Introduction

Patients in acute respiratory failure are not uncommon in the emergency department, and a decisional branch point often lies between intubation and noninvasive support. Noninvasive support typically takes the form of supplemental oxygen via nonrebreather. However, as more literature emerges, noninvasive positive pressure ventilation (NIPPV) has surfaced as an important instrument in the emergency physician’s toolbox.

NIPPV refers to mechanical ventilation that is not delivered via endotracheal or tracheostomy tube (often through a facemask). The benefits of NIPPV include and are not limited to:

• Decreased technical difficulty.
• Avoiding sedation.
• Avoiding complications of intubation, for example, nosocomial infections such as ventilator-associated pneumonia.
• Decreased morbidity/mortality.
• Decreased cost

.

Despite these benefits, there are data showing NIPPV is still underutilized by clinicians.¹

Physiology

NIPPV provides positive end-expiratory pressure and ventilatory support to recruit collapsed alveoli, increase tidal volume and functional residual capacity, and improve lung compliance. The physiological sum manifests as decreased respiratory effort and improved oxygenation. Recruitment of alveolar units maintains gas exchange during the entire respiratory cycle, as well as increasing intra-alveolar forces against pulmonary edema.

In addition to these respiratory benefits, NIPPV can increase cardiac output by decreasing LV preload in heart failure or decreasing LV afterload by reducing systolic wall stress.^2,3,4

Patient Selection

The fundamental success of NIPPV lies in the emergency physician’s selection of the appropriate patient. NIPPV is ultimately used to improve or prevent worsening acute respiratory failure. In objective measures, this can be described as⁵:

• SaO2 less than 90%.
• Use of accessory muscles.
• Inability to speak in full sentences.
• Respiratory rate greater than 24.
• Altered mental status.

Not all disease processes are equally amendable to NIPPV. Table 1 summarizes the disease processes for which NIPPV is most useful; these are addressed later in more detail.

As important as knowing indications for the NIPPV, knowledge of the contraindications is equally vital (Table 2).⁵

Monitoring pH and CO2 is helpful to trend patient status, but these should not be used as exclusion criteria. In 2005, Diaz and colleagues used NIPPV successfully in patients with hyerpcapnic comas.⁶

Disease Processes Appropriate For NIPPV

COPD. Chronic obstructive pulmonary disease (COPD) affects 32 million people in the United States and is the fourth leading cause of death.⁷ Often, this disease presents in respiratory extremis, and NIPPV has quickly emerged as a standard of care in treatment of severe exacerbations. When comparing NIPPV usage to treatment without it, multiple meta-analyses have revealed statistically significant reductions in intubation rates, mortality, and hospital length of stay.^8,9,10

In addition to these mortality and morbidity benefits, Lightowler’s meta-analysis showed significant physiological changes with NIPPV therapy. Within the first hour, patients exhibited improvement in pH, PaCO2, and respiratory rate.⁸ NIPPV can be utilized successfully in hypercapnic patients with a GCS less than 8 secondary to acute respiratory failure.⁶

As previously noted, the key to success with NIPPV usage is selection. A randomized, controlled trial by Keenan and colleagues showed that NIPPV therapy had no benefit versus standard therapy in mild COPD exacerbation.¹¹ One meta-analysis specifically analyzed NIPPV benefits in COPD exacerbations with hypercapnia (defined as PaCO2 greater than 45 mm Hg), and another meta-analysis defined severe COPD exacerbation as a pH less than 7.3.^8,9

In addition, the emergency physician must use the clinical picture to delineate between mild and severe COPD exacerbations. However, in severe COPD, noninvasive positive pressure ventilation must be considered standard therapy.

Congestive heart failure. Every year, congestive heart failure accounts for more than 1 million hospitalizations, and for patients older than 65 years, it is the leading discharge diagnosis in the United States.¹² Severe congestive heart failure exacerbations commonly manifest with pulmonary edema in the emergency department.

The use of NIPPV versus traditional therapy in cardiogenic pulmonary edema has been supported by several meta-analyses, most recently by Vital and colleagues in the Cochrane Database in 2008. NIPPV has demonstrated statistically significant decreased risk of intubation, as well as decreased in-hospital mortality.^13,14,15,16 Studies have also shown significant physiological improvements with NIPPV usage in respiratory rate, pH, PaCO2, PaO2, heart rate, work of breathing, afterload, preload, cardiac index, and ejection fraction.^{17,18,19,20,21,22}

Despite proven benefits of NIPPV in cardiogenic pulmonary edema, controversies still exist regarding its safety and efficacy. A trial by Mehta and colleagues in 1997 raised a concern of increased incidence of myocardial infarction with use of bilevel positive airway pressure (BiPAP) support versus continuous positive airway pressure (CPAP).¹⁷ However, subsequent trials have contradicted these findings and found no difference in myocardial infarction rate with any group.^23,24

In addition, Gray and colleagues recently published a multicenter randomized trial in the New England Journal of Medicine that showed no benefit in 7-day mortality and intubation rates with noninvasive ventilation versus standard oxygen therapy.

However, per the authors, the difference in intubation rates may be a reflection of the relatively low number of intubations in the trial.²⁴ Also, when comparing supportive ventilation versus standard oxygen therapy, patients showed earlier improvements in resolution of dyspnea, respiratory distress, and metabolic disturbances. Because of the physiological benefits, the authors continue to recommend NIPPV as an adjunctive therapy.

In decompensated heart failure, NIPPV has been shown to be a safe and effective treatment that should be part of emergency medicine’s standard approach.

Asthma. Asthma is another disease that is all too familiar to the emergency physician. NIPPV usage versus standard therapy has shown to be effective in correcting gas exchange abnormalities, decreasing work of breathing, improving peak expiratory flow, and increasing albuterol delivery.^25,26 A prospective, randomized control trial has shown that NIPPV therapy reduces admission rates, improves FEV1, and alleviates an asthma attack faster.²⁷ Currently, the studies are limited to morbidity indicators. However, the data and anecdotal evidence show that NIPPV is effective as a therapeutic option in severe asthma exacerbations. NIPPV, as a therapeutic option, becomes even more pertinent when considering the unique hazards of intubating the asthmatic patient.

Other disease processes. While most data and experience focus on COPD, congestive heart failure, and asthma, NIPPV is certainly not limited to these diseases. Studies with pneumonia patients in respiratory distress have shown that, as long as secretions are controlled, NIPPV decreases intubation rates and respiratory rates.²⁸

Furthermore, very strong arguments for NIPPV versus intubation extend to immunocompromised patients with hypoxemic respiratory failure and pulmonary infiltrates.

In a prospective randomized trial, Hilbert and colleagues found that NIPPV decreased intubation rates and serious complications and increased likelihood of survival to hospital discharge.29 The subsequent decrease in complications is thought to be from the decreased infection rates with NIPPV versus intubation.²⁹

While the mortality benefit may be nonexistent, patients who are DNR/DNI remain an important subset for whom to consider NIPPV. Shortness of breath is often reported as a major source of discomfort, and NIPPV therapy can effectively and comfortably relieve dyspnea.30 Also, there is evidence that NIPPV is effective for pulmonary contusion, and case reports suggest effectiveness in flail chest and cystic fibrosis.^31,32,33,34

Setup

NIPPV success revolves around selection of the appropriate patient and early initiation of therapy. Once the decision is initiated, the physician must choose from a variety of delivery modalities and settings. Face mask delivery shows no difference in outcomes when compared with nasal delivery. However, because of excessive air leaks in the mouth, nasal delivery is not tolerated as well as face mask delivery.³⁵ Of note, BiPAP has shown no difference in treatment success when compared to CPAP.^24,36

While there is no standard setting to initiate, most studies have a mean NIPPV setting of an inspiratory pressure of 10-15 cm of water and maximum expiratory pressure of 5 cm of water.^24,37 Expert guidance from emergency physicians and critical care physicians suggests that starting at an inspiratory pressure of 15 cm of water and a maximum expiratory pressure of 5 cm of water leads to more successful therapy than titrating up from lower settings. Once NIPPV is initiated, the emergency physician must continue to monitor the patient to assess need for escalation or discontinuation of therapy.

The patient’s progress should be measured every 30 minutes to 2 hours to determine treatment success or failure. As an adjunct to clinical exam, serial arterial blood gases may be helpful. If tolerated and needed, then increasing the inspiratory pressure by 2 cm of water every 20-30 minutes may increase the pressure support to a maximum inspiratory pressure of 20-25 cm of water and a maximum expiratory pressure of 15 cm of water. The expiratory pressure should be adjusted in patients with persistent hypoxemia or diffuse lung parenchyma involvement.³⁸

Patient tolerance of BiPAP is variable and can be improved by efficient troubleshooting by the emergency physician (Table 3).

Discontinuation of therapy should not be the initial option if the patient has difficulty tolerating the treatment. If the patient does not tolerate NIPPV, then the first step is to assess for air leaks within the unit. As the default pressure support system is flow limited, any air leaks will prevent the machine from reaching the preprogrammed flow rate/pressure limit, thereby prolonging the inspiratory time.

If there is a persistent air leak, then a time-limited setting should be attempted in order to limit the inspiratory time.

Finally, if there still remains no improvement, then the clinician can use a proportional assist ventilation (PAV) mode. When viewing clinical outcomes, PAV is not different from pressure support, but this mode may be better tolerated. As a final step of therapy escalation, the patient may be changed to an assist-control (AC) setting. This particular mode is not as well tolerated but will decrease the work of breathing by delivering a set volume.³⁹

If the patient shows clinical signs of improvement during the emergency department visit, then the physician should attempt to wean the patient from ventilatory support. The clinician must take a stepwise approach by incrementally decreasing the amount of pressure support or increasing the time off of NIPPV in intervals.

Summary

Acute respiratory failure is a multifactorial presentation that the emergency physician must be able to handle deftly. Intubation of patients is a common treatment that may be necessary in patients presenting with acute respiratory failure. However, this remains a procedure that is fraught with complications in the short and long term.

NIPPV has been shown, in specific disease processes, to decrease intubation rates, as well as mortality and various indicators of morbidity. The evidence for usage in COPD, congestive heart failure, asthma, and respiratory failure in the immunocompromised patient is very compelling, and noninvasive positive pressure has become standard therapy. Support for NIPPV in other disease processes is also growing as the evidence continues to mount.

References

1. Sweet DD, Naismith A, Keenan SP, et al. Missed opportunities for noninvasive positive pressure ventilation: A utilization review. J. Crit. Care 2008;23(1):111-7.
2. Baratz DM, Westbrook PR, Shah PK, et al. Effect of nasal continous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure. Chest 1992;102(5):1397-401.
3. Chadda K, Annane D, Hart N, et al. Cardiac and respiratory effects of continuous positive airway pressure and noninvasive ventilation in acute cardiac pulmonary edema. Crit. Care Med. 2002;30(11):2457-61.
4. Pinsky MR, Summer WR, Wise RA, et al. Augmentation of cardiac function by elevation of intrathoracic pressure. J. Appl. Physiol. 1983;54(4):950-5.
5. Shrank K. Better ventilation. The science to support your CPAP protocol. JEMS 2007;32(10):S17-9.
6. Diaz GG, Alcaraz AC, Talavera JC, et al. Noninvasive positive-pressure ventilation to treat hypercapnic coma secondary to respiratory failure. Chest 2005;127(3):952-60.
7. Kleinschmidt, P. Chronic Obstructive Pulmonary Disease and Empysema. eMedicine Specialities. http://emedicine.medscape.com/article/807143-overview. Accessed July 31, 2009.
8. Lightowler JV, Wedzicha JA, Elliot MW, et al. Noninvasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis. BMJ 2003;326(7382):185.
9. Keenan S, Sinuff T, Cook DJ, et al. Which patients with acute exacerbation of chronic obstructive pulmonary disease benefit from noninvasive positive-pressure ventilation? A systematic review of the literature. Ann. Intern. Med. 2003;138(11):861-70.
10. Brochard L, Mancebo J, Wysocki et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N. Engl. J. Med. 1995;333(13):817-22.
11. Keenan SP, Powers CE, McCormack DG. Noninvasive positive-pressure ventilation in patients with milder chronic obstructive pulmonary disease exacerbations: a randomized controlled trial. Respir. Care 2005;50(5):610-6.
12. American Heart Association. Heart Disease and Stroke Statistics: 2006 Update. Dallas, TX. American Heart Association, 2006.
13. Masip J, Roque M, Sanchez B, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA 2005;294(24):3124-30.
14. Peter JV, Moran JL, Phillips-Hughes J, et al. Effect of noninvasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary edema: a meta-analysis. Lancet 2006;367(9517):1155-63.
15. Winck JC, Azevedo LF, Costa-Pereira A, et al. Efficacy and safety of noninvasive ventilation in the treatment of acute cardiogenic pulmonary edema—a systematic review and meta-analysis. Crit. Care 2006;10(2):R69.
16. Vital FM, Saconato H, Ladeira MT, et al. Noninvasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database Syst. Rev. 2008;(3):CD005351.
17. Mehta S, Jay GD, Woolard RH, et al. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit. Care Med. 1997;25(4):620-8.
18. 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 Med. 1997;155(2):500-5.
19. Pang D, Keenan SP, Cook DJ, 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(4):1185-92.
20. Bellone A, Barbieri A, Ricci C, et.al. Acute effects of noninvasive ventilatory support on functional mitral regurgitation in patients with exacerbation of congestive heart failure. Intensive Care Med. 2002 Sep;28(9):1348-50.
21. L’Her E. Noninvasive mechanical ventilation in acute cardiogenic pulmonary edema. Curr. Opin. Crit. Care 2003;9(1):67-71.
22. 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 Med. 2004;32(9):1860-5.
23. Gray A, Goodacre, S, Newby DE, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. N. Engl. J. Med. 2008;359(2):142-51.
24. Meduri GU, Cook TR, Turner RE, et al. Noninvasive positive pressure ventilation in status asthmaticus. Chest. 1996;110(3):767-74.
25. Pollack CV Jr, Fleisch KB, Dowsey K. Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by a nasal bilevel positive airway pressure circuit. Ann. Emerg. Med. 1995;26(5):552-7.
26. Soroksky A, Stav D, Shpirer I. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest 2003;123(4):1018-25.
27. Confalonieri M, Potena A, Carbone G, et al. Acute respiratory failure in patients with severe community-acquired pneumonia. A prospective randomized evaluation of noninvasive ventilation. Am. J. Respir. Crit. Care Med. 1999;160(5 Pt 1):1585-91.
28. Hilbert G, Gruson D, Vargas F, et al. Noninvasive ventilation in immunosuppressed patients with pulmonary infiltrates, fever, and acute respiratory failure. N. Engl. J. Med. 2001;344(7):481-7.
29. Meduri GU, Fox RC, Abou-Shala N, et al. Noninvasive mechanical ventilation via face mask in patients with acute respiratory failure who refused endotracheal intubation. Crit. Care Med. 1994;22(10):1584-90.
30. Garfield MJ, Howard-Griifin RM. Noninvasive positive pressure ventilation for severe thoracic trauma. Br. J. Anaesth. 2000;85(5):788-90.
31. Antonelli M, Conti G, Moro ML, et al. Predictors of failure of noninvasive positive pressure ventilation in patients with acute hypoxemic respiratory failure: a multi-center study. Intensive Care Med. 2001;27(11):1718-28.
32. Al-Ansari MA. Successful use of noninvasive positive pressure ventilation in a complicated flail chest. Saudi Med. J. 2006;27(8):1244-7.
33. Madden BP, Kariya-wasam H, Siddiqi AJ, et al. Noninvasive ventilation in cystic fibrosis patients with acute or chronic respiratory failure. Eur. Respir. J. 2002;19(2):310-3.
34. Kwok H, McCormack J, Cece R, et al. Controlled trial of oronasal versus nasal mask ventilation in the treatment of acute respiratory failure. Crit. Care Med. 2003;31(2):468-73.
35. Moritz F, Brousse B, Gelle B, et al. Continuous positive airway pressure versus bilevel noninvansive ventilation in acute cardiogenic pulmonary edema: a randomized multicenter trial. Ann. Emerg. Med. 2007;50:666-75.
36. Masip J. Noninvasive ventilation in acute cardiogenic pulmonary edema. Curr. Opin. Crit. Care 2008;14(5):531-5.
37. Liesching T, Kwok H, Hill NS. Acute applications of noninvasive positive pressure ventilation. Chest 2003;124(2):699-713.
38. Girault C, Richard JC, Chevron V, et al. Comparative physiologic effects of noninvasive assist-control and pressure support ventilation in acute hypercapnic respiratory failure. Chest 1997;111(6):1639-48.