The AMI rate was not different with n-CPAP and n-IPPV, which resulted to be equally effective in the treatment of ACPE.

Trial registration: Clinicaltrials.gov Identifier: NCT00453947.

Figures in this Article

The application of positive pressure to airways, either by noninvasive continuous positive airway pressure (n-CPAP) or noninvasive intermittent positive pressure ventilation (n-IPPV), in addition to medical treatment, improves the outcome of patients with acute respiratory failure secondary to acute cardiogenic pulmonary edema (ACPE).15 By increasing intrathoracic pressure, the application of positive pressure to the airways has both respiratory and hemodynamic effects.6 The addition of n-CPAP or n-IPPV to standard treatment has been shown to improve gas exchange,14 lung mechanics,78 work of breathing,79 and afterload of the left ventricle,78,10 and to reduce the need for endotracheal intubation and invasive ventilation.5,11

A few studies have compared n-CPAP and n-IPPV; of these, one study12observed an increased rate of acute myocardial infarction (AMI), and another study13showed a trend toward an increase in creatine kinase associated with the use of n-IPPV, as opposed to n-CPAP. A third study14 reported a higher incidence of AMI in the patients receiving n-IPPV, compared to those receiving only medical therapy. Although further studies4,1516 did not confirm these observations, a few recent metaanalyses11,17 could not eliminate all the doubts at this regards because of the paucity of data available and of the presence of confounding factors.

This study has been designed and powered to assess whether the application of n-IPPV, as opposed to n-CPAP, increases the rate of AMI in ACPE patients (primary end point). In addition, we compared the two techniques with respect to rate of endotracheal intubation, death, duration of ventilatory assistance, and hospital length of stay. Trends of heart rate, respiratory rate, and arterial blood gas levels over time were also assessed and compared.

Patients and Setting

The study was performed between July 2002 and December 2003 in the High Dependency Unit (HDU) of the Emergency Department of the San Giovanni Bosco Hospital in Turin, Italy. At the time of the study, the HDU staff were well experienced with noninvasive ventilation. The institutional ethic committee of the hospital approved the study. Patients gave their informed consent to participate in the study, which was conducted in accordance with the Declaration of Helsinki.

All patients ≥ 18 years old admitted to the HDU for acute respiratory failure secondary to severe ACPE were considered eligible. Inclusion criteria were as follows: rapid onset of symptoms, severe dyspnea at rest, respiratory rate > 30 breaths/min, use of accessory respiratory muscles, oxygen saturation by pulse oximetry (Spo2) < 90% with a fraction of inspired oxygen (Fio2) of 60% via a Venturi mask, radiologic findings of ACPE. Exclusion criteria were as follows: acute coronary syndrome on hospital admission,18 hemodynamic instability (systolic BP < 90 mm Hg with dopamine or dobutamine infusion ≥ 5 μg/kg/min) or life-threatening arrhythmias, need for immediate endotracheal intubation (respiratory arrest, bradypnea, or gasping for air), inability to protect the airways, impaired sensorium (unconsciousness or agitation), inability to clear secretions, respiratory tract infection, recent esophageal/gastric surgery, GI bleeding, facial deformities, hematologic malignancy or cancer with an Eastern Cooperative Oncology Group performance status ≥ 2, chronic respiratory failure necessitating long-term oxygen therapy, diagnosis of myocardial infarction, pulmonary embolism, pneumonia, exacerbation of COPD, pneumothorax in the previous 3 months, and denial or refusal of intubation.

Before enrollment, all patients were maintained in a semiortopnoic position and received the following standard medical treatment: oxygen therapy, with Fio2 of 60% via a Venturi mask; furosemide (60 mg IV, eventually repeated); glycerol trinitrate in continuous infusion titrated at the highest tolerated dose (ie, systolic arterial pressure > 90 mm Hg), while the patients unresponsive to nitrate (ie, unable to maintain systolic arterial pressure < 140 mm Hg) received sodium nitroprusside; and morphine clorohydrate (2 mg IV, eventually repeated). Arrhythmias were treated as indicated according to American College of Cardiology/American Heart Association/European Society of Cardiology guidelines.1920

Measurements and Protocol

Patients were assigned to n-CPAP or n-IPPV according to a random sequence previously generated from a table of random numbers. The assignments were placed in closed boxes, with identification numbers, stored in the HDU. The attending physician made the assignment at the time of hospital admission. It was impossible to blind the treatment.

Both n-CPAP and n-IPPV were delivered by oronasal mask. ECG, breathing frequency, Spo2, and noninvasive systemic arterial pressure were continuously monitored. Twelve-lead ECG and serum creatine phosphokinase, creatine kinase isoenzyme MB, and troponin-I measurements were performed on study entry and then every 6 h during the first 2 days. The simplified acute physiologic score-II was measured within the first 24 h after HDU admission.

n-CPAP was applied by means of a flow generator (WhisperFlow; Caradyne; Parkmore West, Galway, Ireland) able to deliver a flow of 140 L/min and a spring-loaded expiratory pressure valve (disposable adjustable positive end-expiratory pressure [PEEP] valve; GaleMed Corporation; Taiwan). Fio2 was regulated with an external oxygen analyzer to maintain Spo2 between 92% and 94% with n-CPAP set at 5 cm H2O. n-CPAP was then progressively increased by 2 cm H2O increments up to a maximum of 12 cm H2O until a target Spo2 ≥ 96% was achieved. n-IPPV was delivered with a mechanical ventilator (LTV 1000; Pulmonetics Systems; Minneapolis, MN). Fio2 was regulated on the ventilator to achieve a Spo2 between 92% and 94% with an initial PEEP of 5 cm H2O and an inspiratory pressure such to obtain an expiratory tidal volume ranging between 6 and 8 mL/kg. PEEP was then progressively increased by 2 cm H2O up to a maximum of 12 cm H2O until a target Spo2 ≥ 96% was achieved. The trigger of the ventilator was adjusted at the most sensible value with no visible autotriggering. The threshold at which the ventilator cycled off inspiration was always 25% of peak inspiratory flow. To avoid that unavoidable air leaks could interfere with the flow-based cycling off criteria, determining an unwarranted prolongation of the mechanical insufflation into the patient’s neural expiration (so-called inspiratory hang-up), a maximum inspiratory time of 1.2 s was preset.21

Arterial blood gas levels, Spo2, heart rate, systemic arterial pressure, and respiratory rate were recorded on study entry, after 30 and 60 min, and at the end of the ventilatory treatment. The ventilatory treatment was considered successful and interrupted when the following criteria were all satisfied: respiratory rate < 24 breaths/min, heart rate < 110 beats/min, pH ≥ 7.35, and Spo2 ≥ 92% with low-flow oxygen. Treatment was considered a failure and the patients required endotracheal intubation and invasive ventilation whenever one of the following occurred: cardiac arrest or gasping for air, Pao2/Fio2 < 100, inability to improve respiratory distress and arterial blood gas levels within 60 min, coma or psychomotor agitation, hemodynamic instability, or life-threatening ventricular arrhythmias.

End Points and Data Analysis

The primary end point of the study was to assess and compare the rate of AMI with the two techniques. A priori power analysis showed that a sample size of 50 patients would allow detecting a 40% difference in the rate of AMI between the two groups, with a 80% power at the 5% two-sided level of significance.12

According to the international guidelines,22 AMI was diagnosed when chest pain, modifications of 12-lead ECG, and increase of the cardiac markers were all present. The cut-off value for troponin-I (third generation) [Roche/Elecsys; Basel, Switzerland] was 0.04 ng/mL.18 Secondary end points were rate of endotracheal intubation, death, duration of ventilatory assistance, HDU and hospital length of stay. Trends of heart rate, respiratory rate, and arterial blood gas levels over time were also assessed with both forms of ventilatory treatments, excluding from the analysis the values obtained after endotracheal intubation for those patients with treatment failure.

Statistical analysis was performed using software (SPSS v 13.0; SPSS; Chicago, IL). Data are presented as mean ± SD unless otherwise specified. The unpaired Student t test was utilized for comparisons of variables between the two groups, whenever indicated. Variables without homogeneous variance and normal distribution were compared using the Mann-Whitney test. Qualitative or categorical variables were compared with the χ2 test or Fisher exact test, as appropriated. To evaluate trends over time, we used the analysis of variance for repeated measures and the Bonferroni test for comparisons between specific time points. For variables without homogeneous variance, the analysis of variance for repeated measures on ranks was utilized, as indicated. A two-tailed level of significance < 0.05 was considered significant for all comparisons.

During the study period, 60 patients admitted to the HDU for an episode of ACPE were considered eligible (Fig 1 ); of these, 3 patients had pneumonia and 3 patients had chest pain on admission and were excluded. Two patients refused to participate. Of 52 patients enrolled, 27 patients and 25 patients were randomized to n-CPAP and n-IPPV, respectively. Patient characteristics at enrollment (Table 1 ) were not significantly different between the two groups. In the n-CPAP group, the mean pressure applied was 8.8 ± 1.9 cm H2O. In the n-IPPV group, PEEP and inspiratory pressure above PEEP were 7.0 ± 1.2 cm H2O and 15.0 ± 3.1 cm H2O, respectively.

An increase in troponin-I > 0.04 μg/L within the first 24 h of ventilation associated with chest pain and/or ECG modifications was observed in eight patients and four patients in the n-CPAP and n-IPPV groups, respectively (p = 0.244). None of these patients died or underwent endotracheal intubation. In addition, we observed a slight troponin-I increase not associated with any other sign of acute coronary syndrome criteria18 in six patients and four patients in the n-CPAP and n-IPPV groups, respectively (p = 0.738); none of these patients died or required endotracheal intubation.

No patient in the n-CPAP group and one patient in the n-IPPV group (worsening of gas exchange after 60 min) required endotracheal intubation (p = 0.481). Two patients (7.4%) and three patients (12%) died in the n-CPAP and n-IPPV groups, respectively (p = 0.662). The two patients in the n-CPAP group died because of ventricular arrhythmias and cardiac arrest; of the three patients in the n-IPPV group, one died of ventricular arrhythmia and two died of cardiac arrest.

n-CPAP and n-IPPV were applied for a mean of 8.1 ± 8.3 h and 6.0 ± 4.7 h, respectively (p = 0.525). There was no difference between the two groups with respect to HDU length of stay (4.0 ± 2.5 days vs 4.1 ± 3.2 days, respectively, p = 0.437) and hospital length of stay (12.9 ± 23.7 days vs 9.9 ± 7.4 days, respectively, p = 0.529).

Pao2/Fio2, pH, respiratory rate, heart rate, and Spo2 significantly improved after 60 min in both groups. We also analyzed the effects of the two ventilatory techniques on Paco2 in the subgroup of patients (21 patients and 17 patients in the n-CPAP and n-IPPV groups, respectively) who were hypercapnic (Paco2 > 45 mm Hg) at enrollment. As depicted in Figure 2 , both techniques were effective in determining a significant improvement in Paco2 after 60 min of treatment; a further improvement was observed at the end of treatment in both groups.

We found that the rate of AMI in the n-IPPV group was not higher than in the n-CPAP group. The improvements in Pao2/Fio2, pH, respiratory rate, heart rate, and Spo2 produced by n-CPAP and n-IPPV were similar; the decrease in Paco2 over time was also not significantly different with the two techniques, despite a trend toward a faster reduction with n-IPPV. Rate of endotracheal intubation, death, duration of ventilatory support, and HDU and hospital lengths of stay were not different with the two techniques.

A previous study12 comparing n-CPAP with n-IPPV was abruptly interrupted because of a higher proportion of AMI in the patients who received n-IPPV, compared to those treated by n-CPAP; however, 10 of 14 patients (71%) in the n-IPPV group, as opposed to 4 of 13 patients (31%) in the n-CPAP group, had chest pain on study entry,12 which raises the doubt that the observed difference in AMI rate between the two groups was consequent to a bias in the selection and allocation of the patients rather than to the ventilatory treatment received. To avoid any bias from potential confounding factor, we excluded from the study all patients with history of chest pain, ECG modifications such as ST-segment elevation or depression, T-wave inversion, new onset of left bundle-branch block, and elevated markers of cardiac ischemia at emergency department presentation. In another study, Sharon and coworkers14 compared in patients with ACPE the efficacy and safety of n-IPPV plus low doses of isosorbide dinitrate vs no ventilatory treatment plus high doses of isosorbide dinitrate. They reported a higher percentage of AMI and death in the first group, as opposed to the group of patients treated with the medical therapy only. It should be noted, however, that in this study the two groups of patients received remarkably different amounts of IV nitrate, which makes the comparison unfair; moreover, the amount of inspiratory and expiratory pressure applied to the airway during n-IPPV was extremely low. In our study, the medical treatment was identical for the two groups, and the pressure applied with both n-CPAP and n-IPPV was similar to that reported by the large majority of the previous studies4,13,1516; it is also important to remark that our staff was well trained and largely experienced with both techniques. The study by Bellone et al15 prospectively compared n-CPAP and n-IPPV, having the AMI rate as the primary end point, and found no difference between the two forms of ventilatory treatment. While the study by Bellone et al15 included patients who had an airway tract infection as the precipitating cause of ACPE, we excluded patients with respiratory tract infections and thus included only patients with a cardiogenic precipitating factor (Table 1).

In 10 patients, we observed a slight troponin-I increase not associated with ECG modification, chest pain, or clinical history of acute coronary syndrome. A troponin-I increase may occur as a consequence of a myocardial injury secondary to an imbalance between demand and supply, even in absence of coronary stenosis. It should be noted, however, that these patients were equally distributed between the two groups.

In keeping with the results of previous studies,4,12,15,23 improvement in vital signs, duration of ventilatory assistance, and hospital length of stay were not different between the two groups; rate of endotracheal intubation and death were also not significantly different between the two groups.

Acute hypercapnia and respiratory muscle failure occurs when, because of the increased mechanical load, energy demand of the respiratory muscles cannot be met by the energy supplied.24 Chadda and coworkers9 observed that n-IPPV was more effective than n-CPAP in unloading the respiratory muscles in patients with acute respiratory failure secondary to ACPE. Bellone et al23 did not find any significant advantage of n-IPPV compared to n-CPAP in reducing Paco2 in patients with hypercapnia and ACPE. In keeping with this latter study, at a post hoc analysis comparing the effects of the two ventilatory techniques in the subgroup of patients who were hypercapnic at enrolment, we found that n-CPAP was as effective as n-IPPV in correcting respiratory acidosis.

In conclusion, our study indicates that n-CPAP and n-IPPV are equally effective in treating patients with severe acute respiratory failure secondary to ACPE, and that the rate of AMI is not different with the two techniques. Because of the ease of use and the lower cost, we suggest that n-CPAP should be considered first-line ventilatory treatment.

Abbreviations: ACPE = acute cardiogenic pulmonary edema; AMI = acute myocardial infarction; Fio2 = fraction of inspired oxygen; HDU = High Dependency Unit; n-CPAP = noninvasive continuous positive airway pressure; n-IPPV = noninvasive intermittent positive pressure ventilation; PEEP = positive end-expiratory pressure; Spo2 = oxygen saturation by pulse oximetry

This study was performed at the High Dependency Unit of the S. Giovanni Bosco Hospital, Turin, Italy.

Study registered at ClinicalTrials.gov; registration No. NCT00453947.

All the authors declare that this study has been performed without any financial support and disclose that no financial or other potential conflicts of interest exist.

Figure Jump LinkFigure 1. Trial profile showing the flow of patients through the trial.Grahic Jump Location
Table Graphic Jump Location
Table 1. Baseline Characteristics of Patients at Study Entry*
* 

Data are presented as mean ± SD unless otherwise indicated.

Figure Jump LinkFigure 2. Box plot of Paco2 trend over time in hypercapnic patients. Compared to baseline values (T0), in the subgroup of hypercapnic patients, Paco2 did not significantly change after 30 min (T1), while it improved after 60 min (T2) of noninvasive ventilation and improved at the end of the treatment (T3) with both n-CPAP (baseline, 69.7 ± 18.4; 30 min, 65.6 ± 14.1; 60 min, 55.6 ± 9.7; end of treatment, 44.2 ± 4.5) and n-IPPV (baseline, 66.1 ± 16.0; 30 min, 57.8 ± 24.0; 60 min, 53.7 ± 20.4; end of treatment, 48.4 ± 20.2); *not significant; †p < 0.05; ‡p < 0.001.Grahic Jump Location
Räsan̈en, J, Heikklia, J, Downs, J, et al (1985) Continuous positive airway pressure by face mask in acute cardiogenic pulmonary edema.Am J Cardiol55,296-300. [PubMed] [CrossRef]
 
Bersten, AD, Holt, AW, Vedig, AE, et al Treatment of severe cardiogenic pulmonary edema with continuous positive pressure delivered by face mask.N Engl J Med1991;325,1825-1830. [PubMed]
 
L’Her, E, Duquesne, F, Girou, E, et al Noninvasive continuous positive airway pressure in elderly cardiogenic pulmonary edema patients.Intensive Care Med2004;30,882-888. [PubMed]
 
Park, M, Sangean, MC, de Volpe, M, et al Randomized, prospective trial of oxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema.Crit Care Med2004;32,2407-2415. [PubMed]
 
Masip, J, Roque, M, Sanchez, B, et al Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis.JAMA2005;294,3124-3130. [PubMed]
 
Navalesi, P, Maggiore, SM Positive end-expiratory pressure. Tobin, MJ eds.Principle and practice of mechanical ventilation.2006,273-326 McGraw-Hill. New York, NY:
 
Lenique, F, Habis, M, Lofaso, F, et al Ventilatory and hemodynamic effects of continuous positive airway pressure in left heart failure.Am J Respir Crit Care Med1997;155,500-505. [PubMed]
 
Baratz, DM, Westbrook, PR, Shah, PK, et al Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure.Chest1992;102,1397-1401. [PubMed]
 
Chadda, K, Annane, D, Hart, N, et al Cardiac and respiratory effects of continuous positive airway pressure and non-invasive ventilation in acute cardiac pulmonary edema.Crit Care Med2002;30,2457-2461. [PubMed]
 
Naughton, MT, Rahman, MA, Hara, K, et al Effect of continuous positive airway pressure on intra-thoracic and left-ventricular pressures in patients with congestive heart failure.Circulation1995;91,1725-1731. [PubMed]
 
Peter, JV, Moran, JL, Phillips-Hughes, J, et al Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis.Lancet2006;367,1155-1163. [PubMed]
 
Mehta, S, Jay, GD, Woolard, RH, et al Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema.Crit Care Med1997;25,620-628. [PubMed]
 
Crane, SD, Elliot, MV, Gilligan, P, et al Randomized controlled comparison of continuous positive airway pressure, bilevel non-invasive ventilation and standard treatment in emergency department patients with acute cardiogenic pulmonary oedema.Emerg Med J2004;21,155-161. [PubMed]
 
Sharon, A, Shpirer, I, Kaluski, E, et al High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema.J Am Coll Cardiol2000;36,832-837. [PubMed]
 
Bellone, A, Monari, A, Cortellaro, F, et al Myocardial infarction rate in acute pulmonary edema: noninvasive pressure support ventilation versus continuous positive airway pressure.Crit Care Med2004;32,1860-1865. [PubMed]
 
Masip, J, Betbesè, AJ, Pàez, J, et al Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomized trial.Lancet2000;356,2126-2132. [PubMed]
 
Ho, KM, Wong, K A comparison of continuous and bi-level positive airway pressure non-invasive ventilation in patients with acute cardiogenic pulmonary oedema: a meta-analysis.Crit Care2006;10,R49. [PubMed]
 
Panteghini, M Acute coronary syndrome: biochemical strategies in the troponin era.Chest2002;122,1428-1435. [PubMed]
 
ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary; a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology.Circulation2001;104,2118-2150. [PubMed]
 
Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 5: Pharmacology I: Agents for arrhythmias.Circulation2000;102(suppl),I-112-I-118
 
Calderini, E, Confalonieri, M, Puccio, PG, et al Patient-ventilator asynchrony during noninvasive ventilation: the role of expiratory trigger.Intensive Care Med1999;25,662-667. [PubMed]
 
The Joint European Society of Cardiology/American College of Cardiology Committee.. Myocardial infarction redefined: a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction.Eur Heart J2000;21,1502-1513. [PubMed]
 
Bellone, A, Vettorello, M, Monari, A, et al Noninvasive pressure support ventilation vs. continuous positive airway pressure in acute hypercapnic pulmonary edema.Intensive Care Med2005;31,807-811. [PubMed]
 
Roussos, C, Koutsoukou, K Respiratory failure.Eur Respir J2003;22,3S-14S
 

Figures

Figure Jump LinkFigure 1. Trial profile showing the flow of patients through the trial.Grahic Jump Location
Figure Jump LinkFigure 2. Box plot of Paco2 trend over time in hypercapnic patients. Compared to baseline values (T0), in the subgroup of hypercapnic patients, Paco2 did not significantly change after 30 min (T1), while it improved after 60 min (T2) of noninvasive ventilation and improved at the end of the treatment (T3) with both n-CPAP (baseline, 69.7 ± 18.4; 30 min, 65.6 ± 14.1; 60 min, 55.6 ± 9.7; end of treatment, 44.2 ± 4.5) and n-IPPV (baseline, 66.1 ± 16.0; 30 min, 57.8 ± 24.0; 60 min, 53.7 ± 20.4; end of treatment, 48.4 ± 20.2); *not significant; †p < 0.05; ‡p < 0.001.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Baseline Characteristics of Patients at Study Entry*
* 

Data are presented as mean ± SD unless otherwise indicated.

References

Räsan̈en, J, Heikklia, J, Downs, J, et al (1985) Continuous positive airway pressure by face mask in acute cardiogenic pulmonary edema.Am J Cardiol55,296-300. [PubMed] [CrossRef]
 
Bersten, AD, Holt, AW, Vedig, AE, et al Treatment of severe cardiogenic pulmonary edema with continuous positive pressure delivered by face mask.N Engl J Med1991;325,1825-1830. [PubMed]
 
L’Her, E, Duquesne, F, Girou, E, et al Noninvasive continuous positive airway pressure in elderly cardiogenic pulmonary edema patients.Intensive Care Med2004;30,882-888. [PubMed]
 
Park, M, Sangean, MC, de Volpe, M, et al Randomized, prospective trial of oxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema.Crit Care Med2004;32,2407-2415. [PubMed]
 
Masip, J, Roque, M, Sanchez, B, et al Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis.JAMA2005;294,3124-3130. [PubMed]
 
Navalesi, P, Maggiore, SM Positive end-expiratory pressure. Tobin, MJ eds.Principle and practice of mechanical ventilation.2006,273-326 McGraw-Hill. New York, NY:
 
Lenique, F, Habis, M, Lofaso, F, et al Ventilatory and hemodynamic effects of continuous positive airway pressure in left heart failure.Am J Respir Crit Care Med1997;155,500-505. [PubMed]
 
Baratz, DM, Westbrook, PR, Shah, PK, et al Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure.Chest1992;102,1397-1401. [PubMed]
 
Chadda, K, Annane, D, Hart, N, et al Cardiac and respiratory effects of continuous positive airway pressure and non-invasive ventilation in acute cardiac pulmonary edema.Crit Care Med2002;30,2457-2461. [PubMed]
 
Naughton, MT, Rahman, MA, Hara, K, et al Effect of continuous positive airway pressure on intra-thoracic and left-ventricular pressures in patients with congestive heart failure.Circulation1995;91,1725-1731. [PubMed]
 
Peter, JV, Moran, JL, Phillips-Hughes, J, et al Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis.Lancet2006;367,1155-1163. [PubMed]
 
Mehta, S, Jay, GD, Woolard, RH, et al Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema.Crit Care Med1997;25,620-628. [PubMed]
 
Crane, SD, Elliot, MV, Gilligan, P, et al Randomized controlled comparison of continuous positive airway pressure, bilevel non-invasive ventilation and standard treatment in emergency department patients with acute cardiogenic pulmonary oedema.Emerg Med J2004;21,155-161. [PubMed]
 
Sharon, A, Shpirer, I, Kaluski, E, et al High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema.J Am Coll Cardiol2000;36,832-837. [PubMed]
 
Bellone, A, Monari, A, Cortellaro, F, et al Myocardial infarction rate in acute pulmonary edema: noninvasive pressure support ventilation versus continuous positive airway pressure.Crit Care Med2004;32,1860-1865. [PubMed]
 
Masip, J, Betbesè, AJ, Pàez, J, et al Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomized trial.Lancet2000;356,2126-2132. [PubMed]
 
Ho, KM, Wong, K A comparison of continuous and bi-level positive airway pressure non-invasive ventilation in patients with acute cardiogenic pulmonary oedema: a meta-analysis.Crit Care2006;10,R49. [PubMed]
 
Panteghini, M Acute coronary syndrome: biochemical strategies in the troponin era.Chest2002;122,1428-1435. [PubMed]
 
ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary; a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology.Circulation2001;104,2118-2150. [PubMed]
 
Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 5: Pharmacology I: Agents for arrhythmias.Circulation2000;102(suppl),I-112-I-118
 
Calderini, E, Confalonieri, M, Puccio, PG, et al Patient-ventilator asynchrony during noninvasive ventilation: the role of expiratory trigger.Intensive Care Med1999;25,662-667. [PubMed]
 
The Joint European Society of Cardiology/American College of Cardiology Committee.. Myocardial infarction redefined: a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction.Eur Heart J2000;21,1502-1513. [PubMed]
 
Bellone, A, Vettorello, M, Monari, A, et al Noninvasive pressure support ventilation vs. continuous positive airway pressure in acute hypercapnic pulmonary edema.Intensive Care Med2005;31,807-811. [PubMed]
 
Roussos, C, Koutsoukou, K Respiratory failure.Eur Respir J2003;22,3S-14S
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543