Abstract & Commentary
Chadda and associates explored the hypothesis that noninvasive positive-pressure ventilation (NPPV) would unload the respiratory muscles and improve cardiac and hemodynamic function more effectively than continuous positive airway pressure (CPAP). The study included 6 patients with acute cardiogenic pulmonary edema. In random order, the patients were treated with 5 cm H2O CPAP, 10 cm H2O CPAP, and NPPV with an inspiratory pressure of 10 cm H2O and an expiratory pressure of 5 cm H2O. Each treatment lasted 20 minutes, and patients were enrolled approximately 1 day after presenting with acute cardiogenic pulmonary edema. Oxygen was administered to maintain SpO2 > 90%. CPAP and NPPV were applied using an oronasal mask. Respiratory assessments included flow measurements at the mask and pressure from an esophageal balloon catheter. Hemodynamic measurements included heart rate, blood pressure, cardiac output, and pressures from a pulmonary artery catheter.
NPPV reduced the esophageal pressure swings and esophageal pressure time product compared with baseline, whereas there was no reduction in either of these measures with CPAP. NPPV and 10 cm H2O CPAP both reduced the right and left atrial filling pressures without a change in cardiac index. Chadda et al concluded that both NPPV and CPAP at 10 cm H2O reduced ventricular preload, and thus improved cardiac performance, but that NPPV was more effective at unloading the respiratory muscles (Chadda K, et al. Cardiac and respiratory effects of continuous positive airway pressure and noninvasive ventilation in acute cardiac pulmonary edema. Crit Care Med. 2002;30:2457-2461).
Comment by Dean R. Hess, PhD, RRT
In the past 10 years, a plethora of high-level evidence has accumulated to support the use of NPPV. In appropriately selected patients, NPPV reduces the need for endotracheal intubation, improves survival, and decreases the risk of ventilator-associated pneumonia.1-3 The strongest evidence of NPPV’s effectiveness is in patients with acute decompensation of COPD. The role of NPPV in patients with acute cardiogenic pulmonary edema is unclear. Although some have reported benefit from NPPV in this patient population,4,5 others have urged caution.6 Mehta and associates7 reported a higher rate of acute myocardial infarction (AMI) in patients with acute cardiogenic pulmonary edema who were randomized to receive NPPV as compared to those who received mask CPAP. In patients with acute cardiogenic pulmonary edema, Rusterholtz and colleagues8 reported a high rate of NPPV failure in patients with AMI. Sharon and associates9 reported that high-dose nitrates were safer and more effective than NPPV in these patients. There is considerable evidence for the effectiveness of mask CPAP10 (without NPPV) for the treatment of acute cardiogenic pulmonary edema.
It is against this background that the present study was conducted. Not surprisingly, Chadda et al reported that NPPV unloaded respiratory muscles to a greater extent than CPAP. However, NPPV and CPAP were equally effective in reducing right and left ventricular preload. An appropriate question might be, "So what?" Chadda et al conclude that this study supports the use of NPPV in patients with acute cardiogenic pulmonary edema. I take issue with this conclusion for several reasons. First, this was a short (20-minute) physiologic study. There is no way that we can know if these findings would result in better outcomes in patients receiving NPPV rather than CPAP. Second, the study was conducted almost 1 day after the patients presented with acute cardiogenic pulmonary edema. By the time the patients were enrolled, they had already been treated with diuretics, vasodilators, and inotropic drugs. This is not the time at which most clinicians use either CPAP or NPPV for patients with acute cardiogenic pulmonary edema; rather, we apply this therapy soon after the patient presents to the emergency department.
So how might I apply these findings in my practice? Given the high-level evidence for its use, I will continue to use mask CPAP at 10 cm H2O for patients with acute cardiogenic pulmonary edema. For those patients who remain hypercarbic with CPAP therapy, I will, as I have in the past, consider the addition of NPPV before intubation. I strongly consider emergent endotracheal intubation for patients with AMI, pulmonary edema, and respiratory failure.
1. Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med. 2001;163:540-577.
2. Peter JV, et al. Noninvasive ventilation in acute respiratory failure—A meta-analysis update. Crit Care Med. 2002;30:555-562.
3. Girou E, et al. Association of noninvasive ventilation with nosocomial infections and survival in critically ill patients. JAMA. 2000;284:2361-2367.
4. Masip J, et al. Noninvasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary edema: A randomised trial. Lancet. 2000;356:2126-2132.
5. Hoffman B, Welte T. The use of noninvasive pressure support ventilation for severe respiratory insufficiency due to pulmonary edema. Intensive Care Med. 1999;25:15-20.
6. Wysocki M. Noninvasive ventilation in acute cardiogenic pulmonary edema: Better than continuous positive airway pressure. Intensive Care Med. 1999;25:1-2.
7. Mehta S, et al. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit Care Med. 1997;25:620-628.
8. Rusterholtz T, et al. Noninvasive pressure support ventilation (NIPSV) with face mask in patients with acute cardiogenic pulmonary edema (ACPE). Intensive Care Med. 1999;25:21-28.
9. Sharon A, 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 Cardiol. 2000;36:832-837.
10. Pang D, et al. The effect of positive pressure airway support on mortality and the need for intubation in cardiogenic pulmonary edema: A systematic review. Chest. 1998;114:1185-1192.