Use of Short Release Time in Airway Pressure Release Ventilation

The mortality rate for acute lung injury (ALI) and the adult respiratory distress syndrome (ARDS) is approximately 40% to 50%.¹ The American-European Consensus Conference on ARDS defined ALI as a syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiological, and physiological abnormalities.² The criteria defining ALI and ARDS are similar: the acute onset and persistent nature of the disorders, lasting days to weeks; chest radiographs showing bilateral infiltrates; and pulmonary wedge pressures of less than 18 mm Hg without clinical evidence of left atrial hypertension. Arterial hypoxemia is the major difference in classification criteria, with ALI having a ratio of arterial Po2 to fraction of inspired oxygen (Fio2) of less than 300 mm Hg and ARDS having a ratio of less than 200 mm Hg.

Endotracheal intubation and mechanical ventilatory support are imminent when hypercarbia and hypoxemia progress to respiratory failure. The physiological goals of mechanical ventilation are to support pulmonary gas exchange, to increase lung volume, and to reduce the work of breathing.^3,4 With reduced lung compliance, the inflation capacity of the lungs may be less than one third of the normal amount. To achieve ventilation goals and to avoid further lung injury caused by stretching-induced hyperinflation, adjunctive therapies such as prone positioning, partial liquid ventilation, nitric oxide inhalation, and tracheal gas insufflation have been used.

Animal studies^5,6 have shown that high Fio2s high cycling pressures are potentially injurious to the lungs. Employing protective ventilation strategies using tidal volumes (Vts) of less than 6 mL/kg and maintaining end-inspiratory pressures of less than 30 cm H2O have been shown to produce a reduction in mortality.^1,7 A reduced Vt may result in an intentional elevation of Paco2; this is commonly referred to as permissive hypercapnia. In animal models, periodic inflation with a large, sustained volume has been used to prevent collapse when small Vts are used. Oxygen should be used judiciously to maintain a somewhat lower than usually acceptable arterial oxygenation and saturation level whenever the Fio2 exceeds 0.65. Atelectasis can be prevented by adding positive end-expiratory pressure (PEEP) or extending the inspiratory time. Sedation and neuromuscular blockade may be needed to achieve the goals of avoiding increases in ventilator support or ventilator intolerance. Alternative ventilatory modes have been used to avoid high ventilating pressures and large swings in baseline-to-peak airway pressures; these include pressure-controlled ventilation, pressure-controlled inverse-ratio ventilation, high-frequency ventilation, and airway pressure release ventilation (APRV).

APRV Characteristics
APRV was first described by Stock et al,⁸ Downs and Stock,⁹ and Stock and Downs¹⁰ in 1987. The system described consisted of a 50-psi gas source directed through a Venturi device delivering a total gas flow of 90 to 100 L/min. The gas reached the experimental animal’s tracheotomy tube via inspiratory tubing connected to a T-piece. To complete the circuit, the expiratory limb allowed the fresh gas and expired gases to flow continuously through the tubing, with two possible routes to travel for exhalation. First, a threshold resistor expiratory valve was set to deliver the high pressure at the maximum pressure limit, resulting in an elevated resting lung volume. Second, a timed switch opened periodically and bypassed the expiratory valve, causing a dumping of the expired gas to ambient pressure. This is commonly called the release time.

This change from a resting high lung volume to a lower lung volume caused carbon dioxide–rich gas to be expelled from the lungs. In addition to the change from high to low pressure, several other factors contributed to carbon dioxide elimination, including lung-thorax compliance, release time, and airway and circuit resistance. Another key factor was the continuous gas flow, which allowed the patient to breathe spontaneously throughout the entire respiratory cycle. This was possible even at the maximum pressure limit, thus increasing exhaled minute ventilation. Because spontaneous ventilation could occur virtually at any time, without a significant fluctuation in airway pressure, many have called this form of ventilation two-level continuous positive airway pressure. In an effort to standardize mode names for mechanical ventilation, Chatburn and Primiano11 have stated that APRV is simply a form of pressure-controlled intermittent mandatory ventilation (IMV).

Case Study
A 2 1/2-year–old, 17-kg male residing at an extended care facility was admitted to our pediatric intensive care unit on March 7, 2000, for respiratory failure. His medical history was significant for mental retardation, cerebral palsy, epilepsy, and asthma. Three days prior to admission, the patient had developed a fever, a cough, tachypnea, and wheezing. Therapy with oxygen, albuterol aerosols, and systemic anti-inflammatories was started. One day prior to admission, a chest radiograph had demonstrated a left lower lobe infiltrate with an effusion. A diuretic and a course of antibiotics were given. The patient was then transferred to MetroHealth Medical Center, Cleveland.

On admission, the patient had a temperature of 38.1°C, a respiratory rate of 64 breaths per minute, a heart rate of 70 beats per minute, a blood pressure of 115/46, and an oxygen saturation of 98%. The physical examination revealed dehydration, rhinorrhea, absence of wheezing, and diminished air exchange on the left, with crackles at the bases of both lungs. The patient was intubated for respiratory distress and increased work of breathing. The nasopharyngeal swab was positive for respiratory syncytial virus. Initially, the patient was supported with volume-targeted ventilation using synchronized IMV (SIMV) with pressure support and autoflow (in which each breath is pressure-limited and the pressure limit is automatically minimized between breaths so as to be consistent with preset Vt).¹¹ The ventilator was set to provide a Vt of 170 mL, a respiratory rate of 20 breaths per minute, an Fio2 of 1, and a PEEP of 5 cm H2O. On the second day, the Vt and Fio2 were reduced to 120 mL and 0.5, respectively. On the fourth day, the patient’s chest radiograph showed bilateral patchy infiltrate consistent with ARDS. On the fifth day, due to deterioration in the patient’s respiratory status, the ventilator settings were changed to pressure-controlled ventilation with a peak pressure of 36 cm H2O, a PEEP of 10 cm H2O, an inspiratory time of 1.2 seconds, an inspiratory-to-expiratory ratio of 1:1.5, and 100% oxygen. Shortly after changing to pressure-controlled ventilation, despite bag-valve and conventional ventilation, a rapid deterioration in the patient’s oxygenation warranted a trial of APRV. Initially, the release time was set at 2.2 seconds. This was then reduced to 0.2 seconds, resulting in a marked improvement in oxygenation. The patient tolerated the short release time and prolonged time at the high pressure level without further sedation or use of neuromuscular blockade.

The patient continued to be weaned from ventilatory support and, by the third day of APRV, had reached an Fio2 of 0.35, a peak pressure of 12 cm H2O, a low pressure of 5 cm H2O, a 1.5-second period spent at the high pressure, and a 6-second period at the low pressure. In preparation for extubation, the patient began using SIMV with a 150-mL Vt, a respiratory rate of eight breaths per minute, and PEEP of 5 cm H2O. Following extubation to a nasal cannula, the patient developed upper-airway obstruction. The cannula was exchanged for noninvasive ventilation with a full-face mask. The patient was gradually weaned to room air and was discharged to the original chronic care facility.

Discussion
APRV is a mode of ventilatory support that achieves ventilation by intermittently lowering airway pressure from a previously determined high level of positive pressure. This change results in exhalation through a reduction in lung volume. This is in contrast to conventional forms of ventilation, which increase lung volume from a resting functional residual capacity. Many advantages have been cited for this form of support, including lower peak airway pressures, improvement in ventilation-perfusion mismatching, lower intrathoracic pressures, and a reduction in the use of analgesics, sedatives, and paralytics.

Valentine et al¹² randomly compared APRV, SIMV, and pressure support in patients deemed ready for weaning following cardiac surgery. In the absence of parenchymal lung disease, they concluded, all three modes provide acceptable oxygenation and ventilatory support, with APRV providing the lowest peak pressure. Use of APRV in experimental animals with oleic acid–induced lung injury and in human subjects with ARDS showed additional benefits, as compared with conventional ventilation. Improvements in ventilation-perfusion matching, cardiac output, oxygen delivery, and arterial oxygenation, along with a decrease in dead space, have been documented.^8,13 This may be, in part, due to spontaneous breathing during the entire respiratory cycle, and to the longer time spent at an elevated resting lung volume (further promoting alveolar recruitment).

Anxiety control, comfort measures, and, sometimes, control of ventilation require the use of sedatives and neuromuscular blockade. Excessive use of sedatives and paralytics may have consequences by impairing cardiovascular function and gastrointestinal motility, as well as by promoting atelectasis caused by the inability to cough and clear airway secretions. A prospective analysis¹⁴ of 596 postoperative adult patients with normal results of pulmonary function studies prior to cardiac surgery showed a reduction in the consumption of analgesics and sedatives in patients ventilated using APRV, as compared with assist-control ventilation and IMV. Another added benefit was a significantly shorter mean duration of intubation in the APRV group.

There are several potential disadvantages of APRV. It is a form of pressure-controlled ventilation, and Vts are subjected to changes in lung compliance and in circuit and airway resistance. As the lungs become less compliant and/or resistance increases, exhaled Vts will diminish. In the absence of spontaneous breathing, carbon dioxide levels will rise. Caution should be used when ventilating patients with airflow obstructions. Patients with chronic obstructive lung disease and acute asthma exacerbations may be difficult to ventilate when the release times are too short. In animal models and adult humans without airflow obstruction, 1.5 seconds has been used as a starting point for complete cessation of expiratory airflow during the release time. The presence of wheezing and prolonged expiratory times excluded patients from the use of APRV in one study.10 APRV is a form of timed-cycled nonsynchronized IMV. The potential for patient-ventilator dyssynchrony exists when cycling between pressures interferes with spontaneous breathing efforts. Our use of a short release time prohibited complete exhalation and the need to breathe before the machine quickly cycled to the high pressure level.

Conclusion
Infants and children are at particular risk for loss of lung volume, airway closure, and hypoxemia due to a functional residual capacity close to the residual volume. With APRV’s inherent possibility of alveolar derecruitment, atelectasis, and airway closure during the release phase,¹⁵ we intentionally prevented a lengthy release time, thereby preventing expired flow from returning to baseline values. The result was a measured total PEEP of 15 cm H2O (which was the goal targeted as likely to be at or above the estimated inflection point of the pressure-volume curve).⁷

This was not our first attempt at using a short release time. Previously, a 14-year-old female trauma patient with bilateral lung contusions who was using SIMV was supported with APRV and a 0.5-second release time following a Pao2 result of 54 mm Hg while breathing 100% oxygen. Four hours later, while still using APRV, the patient was weaned to an Fio2 of 0.6 with a Pao2 of 72 mm Hg.¹⁶ We were able to oxygenate and ventilate our patient at a release time not previously described in the literature without the additional use of sedation and neuromuscular blockade. A stable minute ventilation was achieved by both the machine’s released exhaled Vt and the patient’s own spontaneous Vt. The peak airway pressure was slightly lower during APRV than during conventional ventilation, and was below the 30 cm H2O threshold for the prevention of pulmonary injury. A large pediatric clinical trial needs to be conducted to justify the safety and efficacy of the use of a short release time further.

James E. Martin, RRT, is a clinical specialist, Division of Pediatric Pulmonology, MetroHealth Medical Center, Cleveland.

References
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