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CE Article: BiPAP Essentials for Prehospital Providers

Figure 1: A graphical representation of IPAP, EPAP and pressure support.

Objectives

  • Provide an introduction and overview of bilevel positive airway pressure (BiPAP); 
  • Identify differences in mechanism and applications between BiPAP and continuous positive airway pressure (CPAP); 
  • Outline the technical components of BiPAP administration for prehospital providers. 

Over the years, continuous positive airway pressure (CPAP) has become an accepted and routinely used prehospital emergency treatment for acute respiratory failure. Evidence shows noninvasive ventilatory management can reduce intubation rates and improve patient recovery,1 and with the arrival of CPAP several years ago, many alterations and advances have improved this therapy, resulting in better patient outcomes. Among these advances has been bilevel positive airway pressure, or BiPAP.

BiPAP, more commonly observed in hospital emergency departments and intensive care units, has also made its way to the prehospital setting.2 Many prehospital providers seem to have a natural curiosity about this lifesaving intervention. This article will discuss the pulmonary mechanism of BiPAP, how it differs from CPAP and technical aspects providers can utilize in their practice where BiPAP is offered.

Pulmonary Mechanics

As the name implies, bilevel positive airway pressure offers two different levels of noninvasive pressure that correspond to the respiratory cycle. These levels are called the inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). These are also known as the inspiratory baseline and the expiratory baseline pressures. When a patient receives BiPAP, the noninvasive ventilator functions to provide a preset expiratory pressure during the expiratory phase and a preset inspiratory pressure during the inspiratory phase of the respiratory cycle.

This mechanism creates an astonishingly powerful method of reducing the patient’s work of breathing and increasing the functional residual capacity (FRC) of the lungs (FRC is the volume of air left in the lungs at the end of exhalation).3 It is important to note there are two separate physiological processes working in the lungs: ventilation and oxygenation. Ventilation specifically deals with the removal of carbon dioxide from the lungs. The effectiveness of ventilation is measured by arterial carbon dioxide levels, or PaCO2; in the prehospital environment this is often correlated with end-tidal carbon dioxide, or EtCO2. From a mechanical ventilation standpoint, ventilation is monitored and even controlled by adjusting values such as tidal volume, minute ventilation and respiratory rate. Oxygenation specifically deals with the ability of the lungs to deliver oxygen to the pulmonary capillaries. Oxygenation is measured most accurately by obtaining the partial pressure of arterial oxygen, or PaO2; this is most commonly related to the patient’s SpO2 value in the prehospital environment. In mechanical ventilation the PaO2 and/or SpO2 is improved by increasing the positive end expiratory pressure (PEEP, which coincidentally is directly proportional to the FRC in the lungs) and the fraction of inspired oxygen (FiO2, 21%–100%).

The removal of carbon dioxide in BiPAP is done through the use of pressure support. Pressure support is a value determined by the difference between IPAP and EPAP (Figure 1). Pressure support is primarily used for ventilation, meaning it’s inversely proportional to arterial carbon dioxide levels. As pressure support increases, PaCO2 should decrease; when pressure support decreases, PaCO2 should increase. The pressure support is directly proportional to tidal volume: As pressure support increases, tidal volume should increase, and vice versa.

Patients who present in the latter stages of acute respiratory failure often present with arterial blood gases reflective of uncompensated respiratory acidosis, usually as a result of decreased tidal volumes and minute ventilation due to muscle fatigue and/or abnormal ventilatory rates. BiPAP may benefit these patients by accelerating their recovery from respiratory failure.The ventilating pressure support augments the patient’s compromised respiratory effort by alleviating muscle demand for ventilation. Thus, the addition of pressure support utilizing IPAP effectively and safely ventilates the patient, much in the same way bag-valve mask ventilation works, a service CPAP does not perform.5  

BiPAP offers another pulmonary mechanism that CPAP already offers: positive end expiratory pressure. CPAP provides a constant airway pressure in the lungs during both inspiration and expiration. This constant baseline provides the lungs with PEEP, which increases the pulmonary reserve, or functional residual capacity. BiPAP does this through expiratory positive airway pressure. During the expiratory phase, the noninvasive ventilator lowers airway pressure to a preset EPAP, which is synonymous with the PEEP. This maintains small-airway patency, prevents atelectasis and increases FRC, drastically improving oxygenation.6 While CPAP works to improve only oxygenation (hypoxemic respiratory failure), the use of BiPAP improves not only oxygenation but also ventilation with the use of pressure support.12 

Technical Aspects

There are different types of BiPAP modes. Some models provide a time-triggered mode, where the IPAP and EPAP cycles occur at a prescribed respiratory rate. This type of BiPAP is less frequently used because it is associated with patient-ventilator dyssynchrony and increased respiratory distress.7 The more commonly used mode of BiPAP is known as spontaneous timed. This mode allows the operator to set a minimal respiratory rate, usually around 8–12 bpm. The idea is that the patient continues to breathe spontaneously, and the IPAP and EPAP are triggered according to the patient’s spontaneous effort; however, if the patient experiences a period of apnea or their respiratory rate drops below the rate set on the ventilator, the machine will switch to a prescribed respiratory rate until the patient begins to breathe spontaneously again.7 

This approach is not designed to actually ventilate the patient, but it is meant as a safety mechanism to allow for some positive pressure ventilation to occur should the patient begin deteriorating. Most models have built-in alarms that alert providers that the BiPAP has switched to a prescribed respiratory rate or if no spontaneous effort is noted from the patient. This is most helpful when BiPAP is used in patients who have central sleep apnea, a form of sleep apnea in which efforts to breathe do not occur (versus obstructive sleep apnea, where the airway is compromised by decreased muscle tone or from some other obstruction).8 The machine time-cycled IPAP and EPAP are meant to prompt the patient to begin spontaneously breathing again.

In the emergency setting, noninvasive ventilation (NIV) is often used for two distinct types of respiratory disorders: restrictive lung disease and obstructive airway disease. Most of the time this is due to acute cardiogenic pulmonary edema, asthma or chronic obstructive pulmonary disease. Other conditions that benefit from the use of NIV are acute hypoxemia, acute respiratory distress syndrome and palliative care. Settings for NIV are most often determined based upon presentation and titrated to effect. Most clinicians start at an IPAP of 10 cm H2O and an EPAP of 5 cm H2O, leaving a pressure support of 5 cm H2O. Sources recommend titrating the pressure support to meet appropriate tidal volumes of 6 ml/kg of ideal body weight. If the presenting tidal volume is lower than predicted, it is important for the clinician to increase the pressure support to assure adequate ventilation. Other sources seriously recommend not exceeding an IPAP of 20–25 cm H2O due to the risk of gastric distention.13 

It is helpful to distinguish which respiratory process is compromised, oxygenation or ventilation. If the patient is oxygenating well with respiratory distress, increased levels of PEEP may not be necessary, allowing the clinician to leave EPAP at a normal level of 5 cm H2O. However, in some cases, such as acute pulmonary edema, increased levels of PEEP may be necessary to maintain alveoli patency and reduce fluid infiltration to improve oxygenation. EPAP levels of 5, 8 or 10 cm H2O may be necessary in the presence of hypoxia. It is theorized that consistently high levels of intrathoracic pressure due to PEEP decrease preload on the heart, reducing the circulating volume of blood and fluid through the lungs, reducing pulmonary edema and decreasing hydrostatic pressures in the pulmonary vasculature.9  

Most prehospital providers are comfortable with determining the liter flow required for oxygen devices such as a nasal cannula or nonrebreather; however, when using a noninvasive ventilator for BiPAP, oxygen is most often determined by the fraction of inspired oxygen, or FiO2. FiO2 is the percentage of oxygen inspired, room air being 21% and a nonrebreather with 15 lpm of oxygen at 100% FiO2 (theoretically). When initiating BiPAP it is also important to determine the amount of oxygen the patient needs. The use of CPAP (PEEP) or EPAP (in the case of BiPAP) often eliminates the need for high levels of FiO2; some clinicians with experience using BiPAP often find the mechanism of expiratory pressure allows clinicians to supply lower levels of oxygen, sometimes between 30%–50% (which is roughly equivalent to using a nasal cannula for oxygenation), and maintain SpO2 levels. Oxygen toxicity has become a hot topic in prehospital literature; make all attempts to avoid excessive oxygen administration. In mechanical ventilation, the amount of PEEP used often corresponds with the level of FiO2 required. For example, when using high levels of PEEP, a lower amount of oxygen is needed to maintain oxygenation, and vice versa for circumstances using low levels of PEEP. The same concept holds true for noninvasive BiPAP. Clinicians may titrate EPAP according to the amount of FiO2 required to maintain SpO2 or PaO2. Most sources recommend maximum EPAP levels between 10–15 cm H2O, and of course FiO2 can be adjusted to maintain appropriate SpO2.13 Patients requiring high levels of both EPAP and FiO2 may have decompensated to the point where intubation and invasive mechanical ventilation are required. 

Prehospital Clinical Applications

A common complaint of 9-1-1 callers is respiratory distress or difficulty breathing. Since this has a high occurrence, it’s important for prehospital providers to know when BiPAP is appropriate for those experiencing it. First and foremost, BiPAP is not indicated for patients who are unable to maintain their airway, are hemodynamically unstable, have an altered level of consciousness or are apneic or require immediate intubation. Complications or adverse effects of BiPAP include gastric distention, hypotension, anxiety and (less likely) pneumothorax.12 

COPD is an obstructive disorder characterized by increased airway resistance and decreased expiratory flow rates. This makes it difficult for COPD patients to fully exhale their tidal volume. Although most people associate it with smoking and emphysema, COPD is actually an umbrella term that includes other respiratory conditions, such as asthma and chronic bronchitis. During an exacerbation of this disease, increased airway resistance leads to air trapping and a retained volume of air in the distal airways and alveoli. As the exacerbation worsens, trapped gases decrease the volume of air the patient can inspire. 

The solution to this is to open the airways and maintain their patency. This can be done with medications such as bronchodilators, steroids and smooth muscle relaxers. However, BiPAP offers the ability to “stint” airways by providing PEEP. This maintains the patency of lower airways and allows the patient to exhale with much more ease. The addition of pressure support decreases muscle fatigue by augmenting the amount of work the patient performs to breathe. Patients in acute respiratory failure, a common occurrence with COPD, benefit from the pressure support because it decreases arterial carbon dioxide by increasing the patient’s tidal volume with the increased positive pressure during the inspiratory phase of the respiratory cycle. 

Patients with congestive heart failure and/or pulmonary edema benefit greatly from BiPAP.10 Not only does BiPAP decrease muscle fatigue, increase tidal volume and maintain alveolar/distal airway patency,11 but therapeutically BiPAP benefits “wet” lungs by decreasing central venous return. This decreases the amount of circulating blood volume that goes through the pulmonary vasculature, which in turn decreases hydrostatic vessel pressure and prevents fluid from crossing the capillary membrane in the alveoli and flooding the interstitial spaces. The decreased venous return is caused by the PEEP or, in the case of BiPAP, the EPAP. The increased expiratory pressure increases intrathoracic pressures, putting stress on the venous return system, decreasing central venous pressures. This increased EPAP increases the functional residual capacity of the lungs, leading to an increase in arterial oxygen and/or SpO2. Note also that pulmonary edema does not have to be a result of CHF for BiPAP to be effective. Other causes of noncardiogenic pulmonary edema, such as acute respiratory distress syndrome (ARDS), sepsis/systemic inflammatory response syndrome and renal failure (with fluid overload) with respiratory distress, warrant noninvasive ventilation if immediate intubation is not required. 

When differentiating the appropriate use of CPAP versus BiPAP, it is important to consider whether the patient is suffering from type 1 or type 2 respiratory failure. In type 1 (hypoxemic) respiratory failure, the patient suffers from hypoxemia alone, usually defined as a PaO2 less than 50 mmHg.14 In type 2 (ventilatory/hypercapnic) respiratory failure, the patient suffers from hypercapnia, usually defined as a PaCO2 greater than 50 mmHg, which can be accompanied by type 1.14 CPAP itself is an effective first-line agent for type 1 patients, as it is effective for increasing FRC by applying PEEP.12 Type 2 patients are recommended to be placed on BiPAP as an effective means of improving gas exchange and normalizing arterial blood gases.12 When considering changes in practice and purchasing equipment, it may be prudent to utilize devices that can provide BiPAP since BiPAP utilizes EPAP, which essentially is PEEP. This may be why BiPAP does not display a clinical benefit in outcomes over CPAP in cases of acute cardiogenic pulmonary edema that may initially present as type 1 respiratory failure.4

Conclusion

This article in no way fully expresses the scope and technical aspects of bilevel positive airway pressure ventilation. The reader is encouraged to seek further knowledge through reading, clinical observation and skill practice. 

BiPAP is an amazing innovation in the treatment of pulmonary disorders. It is proven to prevent and delay endotracheal intubation in patients experiencing acute respiratory failure. Paramedics interested in providing advanced emergency and critical care in the field will find BiPAP a tool that can be applied in situations where emergency CPAP may have been used. With the proper training, didactic opportunity and clinical practice, prehospital providers can and should be comfortable applying this therapy with the potential to reduce the burdens of endotracheal intubation and respiratory arrest in patients experiencing pulmonary disease exacerbations. 

References

1. McNeill GBS, Glossop AJ. Clinical applications of non-invasive ventilation in critical care. Contin Educ Anaesth Crit Care Pain, 2012; 12(1): 33–7.

2. Daily JC, Wang HE. Noninvasive positive pressure ventilation: resource document for the National Association of EMS Physicians position statement. Prehosp Emerg Care, 2011 Jul–Sep; 15(3): 432–8.

3. Vines D. Respiratory Monitoring in the Intensive Care Unit. In: Wilkins R, Dexter J, Heuer A. Clinical Assessment in Respiratory Care, 6th ed. St. Louis, MO: Elsevier, 2009.

4. Nouira S, Boukef R, Bouida W, et al. Non-invasive pressure support ventilation and CPAP in cardiogenic pulmonary edema: a multicenter randomized study in the emergency department. Intensive Care Med, 2011 Feb; 37(2): 249–56.

5. Yosefy C, Hay E, Ben-Barak A, et al. BiPAP ventilation as assistance for patients presenting with respiratory distress in the department of emergency medicine. Am J Respir Med, 2003; 2(4): 343–7.

6. Crouser ED, Exline MC, Fahy RJ. Acute Lung Injury, Pulmonary Edema, and Multiple System Organ Failure. In: Kacmarek RM, Stoller JK, Heuer A. Egan’s Fundamentals of Respiratory Care, 10th ed. St. Louis, MO: Elsevier, 2013.

7. Respironics. V60 Ventilator User Manual, p. 4–10.

8. American Academy of Sleep Medicine, Sleep Education. Central Sleep Apnea—Overview & Facts, www.sleepeducation.org/sleep-disorders-by-category/sleep-breathing-disorders/central-sleep-apnea/overview-facts.

9. Torres JD, Radeos MS. Noninvasive Ventilation: Update on Uses for the Critically Ill Patient. EM Crit Care, 2011; 1(2): 1–18.

10. Hoffmann B, Welte T. The use of noninvasive pressure support ventilation for severe respiratory insufficiency due to pulmonary oedema. Intensive Care Med, 1999 Jan; 25(1): 15–20.

11. Antonescu-Turcu A, Partasarathy S. CPAP and bi-level PAP therapy: new and established roles. Respir Care, 2010 Sep; 55(9): 1,216–29.

12. Montgomery H, Camporota L, Orhan O, et al. Handbook of Mechanical Ventilation. London: Intensive Care Society, 2015.

13. Soo Hoo GW. Noninvasive Ventilation. Medscape, http://emedicine.medscape.com/article/304235-overview#a4.

14. Melanson P. Acute respiratory failure. McGill Critical Care Medicine, https://www.mcgill.ca/criticalcare/teaching/files/acute.

Dustin Britt, AAS, RRT-ACCS, CPFT, NRP, FP-C, is a paramedic with Stanly County EMS and a respiratory therapist with Carolinas Healthcare System in Albemarle, NC. His recent experience includes working as a flight paramedic with Eagle Air Med in Gallup, NM.

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