• Obstructive sleep apnea. Traditionally, CPAP has been used in OSA to provide a pneumatic splint to the upper airway to prevent obstruction during sleep. BiPAP provides both PEEP and PSV during inspiration, both assisting with ventilation and treating hypercarbia.1,3,4 In some patients with OSA, this method is more effective, especially in those with nighttime hypoventilation. Patients with OSA admitted to a critical care unit may need intubation and higher levels of ventilatory support than is possible to provide with NPPV. Others have conditions that may be managed on NPPV, but support levels may be higher than home NPPV settings.

• Cardiogenic pulmonary edema. Many studies have been accomplished that demonstrate the efficacy of NPPV in patients with congestive heart failure (CHF) and pulmonary edema.10,11,14,16,17,19,21,24,25 In these patients, the positive pressure results in preload and afterload reduction and restoration of functional residual capacity. NPPV works synergistically with diuretics and other medical interventions, enhancing their effect. In patients with a chronic condition, such as those with OSA and CHF, treatment with CPAP for 1 month significantly decreased systolic blood pressure (BP) and improved left ventricular function.¹⁴ Improved quality of life appears to be an additional benefit.¹⁶ In the patient with an acute illness, studies with PSV through a face mask suggest that intubation may be prevented¹⁰ and that its early use also accelerates improvement in partial pressure of arterial oxygen/fraction of inspired oxygen (PaO₂/FiO₂) ratio, partial pressure of arterial carbon dioxide (PaCO₂), dyspnea, and respiratory rate but not overall clinical outcomes.¹⁷ Interestingly, both CPAP and BiPAP appear to be equally effective in this patient population. In an randomized controlled trial (RCT) that compared the modes, both resulted in improved vital signs and arterial blood gas values and a lower rate of endotracheal intubation without cardiac ischemic complications.¹⁹ In the patient with an acute illness with cardiogenic pulmonary edema, the evidence supports a trial of NPPV with exception of those with extubation failure.^4,23

• Acute or chronic respiratory failure (i.e., chronic obstructive pulmonary disease [COPD]). A high level of evidence supports the use of trial of NPPV in hypercapnic respiratory failure (particularly related to COPD).⁴ The only exception to this recommendation is in those with extubation failure.⁴ NPPV in patients with hypercapnia has been effective in reducing intubation rates^17,23 and is associated with reductions in mortality and the need for invasive mechanical ventilation but not hospital length of stay.²⁰

• Acute hypoxemic respiratory failure. Although some studies suggest that NPPV may be effective in selected instances of acute hypoxemic respiratory failure,2,11–13 perhaps the most compelling category for use is in patients with immunosuppression with pneumonia.^12,22 In an RCT, early initiation of NPPV in these patients was associated with significant reductions in the rates of endotracheal intubation and serious complications. In addition, an improved likelihood of survival to hospital discharge was found.¹² Unfortunately, with this exception, study findings have not conclusively supported the routine use of NPPV in hypoxemic respiratory failure patient populations.^15,23

• To prevent reintubation after extubation. The use of NPPV has not been associated with prevention of need for reintubation or a reduction in mortality in patients with respiratory failure after extubation.5,7 However, careful selection of patients for NPPV after extubation did appear to improve outcomes in one RCT.⁹ In this study, the early use of NPPV (BiPAP) in those “at risk of respiratory failure following extubation”⁹ resulted in a decreased intensive care unit mortality. The risk factors included cardiac failure as cause of intubation, age more than 65 years, and increased severity of illness as identified by an Acute Physiology and Chronic Health Evaluation (APACHE) II score of more than 12 on the day of extubation.⁹

• Failure to wean. Although this population is underrepresented in the literature, at least one recent study suggests that the use of NPPV in patients with failure to wean successfully for three consecutive days may show better outcomes than in those weaned in a more traditional manner. In the study, BiPAP was used after early extubation and resulted in fewer days of mechanical ventilation and length of stay, less need for tracheostomy, lower incidence of complications, and improved survival.⁸

• Invasive ventilation not desired: Palliative or end-of-life care. In 2007, the Society of Critical Care Medicine’s Palliative Noninvasive Positive Pressure Ventilation Task Force proposed recommendations for the use of NPPV for patients and families of the patients wishing to forego endotracheal intubation.⁶ The recommendations focus on ensuring that patients and families understand the goals of the therapy (reduction of air hunger, etc), the criteria for determining success or failure of the NPPV, that the healthcare providers be experienced in the use of NPPV and the setting appropriate.⁶ The use of the therapy for end-of-life care is controversial because some believe it unduly prolongs death and others maintain it is a means of decreasing uncomfortable symptoms such as dyspnea.

• Status asthmaticus. Because of the instability of these patient conditions and the difficulty inherent in providing ventilatory support during the acute phase (e.g., preventing hyperinflation, auto-PEEP, and barotrauma), the use of NPPV is not recommended. Few studies are available supporting its use in this category of patient condition.

• Hemodynamic instability. Generally, this condition refers to patients with high vasopressor requirements or other supportive therapies. These patients need full ventilatory support to ensure acid-base stability and the adequacy of oxygenation and ventilation.

• Inadequate airway protective reflexes. Cough and swallow are essential for airway protection. Absence of these reflexes puts the patient at risk for aspiration.

• Encephalopathy or coma. As noted previously, the inability to protect the airway or remove a mask (especially full face masks) when necessary puts the patient at risk for aspiration.

• Mask fit or intolerance (claustrophobia, facial deformities, and occasionally, the absence of teeth). Different noninvasive options are available and should be considered if intolerance of masks (nasal or full face) or other interfaces is evident.

• Excessive secretions. The presence of secretions necessitates that the patient be able to effectively clear the airway. When excessive secretions are present, the work associated with effective airway clearance may quickly overwhelm the patient’s endurance and result in respiratory failure.

• Severe agitation. Agitation makes adjustment to the use of a noninvasive interface difficult. Further, leaks are increased when the interface is displaced, which makes ventilation unreliable and ineffective.

• High FiO₂ requirements. Most of the NPPV ventilators do not provide a high level of FiO₂ (this varies with the make, model, and manufacturer of the ventilator). In these cases, the patient may need invasive ventilation or NPPV with a conventional ventilator to ensure provision of the required FiO₂.

• Noninvasive interfaces are selected on the basis of patients’ unique facial features, patient preferences, comfort, ease of use, availability, and provider experience and preference and include full face masks, nasal masks, nasal pillows, and helmets. Of these, full head helmets are the least commonly used (and not discussed further in this procedure) but may be more prevalent in the future as experience with the interfaces increases.¹⁸ See Fig. 28-1 for NPPV interfaces.

• When NPPV fails, as evidenced by lack of improvement or further deterioration, invasive ventilation is necessary. Equipment and personnel to ensure safe intubation and application of invasive ventilation are necessary and should be ensured (see Procedures 2, 3, 35) Some potential causes of NPPV failure follow:

• Poor patient selection. See previous potential applications and exclusions.

• Mask intolerance and leaks. As noted previously, careful selection of the interface is essential to ensure success. In addition to patient facial characteristics, the actual process of applying the mask may be the reason for failure. In general, application of the mask as gently and gradually as possible is important to help the patient acclimate. Simultaneous and gradual adjustment of the mode parameters is a useful technique if the situation allows for the use of such a strategy. If mask leaks are present, patient-generated cycling may be adversely affected and result in dyssynchrony. Time-cycled modes may be helpful in these cases. Other mask complications that limit use include gastric distention and vomiting, nasal congestion, eye irritation from leaks, discomfort, claustrophobia, and nasal and facial skin breakdown.

• Development of serious complications. These complications include myocardial infarction, gastrointestinal bleeding, and sepsis.

• Limitation of the ventilator. Most NPPV ventilators do not provide for the delivery of high FiO₂, as noted previously. Flow capabilities may also vary and, if inadequate, result in dyssynchrony. In one study that compared bilevel devices with standard adult critical care ventilators, the bilevel devices were found to provide superior flow delivery.¹⁴

• Patient ventilator dyssynchrony. Many reasons for dyssynchrony exist and may include both physical and mechanical reasons such as auto-PEEP, worsening condition or other complications, and ventilator limitations (e.g., CO₂ elimination from partial rebreathing with some NPPV circuits).

• Complications of NPPV are similar to invasive positive pressure ventilation (PPV) and include hemodynamic changes and pulmonary barotrauma. These complications are described subsequently in this procedure.

• Assess for the following signs and symptoms of fatigue and impending acute ventilatory failure:

Rationale: These signs and symptoms demonstrate failure to adequately ventilate with NPPV. If the situation is not corrected, the patient may need intubation and initiation of PPV. While PPV is considered and assembled, support ventilation via a manual self-inflating resuscitation bag, if necessary.

• Assess for the following signs and symptoms of inadequate oxygenation:

Rationale: If hypoxemia noted by a saturation of arterial oxygen (SaO₂) is less than 90% or PaO₂ less than 60 mm Hg) cannot be immediately corrected on NPPV, the patient may need invasive PPV. While PPV is considered and assembled, provide 100% oxygen via manual resuscitation bag and mask.

• Determine pH and arterial carbon dioxide tension. Rationale: Acute ventilatory failure is confirmed by an uncompensated respiratory acidosis. Ventilatory failure is an indication for immediate adjustment of settings and possibly invasive PPV. See previous bullet.

• Verify correct patient with two identifiers. Rationale: Prior to performing a procedure, the nurse should ensure the correct identification of the patient for the intended intervention.

• Ensure that the patient understands pre-procedural teachings. Answer questions as they arise, and reinforce information as needed. Rationale: This communication evaluates and reinforces understanding of previously taught information.

• Premedicate as needed. Rationale: Cautious use of narcotics, sedatives, or anxiolytics may be necessary for comfort, to help allay anxiety, and to improve the patient’s tolerance of NPPV. However, the use of the drugs should not adversely affect spontaneous breathing or consciousness.