help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bersten, A. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bersten, A. D.
American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 1406-1408, (2003)
© 2003 American Thoracic Society


Editorial

Noninvasive Ventilation for Cardiogenic Pulmonary Edema

Froth and Bubbles?

Andrew D. Bersten, M.D.

Department of Critical Care Medicine Flinders Medical Centre and School of Medicine Flinders University Adelaide, South Australia, Australia

Acute cardiogenic pulmonary edema usually presents with the sudden onset of acute hypoxemic respiratory failure that requires rapid assessment and treatment. Although this may be secondary to sudden decompensation of chronic heart failure, myocardial ischemia is also common. Typically, patients are hypoxemic with increased work of breathing, acidemic because of both respiratory and metabolic factors (1), and hypertensive and tachycardic. Diastolic dysfunction is the major contributor to raised hydrostatic pressure and pulmonary edema (2). Despite standard medical therapy with oxygen, nitrates, and diuretics, ventilator assistance may be needed.

Noninvasive ventilation is widely used in cardiogenic pulmonary edema (3, 4), usually resulting in rapid relief of dyspnea. Although this simple but dramatic clinical observation was made many years ago (5), there are many unanswered questions. In this issue of the Journal (pp. 1432–1437), Nava and coworkers (6) report important findings from a multicenter study that helps focus some of these issues.

While the term noninvasive ventilation covers numerous methods of ventilator assistance without endotracheal intubation, it is most commonly applied as positive airway pressure using a mask as the interface. The simplest and most commonly used technique in cardiogenic pulmonary edema is continuous positive airway pressure (CPAP). There has been growing interest, however, in the use of modes where inspiratory effort is supported by a greater level of positive pressure (pressure support) interposed on top of positive end-expiratory pressure (PEEP), also termed bilevel positive airway pressure. Raised intrathoracic pressure increases functional residual capacity and oxygenation, improves lung mechanics, and reduces work of breathing (7, 8). There may also be beneficial cardiovascular effects resulting in reduced afterload and preload; clinical studies, necessarily performed some hours after onset, show reduced transmural ventricular filling pressures (7). As mask CPAP leads to more rapid physiologic improvement, consistently reduced intubation rate, and a tendency to reduced mortality (9), there are qualified recommendations for its use in cardiogenic pulmonary edema (1012).

Nava and colleagues (6) prospectively randomized 130 patients with cardiogenic pulmonary edema, receiving standard medical therapy, to either oxygen at ambient pressure or oxygen with mask pressure support plus PEEP. Consistent with previous studies, this led to a more rapid improvement in physiologic variables, such as oxygenation, arterial carbon dioxide tension, respiratory rate, dyspnea, blood pressure, and heart rate. Mortality and intubation rate, however, were unchanged. How do the new data add to our understanding and use of noninvasive ventilation?

Compared with CPAP, where airway pressure is designed to be constant, pressure support plus PEEP augments tidal volume and inspiratory unloading. This may be advantageous in cardiogenic pulmonary edema, in which there already appears to be an inverse relationship between initial arterial pH and intubation risk reduction with CPAP (9). Consistent with these data, subgroup analysis by Nava and colleagues (6) found a reduced risk of intubation in patients who were hypercapnic at baseline (2/33 versus 9/31, p = 0.015), supporting their contention that future trials need to stratify for this factor.

Although Masip and colleagues (13) had reported that noninvasive pressure support reduced intubation risk, but not mortality, Sharon and coworkers (14) found that intubation and myocardial infarction were increased when compared with high-dose nitrates. The 80% intubation rate in their noninvasive ventilation group, however, well exceeds that expected from previous studies, and may reflect the low inspired oxygen concentration and low airway pressures used. An earlier study (15) comparing mask CPAP with pressure support plus PEEP, with comparable inspired oxygen concentrations, also found a greater rate of myocardial infarction with pressure support, but this may have been due to small sample size and a trend toward fewer patients with chest pain at baseline in the CPAP group. Importantly, Nava and coworkers (6) found no increased risk of myocardial infarction with mask pressure support ventilation.

With this important safety issue now clarified, it is appropriate for studies to compare mask CPAP with noninvasive pressure support ventilation, and for there to be adequate power to detect different intubation risks, and possibly mortality differences. As blinding of these modes is difficult, robust guidelines for intubation, protocolized standard medical therapy, titration, and weaning of airway pressure, equivalence of inspired oxygen concentration, and ease of delivering airway pressure will all be important. For example, the average expiratory and inspiratory airway pressures used by Nava and colleagues (6) were 6.1 and 14.5 cm H2O, respectively. Is this equivalent to 10 cm H2O CPAP, which has been commonly used and recommended? Rather than augment systolic function, standard medical therapy for cardiogenic pulmonary edema targets the consequences and cause of diastolic dysfunction. If a parallel (systole with inspiration and diastole with expiration) can be made with the approach to prescribing noninvasive ventilation, it may be worth reexamining the prescription of PEEP when pressure support is used.

Where are these patients best treated? Nava and colleagues (6) managed their patients in the emergency department, with an average period of 11.4 hours noninvasive ventilation—consistent with previous studies. While emergency department presentation is common, other investigators have managed these patients in their intensive or coronary care units. Practical issues, including local hospital setup and staffing, usually combine to determine where noninvasive ventilation is performed, although there is also the influence of multiple stakeholders. It is also important to recognize that the workload in the first 6–8 hours may be greater than required for a conventionally managed intensive care patient (16). In acute hypoxemic respiratory failure, the ability to rapidly respond with intubation and cardiorespiratory support is crucial. In cardiogenic pulmonary edema, there are additional demands, such as the recognition and treatment of arrhythmias and myocardial ischemia. Consequently, patients with severe cardiogenic pulmonary edema requiring noninvasive ventilator support need to be triaged to a high acuity environment with an adequate nurse–patient ratio and 24 hour medical care. In addition to standard medical care and noninvasive ventilation, the possibility that this represents an acute coronary syndrome needs to be considered. Unlike Nava and coworkers, who excluded or intubated patients requiring thrombolysis, many centers would concurrently provide support with noninvasive ventilation while administering thrombolytics or proceeding to percutaneous revascularization.

FOOTNOTES

Conflict of Interest Statement: A.D.B. has no declared conflict of interest.

REFERENCES

  1. Anthonisen NR, Smith HJ. Respiratory acidosis as a consequence of pulmonary edema. Ann Intern Med 1965;62:991–999.
  2. Gandhi SK, Powers JC, Nomeir A-M, Fowle K, Kitzman DW, Rankin KM, Little WC. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 2001;344:17–22.[Abstract/Free Full Text]
  3. Sinuff T, Cook DJ, Randall J, Allen CJ. Evaluation of a practice guideline for noninvasive positive-pressure ventilation for acute respiratory failure. Chest 2003;123:2062–2073.[Abstract/Free Full Text]
  4. Carlucci A, Richard J-C, Wysocki M, Lepage E, Brochard L, and the SRLF Collaborative Group on Mechanical Ventilation. Noninvasive versus conventional mechanical ventilation: an epidemiologic survey. Am J Respir Crit Care Med 2001;163:874–880.[Abstract/Free Full Text]
  5. Poulton EP. Left-sided heart failure with pulmonary oedema: its treatment with the "pulmonary plus pressure machine." Lancet 1936;2:981–983.
  6. Nava S, Carbone G, DiBattista N, Bellone A, Baiardi P, Cosentini R, Marenco M, Giostra F, Borasi G, Groff P. Noninvasive ventilation in cardiogenic pulmonary edema: a multicenter randomized trial. Am J Respir Crit Care Med 2003;168:1432–1437.[Abstract/Free Full Text]
  7. Lenique F, Habis M, Lofaso F, Dubois-Rande J-L, Harf A, Borchard L. Ventilatory and hemodynamic effects of continuous positive airway pressure in left heart failure. Am J Respir Crit Care Med 1997;155:500–505.[Abstract]
  8. Chadda K, Annane D, Hart N, Gajdos P, Rapael JC, Lofaso F. Cardiac and respiratory effects of continuous positive airway pressure and noninvasive ventilation in acute cardiac pulmonary edema. Crit Care Med 2002;30:2457–2461.[CrossRef][Medline]
  9. Pang D, Keenan SP, Cook DJ, Sibbald WJ. 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.[Abstract/Free Full Text]
  10. International Consensus Conferences in Intensive Care Medicine. Noninvasive positive pressure ventilation in acute respiratory failure. Am J Respir Crit Care Med 2001;163:283–291.
  11. Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med 2001;163:540–577.[Free Full Text]
  12. British Thoracic Society standards of care committee. Non-invasive ventilation in acute respiratory failure. Thorax 2002;57:192–211.[Free Full Text]
  13. Masip J, Betbese AJ, Paez J, Vecilla F, Canizares R, Padro J, Paz MA, de Otereo J, Ballus J. Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary edema: a randomized trial. Lancet 2000;356:2126–2132.[CrossRef][Medline]
  14. Sharon A, Shpirer I, Kaluski E, Moshkovitz Y, Milovanov O, Polak R, Blatt A, Simovitz A, Shaham O, Faigenberg Z, 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.[Abstract/Free Full Text]
  15. Mehta S, Jay GD, Woolard RH, Hipona RA, Connolly EM, Cimini DM, Drinkwine JH, Hill NS. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit Care Med 1997;25:620–628.[CrossRef][Medline]
  16. Brochard L. Noninvasive ventilation for acute respiratory failure. JAMA 2002;288:932–935.[Free Full Text]



This article has been cited by other articles:


Home page
Postgrad. Med. J.Home page
R Agarwal, A N Aggarwal, D Gupta, and S K Jindal
Non-invasive ventilation in acute cardiogenic pulmonary oedema
Postgrad. Med. J., October 1, 2005; 81(960): 637 - 643.
[Abstract] [Full Text] [PDF]


Home page
ChestHome page
K. Bendjelid, N. Schutz, P. M. Suter, G. Fournier, D. Jacques, S. Fareh, and J.-A Romand
Does Continuous Positive Airway Pressure by Face Mask Improve Patients With Acute Cardiogenic Pulmonary Edema Due to Left Ventricular Diastolic Dysfunction?
Chest, March 1, 2005; 127(3): 1053 - 1058.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
M. J. Tobin
Critical Care Medicine in AJRCCM 2003
Am. J. Respir. Crit. Care Med., January 15, 2004; 169(2): 239 - 253.
[Full Text] [PDF]


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bersten, A. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bersten, A. D.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2003 American Thoracic Society