Although mechanical ventilation can save lives, it can also cause serious complications—including lung damage, hemodynamic compromise, atelectasis, and ventilator-associated pneumonia (VAP). Some of these complications stem in part from ventilation modes that dictate when the patient breathes and the duration and size (tidal volume) of the breath.

But the custom of adapting the patient to the ventilator is changing. To reduce complications, minimize the negative effects of excessive sedation, and decrease ventilator days, many critical-care clinicians are promoting spontaneous breathing during mechanical ventilation by adapting the ventilator to the patient. Airway pressure release ventilation (APRV) plays a key role in this approach.

Understanding APRV

First described in 1987, APRV is being used increasingly as both a noninvasive and invasive ventilation mode. It provides extended periods of continuous positive airway pressure (CPAP), which alternate with brief releases to a lower pressure level. The releases allow carbon dioxide (CO2)-rich gas to move out of the lung and permit fresh gas to enter, augmenting the patient’s spontaneous breathing during CPAP.

With APRV, the ventilator cycles between two CPAP levels:

•   P high (the higher CPAP level), along with T high (CPAP duration), helps open collapsed alveoli, promotes oxygenation and CO2 diffusion, and may limit ventilator-induced lung injury. Ideally, P high is set at a level that keeps lungs inflated but not overdistended.

•   P low (the lower CPAP level) along with T low (duration of lower CPAP level) maintains end-expiratory lung volume and promotes bulk CO2 elimination.

By combining diffusive and bulk gas exchange, APRV may be a more efficient form of ventilation. As the lung stays open during the CPAP phase, cardiac output delivers CO2 to diffuse into the lung (alveolar space) and oxygen into the blood. The subsequent release phase causes bulk movement of a high concentration of CO2 for removal, offloading some of the metabolic work and preserving spontaneous breathing. APRV allows the patient to breathe spontaneously at any time throughout the respiratory cycle.

Indications

APRV may be used:

•   at the time of intubation as the primary ventilation mode throughout respiratory failure

•   noninvasively as the initial ventilation mode or after extubation

•   into the weaning and extubation phases

•   as a rescue mode.

The spontaneous breathing advantage

Whenever possible, spontaneous breathing should be preserved in mechanically ventilated patients tominimize dependent atelectasis and reduce the risk of acute lung injury (ALI) and infection. By permitting unassisted spontaneous breathing, APRV helps patients achieve preferential recruitment to dependent lung regions without the use of increased airway pressure. With an unassisted spontaneous breath, the diaphragm contracts, pulling gas into dependent lung regions as gas flow is coupled with patient effort. As a result, patients receive the flow they want—not the flow the machine is set to deliver.

Assisted spontaneous breathing, on the other hand, pushes most of the gas into nondependent lung regions and may perpetuate dependent lung derecruitment (alveolar collapse) and respiratory infections. Pressure support ventilation, for instance, uses a fixed preset pressure and reacts to the initial patient effort. The resultant high flow rapidly outpaces the demand (patient effort), effectively transitioning from patient-controlled to ventilator-controlled gas flow and pushing rather than pulling gas into the lung.

Responding to the demands of critical illness

Spontaneous breathing during APRV allows greater flexibility to the dynamic and rapidly changing metabolic demands of critical illness. When used as a preventive lung recruitment measure to maintain lung aeration, unassisted spontaneous breathing may reduce the need for reactive recruitment maneuvers. Also, the cardiopulmonary benefits of unassisted spontaneous breathing may reduce the negative physiologic effects of mechanical breaths on the circulation.

In contrast, lack of spontaneous breathing may contribute to worsening respiratory dysfunction by increasing the risk of atelectasis and pulmonary infections. Complications of mechanical ventilation increase over time, and successful extubation depends on spontaneous breathing.

How APRV maintains lung recruitment and preserves spontaneous breathing

In respiratory failure, the lungs become edematous and heavy, causing alveolar collapse (atelectasis) and opposing the patient’s effort to breathe efficiently. Typically, critically ill patients lack the strength to expand the lungs against these opposing forces without developing increased work of breathing.

Air remaining in the lungs after exhalation is called end-expiratory lung volume (EELV). In adult males, normal EELV measures approximately 3 L. As atelectasis progresses, EELV may decrease by as much as one-third. As the weight of the heart, lungs, and abdominal contents causes additional compression, EELV decreases further. The resulting lung volume loss forces the lungs to expand from a lower EELV, causing excessive elastic work of breathing.

With traditional modes of ventilation, such as synchronized intermittent mandatory ventilation (SIMV), the expiratory phase accounts for most of the ventilator time cycle. SIMV permits spontaneous breaths between set mandatory breaths at the positive end-expiratory pressure (PEEP) level. During the expiratory phase, PEEP is used to prevent alveolar collapse and maintain EELV. However, the PEEP level may be too low to overcome the reduced EELV and increased elastic work of breathing. As a result, the patient may require increased mandatory support from the ventilator, possibly limiting or eliminating spontaneous breathing.

With APRV, on the other hand, most of the time cycle is spent at the upper CPAP level above EELV. Because APRV uses a brief release phase, the extended CPAP phase (90% and above) limits shear forces from cyclic opening and closing; this is crucial because shear forces may lead to stress failure of the lung.

Thus, APRV improves dead space and shunt, resulting in less frequent and extreme changes between lung volumes than traditional ventilation. These effects decrease the elastic work of breathing and help preserve spontaneous breathing.

Improved cough and secretion control

By allowing spontaneous breathing and increasing patient comfort, APRV helps preserve the cough reflex—a major respiratory defense mechanism. In mechanically ventilated

patients, inability to breathe spontaneously because of excessive sedation may diminish or completely eliminate the ability to cough and reject recurrent pharyngeal aspirations. Artificial airway suctioning can’t replace cough in clearing aspirated secretions, as most secretions are beyond a suction catheter’s reach.

In critically ill patients with artificial airways, aspiration occurs despite balloon cuff inflation because the seal isn’t complete. Secretions pool in the pharynx and trickle down between the creases and folds of the inflated balloon. Once secretions reach the distal tip of the artificial airway, gas delivery from the ventilator aerosolizes and propels the aspirated pharyngeal secretions deep into the airways. Patients who lack the cough reflex can’t reject this aspirate, and these recurrent “silent” aspirations increase the risk of VAP.

Reduced sedation requirements

Preset ventilator settings that force the patient to breathe at a particular frequency and flow rate for a defined time at a clinician-prescribed tidal volume cause the patient’s breathing to become out of synch with the ventilator. This asynchrony decreases patient comfort and may necessitate increased sedation or even paralytic agents. APRV reduces asynchrony by permitting the patient to breathe spontaneously at any time during the respiratory cycle, thus decreasing the need for sedation.

Weaning patients from APRV

APRV may permit earlier weaning and thereby reduce the risk of complications, such as ALI and VAP. Data suggest that 24% of patients without ALI at the onset of mechanical ventilation developed it after being on the ventilator for more than 48 hours. The risk of VAP increases every ventilator day.

During weaning, APRV gradually evolves to pure CPAP using a method called “Drop and Stretch.” In this method, P high is decreased (dropped) and T high is increased (stretched). “Drop and Stretch” progressively eliminates the brief release phases, allowing APRV to evolve to pure CPAP. Once the patient tolerates pure CPAP and the fraction of inspired oxygen is 40% or lower, weaning is simplified because the CPAP level is the only variable that needs to be reduced.

If respiratory failure worsens during weaning, the release phases are reestablished using the “Raise and Reduce” method, in which P high is raised and T high is reduced. This method produces more release phases, unloading a greater percentage of the metabolic burden by increasing CO2 clearance. Elevating the P high reduces the increased elastic work of breathing.

Is APRV right for your patient?

No one mechanical ventilation mode fits every patient’s needs. But by learning about the benefits of APRV, you may help reduce complications of mechanical ventilation and increase patient comfort.O

Selected references

Downs JB, Stock MC. Airway pressure release ventilation: a new concept in ventilatory support. Crit Care Med. 1987;15:459-461.

Gajic O, Dara S, Mendez J, et al. Ventilator-associated lung injury in patients without acute lung injury at the onset of mechanical ventilation. Crit Care Med. 2004;32(9):1817-1824.

Habashi N. Other approaches to open-lung ventilation: airway pressure release ventilation. Crit Care Med. 2005; 33(suppl):S228-S240.

Habashi N, Andrews A. Ventilator strategies for posttraumatic acute respiratory distress syndrome: airway pressure release ventilation and the role of spontaneous breathing in critically ill patients [published correction appears in Curr Opin Crit Care. 2005;11(3):294]. Curr Opin Crit Care. 2004;(10):549-557.

Tokics L, Hedenstierna G, Svensson L, et al. V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans. J Appl Physiol. 1996;81:1822-1833.

Penny S. Andrews, RN, BSN, is a Full Partner in the Neurotrauma Critical Care Unit at the R Adams Cowley Shock Trauma Center, University of Maryland Medical Center, in Baltimore. Nader M. Habashi, MD, is Medical Director of the Multitrauma Critical Care Unit at R Adams Cowley Shock Trauma Center.