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(Chest. 2005;127:1053-1058.)
© 2005 American College of Chest Physicians

Does Continuous Positive Airway Pressure by Face Mask Improve Patients With Acute Cardiogenic Pulmonary Edema Due to Left Ventricular Diastolic Dysfunction?*

Karim Bendjelid, MD, MS; Nicolas Schütz, MD; Peter M. Suter, MD, FCCP; Gerard Fournier, MD; Didier Jacques, MD; Samir Fareh, MD and Jacques-A Romand, MD

* From the Surgical Intensive Care Unit (Drs. Bendjelid, Schütz, Suter, and Romand), Department of Anesthesiology, Pharmacology and Surgical Intensive Care, Geneva University Hospitals, Genève, Switzerland; Medical Intensive Care Unit (Drs. Fournier and Jacques), Centre Hospitalier Lyon-Sud, Lyon University Hospitals, France; and Intensive Care Unit of Cardiology (Dr. Fareh), Hôpital Cardio-vasculaire et Pneumologique Louis Pradel, Lyon University Hospitals, Lyon, France.

Correspondence to: Karim Bendjelid, MD, MS, Chef de Clinique Scientifique, Surgical Intensive Care Unit, Geneva University Hospitals, CH-1211 Genève 14, Switzerland; e-mail: Karim. Bendjelid{at}hcuge.ch


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Objective: Continuous positive airway pressure (CPAP) by face mask is an effective method of treating severe cardiogenic pulmonary edema (CPE). However, to our knowledge, no study has provided a precise evaluation of the effects of CPAP on cardiac function in patients presenting with CPE and preserved left ventricular (LV) function.

Design: Prospective observational clinical study.

Setting: A 14-bed, medical ICU at a university hospital.

Patients: Nine consecutive patients presenting with hypoxemic acute CPE.

Interventions: All patients were selected for 30 min of CPAP with 10 cm H2O by mask with fraction of inspired oxygen adjusted for a cutaneous saturation > 90%. Doppler echocardiography was performed before CPAP application and during the last 10 min of breathing with CPAP. Two-tailed, paired t-tests were used to compare data recorded at baseline (oxygen alone) and after CPAP.

Measurements and results: Four patients presented CPE with preserved left ventricular (LV) function (a preserved LV ejection fraction [LVEF] > 45%, and/or aortic velocity time integral > 17 cm in the absence of aortic stenosis or hypertrophic cardiomyopathy). Oxygenation and ventilatory parameters were improved by CPAP in all patients. Hemodynamic monitoring and Doppler echocardiographic analysis demonstrated that in patients with preserved LV systolic function, mean arterial pressure and LV end-diastolic volume were decreased significantly by CPAP (p < 0.04). In patients with LV systolic dysfunction, CPAP improved LVEF (p < 0.05) and decreased LV end-diastolic volume (p = 0.001) significantly.

Conclusion: CPAP improves oxygenation and ventilatory parameters in all kinds of CPE. In patients with preserved LV contractility, the hemodynamic benefit of CPAP results from a decrease in LV end-diastolic volume (preload).

Key Words: left ventricular constraint • lung edema • pressure support


   Introduction
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 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Acute cardiogenic pulmonary edema (CPE) is a frequent cause of acute respiratory failure and a common reason for acute hospital admission. Many of these patients are nonresponders to standard medical treatment and need continuous positive airway pressure (CPAP) by face mask.123 Indeed, the acute increase in extravascular lung water resulting from left ventricular (LV) dysfunction reduces lung volume and lung compliance, and increases airway pressure and closing volume. As a consequence, both work and oxygen cost of breathing rise, and CPAP may be required in addition to pharmacologic treatment. Thus, in this situation, CPAP by face mask may improve oxygenation and cardiac function, and may decrease respiratory work.4

Following this (patho)physiologic concept, several randomized controlled studies 125 published over the last decades have reported that patients with CPE may benefit from CPAP delivered by face mask. However, a multicentered, randomized controlled study6 observed that CPAP neither reduced the need for intubation nor improved in-hospital patient survival in hypoxemic patients with CPE. The fact that a large number of patients presenting CPE have preserved LV systolic function789 could explain the discrepancy between these results.10 To our knowledge, no study has performed a precise evaluation of the effects of CPAP on LV function in patients presenting CPE resulting from diastolic dysfunction.11 Observing that CPAP reduces transmural cardiac pressure12 and LV volume in patients with congestive heart failure, we hypothesized that CPAP application by face mask would improve respiratory failure following LV systolic dysfunction and could be deleterious in respiratory failure following LV diastolic dysfunction.10 Thus, we conducted a prospective, observational, Doppler echocardiographic study to analyze the effects of CPAP on LV function in patients with both systolic and diastolic dysfunction presenting with acute CPE.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
The protocol was approved by the hospital institutional ethical board, and no informed consent was required before entering the study, as CPAP is a part of routine therapeutic practice applied to CPE. Over a 6-month period, this study of nine patients with acute CPE was performed in a medical ICU. The criteria for entering the study included clinical signs of hypoxemic CPE with dyspnea, orthopnea, and radiologic evidence of pulmonary congestion on chest radiography despite pharmacologic treatment (diuretics and isosorbide-dinitrate). Criteria for eligibility were as follows: pulmonary edema confirmed by rales over both lungs on auscultation, dyspnea with a respiratory rate (RR) > 25 breaths/min, and a peripheral arterial oxygen saturation (SpO2) < 90% while breathing 100% fraction of inspired oxygen (FIO2) or a SpO2 < 85% while breathing air. Patients were excluded from the study when there was evidence of: requirement for immediate intubation, severe persistence of hemodynamic instability, persistence of a severe acidosis (arterial pH < 7.20), Glasgow coma scale < 7, difficulties with use of the mask (noncooperative patient), known evidence of underlying respiratory insufficiency or cor pulmonale, a history suggesting bronchial aspiration or respiratory infection, non-sinus cardiac rhythm, acute myocardial infarction, tachycardia > 120 beats/min, and moderate-to-severe cardiac valve disease diagnosed using color Doppler ultrasound.

Study Protocol
All patients were selected for CPAP in addition to standard medical therapy. The total duration of CPAP application was 30 min. CPAP was delivered using a system consisting of a gas mixer with an adjustable flow (maximum, 150 L/min) and FIO2, with a positive end-expiratory pressure valve (Whisperflow; Caradyne LTD, Baxter; Deerfield, IL).13 The setting was a flow of at least 60 L/min, positive end-expiratory pressure of 10 cm H2O, and FIO2 adjusted for SpO2 > 90%. A full face mask (VBM; Medizintechnik; Sulz, Germany) was used for all patients. Humidification of inspired gases was achieved by a heat moisture exchange device (Hydro-therm HME; Intersurgical LTD; Wokingham, UK). During the study period, standard medical therapy was not changed. The study was initiated at least 30 min after the last administered dose of any diuretic drug and/or a change in dosage of any vasodilator drugs. Doppler echocardiographic images were recorded before CPAP application (at baseline) and during the last 10 min of the 30-min application of CPAP (at CPAP period).

Data Analyzed
SpO2 was continuously monitored with a pulse oximeter (M3150A; Agilent Technologies; Andover, MA). Data collected before the start of CPAP included simplified acute physiology score II, Glasgow coma scale, RR, heart rate, ECG, mean systemic arterial pressure (MAP), urine output, and complete blood gas analysis. All these variables were monitored before and after the 30-min application of CPAP. Moreover, ICU mortality, the need for endotracheal intubation, and mechanical ventilation (MV) were also recorded.

Echocardiography
All patients underwent an echocardiographic investigation shortly before CPAP. Complete M-mode and two-dimensional echocardiograms and color Doppler ultrasound examination were performed using an ultrasound system (SONOS 2000; Hewlett-Packard; Andover, MA) with the patient in a semirecumbent position with the head at 45°. All tracings were recorded by one investigator, and each value represented the average of three tracings. Doppler echocardiographic traces were analyzed off-line, and the following variables were measured: peak flow velocity in early diastole (E) and during atrial contraction (A), deceleration time of early diastolic flow, velocity time integral of aortic flow (VTIAo), velocity time integral of mitral flow, and LV ejection fraction (LVEF) derived from the standard equation (Simpson rule). LV end-systolic and end-diastolic volumes were measured using the modified biplane Simpson method (method of disks) using the apical four-chamber and two-chamber views.14 The total stroke volume of the left ventricle was calculated as the difference between these volumes. The derived LVEF was calculated directly as the ratio of stroke volume to end-diastolic volume. Patients were considered as having LV systolic dysfunction if the ejection fraction was < 45% and/or the VTIAo was < 17 cm in absence of aortic stenosis or hypertrophic cardiomyopathy. In the absence of those parameters, patients were considered to present with LV diastolic dysfunction.

Statistical Analysis
Data are expressed as mean ± SD. Statistical calculations were made using software (GraphPad Prism V3; GraphPad Software; San Diego, CA) for personal computer. Statistical significance was set at p < 0.05. Two-tailed, paired t tests were used to compare data recorded at baseline (oxygen alone) and after 30 min of CPAP.


   Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
During 6 months, 13 patients met the study criteria. Four patients were excluded for the following reasons: atrial fibrillation (n = 2), tachycardia > 120 beats/min (n = 1), and hemodynamic instability (n = 1). The protocol was conducted in nine patients with CPE (six men and three women; mean age, 65 years; range, 34 to 93 years). Six patients had a medical history of hypertensive cardiomyopathy, and three patients had coronary diseases. No patients presenting with acute CPE had hypoalbuminemia. For the nine patients, mean baseline PaCO2 was 39 ± 3 mm Hg (range, 34 to 44 mm Hg) and pH was 7.39 ± 0.04 (range, 7.34 to 7.51) [± SD]. Demographic characteristics are presented on Table 1 .


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  		Table 1. Demographic Characteristics and Baseline Clinical, Hemodynamic, Respiratory, and Doppler Echocardiographic Parameters

 
Four of the nine patients presented with CPE and preserved LF systolic function. MAP was higher in patients with preserved LV function than in patients with LV dysfunction (p = 0.03). Two patients with LV dysfunction required orotracheal intubation and MV 12 h after the beginning of the CPE. Oxygenation (SpO2 and PaO2) was improved by CPAP in all patients (Table 2 ). Similarly, the RR decreased significantly during CPAP in all patients (Table 2). Hemodynamic monitoring and Doppler echocardiographic analysis showed that in patients with preserved LV systolic function, MAP and LV end-diastolic volume were decreased significantly by CPAP (p < 0.04) [Table 3 ]. In patient with LV systolic dysfunction, CPAP improved LVEF (p < 0.05) and decreased LV end-diastolic volume (p = 0.001) significantly (Table 3).


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  		Table 2. Effects of CPAP on Hemodynamic, Respiratory, and Doppler Echocardiographic Parameters in All Patients (n = 9)*

 

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  		Table 3. Effects of CPAP on Hemodynamic, Respiratory, and Doppler Echocardiographic Parameters*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The present study shows that in all types of CPE, CPAP by mask improves oxygenation and decreases RR. In patients with LV diastolic dysfunction, the hemodynamic benefit of CPAP results from a decrease in LV end-diastolic volume (preload). However, in patients with altered systolic function, the utility of CPAP is due to both an increase in LVEF and a decrease in preload.

LV diastolic dysfunction is defined as an impaired ventricular filling and is the mechanism of diastolic heart failure with LVEF > 55%. General practitioners are not always familiar with this concept, as nearly 50% of them were unaware of it in a survey.15 After years of the spotlight on heart failure related to altered LV systolic function, there has been a contemporary increased interest in the cardiac failure related to LV diastolic dysfunction.161718 However, to our knowledge, no study has evaluated the impact of the nature of LV dysfunction on the benefit of CPAP in patients with CPE. Because comprehensive Doppler echocardiography can characterize diastolic function directly in addition to measurement of LVEF,1920 the present study possibly has provide the information required.

Several reports indicated that heart failure resulting from diastolic dysfunction is difficult to understand,21 that the precise mechanism is not completely understood,22 and that the treatment has not been validated.23 Interestingly, Gandhi and colleagues24 hypothesized that patients with CPE and hypertension have transient LV dysfunction that is not longer present after resolution of the acute event. Thus, they studied echocardiographic LVEF of 38 patients with cardiopulmonary edema associated with hypertension during the first 6 h and 72 h after the acute event.24 The results of their study24 showed that 18 patients had normal LVEF during the CPE and 72 h after. This study has been confirmed by other studies2526 demonstrating that in patients with CPE related to diastolic dysfunction, LVEF was unchanged over time.

Once LV end-diastolic pressure exceeds the pulmonary capillary transudation point, free fluid rapidly passes into the pulmonary interstitial and alveolar spaces. Typically, patients with acute CPE are hypoxemic and have increased work of breathing.27 The majority of them should be managed using CPAP by mask when they do not respond to conventional medical treatment.2829 A systematic review28 concluded that CPAP was associated with a 26% lower risk of intubation and a trend toward decreased mortality. The rational supporting the use of CPAP in patients with CPE is very strong. Indeed, CPAP improves oxygenation, increases functional residual capacity, and enhances lung compliance. From a hemodynamic standpoint, it rises extracardiac pressure, lowers transmural pressure, and decreases afterload and LV work.3031 However, this positive hemodynamic effect is most likely to occur when LV systolic function is altered and can be unfavorable when cardiac function is preserved.32

To our knowledge, the present study is the first investigating the hemodynamic effects of CPAP by mask on patients presenting with CPE and LV diastolic dysfunction. Our four patients with preserved LV systolic function (LVEF, 49 ± 2%; MAP, 91 ± 13 mm Hg during the acute event) had hemodynamic values similar to the 18 patients studied by Gandhi and colleagues.24 Moreover, as demonstrated by MacCarthy et al,33 our data confirm that LV end-diastolic volume is lower in patients with preserved LV systolic function when compared to those with altered systolic function. We have also demonstrated that LVEF is not improved by CPAP in patients with preserved systolic function, as it was case in patients with altered systolic function. In addition, there is a real decrease of MAP (nearly similar to LV impedance) in patients with diastolic dysfunction, whereas this parameter is unchanged when systolic dysfunction occurs (Table 3). The latter phenomena emphasize the magnitude of systemic arterial pressure value in the occurrence of diastolic dysfunction.

The present data show that CPAP is beneficial for all types of CPE and confirms that its utility, in patients with altered systolic function, is due to both increase in LVEF and decrease in preload. Moreover, the new information provided is that in patients with preserved LV contractility, the hemodynamic benefit of CPAP on CPE only results from a decrease in LV end-diastolic volume (preload), by diminishing venous return. According to our results, an overloaded circulation seems to be a key predisposing substrate to acute CPE, which might then be precipitated by a relatively modest additional volume load without necessarily involving LV systolic dysfunction.34 Furthermore, because high aortic pressure decreases LV ventricular compliance and increases left atrial pressures, CPAP mechanically squeezes blood back into the venous compartment decompressing the overdistended heart. This decrease in venous return sets the left ventricle in a more favorably position on its compliance curve. This concept is confirmed by the significant decrease in high arterial pressure values observed after CPAP in our patients with preserved LV contractility. Moreover, we may expect that CPAP, by decreasing respiratory work in patients with cardiopulmonary edema,4 unloads the heart from the amount of cardiac output that supplies the respiratory muscles 3536 and improves oxygen delivery for others tissues. Indeed, during CPE, the respiratory muscles work hard; therefore, metabolic demands are increased.37 Then the respiratory muscles receive inordinately large amounts of blood and deprive the rest of the body.37 Moreover, in CPE, the RR is increased and the driving pressure of the diaphragmatic blood flow is decreased due to the impedance of flow during contractions.37 Subsequently, the significant decrease in RR during CPAP observed in the present study (Table 2) has probably permitted, as well, a better diaphragmatic perfusion.

Study Limitations
Some limitations of this work should be acknowledged. First of all, patients were considered as having diastolic heart failure because their LV systolic function was preserved.38 To fully characterize diastolic function, cardiac catheterization remains the "gold standard." However, there are ethical concerns with the use of these techniques in patients with CPE. New invasive measurements of diastolic function (such as tissue Doppler echocardiography) could have been used in our study, as they have a better sensitivity and specificity than conventional Doppler echocardiography. However, this equipment was not available when our study was performed. Nevertheless, one study39 has shown that it may not be necessary to directly measure diastolic function in every patient to prove that they have heart failure caused by a predominant abnormality in diastolic function. The measurement of diastolic function is not mandatory but may be confirmatory.38 Second, because our sample size was small and diastolic heart failure occurred in few patients, our results should be confirmed by further studies.

In summary, the present study shows that CPAP should be used for the management of CPE in patients with diastolic LV dysfunction. In patients with preserved systolic function, CPAP decreases LV end-diastolic volume. Moreover, our data confirm that in patients with altered systolic function, the benefit of CPAP is due to both an increase in LVEF and a decrease in preload. This work should stimulate cardiologists to confirm our data with further much larger studies involving new methodology as Doppler echocardiographic tissue imaging.


   Acknowledgements
 
We thank Prof. Claude Guerin, University of Lyon (France), for his helpful suggestions during the planning phase of the study, and Samia Brunner for translation support.


   Footnotes
 
Abbreviations: A = peak flow velocity during atrial contraction; CPE = cardiogenic pulmonary edema; CPAP = continuous positive airway pressure; E = peak flow velocity in early diastole; FIO2 = fraction of inspired oxygen; LV = left ventricular; LVEF = left ventricular ejection fraction; MAP = mean systemic arterial pressure; MV = mechanical ventilation; RR = respiratory rate; SpO2 = peripheral arterial oxygen saturation; VTIAo = velocity time integral of aortic flow

Preliminary data have been presented to the Fifteenth International Congress of Echocardiography. June 11–13, 2003, Paris, France.

This study was been performed at the medical ICU of Lyon-Sud, and was supported by the Gold Medal fund of Lyon University Hospitals (Dr. Bendjelid), Lyon, France.

Received for publication March 31, 2004. Accepted for publication September 28, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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