COPD patients who are willing to comply with NPPV therapy can experience significant improvements in function, activities of daily living, and quality of life.
Noninvasive positive-pressure ventilation (NPPV) is the use of positive-pressure ventilation without the use of an invasive artificial airway. Nocturnal bilevel ventilation is the use of NPPV at two pressures (for inhalation and exhalation) for at least 4 hours per night. Ventilation is supplied using a variety of nasal masks, full-face masks, and nasal pillows. Positive pressure assists the patient during inhalation, and exhalation is passive due to lung recoil. Diaphragmatic work can be eliminated if the inspiratory pressure is sufficient.1 In addition, the majority of machines used for NPPV provide expiratory positive airway pressure (EPAP) that can increase oxygenation and overcome the effects of autoPEEP (positive end-expiratory pressure) in patients with severe hyperinflation in chronic obstructive pulmonary disease (COPD).2
If the lungs are to function effectively, there must be sufficient respiratory drive, adequate diaphragm and accessory-muscle function and strength, and good lung function (including the capacity needed for normal tidal breathing and enough pulmonary reserve to handle increases in the ventilatory workload as needed). During normal sleep, Pao2 decreases slightly and Paco2 increases slightly in response to shallow breathing. In the absence of lung disease, these fluctuations are well tolerated; sleep is still deep enough, and rest is still sufficient for normal Pao2 and Paco2 levels to be restored, upon awakening, with no adverse effects.
There are, however, certain diseases and conditions in which the decrease in Pao2 and increase in Paco2 are exaggerated during sleep and are not tolerated. These disorders include COPD (emphysema, chronic bronchitis, bronchiectasis, and cystic fibrosis), disorders of ventilatory control, neuromuscular disorders such as muscular dystrophy, and obesity-hypoventilation syndrome. In all of these conditions, lung function is compromised. In severe cases, fluctuations in Pao2 or Paco2 or increased ventilatory workloads will not be tolerated because the patient is already sustaining a maximal workload simply in order to maintain normal, daytime tidal breathing. If, during sleep, such a patient experiences hypoventilation or further desaturation, the resulting effects will compromise daytime lung function and a decreased ability to perform activities of daily living.
Hyperinflation in patients with COPD increases the work of breathing.3 For this reason, it was suggested that there might be some benefit to be gained by resting the patients chronically fatigued muscles (using nocturnal NPPV).4-6 It was further theorized that this period of rest of 4 to 6 hours per day would permit recovery of muscle, increase muscle strength, reduce the length of periods of muscle fatigue, and improve gas exchange, as well as pulmonary function values.3 Some studies4,7-10 have shown improvements in the respiratory muscles obtained through the use of NPPV, while other studies11-13 have found no benefit. The studies that found improvement also correlated it with the reduction of Paco2, rather than with the improvement in respiratory muscle strength.3,14 Hill et al3 also pointed out that the favorable studies showed an average baseline Paco2 level that was 10 mm Hg higher than that seen in the unfavorable studies. This emphasizes the importance of patient selection in the successful use of nocturnal NPPV.
Several adverse effects are common among individuals with lung disease who are not tolerating the changes in Pao2 and Paco2 experienced during sleep; they may be undergoing exaggerated changes (nocturnal hypoventilation). These symptoms, many of which are attributable to insufficient rest, may be used to assess the patients suitability as a candidate for NPPV therapy:
daytime sleepiness and frequent napping;
increased daytime Paco2 levels secondary to insufficient diaphragmatic rest during sleep (one theory holds that large fluctuations in Paco2 may raise central chemoreceptor sensitivity to higher carbon dioxide levels);
morning headaches that usually subside after the patient has been awake for some time;
poor sleep, with frequent awakenings;
poor memory and concentration;
frequent hospitalization15 (particularly because adequate muscle rest is required to generate an adequate cough, and because the immune system can be compromised by poor sleep);
development or exacerbation of cor pulmonale secondary to chronic hypoxemic pulmonary vasoconstriction;
increased work of breathing during the day; and
oxygen desaturation at night.
Patients with severe COPD are known to have a high incidence of sleep-disordered breathing, including sleep apnea and periods of hypoventilation with oxygen desaturation.16 They were also known to have poor-quality sleep and shorter sleep times.17 Since continuous positive airway pressure (CPAP) and bilevel positive airway pressure have been shown to improve sleep in patients without COPD, it was theorized that these therapies would also help COPD patients. Sleep studies18 have shown an improvement in sleep among COPD patients using NPPV. The two pressures used during NPPV are usually referred to as inspiratory positive airway pressure (IPAP) and EPAP. EPAP is a set pressure that has the same function as PEEP or CPAP. It can splint the airway open to offset upper-airway obstructions and help prevent premature airway collapse. It can improve compliance, distribution of ventilation, and collateral ventilation, and will also increase mean airway pressure; this can normalize Pao2 levels at night, thus alleviating the patients symptoms.
When the patient inhales, the flow rate increases, therefore raising the positive pressure to a preset level throughout the inspiratory phase of the respiratory cycle. This change to a higher pressure will increase the patients tidal volume and improve or normalize Paco2 levels. IPAP has the same function as pressure-support ventilation. The IPAP portion of this therapy can also remove some of the workload imposed on the diaphragm, allowing it to rest during sleep. By improving Pao2 and Paco2 and by decreasing the work of breathing during sleep, it is possible to improve cardiovascular function, decrease daytime sleepiness, reduce fatigue, rid the patient of morning headaches, reduce hospitalization, and improve muscular strength. These changes, in turn, increase the patients reserve volume and level of activity. Stabilizing Paco2 at a relatively normal level at night can, in theory, not only prevent the sensitivity level of central chemoreceptors from rising, but may actually reset their sensitivity to a lower level.19 Appetite, memory, and concentration may also improve in response to sufficient rest.
A consensus conference was convened by the National Association of Medical Directors of Respiratory Care in Washington, DC, on February 4 and 5, 1998. The report3 of this conference stated that although there seems to be a need for more controlled long-term studies, NPPV ventilation seems to be better tolerated than negative-pressure ventilation by COPD patients. The report also documented improvement among COPD patients with obstructive sleep apnea. Patients with little or no carbon dioxide retention do not seem to benefit from NPPV, whereas patients with carbon dioxide retention at levels above 50 mm Hg seem to benefit from it. If, in addition, the patient exhibits desaturation during sleep, the benefit from NPPV is even greater.
The members of the consensus conference agreed that before a COPD patient is considered for NPPV, a physician with skills and experience in NPPV must establish and document an appropriate diagnosis on the basis of history, physical examination, and results of diagnostic tests; in addition, he or she must ensure optimal management of COPD through the use of bronchodilators, supplemental oxygen as indicated, and optimal management of underlying disorders. For example, a multichannel sleep study should be performed to exclude associated sleep apnea, if this is clinically indicated.
The most common obstructive lung diseases for which conference participants believed that NPPV might be indicated are chronic bronchitis, emphysema, bronchiectasis, and cystic fibrosis. Clinical indications for its use were determined to be symptoms (such as fatigue, dyspnea, or morning headache) plus one of the following physiologic criteria: a Paco2 level of more than 55 mm Hg; a Paco2 level of 50 to 54 mm Hg in the presence of nocturnal desaturation to a level of less than 88% for 5 continuous minutes while receiving supplemental oxygen at a flow rate of more than 2 L/ min; or a Paco2 level of 50 to 54 mm Hg and hospitalization related to more than two episodes of hypercapnic respiratory failure within one 12-month period.
Settings and Monitoring
In reviewing many studies, it becomes apparent that the reason for poor results or a small number of study subjects is poor patient compliance. As Smith has written, NIMV must be administered through a trained clinician because the patient will go through a period in which he or she will have to adapt to it. There will be many hurdles encountered along the way during that period, and the clinician needs to know how to help the patient overcome them.15
As starting points, an IPAP of 8 mm Hg and an EPAP of 4 mm Hg are generally used. Protocols should be used to adjust the pressure. For example, IPAP should be increased to improve alveolar ventilation or Paco2, and EPAP should be increased to improve oxygenation and/or obstructive sleep apnea. It is important to remember that if the EPAP is increased, the practitioner must also increase the IPAP to maintain the same pressure difference. The minimum EPAP level recommended by most manufacturers is 4 mm Hg. If supplemental oxygen is needed, it can be supplied through the NPPV system. Most manufacturers publish a bleed-in chart for oxygen to help the practitioner maintain the patients ordered flow rate or fraction of inspired oxygen.
Patients should be monitored on a regular basis. Monitoring should include the parameters that were used for patient selection; in addition, patients should be monitored for symptom relief, levels of daytime activity, signs of cor pulmonale, pedal edema, and respiratory rate. In most cases, the practitioner should see improvements in the patients resting respiratory rate, oxygen saturation, level of activity, decreased Paco2, and fewer hospital admissions.
Any therapy for the COPD patient may yield only marginal benefits, but even small improvements may lead to significant functional benefits, improving the quality of life. Due to the short life expectancy of patients with severe COPD, it may be difficult to conduct long-term studies of large populations. For properly selected patients who are willing to comply with this form of therapy, however, nocturnal bilevel NPPV can create significant improvements in function, activities of daily living, and quality of life.
Debra Lierl, MEd, RRT, is program chair of respiratory care and emergency medical services, Cincinnati State Technical & Community College. Mike Chaney, RRT, is a respiratory care instructor at the college.
1. Carrey Z, Gottfried SB, Levy RD. Ventilatory muscle support in respiratory failure with nasal positive pressure ventilation. Chest. 1984;97:150-158.
2. Appendini L, Palessio A, Zanaboni S, et al. Physiologic effects of positive end-expiratory pressure and mask pressure support during exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1994;149:1069-1076.
3. Hill N, Leger P, Criner G. Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventilationa consensus conference report. Chest. 1999;116:521-534.
4. Braun NM, Marino WD. Effect of daily intermittent rest of respiratory muscles in patients with severe chronic airflow limitation. Chest. 1984;85:S59-S60.
5. Nava S, Ambrosino N, Rubini F, et al. Effect of nasal pressure support ventilation and external PEEP on diaphragmatic activity in patients with severe stable COPD. Chest. 1993;103:143-150.
6. Renston JP, Di Marco AF, Supinski GS. Respiratory muscle rest using nasal BiPAP ventilation in patients with stable severe COPD. Chest. 1994;105:1053-1060.
7. Cropp A, Dimarco A. Effects of intermittent negative pressure ventilation on respiratory muscle function in patients with severe chronic obstructive pulmonary disease. Am Rev Respir Dis. 1987;135:1056-1061.
8. Gutierrez M, Berolza T, Contreras G, et al. Weekly cuirass ventilation improves blood gases and inspiratory muscle strength in patients with chronic air-flow limitation and hypercarbia. Am Rev Respir Dis. 1988;138:617-623.
9. Scano C, Gigliotti F, Duranti R, et al. Changes in ventilatory muscle function with negative pressure ventilation in patients with severe COPD. Chest. 1990;97:322-332.
10. Ambrosino N, Montagna T, Nava S, et al. Short term effect of intermittent negative pressure ventilation in COPD patients with respiratory failure. Eur Respir J. 1990;3:502-508.
11. Zibrak JD, Hill NS, Federman ED, et al. Evaluation of intermittent long-term negative pressure ventilation in patients with severe chronic obstructive pulmonary disease. Am Rev Respir Dis. 1988;138:1515-1518.
12. Celli B, Lee H, Criner C, et al. Controlled trial of external negative pressure ventilation in patients with severe airflow obstruction. Am Rev Respir Dis. 1989;140:1251-1256.
13. Shapiro SH, Ernst P, Grav-Donald K, et al. Effect of negative pressure ventilation in severe chronic obstructive pulmonary disease. Lancet. 1992;340:1425-1429.
14. Juan G, Calverley P, Talamo C, et al. Effect of carbon dioxide on diaphragmatic function in human beings. N Engl J Med. 1984;310:874-879.
15. Smith R. Noninvasive mechanical ventilation. Home Health Care Dealer. 1998;10(6):91-93.
16. Fleetham J, West P, Mezon B, et al. Sleep, aerosol and oxygen desaturation in chronic obstructive pulmonary disease. Am Rev Respir Dis. 1982;126:429-433.
17. Catterall JR, Douglas NJ, Calverley PMA, et al. Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome. Am Rev Respir Dis. 1983;128:24-29.
18. Krachman SL, Quaranta AJ, Berger TJ, Criner GJ. Effects of noninvasive positive pressure ventilation on gas exchange and sleep in COPD patients. Chest. 1997;112:623-628.
19. Schneerson JM. The changing role of mechanical ventilation in COPD. Eur Respir J. 1996;9:393-398.