Peter M. C. DeBlieux
Kerry B. Broderick
Introduction
Patients with severe respiratory complaints frequently present to the emergency department (ED) and comprise more than 10% of all presentations. Over the past decade, ED presentations of asthma, pneumonia, and chest pain have increased. A thorough knowledge of mechanical ventilatory support, both invasive and noninvasive is essential for practicing emergency medicine clinicians. Chapter 37focuses on the institution of invasive mechanical ventilation, and this chapter covers noninvasive positive-pressure ventilation (NPPV or NIVS). Recently, the use of NPPV has grown steadily due to evidence-based research, cost effectiveness, and consideration of patient comfort and complications.
The advantages of NPPV over mechanical ventilation include preservation of speech, swallowing, and physiological airway defense mechanisms; reduced risk of airway injury; reduced risk of nosocomial infection; and probably a decreased length of stay in the intensive care unit (ICU).
Technology of Noninvasive Mechanical Ventilation
Noninvasive mechanical ventilators have several characteristics that are distinct from standard critical care ventilators. NPPV offers a more portable technology due to the reduced size of the air compressor. Because of this reduction in size, these noninvasive ventilators do not develop pressures as high as their critical care ventilator counterparts. Noninvasive ventilators have a single-limb tubing circuit that delivers oxygen to the patient and allows for exhalation. To prevent an accumulation of carbon dioxide, this tubing is continuously flushed with supplemental oxygen delivered during the expiratory phase. Exhaled gases are released through a small exhalation port near the patient's mask. During the respiratory cycle, the machine continuously monitors the degree of air leak and compensates for this loss of volume. NPPV is designed to tolerate air leak and compensates by maintaining airway pressures. This is in sharp contrast to the closed system found in critical care ventilators comprised of a dual, inspiratory and expiratory tubing system that does not tolerate air leak or compensate for lost volume. The device that makes physical contact between the patient and the ventilator is termed the interface. Interfaces for NPPV come in a variety of shapes and sizes designed to cover the individual nares, the nose only, the nose and mouth, the entire face, or the helmet. Ideally, interfaces should be comfortable, offer a good seal, minimize leak, and limit dead space.
Modes of Noninvasive Mechanical Ventilation
In a manner analogous to invasive mechanical ventilation, understanding the modes of NPPV is based on knowledge of three essential variables: the trigger, the limit, and the cycle. The trigger is the event that initiates inspiration: either patient effort or machine-initiated positive pressure. The limit refers to the airflow parameter that is regulated during inspiration, either airflow rate or airway pressure. The cycle terminates inspiration: either a pressure is delivered over a set time period or the patient ceases inspiratory efforts.
Continuous Positive Airway Pressure
Continuous positive airway pressure (CPAP) is a mode for invasive and noninvasive mechanical ventilation. As mentioned in Chapter 37, CPAP is not a stand-alone mode of assisted mechanical ventilation. It is equivalent to positive end-expiratory pressure (PEEP) and facilitates inhalation by reducing pressure thresholds to initiate airflow. It provides positive airway pressure throughout the respiratory cycle. This static, positive pressure is maintained constantly during inhalation and exhalation. This mode should never be used in patients who may have apneic episodes because of the lack of a backup rate.
Spontaneous and Spontaneous/Timed Modes
In spontaneous mode, the airway pressure cycles between an inspiratory positive airway pressure (IPAP) and an expiratory positive airway pressure (EPAP). This is commonly referred to as bilevel or biphasic positive airway pressure (BL-PAP or BiPAP). The patient's inspiratory effort triggers the switch from EPAP to IPAP. The limit during inspiration is the set level of IPAP. The inspiratory phase cycles off, and the machine switches back to IPAP when it detects a cessation of patient effort, indicated by a decrease in inspiratory flow rate, or a maximum inspiratory time is reached, typically 3 seconds. Tidal volume (Vt) varies breath to breath and is determined by degree of IPAP, patient effort, and lung compliance. Work of breathing (WOB) is primarily dictated by initiation and maintenance of inspiratory airflow, with additional WOB linked to active contraction of the expiratory muscles.
Spontaneous mode depends on patient effort to trigger inhalation. A patient breathing at a low rate can develop a respiratory acidosis. The spontaneous/timed (ST) mode prevents this clinical consequence. The trigger in the ST mode can be the patient's effort or an elapsed time interval, predetermined by a set respiratory backup rate. If the patient does not initiate a breath in the prescribed interval, then IPAP is triggered. For machine-generated breaths, the ventilator cycles back to EPAP based on a set inspiratory time. For patient-initiated breaths, the ventilator cycles as it would in the spontaneous mode.
Conceptually, one can consider BiPAP as CPAP with pressure support (PS). The pressure during the inspiratory phase is termed IPAP and is analogous to PS, a pressure boost during inspiratory efforts. The pressure during the expiratory phase is termed EPAP and is analogous to CPAP, or PEEP, positive pressure during the entire respiratory cycle. The IPAP is necessarily set higher than EPAP by a minimum of 5 cm H2O, and the difference between the two settings is equivalent to the amount of PS provided.
The keys to successfully using NPPV on an emergency basis are patient selection and appropriate aggressiveness of therapy—that is, before resorting to endotracheal intubation and mechanical ventilation.
Indications and Contraindications
The indications for NPPV in the emergency setting are straightforward. The eligible patient must have a patent, nonthreatened airway; be conscious and cooperative; and have an existing, although insufficient, ventilatory drive. Patients who may benefit from NPPV may be hypercarbic, hypoxemic, or both. Patients with an acute exacerbation of chronic obstructive pulmonary disease (COPD), congestive heart failure exacerbation, severe pneumonia, status asthmaticus, or mild postextubation stridor might all be considered for NPPV. NPPV is contraindicated if the patient has a threat to his or her airway, is unable to cooperate, or is apneic. If the patient is in extremis, with very poor oxygen tensions and severe and worsening ventilatory inadequacy, immediate intubation is usually indicated, and it is not appropriate to delay intubation for a trial of NPPV. This is a relative contraindication, though, and clinical judgment is required.
The objectives of NPPV are the same as those for invasive mechanical ventilation: to improve pulmonary gas exchange, alleviate respiratory distress, alter adverse pressure/volume relationships in the lungs, permit lung healing, and avoid complications. Patients on NPPV must be monitored closely, using familiar parameters such as vital signs, oximetry, capnography, chest radiograph, bedside spirometry, and arterial blood gases (ABGs).
Initiating Noninvasive Mechanical Ventilation
Either a face mask or a nasal mask can be used, but a nasal mask is generally better tolerated. There are varying mask sizes and styles, and a respiratory therapist must measure the patient to ensure a good fit and seal. First, explain the process to the patient prior to applying the mask. Initially supply 3 to 5 cm H2O of CPAP with supplemental oxygen. Acceptance on the patient's part may improve if the patient is allowed to hold the mask against his or her face. The mask is secured with straps once the patient demonstrates acceptance. Next, explain to the patient that the pressure will change and either sequentially increase the CPAP pressure by 2 to 3 cm H2O increments every 5 to 10 minutes, or initiate BiPAP to support the patient's respiratory effort. Recommended initial settings for BiPAP machines in the noninvasive support of patients in respiratory distress or failure are IPAP of 8 cm H2O and EPAP of 3 cm H2O, for a pressure support (IPAP minus EPAP) of 5 cm H2O. The level of supplemental oxygen flowing into the circuit should be governed by goal pulse oximetry and corroborated by ABG results as necessary; it is appropriate to initiate therapy with 2 to 5 L/minute, but this amount should be adjusted with each titration of IPAP or EPAP.
As the patient's response to ventilatory and other therapy is monitored (using cardiac, respiratory, and blood pressure monitors; oximetry; capnography; ABGs as indicated; and the patient's voiced assessment of tolerance and progress), support pressures are titrated. One approach that has been used successfully in hypoxemic patients in impending respiratory failure is to titrate by raising EPAP and IPAP in tandem in 2 cm H2O steps, allowing a reasonable trial period (e.g., 5 minutes) at each level before increasing further. If the patient is hypercapnic, it may be better to raise the IPAP in 2 cm H2O steps, with the EPAP being increased in a ratio to IPAP of approximately 1:2.5. The intrinsic positive end-expiratory pressure (PEEPi), or auto-PEEP, cannot be measured by a noninvasive ventilator; therefore, EPAP should generally be maintained below 8 to 10 cm H2O to be certain that it does not exceed PEEPi in patients with obstructive lung disease. The IPAP must always be set higher than EPAP. The goals are to reduce the patient's WOB, meet oxygen saturation goals, improve gas exchange, foster patient cooperativity, and maintain a respiratory rate of <30 breaths per minute. If the patient is not approaching these goals after the first hour of NPPV, then strong consideration should be made for rapid sequence intubation and institution of invasive mechanical ventilation.
Tips and Pearls
· Patients who need airway protection must be differentiated from those who need intensive ventilatory support. None of the modes of NPPV provide airway protection.
· Patients with both a patent airway and some preserved respiratory drive—even if that drive is clearly insufficient—may be candidates for NPPV.
· Patients most likely to respond to NPPV in the ED (and therefore avoid intubation) are those with more readily reversible etiologies of distress, such as COPD exacerbation with fatigue, pneumonia with hypoxemia-induced fatigue, or cardiogenic pulmonary edema.
· The ventilatory management of patients in frank or impending respiratory failure with NPPV is a minute-to-minute, ongoing strategic decision. Virtually every modern ventilator is capable of delivering noninvasive ventilation (BiPAP, CPAP) and should be readily accessible to the ED or other areas in the hospital where respiratory emergencies arise. Physicians, nurses, and respiratory care personnel must be comfortable with ventilator use and knowledgeable of the limitations.
· Patient selection must take into account the overall condition of the patient, the patient's tolerance of mask support versus intubation, and the anticipated degree of reversal of the underlying insult with ventilatory and pharmacological support.
· One must be prepared for prompt intubation (i.e., difficult airway assessment done, drugs and equipment readily at hand) if therapeutic failure occurs.
· NPPV should be accompanied by aggressive medical therapy of the underlying condition (e.g., angiotensin-converting enzyme inhibitors, diuretics and nitrates for pulmonary edema, beta-adrenergic agonist and anticholinergic aerosols and corticosteroids for reactive airways disease).
· Finally, the patient should be carefully monitored for progress of therapy, tolerance of the mode of support, and any signs of clinical deterioration that indicate a need for intubation with mechanical ventilation.
· Patients treated in the ED with NPPV may require judicious sedation for anxiety in order to tolerate the mask, but doses used, if any, are small because preservation of respiratory drive is essential to the use of these modes.
Evidence
In some published series, patients successfully supported in the ED with NPPV were frequently able to be admitted to telemetry units instead of ICUs, thereby incurring a significant cost savings. Uncontrolled studies without definitive inclusion criteria have found NPPV successful in avoiding intubation and mechanical ventilation in a large variety of patients on whom it has been clinically tested. Most of the studies done with NPPV compare NPPV to standard medical care (SMC) with outcome measures of intubation, ICU length of stay, and mortality. Unfortunately, most of the studies are quite small and have either enrollment criteria or end points that are somewhat subjective. Nonetheless, there is a considerable body of literature analyzing the use of NPPV.
1. NPPV and COPD. Two meta-analysis studies have been performed analyzing the use of NPPV in COPD. The most recent meta-analysis was by Peters (1) in 2002 of 15 randomized control trials of NPPV versus SMC. Eight trials enrolled patients with COPD, and seven enrolled patients characterized as a mixed-disease group. NPPV wass associated with an overall 8% reduction in mortality (p = .03), 19% reduced need for intubation (p = .001), and 2.74 days shorter hospital stay (p = .004). The COPD group had more significant reductions with 13% decrease in mortality (p = .001), 18% decreased need for MV (p = .02), and decrease in hospital stay by 5.66 days (p = .01). In 1997, Keenan et al. (2) published a meta-analysis of such trials and identified only 7 out of 212 that met rigorous inclusion criteria for analysis. The analysis showed NPPV to have a decreased mortality (odds ratio, 0.29; 95% confidence interval [CI], 0.15–0.59), and a decreased need for intubation (odds ratio, 0.20; 95% CI, 0.11–0.36) (2).
2. NPPV and asthma. Shivaram et al. (3,4) demonstrated both a decreased WOB and an increased patient comfort level during CPAP support of acute asthma exacerbations. Meduri (5) studied NIVS in 17 patients with asthma and acute respiratory failure over a 3-year period and demonstrated marked improvements in pH, PaCO2, and respiratory rates, even at lower pressures of support (2.5 cm H2O). These small studies should not be considered to constitute evidence that NPPV is of benefit in acute asthma, and NIVS should be used in asthma only with extreme caution.
3. NPPV and pulmonary edema (PE). In small studies, there appears to be a benefit to NPPV in the PE patients; however, larger prospective trials are needed before firm conclusions can be drawn. A randomized prospective study of 39 patients with PE compared CPAP to SMC and found a significant decrease in need for intubation (p = .005) in the CPAP group. Bersten (6) reported no significant difference in mortality and hospital length of stay. An open nonrandomized study on 29 patients with NPPV found oxygen saturation increased from 73.8 ± 11% to 93 ± 5%, mean pH increased from 7.22 ± 0.1 to 7.31 ±.07 (p <.01), and PaCO2 decreased from 62 ± 18.5 mm Hg to 48.4 ± 11.5 mm Hg (7). A randomized, controlled, prospective clinical trial on 27 patients comparing nasal CPAP to nasal BiPAP against historical controls for intubation rates and myocardial infarction (MI) found that BiPAP improved ventilation and vital signs more rapidly than CPAP. However, intubation rates, hospital stay, and overall mortality between the two modes of NPPV showed no significant differences in this study. Mehta (8) also reported a higher rate of MI in patients with BiPAP (71%) as compared to CPAP (31%) and usual medical care from historical controls (38%). A randomized prospective study of 40 patients comparing BiPAP to high-dose isosorbide (HDI) reported that 80% of patients in the BiPAP group required intubation as compared with 20% in the HDI group, MI rates of 55% and 10%, and death in two and zero patients, respectively (9). A meta-analysis of NPPV studies in pulmonary edema from 1983 through 1997 found that only 3 of 497 studies were sufficiently rigorous to fulfill their study criteria. These three randomized control trials showed NPPV patients to have a decreased need for intubation (-26%; 95% CI, -13% to -38%), but the decrease in hospital mortality was not significant (-6.6%; 95% CI, +3% to -16%) as compared to standard therapy alone (10). A more recent study compared BiPAP to standard medical therapy in a mixed population of COPD and acute respiratory failure patients. The study ended prematurely after interim analysis of the first 20 patients because the data showed clear benefit in the BiPAP group (11).
References
1. Peters JV. Noninvasive ventilation in acute respiratory failure—a meta-analysis update. Crit Care Med 2002;30:555–562.
2. Keenan SP, Kernerman PD, Cook DJ, et al. Effect of noninvasive positive pressure ventilation on mortality in patients admitted with acute respiratory failure: a meta-analysis. Crit Care Med 1997;25:1685.
3. Shivaram U, Donath J, Khan FA, et al. Effects of CPAP in acute asthma. Respiration 1987;52:157.
4. Shivaram U, Miro AM, Cash ME, et al. Cardiopulmonary responses to CPAP in acute asthma. J Crit Care 1993;8:87.
5. Meduri GM. Noninvasive positive-pressure ventilation in patients with acute respiratory failure. Clin Chest Med 1996;17:513.
6. Bersten AD. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. N Engl J Med 1991;325:1825–1830.
7. Hoffman B. The use of noninvasive pressure support ventilation for severe respiratory insufficiency due to pulmonary oedema. Intensive Care Med 1999;25:15–20.
8. Mehta S. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit Care Med 1997;25:620–628.
9. Sharon A. 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. 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.
11. Thys F. Noninvasive ventilation for acute respiratory failure: a prospective randomised placebo-controlled trial. Eur Respir J 2002;20:545–555.