New ventilatory technology provides lung protection and shorter time on the ventilator for burn patients.

 Ventilatory management of burn patients has historically been a challenge for the clinical team.1 Often, many patients in this population sustain inhalation injury, which can cause airway obstruction and the development of pneumonia.2 A high percentage of these patients also have burns over a portion of their body surface. This can result in the inability to provide good pulmonary hygiene, which can lead to pneumonia and, thus, impaired oxygenation.3 Contributing to the impairment of gas exchange are the fluid requirements during resuscitation. Much of the fluid administration leaks into the lung, causing the peak airway pressures to elevate and increasing the chance of ventilator-induced trauma. Also, paralytic administration is required to maintain optimal ventilator-patient interfacing.4 This in itself can result in unwanted side effects and prolonged ventilator duration.5 A new ventilatory option for this patient population is airway pressure release ventilation (APRV).

Clinical rationale
Barotrauma is a complication that can occur at any time during the clinical course of ventilation.6 APRV theoretically provides and maintains gas exchange while reducing the chance of ventilator-induced lung injury.7 Lung-protective ventilatory strategies such as pressure control ventilation (PCV) via a conventional ventilator or high frequency percussive ventilation (HFPV) via the volumetric diffusive respirator (VDR) are commonly used in the burn-patient population.8 During PCV, a change in lung compliance can cause a loss of delivered gas inflation that can impair both ventilation and oxygenation. This results in an increase in driving pressure and a higher risk of barotrauma. The VDR can be difficult to use because of technical limitations, and humidification delivery is suspect. Often, a paralytic is employed for optimal patient-ventilator interface with the VDR. APRV is a mode of ventilation that allows the mean airway pressure (MAP) to be maintained for adequate alveolar ventilation while keeping a lower alveolar distending pressure9 and increasing lung ventilation to atelectatic regions through an increase in inspiratory time throughout the entire ventilator cycle. In theory, by not allowing complete loss of distending pressure, the conducting airways can maintain open architecture, thus splinting the airway to prevent dynamic collapse or airway obstruction from sloughing debris.

The airway pressure waveform of APRV appears similar to that of continuous positive airway pressure (CPAP), but during APRV the high CPAP level is intermittently released at regular short intervals.10 These brief releases facilitate tidal movement of gas, improving carbon dioxide clearance.11 During APRV, the sustained positive airway pressure facilitates recruitment and oxygenation.12 This increases the pulmonary surface area available for gas exchange, improving ventilation while using a lower minute ventilation. A major benefit of APRV is that it allows the patient to breathe spontaneously throughout the entire respiratory cycle, while maintaining an elevated mean airway pressure without an excessive peak airway pressure.13 Spontaneous breathing is enabled via a floating exhalation valve that functions similarly to a CPAP system. The duration of the positive airway pressure level (Phigh) is maintained during the respiratory cycle as long as possible. The relationship of the entire ventilator cycle can be expressed as an inspiratory to expiratory ratio that can vary from 3:1 to 7:1. The release of pressure (Plow) at a short duration is used to augment carbon dioxide removal but at the same time prevent alveolar collapse.14,15 Spontaneous breathing increases ventilation to poorly or nonventilated lung units and helps to reduce ventilation-perfusion mismatch.16 Also, during spontaneous breathing, the posterior muscular sections of the diaphragm remain functional, which minimizes posterior lung consolidation and atelectasis.17

In anecdotal clinical trials, use of APRV has proven to decrease ventilator length of stay and has been shown to decrease mortality.18 APRV has been beneficial in the management of our burn population secondary to the aspect of maintaining the MAP. The maintenance of continuous pressure allows for lung recruitment during the fluid resuscitation phase. APRV allows for spontaneous breathing throughout the respiratory phase. This allows for ventilation to the dependent lung regions secondary to the inspiratory effort and the diaphragmatic movement. The technological innovation of a floating exhalation value provides for spontaneous breathing, which can help facilitate the weaning process.

Ventilatory settings
Stock and colleagues first described APRV in 1987.19 It has been successfully used in a variety of patient populations, although most reported outcomes have been for the trauma patient population.20 APRV may hold advantages over conventional forms of ventilation, particularly the volume-targeted modes. Two pressure settings are used: The higher pressure, referred to as Phigh, is instrumental in alveolar recruitment and oxygenation. The Phigh is usually set for greater than 4 seconds. The lower pressure, referred to as Plow, aids in carbon dioxide elimination. The Plow is usually set for less than 1 second. Unlike with many modes of mechanical ventilation, the patient is allowed to breathe spontaneously at both pressure levels and at any time during the respiratory cycle. APRV acts by opening collapsed alveoli through sustained airway pressure. Constant airway pressure facilitates alveolar recruitment, gas diffusion, and prevention of ventilator-induced trauma.21 These advantages may appear more evident in patients where deflated lung units may be more readily recruited.22

Once the decision is made to utilize APRV, users should consider setting the Phigh equal to the targeted mean airway pressure of the previous mode. Using this strategy, the Phigh is usually set between 25 and 30 cm/H2o. The Plow is set at zero to reduce the impedance of expiratory gas flow and optimize co2 elimination. By accelerating the expiratory flow rate, secretion removal is enhanced, and the Phigh is quickly reestablished. Initially, the Thigh is set between 5 and 6 seconds to facilitate lung inflation and to increase mean airway pressure. The Tlow is usually set between .7 and 1 second. The Tlow is set so expiratory flow drops to 25% to 75% of peak expiratory flow. To minimize derecruitment or alveolar collapse, it is important not to allow expiratory gas flow to drop to zero. As the patient’s oxygenation improves, the Phigh is “dropped” and the Thigh is “stretched.” This approach of “drop and stretch” reduces airway pressure and the number of releases but still maintains a high mean airway pressure.

When weaning is considered, the Phigh is continually reduced and the Thigh is extended until the patient is virtually on a high-level CPAP. Once the settings are reduced to a Phigh of approximately 16 cm H2o and a Thigh of greater than 10 seconds, a spontaneous breathing trial is warranted. Often, the weaning process during APRV makes a natural transition from time-cycled ventilation to assisted spontaneous breathing.23 During APRV, the patient is encouraged to breathe spontaneously during Phigh and Thigh. This spontaneous breathing helps remove co2 and also aids in maintaining respiratory muscle tone and strength. Because lower levels of sedation and less neuromuscular blockade are required during APRV than conventional ventilatory strategies, the sensation of breathing is more comfortable and necessitates less work.24 Breathing from an inflated lung causes less work of breathing and more effective co2 elimination.25,26 If there is either increased work of breathing or decreased compliance, pressure support can be added to the CPAP mode, and spontaneous tidal volume can be augmented. In rare instances, postoperative, the patient can be placed on conventional ventilation until spontaneous breathing is restored or when the patient is clinically stable.27 One can say that APRV is a weaning mode, since spontaneous breathing can take place and is always encouraged when the patient is clinically stabilized.

Ventilatory duration regarding APRV varies. Often, APRV will be employed during fluid resuscitation or in the initial phase of an acute disease process. In some instances, once the patient’s gas exchange is stabilized, the patient is transitioned to a conventional ventilatory strategy. In some cases, the patient will be maintained on APRV to optimize gas exchange for additional procedures that may stress the lungs. If the patient needs to be supine for a prolonged time, APRV may be used to prevent lung collapse or pneumonia.28

In our experience, we have used APRV for as short a time as several hours and as long as 81 days.

Case study
Over the last 24 months, our burn center has employed APRV as a ventilatory strategy on 98 patients, both during the initial resuscitation phase of care and as a bridge of transition from HFPV to ventilatory liberation. Ventilatory duration has been reduced by several days and oxygenation has been maintained in all of the patients transitioned from HFPV, while ventilator-associated pneumonia has decreased.

A case in particular is that of a 17-year-old male patient admitted for extensive full-thickness burns over 45% of his body surface. He had both an inhalation injury and crush injuries to his lower extremities from an auto entrapment and fire. As we commonly do, we initiated HFPV via VDR ventilator for management of inhalation injury and then transitioned to APRV. He was managed on the VDR ventilator for 11 days and maintained on APRV ventilation for 60 days with release volumes between 800 mL and 1,000 mL and a release rate of 8. Since APRV encourages spontaneous breathing, we transitioned him to CPAP mode with pressure-support augmentation. He was liberated from mechanical ventilation after 92 ventilator days to trach mask without difficulty. We maintained frequency to tidal volume (f/tv) between 50 and 80 to exercise his respiratory muscles. We monitored his Pao2/FIo2 ratio and maintained oxygenation via pulse oximetry and examined chest x-rays to detect atelectasis. He had 12 operating room days along with multiple days in the supine position, which required prolonged paralytic and sedative agents to promote graft healing. Most interesting is that he did not develop ventilator-associated pneumonia, which is a frequent consequence of prolonged mechanical ventilation in the intensive care unit. His routine chest x-rays were clear of consolidation.

Clinical implications
APRV introduces not only different technology, but also a different ventilatory philosophy. Historically, the basic principles of mechanical ventilation were based on patients who had nonparenchymal respiratory dysfunction with no loss of lung inflation. Large tidal volumes and minimal PEEP levels were standard practice. Today, the emphasis is on maintaining lower airway pressures and using a longer inspiratory time to combat lung deflation. Still, the concept of allowing patients with early stages of acute lung injury to breathe spontaneously is a foreign concept to many clinicians.

APRV is a ventilatory strategy that promotes the benefits of lung recruitment and allows for spontaneous breathing. In the burn-patient population, APRV has been shown to maintain optimal oxygenation and ventilation in conjunction with reducing ventilatory duration. The ventilator industry will benefit by incorporating APRV into their ventilatory arsenal. The clinical team must meet the challenge of proficiency, in both theory and practice, of this new complex ventilatory modality.
Kenneth Miller, MEd, RRT-NPS, is clinical educator, respiratory care and Robert Lichtenstein, BSRT, RRT-NPS, is clinical educator for respiratory care services at Lehigh Valley Hospital-Muhlenberg, Bethlehem, Pa.

Kenneth Miller, MEd, RRT-NPS, is clinical educator, respiratory care and Robert Lichtenstein, BSRT, RRT-NPS, is clinical educator for respiratory care services at Lehigh Valley Hospital-Muhlenberg, Bethlehem, Pa.

1. Silver GM, Freiburg C, Halerz M, Tojong J, Supple K, Gamelli RL. A survey of airway and ventilator management strategies in North American pediatric burn units. J Burn Care Rehabil. 2004;25(5):435-40.
2. Goretsky MJ, Greenhalgh DG, Warden GD, Ryckman FC, Warner BW. The use of extracorporeal life support in pediatric burn patients with respiratory failure. J Pediatr Surg. 1995;30(4):620-3.
3. Cioffi WG Jr, Rue LW 3rd, Graves TA, McManus WF, Mason AD Jr, Pruitt BA Jr. Prophylactic use of high-frequency percussive ventilation in patients with inhalation injury. Ann Surg. 1991;213(6):575-80; discussion 580-2.
4. Bergogne-Berezin E. The increasing significance of outbreaks of Acinetobacter spp: the need for control and new agents. J Hosp Infect. 1995;30 Suppl:441-52.
5. Sheridan RL, Kacmarek RM, McEttrick MM, et al. Permissive hypercapnia as a ventilatory strategy in burned children: effect on barotrauma, pneumonia, and mortality. J Trauma. 1995;39(5):854-9.
6. Cartotto R, Cooper AB, Esmond JR, Gomez M, Fish JS, Smith T. Early clinical experience with high-frequency oscillatory ventilation for ARDS in adult burn patients. J Burn Care Rehabil. 2001;22(5):325-33.
7. Wahl WL, Ahrns KS, Brandt MM, Rowe SA, Hemmila MR, Arbabi S. Bronchoalveolar lavage in diagnosis of ventilator-associated pneumonia in patients with burns. J Burn Care Rehabil. 2005;26(1):57-61.
8. Cook DJ, Walter SD, Cook RJ, et al. Incidence of and risk factors for ventilator-associated pneumonia in critically ill patients. Ann Intern Med. 1998;129(6):433-40.
9. Carmen B, Cahill T, Warden G, McCall J. A prospective, randomized comparison of the Volume Diffusive Respirator vs conventional ventilation for ventilation of burned children. 2001 ABA paper. J Burn Care Rehabil. 2002;23(6):444-8.
10. Rodenberg DA, Maschinot NE, Housinger TA, Warden GD. Decreased pulmonary barotrauma with the use of volumetric diffusive respiration in pediatric patients with burns: the 1992 Moyer Award. J Burn Care Rehabil. 1992;13(5):506-11.
11. Gattinoni L, Pesenti A. The concept of “baby lung.” Intensive Care Med. 2005;31(6):776-84. Epub 2005 Apr 6.
12. Imai Y, Slutsky AS. High-frequency oscillatory ventilation and ventilator-induced lung injury. Crit Care Med. 2005;33(3 suppl):S129-34. Review.
13. Carney D, DiRocco J, Neiman G. Dynamic alveolar mechanics and ventilator-induced lung injury. Crit Care Med. 2005;33(3 suppl):S122-8. Review.
14. Mentzelopouls SD, Roussos C, Zakynthinos SG. Prone position reduces lung stress and strain in severe acute respiratory distress syndrome. Eur Respir J. 2005;25(3):534-44.
15. Habashi N, Andrew P. Ventilator strategies for posttraumatic acute respiratory distress syndrome: airway pressure release ventilation and the role of spontaneous breathing in critically ill patients. Curr Opin Crit Care. 2004;10(6):549-57.
16. Salim A, Martin M. High-frequency percussive ventilation. Crit Care Med. 2005;33(3 suppl):S241-5. Review.
17. Lucangelo U, Fontanesi L, Antonaglia V, et al. High frequency percussive ventilation (HFPV). Case reports. Minerva Anestesiol. 2003;69(11):853-7, 858-60.
18. Reper P, Van Bos R, Van Loey K, Van Laeke P, Vanderkelen A. High frequency percussive ventilation in burn patients: hemodynamics and gas exchange. Burns. 2003;29(6):603-8.
19. Reper P, Dankaert R, van Hille F, van Leake P, Duinslager L, Vanderkelen A. The usefulness of combined high-frequency percussive ventilation during acute respiratory failure after smoke inhalation. Burns. 1998;24(1):34-8.
20. Habashi NM. Other approaches to open-lung ventilation: airway pressure release ventilation. Crit Care Med. 2005;33(3 suppl):S228-40. Review.
21. Varpula T, Valta P, Niemi R, Takkunen O, Hynynen M, Pettila VV. Airway pressure release ventilation as a primary ventilatory mode in acute respiratory distress syndrome. Acta Anaesthesiol Scand. 2004;48(6):722-31.
22. Varpula T, Jousela I, Niemi R, Takkunen O, Pettila V. Combined effects of prone positioning and airway pressure release ventilation on gas exchange in patients with acute lung injury. Acta Anaesthesiol Scand. 2003;47(5):516-24.
23. Neumann P, Golisch W, Strohmeyer A, Buscher H, Burchardi H, Sydow M. Influence of different release times on spontaneous breathing pattern during airway pressure release ventilation. Intensive Care Med. 2002;28(12):1742-9. Epub 2002, October 10.
24. Kaplan LJ, Bailey H, Formosa V. Airway pressure release ventilation increases cardiac performance in patients with acute lung injury/adult respiratory distress syndrome. Crit Care. 2001;5(4):221-6. Epub 2001, July 2.
25. Putensen C, Zech S, Wriggle H, et al. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med. 2001;164(1):43-9.
26. Putensen C, Mutz NJ, Putensen-Himmer G, Zinserling J. Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med. 1999;159(4 Pt 1):1241-8.
27. Smith RA, Smith DB. Does airway pressure release ventilation alter lung function after acute lung injury? Chest. 1995;107(3):805-8.
28. Sydow M, Burchardi H, Ephraim E, Zielmann S, Crozier TA. Long-term effects of two different ventilatory modes on oxygenation in acute lung injury. Comparison of airway pressure release ventilation and volume-controlled inverse ratio ventilation. Am J Respir Crit Care Med. 1994;149(6):1550-6.