Continuing Education Activity
Non-invasive positive pressure ventilation involves the delivery of oxygen into the lungs via positive pressure without the need for endotracheal intubation. It is used in both acute and chronic respiratory failure but requires careful monitoring and titration to ensure its success and avoid complications. This activity reviews the physiology behind non-invasive positive pressure ventilation, its indications and contraindications, preparation and techniques, and highlights the role and importance of the interprofessional team during initiation and maintenance of this procedure.
- Describe the physiology of non-invasive positive pressure ventilation.
- Identify the indications and contraindications of non-invasive positive pressure ventilation.
- Summarize the technique for initiation and monitoring of non-invasive positive pressure ventilation.
- Identify the complications that can arise with non-invasive positive pressure ventilation.
Non-invasive ventilation (NIV) was first reported in the mid-eighteen century by a Scottish physician, John Dalziel. In 1864, Alfred F. Jones' patented the first American tank respirator in the iron lung, known as non-invasive negative pressure ventilation. In 1938 a new form of NIV was described by Barach et al. as a treatment for pulmonary edema. However, Oertel described the use of intermittent positive pressure (NPPV) earlier by Oertel (1878).
During the polio epidemic and due to very high mortality (more than 80%), innovation was sparked by physicians such as Bjorn Ibsen, an anesthesiologist from Copenhagen, Denmark, who applied positive pressure ventilation in 1952 via trach but required manual delivery. The approach dropped the mortality by more than half (to nearly 40%); however, the delivery of pressure was a logistical problem, as there were no positive pressure ventilators, and patients needed to be bagged by hand.
Over the past century, positive pressure ventilation (NPPV) has been dramatically improved and used to treat respiratory failure from multiple etiologies. It has been proven effective in preventing intubation compared to standard oxygen therapy in the acute setting. NPPV encompasses several methods of respiratory support, the most common being Bilevel Positive Airway Pressure (BPAP).
The latest American Thoracic Society/European Respiratory Journal guidelines support the use of NPPV in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and acute respiratory failure secondary to cardiogenic pulmonary edema, where evidence and level of recommendation are the strongest. However, there is a body of evidence and conditional recommendations that NPPV is effective in other settings of acute respiratory failure, such as post-operative and chest trauma. In addition, several studies support the use of NPPV in various chronic respiratory diseases.
Anatomy and Physiology
Lung compliance refers to the change in volume that accompanies a change in pressure in the lung. Compliance is calculated according to the formula dV/dP, where V refers to the volume of the lung and P refers to the transpulmonary pressure (TPP), which can be otherwise expressed as alveolar pressure (Palv) – intrapleural pressure (Ppl). TPP can be thought of as the pressure that prevents the inward recoil of the lung, or rather the pressure that keeps the lung from collapsing on itself.
At rest, TPP is slightly positive, and during inspiration, as the diaphragm contracts, Ppl will decrease, causing TPP to increase and subsequently the lung to expand. Normal lung tissue is based on a compliance curve in which a change in TPP will generate a maximum increase in lung volume.
Lung diseases can either cause an increase or decrease in the lung's compliance and distortion of the curve, resulting in an increased TPP to generate the appropriate change in lung volume. For example, emphysema will cause the compliance curve to be displaced upwards, resulting in the TPP being in a region where increased TPP will result in a minimal increase in lung volume. In contrast, diseases such as acute respiratory distress syndrome and cardiogenic pulmonary edema will cause an overall decrease of compliance due to liquid-filled alveoli exerting mechanical stress on air-filled alveoli.
NPPV reduces the work of breathing through three different methods. By applying positive end-expiratory pressure (PEEP) through expiratory positive airway pressure (EPAP), NPPV allows the body to overcome the dynamic intrinsic positive end-expiratory pressure threshold required to initiate a breath, as well as increasing lung compliance. By applying inspiratory positive airway pressure (IPAP), NPPV contributes a more significant portion of the TPP required during inspiration, thus reducing the body's breathing work.
According to the latest ATS/ERJ guidelines from 2020 for acute respiratory failure, NPPV carries a strong recommendation for the following in the setting of acute respiratory failure (ARF):
- BPAP for acute or acute-on-chronic respiratory acidosis secondary to COPD exacerbation where pH </= 7.35
- BPAP is the prevention of endotracheal intubation and mechanical ventilation in a patient that is not immediately deteriorating
- BPAP or continuous positive airway pressure (CPAP) for cardiogenic pulmonary edema
ATS/ERJ guidelines carry a conditional recommendation for the following in the setting of ARF:
- Early NIV for immunocompromised patients with ARF
- Post-operative ARF
- As palliation to dyspneic patients in the setting of terminal cancer or other terminal conditions
- Chest trauma patients with ARF
- Prevention of post-extubation respiratory failure in high-risk patients
In addition, NPPV has been effective in treating various chronic respiratory diseases. These diseases include chronic stable COPD with hypercapnia, obesity hypoventilation syndrome, obstructive sleep apnea, respiratory failure secondary to neuromuscular disease, and restrictive thoracic disorders.
- Facial trauma/burns
- Fixed upper airway obstruction
- Active vomiting
- Respiratory or cardiac arrest
- A recent facial, upper airway, or upper GI tract surgery
- Inability to protect the airway
- Life-threatening hypoxemia
- Medical or hemodynamic instability (hypotensive shock, myocardial infarction requiring intervention, uncontrolled ischemia or arrhythmias)
- Altered mental status/agitation
- Bowel obstruction
- Copious respiratory secretions
- Focal consolidation
- Undrained pneumothorax
- Severe co-morbidity
NPPV Circuit Components
NIV device: While CPAP is delivered using a continuous flow, BPAP is typically produced using two modes: Spontaneous or spontaneous/timed (S/T). Spontaneous mode is where the machine augments the patient's spontaneous breaths, whereas S/T mode includes a backup rate slightly below the patient's respiratory rate. Newer versions of NPPV devices were developed to add more monitoring features and ventilatory assistance, such as averaged volume-assured pressure support (AVAPS). The AVAPS device delivers a constant tidal pressure-volume to patients and uses a specific algorithm that automatically calculates the pressure changes needed to maintain an optimal tidal volume. In addition, AVAPS can be combined with auto–expiratory positive airway pressure (AVAPS-AE) to maintain a patient's upper airway patency.
BPAP S/T mode vs. AVAPS
|BPAP S/T mode
|Minimum and maximum pressure
|EPAP (Auto AE)
Fixed pressure support (PS):
|S/T backup rate
|Assured average volume
- Mask: several types of masks exist, including nose mask, nose-mouth mask, and helmet, each with its own set of advantages and disadvantages
NPPV initiation and titration should be performed by experienced physicians trained in its use and monitoring. Qualified physicians typically come from internal medicine, anesthesiology, surgery, emergency medicine, pulmonary medicine, and critical care. Support staff for the procedure includes personnel proficient with the device and complications, and this typically comprises respiratory therapists or registered nurses with an essential care background.
Technique or Treatment
The initiation of NPPV must occur after careful patient, ventilator, and interface selection. As successful implementation of NPPV is mainly dependent on patient cooperation, the goals, process, and complications of this procedure must be explained to the patient in detail before initiation. Following this, mask fitting is started, and the patient should be given time to acclimate to the mask before securing it. The ventilator is then connected to the mask and turned on with oxygen supplementation.
Initiation and titration of NPPV must be performed carefully with close monitoring by the clinician and nursing and respiratory therapy. Titration protocols often differ by institution and pathology. In addition, few titration protocols have been published in the literature. One such protocol for NPPV titration for OSA has been published in the Journal of Clinical Sleep Medicine. In addition, a recently published review in Annals of ATS details a titration protocol for chronic hypercapnic respiratory failure in the setting of COPD.
Titration of NPPV in an Acute Setting
Clinician experience shows that the titration of NPPV in the acute setting in the intensive care unit can be divided into three categories. The first category is for those patients who have simple airway conditions, such as obstructive sleep apnea, needing end-expiratory positive airway pressure, or CPAP alone. The titration of pressure in this situation requires overcoming the collapsing pressure of the upper airway, which can be estimated from the actual body weight. From our experience, using 10% of the actual bodyweight of the patient in kilograms would be the starting point of the EPAP or CPAP.
The second category is for those with hypercapnic or mixed respiratory failures, such as those with acute exacerbation of COPD and no upper airway obstruction (no obesity or suspicion of OSA). In this category of hypercapnic patients, clinicians can use EPAP of 5 cmH2O and add high-intensity pressure support of 10 to 15 cmH2O, which can be titrated based on response in reducing CO2 (measured by arterial blood gas).
A third category is when patients hospitalized with hypercapnic respiratory failure are associated with obesity or obstructive sleep apnea. This group of patients is the most challenging as they require careful adjustment for both inspiratory and expiratory pressures to prevent upper airway collapse while maintaining adequate ventilation. Therefore in this group of patients, one must combine the strategy used in the previous two categories of patients where clinicians can apply sufficient EPAP to overcome the collapsing upper airway pressure using the 10% rule of actual body weight (in kilograms) and add high-intensity pressure support between 10 to 15 cmH2O to provide adequate ventilation and titrate based on arterial blood gas.
Once pH is normalized, the pressure support can be weaned off slowly to allow a slight decrease in hypercapnia that can be managed in an outpatient setting. Patients with chronic respiratory failure suspected of having OHS should be discharged on NPPV until they undergo outpatient diagnostic polysomnography and laboratory PAP titration. In the meantime, the BPAP S/T mode can be used with empiric settings or auto-titrating NPPV such as VAPS with the auto-expiratory positive airway pressure (VAPS-AE), which can automatically adjust the EPAP to ensure adequate upper airway patency due to OSA.
When monitoring to ensure adequate response to NPPV in the acute setting, the clinician must consider the subjective and physiologic responses of the patient. Clinicians should use caution when asking patients about their respiratory status, as some patients will minimize or deny discomfort, thus confounding the clinical picture. Patients who are likely to succeed on NPPV in the acute setting will have a drop in their respiratory rate after 1 to 2 hours, a decrease in heart rate, and better ventilator synchrony.
A blood gas should be drawn one hour after initiation of BPAP as a decrease in PCO2 and increase in pH is predictive of NPPV success. In addition to the parameters above, tidal volume and air leak must be closely monitored as these can contribute to treatment failure if not corrected. The patient's hemodynamics, including blood pressure and heart rate, must also be closely monitored during treatment as intrathoracic pressure and right ventricular afterload will increase and right ventricular preload will decrease, consistent with prior studies which have demonstrated a reduction in cardiac output after initiation of NPPV.
Titration of NPPV in a Chronic Setting
1) COPD with chronic hypercapnic respiratory failure: NIV is used for patients with COPD and stable hypercapnia (CO2 ≥52 mmHg). Prospective randomized controlled trials have significantly improved survival and clinical outcomes (less exacerbation rate and better disease control). Contrary to previous studies, the clinical benefits of NIV in stable COPD seem to be due to high-intensity pressure support that targets the normalization of CO2 (or at least a 20% decrease in CO2 level). Clinician experience in stable patients with COPD and chronic hypercapnic respiratory failure with no evidence of obstructive sleep apnea or obesity indicates using BPAP S/T mode with IPAP 15-20 cmH2O. However, when there is obstructive sleep apnea suspicion or obesity (OSA/COPD overlap), EPAP level will need to be adjusted based on their opening pressure (from the PAP titration sleep study when obstructive apnea is eliminated), or if not available, pressure is set empirically based on actual body weight using the above 10% rules (e.g., for a patient whose weight is 70 kg, the EPAP will be set at seven cmH2O).
2) Obesity hypoventilation syndrome: OHS is defined as a combination of obesity (body mass index >/=30 kg·m^-2), daytime hypercapnia (arterial CO2 >/= 45 mmHg), and diagnosis of OSA (apnea-hypopnea index ≥ five events/hour) after excluding other causes of alveolar hypoventilation. OHS and coexistent OSA treatment is CPAP; however, when CPAP is not tolerated or fails to correct ventilation (CO2 >/= 45mmHg), NPPV (BPAP S/T mode or VAPS) is recommended (see prescription parameters below). The pressure selection in OHS associated with OSA requires eliminating apnea and hypopnea (AHI <5 event/hour) and fixing the hypoventilation and sustained hypoxia. Therefore, a dedicated pressure titration in the sleep laboratory is recommended with follow-up in the clinic to measure ABG and adherence to device treatment (usually within 4 to 6 weeks).
3) Thoracic restrictive disorder (TRD) with hypercapnic respiratory failure: TRD is defined as ventilatory defects associated with elevated CO2 (≥45 mmHg) due to neuromuscular disorders (amyotrophic lateral sclerosis, spinal cord injury, muscular dystrophy, diaphragm paralysis, spina bifida, and congenital central hypoventilation syndrome), chest wall deformity, and other ventilatory drive defects without evidence of interstitial lung disease. The use of NPPV treatment in TRD is similar to other hypoventilation syndromes. It requires careful assessment of OSA and monitoring of CO2 and oxygenation while the patient is awake and sleeping after initiation of therapy. In this condition, BPAP S/T or VAPS should be considered without sleep testing.
The prescribing physician determines settings.
Settings: Primary Mode:
AVAPS-AE with Target Tidal Volume
VT (Tidal Volume- 8ml/kg): _____
Max Pressure: _____
PS Max (pressure support max): _____
PS Min (pressure support minimum): _____
EPAP Max: _____
EPAP Min: _____
Rate (if rate= “auto” then “N/A”): ____
The most common complication of NPPV is mask discomfort. More serious adverse effects include skin rash secondary to hypersensitivity or infection and rarely nasal bridge ulcers. Aerophagia and sialorrhea are also complications that may arise.
Patients may experience symptoms related to the pressure, including discomfort, ear and sinus pain, or gastric insufflation. Serious side effects from pressure include pneumothorax, pneumocephalus, and more recently, pneumomediastinum from NPPV in the setting of SARS-CoV-2 pneumonia.
Aspiration is a serious complication of NPPV, and steps should be taken during patient selection to ensure that patients on NPPV are at low risk of aspiration. Sedation in NPPV has not been well studied due to the thought process that it can lead to an increased risk of aspiration and hypoventilation.
Rarely when patients co-present with respiratory failure and compromised cardiac output, NPPV will cause hemodynamic compromise due to increased intrathoracic pressure and right ventricular afterload, as well as reduced preload.
The final complication arises from patient-ventilator dyssynchrony with BPAP. This falls under two categories: Failure to trigger and failure to cycle, leading to inadequate gas exchange and unnecessary expiratory muscle use. An example of failure to cycle would be during COPD, where rapid inhalations may not give the BPAP adequate time to cycle from inspiration to expiration. Thus, the patient will be expiring against the ventilator’s effort to deliver inspiratory pressure, leading to respiratory discomfort and distress. Failure to trigger can be seen in neuromuscular diseases such as ALS, where the patient cannot generate enough negative pressure during inspiration to trigger the assisted breath.
Respiratory failure is a life-threatening condition responsible for around 30% of in-hospital mortality. The definitive treatment for respiratory failure is mechanical intubation and ventilation. However, this process is associated with significant morbidity and mortality. These include complications with intubation, such as laryngospasm, bronchospasm, incorrect tube placement, aspiration, and hypotension, as well as complications from prolonged time on mechanical ventilation, including ventilator-induced lung injury, ventilator-associated pneumonia, and GI complications, including peptic ulcers and colonization of the GI tract by aerobic gram-negative bacteria.
NPPV has been shown to reduce intubation in COPD, cardiogenic pulmonary edema, and pneumonia and reduce the need for reintubation in hypercapnic respiratory failure following extubation. However, NPPV is a time-consuming procedure requiring high resource utilization and should only be performed under a clinician and support staff with proficiency in its use.
- Start treatment as early as possible
- When arterial pH is less than 7.35 and elevated PaCO2, it indicates the presence of acute or acute on chronic hypercapnia respiratory failure, which require admission to ICU
- In acute on chronic hypercapnia respiratory failure, the first goal is to correct arterial pH
- In chronic hypercapnic respiratory failure with arterial PaCO2more than 51 mmHg, the use of high-intensity pressure support is indicated. It should be targeted to correct CO2 toward normal or at least reduced by 20% from initial levels.
- When OSA is suspected, the EPAP should be adjusted empirically (use the 10% rule of actual body weight) if no PAP titration was performed.
Enhancing Healthcare Team Outcomes
NPPV is initiated at the physician level but requires the cooperation of an interprofessional team to ensure its success. While the physician performs the initial settings and titration, subsequent patient monitoring is usually done by a team including nurses with critical care training and respiratory therapists.
The patient must have their mental status and vital signs continuously monitored, and any abnormalities must be recognized and reported to the physician expediently. IV access should be secured before initiation of NPPV should hypotension develop. The patient will need frequent arterial/venous blood gas draws during titration of NPPV. During transfers of care, it is vital to communicate the patient’s prior NPPV settings and changes to ensure optimal adjustment and effectiveness of NPPV.